Serious illness in newborns, infants and children
Learning Points: Science & Scholarship
Describe the pathogenesis of Fever
Definition and Temperature Thresholds:
Fever is typically defined as a body temperature exceeding 38°C (100.4°F)
In neonates (0-28 to 30 days old) and young infants (1-3 months), fever is concerning at a rectal temperature ≥38.0°C.
In children aged 3-36 months, fever is defined by rectal temperatures ranging from ≥38.0-39.0°C and concerning at ≥39.0°C without an infection focus.
In older children and adults, fever is defined by oral temperatures ranging from ≥37.8-39.4°C and concerning at ≥39.5°C.
Mechanism:
Pyrogen Entry and Prostaglandin Synthesis:
Fever is initiated by pyrogens (substances that cause fever) entering the bloodstream.
These pyrogens travel to the hypothalamus and induce the synthesis of prostaglandin E2 (PGE2).
Pyrogens can be:
Exogenous: Usually microbes (viruses, bacteria) or their products (endotoxins).
Endogenous: Cytokines such as IL-1, TNF-alpha, IL-6, and others produced by the body.
Hypothalamic Set Point Adjustment:
The induction of PGE2 raises the hypothalamic set point for body temperature.
The hypothalamus then recognizes the current body temperature as too low and initiates processes to raise it to the new set point.
Body's Response to Raise Temperature:
Peripheral Vasoconstriction: Reduces heat loss by shunting blood from the skin to the core.
Increased Muscle Tone and Activity: Shivering and increased metabolic rate generate more heat.
Decreased Heat Loss: Reduced perfusion of the skin conserves heat.
Equilibrium at New Set Point:
The body temperature rises until it reaches the new equilibrium at the elevated set point.
Fever rarely exceeds 41°C unless there is a component of hyperthermia.
Role of Cytokines:
Endogenous pyrogenic cytokines (IL-1, IL-6, TNF, IF-alpha) released by phagocytic cells induce PGE2 synthesis in the hypothalamus.
These cytokines also cause systemic effects:
Acute-Phase Response: Increased synthesis of acute-phase proteins by the liver.
Decreased Serum Iron and Zinc: Inhibits bacterial growth.
Leucocytosis: Increased white blood cell count.
Muscle Proteolysis: Breakdown of muscle proteins.
Slow-Wave Sleep: IL-1 induces slow-wave sleep, explaining the somnolence frequently associated with febrile illnesses.
Myalgias and Arthralgias: Increased peripheral PGE2 may account for the muscle and joint pains that often accompany fever.
Increased Heart Rate: A normal physiological response to fever.
Clinical Effects and Benefits vs. Harms:
Benefits of Fever:
Retards Growth and Reproduction of Some Bacteria and Viruses
Retards Growth and Reproduction: Higher body temperatures can slow down or inhibit the growth and reproduction of certain bacteria and viruses. These pathogens often have optimal temperature ranges for their survival and replication. A fever creates an environment less conducive to their growth.
Decreased Serum Iron: Fever can also lead to a reduction in serum iron levels. Many bacteria require iron to grow and reproduce. When serum iron is decreased, it limits the availability of this essential nutrient to the pathogens, further inhibiting their ability to thrive.
Enhances Immunologic Function at Moderately Elevated Temperatures
Enhances Immunologic Function: Moderate fever can boost various aspects of the immune system. This includes:
Increased Production of White Blood Cells (WBCs): White blood cells are crucial for fighting infections. Fever can stimulate the production of WBCs, including lymphocytes, which are involved in the adaptive immune response.
Enhanced Activity of Immune Cells: Immune cells, such as neutrophils and macrophages, can become more active and efficient at engulfing and destroying pathogens at elevated temperatures.
Improved Function of Cytokines: Cytokines are signaling molecules that help regulate the immune response. Fever can enhance the effectiveness of cytokines, improving communication and coordination within the immune system.
Temperature Limitations: However, these benefits are seen at moderately elevated temperatures. When body temperatures approach 40°C (104°F), some of the positive effects can be reversed. Extremely high fevers can be harmful, leading to cellular damage and impairing the function of proteins and enzymes essential for normal body functions.
Harms of Fever:
Discomfort for the patient.
Associated with increased metabolic rate, oxygen consumption, carbon dioxide production, and demands on the cardiovascular and pulmonary systems → demands may offset any immunologic benefit for the child in shock
Hyperthermia vs. Fever:
Hyperthermia: Abnormal elevation of body temperature without a change in the hypothalamic set point.
Failure of normal homeostasis → heat production that exceeds the body’s capacity for dissipation
Body temperature does not respond to antipyretic agents
Characteristic clinical features
History of environmental heat exposure or use of drugs that interfere with normal thermoregulation (e.g. anticholinergics)
Hot, dry skin
CNS dysfunction (e.g. delirium, convulsions, coma)
Can be rapidly fatal
Adverse physiologic effects begin to occur at temperatures >41C
Describe the pathogenesis of Rash
Categories of Childhood Rashes:
Maculopapular: Flat, red area covered with small confluent bumps.
Pustular: Pus-filled lesions.
Vesiculobullous: Fluid-filled lesions.
Diffuse/Erythematous: Generalized redness.
Petechial/Purpureal: Small <2mm red/purple spots caused by hemorrhage from small blood vessels.
Hypersensitivity Reactions:
Type 1: Immediate hypersensitivity (e.g., urticaria)
Mediated by IgE.
Binding of allergen to IgE on cell surface causes cross-linking and mast-cell activation, releasing histamine.
Occurs within 2-30 minutes.
Examples include allergic rhinitis, allergic asthma, atopic eczema, systemic anaphylaxis, and some drug allergies.
Type 2: Humoral cytotoxic reactions (e.g., blistering, vesicles)
Mediated by IgG and/or IgM.
Cell- or matrix-associated antigen: binding of IgG to allergen → complement activation, FcR+ (monocyte) cells → opsonisation and phagocytosis OR cell lysis (NK cells) (e.g. some drug allergies (e.g. penicillin), blood transfusion rejection)
Cell-surface receptor: binding of IgG to antigen on cell-surface receptors → alters signalling → antibody dependent cell-mediated cytotoxicity (ADCC) OR antibody interference with cell surface receptor → chronic stimulation OR impairment (e.g. chronic urticaria (antibody against FC€RI alpha chain))
Occurs within 5-8 hours.
Examples include some drug allergies, blood transfusion rejection, and chronic urticaria.
Type 3: Immune complex mediated (e.g., vasculitis, petechiae, purpura)
Mediated by IgG and/or IgM.
Humoral IgG binds to blood-borne allergen → insoluble complex → complement and phagocyte activation → tissue damage in vasculature, and locations of complex deposition (e.g. lung, skin, kidneys, joints)
Occurs within 2-8 hours.
Examples include serum sickness and arthus reaction.
Type 4: Cell mediated immune reactions (e.g., macules, papules)
Th1 cells e.g. allergic contact dermatitis, tuberculin reaction
Soluble antigen
1st exposure → CD4+ T cells and MHC-II → differentiate to Th1 cells → cytokine release (IL12, IFNg, IL-2, lymphotoxin) and immune cell (e.g. macrophage) activation → cell damage
Th2 cells e.g. chronic asthma, chronic allergic rhinitis
Soluble antigen
1st exposure → CD4+ T cells and MHC-II → differentiate to Th2 cells → IgE production, eosinophil activation, mastocytosis
CTL e.g. graft rejection, allergic contact dermatitis to poison ivy
Cell-associated antigen
CD8+ T cell recognition of allergen on cell-surface receptor → cytotoxicity
24-72 hours
Pathogenesis:
Viral Infection:
Caused by either an immune response to the virus or damage to skin cells from factors released by the virus.
Common viral rashes include:
Measles: Caused by an RNA paramyxoviridae virus
Rubella (German Measles): Caused by an RNA togavirus
Erythema Infectiosum (Slapped Cheek): Caused by parvovirus B19
Roseola Infantum: Caused by HHV6 and 7
Varicella-Zoster: Almost all cases occur in children under 10 years old.
EBV (Epstein-Barr Virus): Around 15-35% will have a cutaneous eruption, which increases with ingestion of ampicillin or amoxicillin.
CMV (Cytomegalovirus): Primary infection often asymptomatic except in immunocompromised individuals.
HIV: 10-12% will develop an acute seroconversion syndrome with a morbilliform cutaneous eruption.
Hand-Foot-and-Mouth Disease: Most typically caused by coxsackie virus type A16 or enterovirus 71.
Cutaneous Herpes Simplex (HSV-1/2): Causes oral, genital, and ocular ulcers during initial infection.
Molluscum Contagiosum: Lesions appear as pearl-like, smooth papules caused by skin-to-skin or fomite contact.
Inflammatory Dermatoses:
Atopic Dermatitis (Eczema): Type 1 hypersensitivity reaction.
Seborrheic dermatitis: infants and adolescents (in adolescents, sebaceous secretions are altered by the normal skin flora → induces dermatitis)
Irritant contact dermatitis
Allergic contact dermatitis: involves a true allergy (most common precipitating agents are species of Toxicodendron, i.e. poison ivy, poison oak, or poison sumac, and the metal nickel)
Psoriasis: exacerbated by stress, local trauma, infections, some medications
Pityriasis rosea: self-limited papulosquamous disorder (?infectious aetiology)
Mastocytosis: heterogenous group of disorders, characterised by clonal mast cell proliferation and accumulation within various organs → in the skin, urticaria, vesicle and bulla formation may be seen
Local Bacterial/Fungal Infection:
Damage to cells from infection and the body’s inflammatory response.
Examples include:
Impetigo: Superficial skin infection caused by Staphylococcus aureus or group A beta-hemolytic streptococci.
Folliculitis: Pyoderma located within a hair follicle, secondary to follicular occlusion by keratin, over-hydration, or infection → bacterial causes include S. aureus and Pseudomonas
Tinea corporis (ringworm): dermatophytic infection of the skin on the body caused by Trichophyton (most commonly) and Microsporum fungal species
Scabies: an infestation with Sarcoptes scabiei organisms
Cutaneous candidiasis: primary or secondary fungal infection caused by members of the genus Candida → typically involves fold areas with an erythematous patch centrally and surrounding smaller satellite lesions, occasionally has whitish discharge centrally
Drug Eruptions:
Caused by delayed immunological hypersensitivity (type 4 hypersensitivity) to the drug or its metabolite.
Drugs can act as haptens, forming complexes with carrier proteins and eliciting an immune response.
Both humoral and cell-mediated mechanisms are involved.
Commonly implicated drugs include antibiotics (sulfonamides, aminopenicillins) and anticonvulsants.
More severe reactions include Stevens-Johnson syndrome/toxic epidermal necrolysis, erythema multiforme, and systemic hypersensitivity syndrome.
Haematological Disorders:
Often due to hemorrhage from small blood vessels.
Conditions include:
Acute Leukemia: Associated with signs and symptoms of underlying cytopenias.
Immune Thrombocytopenia: Diagnosis of exclusion with no systemic upset or organomegaly.
Petechial Rash with Ecchymosis: May be a presenting feature of thrombocytopenia.
Vasculitic/Rheumatological Diseases:
Involves inflamed or damaged cutaneous vessels.
Examples include:
Kawasaki Disease
Henoch-Schonlein Purpura
Systemic Lupus Erythematous
Juvenile Arthritis
Rheumatic Fever
Sarcoidosis
Systemic bacterial infections
Meningococcal disease: generalised purpuric (non-blanching) rash may be a presenting sign of meningococcal septicaemia (Neisseria meningitidis infection)
Syphilis: caused by the spirochete Treponema pallidum → transmitted by sexual contact or vertical transmission → secondary syphilis lesions result from the haematogenous dissemination of treponemes from a syphilitic chancre → manifests primarily as mucocutaneous rash in association with vague constitutional symptoms, diffuse lymphadenopathy, and highly infectious skin lesions
Gonorrhoea infection: caused by Neisseria gonorrhoeae → disseminated gonococcal infection develops as a consequence of untreated primary infection → commonly causes skin papules that progress into haemorrhagic pustules, bullae, petechiae, or necrotic lesions on the extremities
Bacterial endocarditis: rare skin manifestations are Janeway lesions (painless maculopapular lesions on palms and soles) and Osler nodes (painful nodules on tips of fingers → bacterial aetiologies include S. aureus, Enterococcus, Streptococcus bovis, Streptococcus viridans, and HACEK (Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella species) organisms
Toxin-mediated infections:
Staphylococcal scalded skin syndrome: uncommon manifestation of S.aureus toxin-producing strains → toxin targets the granular layer and cause blister formation
Scarlet fever: caused by an erythrogenic toxin produced by group A beta-haemolytic streptococci → manifests as pharyngitis and an accompanying cutaneous eruption (appears in all areas at the same time without a particular pattern of development)
Toxic shock syndrome (TSS): caused by TSS toxin 1, staphylococcal enterotoxins, streptococcal toxins, or other toxins → consists of a complex of symptoms, including fever, low BP, and a diffuse, erythematous rash on the trunk, palms, and soles of the feet that may be desquamative
Anaphylactic/ hypersensitivity reactions
Urticaria
Consists of transient localised wheals (hives), found anywhere on the body
Most commonly in response to either a drug/food allergy or an bite/sting
Cutaneous findings occur due to histamine release in the skin and increased permeability of blood vessels
Each urticarial lesion lasts for 24-48h, although the eruption itself may last longer due to recurrent crops of lesions
Classic Rashes of Childhood:
First Disease: Measles
Second Disease: Scarlet Fever
Third Disease: Rubella
Fourth Disease: Duke’s Disease (etiology unknown)
Fifth Disease: Erythema Infectiosum
Sixth Disease: Roseola
List and briefly describe the mechanisms for underlying factors that predispose children to particular sites of infection and pathogens
Maternal History:
Maternal Health and Illness:
Maternal infections such as HIV, CMV, and HSV can increase the risk of fetal illness and resultant immunodeficiency.
Risky behaviors during pregnancy, including alcohol (ETOH) consumption, smoking, and exposure to toxins, further elevate the risk of fetal immunodeficiency.
HIV can be transmitted from mother to child during pregnancy, childbirth, or breastfeeding, leading to congenital or perinatally acquired HIV infection.
CMV (Cytomegalovirus) can cause congenital CMV infection, leading to developmental delays, hearing loss, and other health issues.
HSV (Herpes Simplex Virus) can cause neonatal herpes, which can be severe and affect multiple organs.
Birth History:
Length of Gestation:
Premature birth (low length of gestation) is associated with an underdeveloped immune system, increasing susceptibility to infections.
Birth Weight:
Low birth weight is linked to immunodeficiency and higher susceptibility to infections.
Mode of Delivery:
Vaginal delivery exposes the newborn to the maternal birth canal flora, which is vital for initiating the development of the immune system.
Non-vaginal deliveries (e.g., cesarean section) are associated with an increased risk of lower respiratory tract infections (LRTI) and allergies, possibly due to the lack of exposure to beneficial maternal flora during birth.
Social History:
Day Care Attendance:
Increased exposure and transmission of pathogens due to close contact with other children, leading to a higher risk of respiratory infections and other communicable diseases.
Pets and Farm Animals:
Animals can be sources of zoonotic infections (infections transmitted from animals to humans) and other pathogens.
Exposure to Solvents, Smoke, and Toxins:
Environmental exposure to these substances at home or day care can increase the risk of respiratory conditions such as asthma.
Growth and Development:
Growth metrics like weight and height, along with underlying chronic conditions, can predispose children to infections.
Feeding History:
Increased duration of breastfeeding provides protective antibodies and enhances immune function, reducing the risk of infections.
Immunization History:
Poor vaccine adherence or incomplete vaccination schedules leave children vulnerable to vaccine-preventable diseases.
Medications:
Immunosuppressants:
Use of medications that suppress the immune system (e.g., corticosteroids, chemotherapy agents) increases vulnerability to infections by reducing the body’s ability to fight off pathogens.
Family History:
Autoimmune Conditions:
A family history of autoimmune conditions or recurrent infections may increase the likelihood of children developing similar conditions due to genetic predispositions and shared environmental factors.
Exposure to family members with contagious diseases increases the risk of transmission and subsequent infection in children.
Common Sites of Infection and Predisposing Factors:
Tonsillitis:
Red, enlarged tonsils +/- purulent exudate
Some children have large tonsils, inflammation needs to be present to make a diagnosis of tonsillitis
Most commonly caused by rhinovirus → coronavirus → adenovirus
If associated with infectious mononucleosis → EBV
If bacterial (10-30%), most commonly group A beta-haemolytic streptococci
Local inflammatory pathways → oropharyngeal swelling, oedema, erythema and pain
Predisposition: frequent contact with pathogens (childcare, etc.), anatomically primarily accessible site by pathogens
Otitis Media:
Purulent effusion (bulging ear drum) + inflammation (redness of ear drum)
Often over-called, a pink eardrum is not otitis media
Respiratory viruses account for most cases and are self-limiting
Co-infections of the middle ear with a virus and a bacterium → development of acute, suppurative otitis media or pus drum
Most common bacteria: Streptococcus pneumoniae (~40%), non-typable Haemophilus influenzae (25-30%) and Moraxella catarrhalis (10-15%)
Under normal conditions the mucociliary action and ventilatory function of the eustachian tube clear the nasopharyngeal flora that enter the middle ear
Upper respiratory viruses can infect the nasal passages, eustachian tube, and middle ear, causing inflammation and impairing these processes
Short length of eustachian tube in children increases risk for infection
List the causes of early and late onset neonatal sepsis
Early Onset Neonatal Sepsis (EOS):
Definition:
Occurs within the first 72 hours to 7 days of life, with some definitions using 72 hours as the cutoff for both term and preterm infants.
Symptoms often appear within the first 6 hours of birth.
Pathophysiology:
Vertical transmission or perinatal transmission from mother to infant.
Pathogens are typically acquired intrapartum, meaning during the delivery process.
Common Causative Pathogens:
Group B Streptococcus (Streptococcus agalactiae):
Most common in industrialized countries.
Universal screening and intrapartum antibiotic prophylaxis have significantly decreased the rate of early onset Group B Streptococcus sepsis.
Escherichia coli:
A gram-negative enteric organism, significant cause of EOS.
Listeria monocytogenes:
Less common but can occur in clusters.
Other Gram-Negative Enteric Bacilli:
Includes Klebsiella species.
Gram-Positive Bacteria:
Includes Enterococcus faecalis, Group D streptococci, alpha-hemolytic streptococci, and staphylococci.
Less Common Pathogens:
Streptococcus pneumoniae
Haemophilus influenzae (Type A and B)
Neisseria meningitidis
Neisseria gonorrhoeae
Viral Infections Mimicking Bacterial Sepsis:
Neonatal infection with herpes simplex virus (HSV) and enterovirus may present similarly to bacterial sepsis
Late Onset Neonatal Sepsis (LOS):
Definition:
Occurs after the first 72 hours to 7 days of life, extending to one month of age
Typically, for preterm infants, LOS is defined as occurring >72 hours after birth, and for term infants, it is ≥7 days
Pathophysiology:
Infections are usually acquired from the environment, which includes hospital (nosocomial) settings or home environments
Pathogens are acquired at delivery but invade later or are acquired postnatally.
Common Causative Pathogens:
Coagulase-Negative Staphylococci (CONS):
The most common cause of LOS due to high incidence in vascular catheter-associated infections in hospitalized neonatal patients.
Gram-Negative Bacilli:
Includes various enteric bacteria.
Streptococci and Anaerobes:
Includes different species of streptococci and anaerobic bacteria.
Staphylococcus aureus:
Significant pathogen in LOS.
Chlamydia trachomatis:
Can cause late onset neonatal sepsis.
Genital Mycoplasmas:
Includes Mycoplasma species associated with genital infections.
E. coli:
Becoming more recognized as a significant cause of LOS, especially in low birth weight infants.
Less Common Pathogens:
Pseudomonas aeruginosa
Enterobacter cloacae
Candida albicans:
Particularly causative in low birth weight infants and immunocompromised neonates.
Viral Infections:
Disseminated infections with HSV, enterovirus, adenovirus, and respiratory syncytial virus (RSV) may manifest as early or late onset sepsis.
Serious bacterial infections:
Briefly describe the pathophysiology of serious bacterial infections in infants and children
UTI
Overview:
Urinary Tract Infections (UTIs) are among the most common serious bacterial infections in children. They can involve the lower urinary tract (cystitis), the upper urinary tract (pyelonephritis), or both.
Pathophysiology:
Colonization:
UTIs begin with the colonization of the periurethral mucosa by genitourinary bacteria. This initial step is crucial for the development of an infection.
Ascending Infection:
Cystitis:
The infection ascends from the urethra into the bladder
In the bladder, bacteria can multiply and cause inflammation of the bladder mucosa
Pyelonephritis:
If vesicoureteral reflux (VUR) is present, bacteria can ascend further into the upper urinary tract, reaching the kidneys and causing pyelonephritis.
Pyelonephritis involves infection of the renal parenchyma and can lead to renal damage and scarring.
Predisposing Factors:
Anatomical Abnormalities:
Conditions such as neurogenic bladder, obstructive uropathy, and vesicoureteral reflux increase the risk of UTIs.
These conditions can lead to incomplete bladder emptying, which facilitates bacterial growth.
Functional Abnormalities:
Functional issues like chronic constipation can lead to incomplete elimination of urine, allowing bacteria to remain in the bladder and grow
Indwelling Foreign Bodies:
Presence of catheters or other foreign bodies can act as a nidus for bacterial colonization and infection
Virulence Factors:
E. coli isolates from UTIs often express virulence factors that enhance their ability to adhere to the uroepithelial cells and grow
These factors include adhesins that mediate attachment to uroepithelial receptors and aerobactin, which enhances bacterial growth
Epidemiology:
UTIs are the most common serious bacterial infections in children without a focal infection.
Prevalence:
8% of girls and 2% of boys will have had a UTI by age 7.
Higher incidence in uncircumcised male infants.
Risk Factors:
Female Sex:
Females have a shorter urethra, which facilitates the ascent of bacteria into the bladder.
Uncircumcised Infants:
Higher prevalence of UTIs due to potential for increased bacterial colonization around the foreskin.
Urogenital Anomalies:
Congenital anomalies such as vesicoureteral reflux and urinary obstruction increase the risk of UTIs
Functional Anomalies:
Conditions such as chronic constipation and withholding behavior, which lead to incomplete bladder emptying and bacterial retention.
Causative Organisms:
Neonates:
Escherichia coli (E. coli): The most common pathogen.
Other less common pathogens include Citrobacter, Enterobacter, and Klebsiella species.
Older Children:
E. coli: The predominant pathogen.
Other less common pathogens include Klebsiella, Enterobacter, and Enterococcus species.
Clinical Features:
General Symptoms:
Fever, abdominal or loin pain, dysuria (painful urination), and frequency (increased need to urinate).
Young Infants:
Non-specific symptoms such as jaundice, failure to thrive, poor feeding, vomiting, irritability, and strong-smelling urine.
Diagnosis:
Urine Dipstick:
Can guide initial management but should be followed by a urine culture and sensitivity (MCS) before starting antibiotics
Urine Collection:
Older Children:
Midstream urine collection is preferred.
Pre-Continent Children ( those who are not yet able to consistently control their urination and bowel movements. This usually includes infants and toddlers):
Not Seriously Unwell:
Clean catch method, which involves stimulating urination by rubbing the lower abdomen.
Seriously Unwell:
Suprapubic aspirate or in/out catheter is used to collect urine directly from the bladder.
Management:
Empirical Antibiotics:
Uncomplicated UTI:
Oral cefalexin is commonly used.
Complicated Cases or Infants <3 months:
Intravenous antibiotics are administered. Common regimens include:
Gentamicin: Administered intravenously over 3-5 minutes.
Dosing:
Child <10 years: 7.5 mg/kg up to 320 mg
Child ≥10 years with septic shock or requiring intensive care: 7 mg/kg
Child ≥10 years without septic shock and not requiring intensive care: 6 mg/kg up to 560 mg
Amoxicillin or Ampicillin: 50 mg/kg up to 2 g IV, 6-hourly
If gentamicin is contraindicated:
Cefotaxime: 50 mg/kg up to 1 g IV, 8-hourly. For children with septic shock or requiring intensive care, 50 mg/kg up to 2 g IV, 8-hourly.
Ceftriaxone (child ≥1 month): 50 mg/kg up to 1 g IV, daily. For children with septic shock or requiring intensive care, 50 mg/kg up to 1 g IV, 12-hourly.
Adjustment Based on Culture and Sensitivity:
Antibiotic regimen should be adjusted according to the results of urine culture and sensitivity testing to target the specific pathogens causing the infection.
Viral Infections Mimicking UTIs:
Disseminated viral infections such as herpes simplex virus (HSV), enterovirus, adenovirus, and respiratory syncytial virus (RSV) can present with similar symptoms to bacterial sepsis.
Bacteraemia
Definition:
Bacteraemia: The presence of bacteria in the blood, which may or may not be symptomatic.
Septicaemia: A clinical condition involving a systemic inflammatory response to infection, typically referring to sepsis.
Pathophysiology:
Recognition and Immune Activation:
Innate Immune Response:
Innate immune cells recognize invading pathogens through pattern recognition receptors (PRRs)
Activation of immune cells leads to the secretion of pro-inflammatory cytokines.
This triggers the migration of polymorphonuclear leukocytes to the site of infection.
Cytokine Release and Systemic Inflammatory Response Syndrome (SIRS):
Pro-inflammatory cytokines induce vasodilation and increase vascular permeability.
Symptoms of SIRS include elevated temperature, accelerated pulse and breathing, and leucocytosis (increased white blood cells).
Sepsis: Suspected or proven infection plus SIRS.
Severe Sepsis: Sepsis with organ dysfunction (e.g., hypotension, hypoxemia, oliguria, metabolic acidosis, thrombocytopenia, confusion).
Septic Shock: Severe sepsis with hypotension unresponsive to fluid resuscitation.
Pathological Processes:
Endothelial Dysfunction: Damage to the endothelial lining of blood vessels.
Cell Death: Apoptosis and necrosis of cells due to severe infection and immune response.
Bio-energetic Derangement: Disruption of cellular energy metabolism.
Immunoparalysis: A state of immune system suppression following an initial hyper-inflammatory phase.
Early-Onset Neonatal Sepsis (EOS):
Timing: Occurs within the first 72 hours of life.
Common Pathogens:
Group B Streptococcus (GBS)
Gram-negative bacilli (e.g., E. coli)
Late-Onset Neonatal Sepsis (LOS):
Timing: Occurs after 72 hours to 1 month of life
Common Pathogens:
Coagulase-Negative Staphylococci (CONS): Most common due to high incidence in vascular catheter-associated infections in hospitalized neonates.
Other EOS Pathogens: Can also cause LOS.
Infants and Young Children:
Common Pathogens:
Streptococcus pneumoniae: Major cause of invasive bacterial infections in childhood.
Neisseria meningitidis: Affects young children and adolescents, less common since vaccination.
Staphylococcus aureus: Can cause severe sepsis in previously healthy children.
Group A Streptococci: Also a cause of severe sepsis.
Epidemiology:
The introduction of the pneumococcal vaccine has reduced the rate of occult bacteraemia to less than 1% in healthy, immunized infants.
Clinical Features:
General Symptoms:
Fever, lethargy, poor perfusion, cyanosis, marked hypo/hyperventilation.
Apparent Focal Disease:
Pneumonia: Cough, dyspnea, pulmonary crackles.
Cellulitis: Skin erythema.
Septic Arthritis: Joint pain and swelling.
Investigations:
Bedside Tests:
Urinalysis, urine microscopy culture and sensitivity (MCS), stool MCS, viral respiratory panel
Blood Tests:
Blood cultures, full blood count (FBC), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), procalcitonin
Imaging:
Chest X-ray (CXR) if pneumonia is suspected.
Other Tests:
Lumbar puncture (LP) if meningitis is suspected.
Management:
Empirical Antibiotics:
Neonates:
Early Onset Sepsis: Benzylpenicillin plus cefotaxime (if meningitis possible) or gentamicin (if meningitis excluded).
Late Onset Sepsis: Amoxicillin/amoxicillin plus cefotaxime (if meningitis possible) or gentamicin (if meningitis excluded)
Infants 1-2 Months:
Amoxicillin/amoxicillin plus cefotaxime/ceftriaxone (if meningitis possible) or gentamicin (if meningitis excluded).
Children >2 Months:
Gentamicin plus cefotaxime/ceftriaxone plus vancomycin
Adjustment After Culture Results:
Adjust antibiotic regimen based on culture and susceptibility results
Risk Factors for Infection with MRSA:
Residence in areas with high prevalence of MRSA
Previous colonization or infection with MRSA, especially if recent or related to the current episode of care.
Frequent or prolonged hospital stays, especially with recent antibiotic exposure or surgery
Management Protocols for MRSA Risk:
Empirical Regimen:
Gentamicin IV:
Children 2 months to <10 years: 7.5 mg/kg up to 320 mg for the first dose.
Children ≥10 years with septic shock or requiring intensive care support: 7 mg/kg for the first dose.
Children ≥10 years without septic shock and not requiring intensive care support: 6 mg/kg up to 560 mg for the first dose.
Plus either:
Cefotaxime 50 mg/kg up to 2 g IV, 6-hourly.
OR ceftriaxone 50 mg/kg up to 2 g IV, 12-hourly.
Plus vancomycin IV if the child has septic shock or is at increased risk of MRSA infection, considering a 25-30 mg/kg loading dose.
Meningitis
Overview:
Meningitis is an inflammation of the protective membranes covering the brain and spinal cord, known as the meninges.
It can be caused by bacterial, viral, or fungal infections.
Types of Meningitis:
Viral Meningitis:
Most common cause of aseptic meningitis (meningitis that is not caused by bacteria)
Causative Agents: Human enteroviruses (most common), herpes simplex virus (HSV), mumps, arboviruses (e.g., West Nile virus), HIV, and rarely, influenza.
Typically self-limiting without serious sequelae
Bacterial Meningitis:
Less common but more serious than viral meningitis.
Causative Agents: Streptococcus pneumoniae, Haemophilus influenzae type b (Hib), and Neisseria meningitidis are the predominant pathogens in both adults and children.
Fungal Meningitis:
Progressive, life-threatening, chronic, or subacute meningitis.
Causative Agent: Cryptococcus species
Often seen in immunosuppressed patients, including infants and neonates.
Pathophysiology:
Colonization and Invasion:
Nasopharyngeal Colonization: Pathogens colonize the nasopharyngeal epithelium.
Common pathogens include
Streptococcus pneumoniae
Neisseria meningitidis
Haemophilus influenzae type b.
The introduction of routine immunization has significantly decreased infections caused by H. influenzae and meningococcal group C.
Tuberculous meningitis should also be considered.
Bloodstream Invasion:
Pathogens invade the bloodstream, allowing them to disseminate and reach the meninges
Attachment and Invasion of the Meninges:
Bacteria attach to and invade the meninges, leading to inflammation
This process involves the release of pro-inflammatory cytokines, leading to increased permeability of the blood-brain barrier and the infiltration of immune cells.
Inflammation and Cerebral Edema:
Inflammation leads to the leakage of proteins and other substances into the brain tissue, causing cerebral edema.
This can alter cerebral blood flow and metabolism, contributing to cerebral vasculitis and further brain damage.
Clinical Features:
Neonates:
Early Symptoms: Lethargy, muscle hypotonia, irritability, poor appetite, vomiting, hyperthermia or hypothermia, dyspnea, and abnormal breathing patterns
Late Symptoms: Bulging fontanelle, high-pitched crying, seizures.
Children:
Classic Triad: Fever, headache, neck stiffness
Other symptoms include altered mental status, photophobia, nausea, vomiting, malaise, seizures.
N. meningitidis (Meningococcal): Myalgia, petechial or purpuric rash.
Investigation:
Blood Tests:
Full blood count (FBC), urea, electrolytes, creatinine (UEC), liver function tests (LFT), C-reactive protein (CRP), venous blood gas (VBG), serum glucose, and blood cultures.
Imaging:
Head CT scan may be required, especially if there are indications of increased intracranial pressure (e.g., focal neurological deficits, altered mental status).
Lumbar Puncture and CSF Analysis:
Perform lumbar puncture (LP) to obtain cerebrospinal fluid (CSF) for analysis.
Procedure: Position patient in the lateral recumbent position, identify the interspace (L3-L4 or L4-L5), and use sterile technique. Obtain CSF for pressure measurement and analysis.
Complications
Failure to obtain a specimen/traumatic bloody tap (common)
Post-dural puncture headache (uncommon) 5-15%
Transient/persistent paraesthesia/numbness (very uncommon)
Respiratory arrest from positioning (rare)
Infection introduced by needle → meningitis, epidural abscess, osteomyelitis (very rare)
Spinal haematoma (very rare)
Brain herniation (extremely rare in the absence of contraindications above)
Contraindications
Absolute contraindications: GCS < 8 or deteriorating LOC, ↑ ICP (but bulging fontanelles without other signs of ↑ ICP is not a contraindication)
Relative contraindications: septic shock, hemodynamic comprise, significant respiratory distress, new focal neurological signs or seizures, seizure within previous 30 minutes, bleeding predisposition (e.g. INR > 1.5, platelets < 50 or child on anticoagulant)
Management:
Supportive Therapy:
Fluid Therapy:
Normal: 3 mL/kg/hour of Plasma-Lyte 148 or normal saline plus 5% glucose.
Hyponatremia: 2 mL/kg/hour Plasma-Lyte 148 or normal saline plus 5% glucose.
Raised ICP or Generalized Edema: 1-2 mL/kg/hour Plasma-Lyte 148 or normal saline plus 5% glucose.
Shock or Hypovolemia: Fluid resuscitation with 10-20 mL/kg normal saline bolus.
Supplemental Oxygen: Administer as needed.
Medical Therapy:
Empirical Antibiotics:
<2 Months:
Treat as sepsis or septic shock
Early Onset Sepsis: Benzylpenicillin plus cefotaxime
Late Onset Sepsis: Amoxicillin/amoxicillin plus cefotaxime
1-2 Months: Amoxicillin/amoxicillin plus cefotaxime/ceftriaxone
2 Months: Ceftriaxone/cefotaxime plus dexamethasone.
Pathogen-Specific Antibiotics:
N. meningitidis: Benzylpenicillin
S. pneumoniae (Penicillin-sensitive): Benzylpenicillin
S. pneumoniae (Penicillin-resistant): Vancomycin
Hib: Ceftriaxone/cefotaxime.
Gram-negative Bacteria: Ceftriaxone/cefotaxime
GBS, Listeria: Benzylpenicillin
HSV: Aciclovir
Antiviral Therapy: For confirmed viral infections like HSV or varicella-zoster, aciclovir or valaciclovir is recommended.
Complications and Sequelae:
SIADH: Syndrome of inappropriate antidiuretic hormone secretion, affecting about 1/3 of children with meningitis.
Cerebral Edema: Increased permeability of the blood-brain barrier leads to vasogenic cerebral edema.
Sensorineural Hearing Loss: Direct bacterial invasion or inflammatory response damages the 8th cranial nerve, cochlea, or labyrinth.
Other Complications: Seizures, circulatory shock, cerebrovascular complications, motor deficits, subdural effusion, intellectual disability, and behavioral problems.
Contact Tracing:
Probable and confirmed cases of invasive meningococcal disease are notifiable.
Close contacts should be traced and monitored for symptoms.
Pneumonia
Risk Factors:
Neonates and Infants:
Prolonged rupture of membranes (PROM), maternal fever, maternal Group B Streptococcus (GBS) colonization, congenital lung cysts, chronic lung disease, immunodeficiency, cystic fibrosis, sickle cell disease, and presence of a tracheostomy
Prolonged rupture of membranes (PROM) refers to the rupture of the amniotic sac and the leakage of amniotic fluid before the onset of labor, lasting more than 18 hours before delivery.
Children:
Chronic lung disease (e.g., asthma), immunodeficiency, cystic fibrosis, and congenital lung abnormalities.
Cause & Pathophysiology:
Neonates (< 2 months):
Common pathogens include
Group B Streptococcus (Streptococcus agalactiae)
Escherichia coli
Klebsiella species
Staphylococcus aureus
Haemophilus influenzae
Pathogenesis involves infection of the lower respiratory tract and lung parenchyma leading to consolidation.
Infants and Children (> 2 months):
Viral Causes (70%): Influenza A, respiratory syncytial virus (RSV), parainfluenza virus, human metapneumovirus (hMPV), and adenovirus
Bacterial Causes: Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydia trachomatis, Staphylococcus aureus.
Viruses are the most common cause of community-acquired pneumonia (CAP) in children older than 2 months.
Clinical Features:
Non-specific symptoms in neonates (temperature instability, poor feeding, irritability).
In older children: cough, fever, tachypnea, retractions, hypoxemia, congestion, irritability, poor feeding
Investigation:
Bedside Tests: Sputum culture, influenza testing (via nasal swab, PCR)
Blood Tests: Full blood count (FBC) to check for leukocytosis, and urea, electrolytes, and creatinine (UEC) for children receiving IV fluids.
Imaging: Chest X-ray (CXR) showing hazy lungs and distinct infiltrates, which may be challenging to differentiate from transient tachypnea of the newborn (TTN) and respiratory distress syndrome (RDS).
Delayed clearance of fetal lung fluid: Normally, fetal lung fluid is absorbed shortly before or during birth. In TTN, this process is delayed, leading to fluid retention in the lungs.
Surfactant deficiency: Surfactant reduces surface tension in the lungs, preventing alveolar collapse. A deficiency leads to widespread atelectasis and impaired gas exchange.
Complications:
Lung abscess
Parapneumonic effusion
Empyema
Management:
Neonates (< 2 months):
Early-Onset CAP (within 72 hours of birth): Benzylpenicillin (60 mg/kg IV) plus gentamicin IV. Modify treatment based on susceptibility testing.
Late-Onset CAP (≥ 72 hours after birth): Ampicillin (50 mg/kg IV) or amoxicillin (50 mg/kg IV) plus gentamicin IV.
Children (≥ 2 months):
Low Severity: Oral amoxicillin (25 mg/kg up to 1g PO, 8-hourly for 3 days).
Moderate Severity: Oral amoxicillin or IV benzylpenicillin (50 mg/kg IV, 6-hourly) for 5-7 days
High Severity: IV cefotaxime (50 mg/kg up to 2g IV, 8-hourly) or IV ceftriaxone (50 mg/kg up to 2g IV, daily). In case of severe penicillin allergy, ciprofloxacin plus vancomycin IV, or moxifloxacin IV.
Supportive Therapies:
Antipyretics for fever.
IV fluids for dehydration.
Supplemental oxygen to maintain SpO2 > 92%.
Chest drain for empyema.
Connective tissue
Pathophysiology:
Infection Sites:
Infections often occur in the metaphyseal region of bones due to the rich blood supply.
Infection spreads hematogenously from a primary site of entry (e.g., respiratory tract, gastrointestinal tract, ENT, skin).
Direct inoculation can occur from open fractures or penetrating wounds.
Local extension from adjacent infected sites is also possible.
Spread of Infection:
In infants, transphyseal vessels allow infection to spread to adjacent joints, leading to septic arthritis.
In adolescents, infections tend to spread through the medullary canal of the bone.
Common Pathogens:
Age <12 months: Staphylococcus aureus, Group B Streptococcus, Gram-negative bacilli, Candida albicans.
Age 1-5 years: Staphylococcus aureus, Haemophilus influenzae (rare in immunized children), Group A Streptococcus (pyogenes), Streptococcus pneumoniae, Kingella kingae, Neisseria gonorrhoeae (consider child abuse).
Age 5-12 years: Staphylococcus aureus, Group A Streptococcus.
Age 12-18 years: Staphylococcus aureus, Neisseria gonorrhoeae (sexually active).
Commonly Affected Joints:
75% of cases affect the lower limb (knee > hip > ankle).
25% of cases affect the upper limbs.
Complications:
Systemic: Septicemia.
Local: Pathological fractures, sequestration, growth disturbances.
Management Approach:
Medical:
Medical: IV antibiotics for a minimum of 2wks, followed by oral antibiotics for 4 weeks → early liaison with microbiologist required
Treat as sepsis or septic shock with an unknown source (as for bacteraemia above)
Empirical regimens target Staphylococcus aureus as well as other potential pathogens (e.g. beta-haemolytic streptococci, Enterobacteriaceae, Pseudomonas aeruginosa)
Give antibiotics within 1h of the patient presenting to medical care or, for a ward-based patient, developing sepsis or septic shock; antibiotics should be given immediately after appropriate samples are taken for culture
Blood samples should always be taken before antibiotic administration
Other relevant samples (e.g. joint aspirate, pus aspirate, bone biopsy) should be collected as soon as possible but should not delay antibiotic administration
Surgical:
Drainage and debridement are necessary if there is frank pus on aspiration, a sequestered abscess, or a collection not accessible to antibiotics.
Other Connective Tissue Disorders in Children
Chondromalacia Patellae:
Pathophysiology: Softening of the cartilage underneath the patella leads to generalized knee pain, especially when climbing stairs, playing sports with an axial load on the knee, or sitting for long periods.
Management: Physiotherapy, ice, analgesia, and arthroscopic smoothing of the patella undersurface.
Cutis Laxa:
Pathophysiology: Inherited or acquired mutation leads to abnormal elastin metabolism, resulting in reduced skin elasticity. This manifests as loose skin that hangs in folds, gastrointestinal hernias or diverticula, pulmonary emphysema, bronchiectasis, heart failure, and aortic aneurysms.
Management: No specific treatment; physical therapy can help increase skin tone. Sometimes plastic surgery is needed.
Ehlers-Danlos Syndrome:
Pathophysiology: Autosomal dominant mutation in genes that encode collagen affects the amount, structure, or assembly of different collagens, leading to articular hypermobility, dermal hyperelasticity, widespread tissue fragility, and bleeding tendencies.
Types: Classic, hypermobility, vascular, kyphoscoliosis, arthrochalasis, dermatosparaxis.
Complications: Bleeding, synovial effusions, sprains, dislocations, spinal kyphoscoliosis, thoracic deformity, pes planus, hernias, diverticula, gastrointestinal hemorrhage, GI perforation, dissecting aortic aneurysm, valve prolapse.
Investigations: Genetic testing, skin biopsy, echocardiography, vascular imaging.
Management: Supportive care such as protective clothing, padding, meticulous hemostasis during surgeries.
Infrapatellar Tendinitis:
Epidemiology: More common in figure skaters, basketball or volleyball players, ages 10-23 years.
Pathophysiology: Overuse injury to the patella tendon at the attachment of the lower pole of the patella leads to microvascular fractures, causing knee pain, especially when straightening the knee against force (e.g., climbing stairs, jumping).
Management: Activity modification, physical therapy, analgesia, and surgical repair if necessary.
Juvenile Idiopathic Arthritis:
Epidemiology: Uncommon, onset before 16 years, females more affected than males.
Pathophysiology: Autoimmune and/or autoinflammatory disease leads to chronic synovial inflammation, joint capsule hyperplasia, pannus formation, and invasion of the articular surface, resulting in loss of joint function.
Clinical Features: Arthritis, fever, rash, adenopathy, splenomegaly, iridocyclitis.
Investigations: FBC (leukocytosis, anemia, thrombocytosis), increased CRP/ESR, positive ANA, RF usually absent, ultrasound, X-ray, slit lamp examination.
Management: Physiotherapy, NSAIDs (first line), DMARDs (second line), surgery if necessary.
Marfan Syndrome:
Pathophysiology: Autosomal dominant mutation of the fibrillin-1 gene on chromosome 15 leads to defective fibrillin, affecting connective tissue microfibrils and elastin.
Clinical Features: Mitral valve prolapse, aortic dissection/aneurysm/regurgitation, retinal detachment, fibrillin-1 mutation, arm span greater than height, near-sightedness, nasal voice (high arched palate), scoliosis, subluxated lens.
Management: Beta-blockers to prevent cardiac complications, symptom management.
Nail-Patella Syndrome:
Pathophysiology: Autosomal dominant mutation in a gene for a transcription factor involved in limb and kidney development results in abnormal bones, joints, fingernails, toenails, and kidneys.
Management: ACE inhibitors for proteinuria and hypertension, kidney transplantation in severe cases.
Osteochondrodysplasias:
Pathophysiology: Mutations in genes encoding proteins involved in the growth and development of connective tissue, bone, or cartilage lead to skeletal maldevelopment and short-limbed dwarfism.
Management: Surgical limb-lengthening, surgical correction of leg bowing, or joint replacement as needed.
Osteogenesis Imperfecta:
Pathophysiology: Mutations in genes encoding for a type of collagen result in diffuse abnormal fragility of bones and sometimes sensorineural hearing loss, blue sclerae, dentinogenesis imperfecta, and joint hypermobility.
Management: Supportive measures such as walking aids and wheelchairs, bisphosphonates, and surgery to improve mobility and correct skeletal defects.
Pseudoxanthoma Elasticum:
Pathophysiology: Gene mutation in a protein involved in cellular detoxification leads to calcification of elastic fibers in the skin, retina, and cardiovascular system. Manifestations include small yellowish papules on the neck, axillae, and flexural surfaces (cutaneous), angled streaks of the retina and retinal hemorrhages leading to gradual vision loss (ocular), and premature atherosclerosis with intermittent claudication, hypertension, angina, and myocardial infarction (cardiovascular).
Management: Symptomatic management and prevention of complications.
Meningococcal sepsis
Epidemiology:
Primarily affects children under 5 years of age and adolescents.
Approximately 50% of cases occur in children under 2 years old, with 25% in individuals over 30 years old.
Cause:
Caused by Neisseria meningitidis, an aerobic gram-negative diplococcus found exclusively in the human nasopharynx.
There are 13 serogroups of Neisseria meningitidis, with the most common being A, B, C, W, and Y.
Pathophysiology:
Transmission and Initial Infection:
Spread by respiratory droplets.
Bacteria colonize the nasopharynx and can invade the bloodstream.
Bacterial Factors and Immune Response:
Bacterial lipo-oligosaccharide stimulates a pro-inflammatory cytokine response.
Endotoxins released by the bacteria trigger a widespread inflammatory response, leading to endothelial necrosis, intraluminal thrombosis, and perivascular hemorrhage.
Systemic Effects:
Vascular Permeability and Hypotension:
Increased vascular permeability and dysregulation of vascular tone result in hypotension.
Myocarditis and myocardial depression may further impair tissue perfusion.
Disseminated Intravascular Coagulation (DIC):
Activation of the coagulation cascade and downregulation of anticoagulant and fibrinolytic pathways.
DIC is characterized by acquired deficiencies of protein C, protein S, and antithrombin III, increased plasminogen activator inhibitor, and thrombin-activatable fibrinolysis inhibitor.
Small-vessel thrombosis and skin necrosis cause purpura fulminans.
Thrombosis of larger blood vessels leads to ischemia or infarction of digits or extremities.
Meningitis and Neurological Complications:
Local inflammatory responses in the brain cause cerebral edema, raised intracranial pressure (ICP), and vascular thrombosis.
Waterhouse-Friderichsen Syndrome:
Bilateral adrenal hemorrhage and necrosis lead to acute adrenal insufficiency.
Clinical Features:
Early Signs (within 12 hours):
Fever, headache, loss of appetite, nausea, vomiting, sore throat, coryza.
Limb pain, myalgia, refusal to walk, cold hands and feet.
Red rash progressing to petechiae and then purpura.
Signs of Sepsis:
Pallor or mottling, cool peripheries, prolonged capillary refill, tachypnea, hypoxia, grunting.
Late Signs (after 12 hours):
Altered level of consciousness, neck stiffness, headache, photophobia, bulging fontanelles, positive Kernig or Brudzinski signs.
Non-blanching rash (purpuric or petechial lesions).
Increased heart rate, respiratory rate, and capillary refill time ≥2 seconds.
Investigations:
Blood Tests:
Blood culture, serum PCR, full blood count (FBC), urea and electrolytes (UEC), liver function tests (LFT), C-reactive protein (CRP), venous blood gas (VBG), serum glucose.
Imaging:
Head CT scan if there are indications of increased intracranial pressure or other neurological signs.
Other Tests:
Lumbar puncture and synovial fluid analysis.
Management:
Management of Sepsis:
Immediate administration of broad-spectrum IV antibiotics within one hour of presentation or upon developing sepsis or septic shock.
Empirical antibiotics should target Neisseria meningitidis and other potential pathogens.
Specific Management of Meningococcal Infection:
Antibiotics:
Initial Therapy: IV ceftriaxone (50 mg/kg up to 2 g, 12-hourly for 5 days) or IV cefotaxime (50 mg/kg up to 2 g, 6-hourly for 5 days).
De-escalation: If susceptibility to benzylpenicillin is confirmed and the patient is not hypersensitive to penicillin, switch to IV benzylpenicillin (60 mg/kg up to 2.4 g, 4-hourly for 5 days).
Penicillin Allergy: For severe hypersensitivity to penicillins, use IV ciprofloxacin (10 mg/kg up to 400 mg, 8-hourly for 5 days).
Supportive Therapy: Consider antipyretics for fever, IV fluids for dehydration, supplemental oxygen, and chest drain if necessary.
Infection Control:
Isolation and droplet precautions for at least 24 hours after antibiotic administration.
Notify the local public health unit and initiate contact tracing. Provide clearance antibiotics for close contacts.
Complications:
Meningitis:
Complications include cerebral edema, raised ICP, hydrocephalus, and long-term neurological deficits.
Sepsis:
Systemic complications such as septic shock, multi-organ failure, and disseminated intravascular coagulation (DIC).
Local complications include tissue necrosis, limb ischemia, and amputations.
Waterhouse-Friderichsen Syndrome:
Acute adrenal insufficiency due to adrenal hemorrhage and necrosis, leading to hypotension, shock, and metabolic disturbances.
Symptoms include salt craving, weight loss, anorexia, fatigue, lethargy, gastrointestinal complaints, orthostatic hypotension, and signs of meningococcal meningitis.
Management involves treating the underlying cause and supportive care.
Prognosis:
Mortality rate is approximately 8%, with a higher rate for sepsis (15-20%) compared to meningitis alone (5%).
Most deaths occur within the first 24 hours of illness onset.
Describe the management approach to serious bacterial infections in infants and children
Initial Stabilization:
Stabilize Airway, Breathing, and Circulation (ABCs):
Ensure the airway is clear and provide oxygen if necessary.
Support breathing with ventilation if required.
Maintain circulation with intravenous fluids and medications to support blood pressure.
Transfer to Pediatric Intensive Care Unit (PICU) if in Septic Shock:
Continuous monitoring and advanced supportive care are essential in the PICU.
Urgent Investigations (Septic Screen):
Full Blood Count (FBC): To check for leukocytosis or leukopenia.
Blood Culture: To identify the causative pathogen.
C-reactive Protein (CRP): To assess inflammation levels.
Urine Microscopy, Culture, and Sensitivity (MCS): To check for urinary tract infections.
Cerebrospinal Fluid (CSF) MCS: To diagnose meningitis if indicated.
Chest X-ray (CXR): To identify pneumonia or other thoracic infections.
Immediate Antibiotic Administration:
Antibiotic choice depends on the age of the child and the suspected or confirmed pathogen. Empirical antibiotic therapy should be initiated promptly.
Empiric Antimicrobial Regimens:
For febrile infants younger than 90 days without focal infections:
<1 Month with Fever but Well Appearing: Empiric antibiotics such as ampicillin and gentamicin or cefotaxime.
1-2 Months Well Appearing with One Risk Factor (e.g., risk factor, abnormal WCC, elevated CRP, CXR findings): Empiric antibiotics.
Additional Considerations:
Acyclovir: Add when indicated (e.g., mucocutaneous vesicles, seizures, CSF pleocytosis (increased number of white blood cells (WBCs) in the cerebrospinal fluid.)) for possible herpes simplex virus infection.
Gentamicin: Add for broader Gram-negative pathogen coverage.
Vancomycin: Add for MRSA coverage if suspected.
Fluid Resuscitation:
Administer intravenous fluids to maintain adequate perfusion and blood pressure.
Fluid boluses of isotonic saline or lactated Ringer's solution, typically 20 mL/kg, may be given and repeated as necessary.
Circulatory Support:
Inotropes (e.g., dopamine, epinephrine): If fluids alone are insufficient to maintain blood pressure and perfusion.
Management of Disseminated Intravascular Coagulation (DIC)
Fresh Frozen Plasma (FFP) and Platelets: Administer to correct coagulopathy and manage bleeding.
No evidence supports the routine use of steroids in septic shock.
Monitoring and Supportive Care:
Continuous monitoring of vital signs, urine output, and other clinical parameters.
Supportive therapies may include antipyretics for fever, supplemental oxygen, and mechanical ventilation if required.
Ensure adequate nutrition and hydration.
Viral Infections
Briefly describe the pathophysiology of viral infections in children
Measles
Epidemiology:
Typically occurs in regions with low vaccination rates and in resource-limited countries
Peak incidence is in children under 12 months of age, especially before routine vaccination
Cause:
Pathogen: Measles virus, an RNA virus of the Morbillivirus genus belonging to the Paramyxoviridae family
Route of Transmission: Direct contact with or inhalation of virus-containing droplets
Incubation Period: Approximately 2 weeks
Pathophysiology:
Incubation (6 to 21 days):
Virus enters the body via respiratory mucosa or conjunctivae
It replicates locally and then spreads to regional lymphatic tissues
Disseminates to other reticuloendothelial sites via the bloodstream (first viremia).
Initial Infection: The virus enters your body, for example, through your nose or mouth.
Local Replication: It starts to multiply where it first entered.
First Viremia: The virus gets into your blood for the first time.
Dissemination: From the blood, the virus spreads to other parts of your body, like the liver and spleen
Secondary Sites of Infection: The virus multiplies in these new areas, possibly entering the blood again and spreading even more
Contagiousness is estimated from five days before the appearance of the rash to four days afterward
A second viremia occurs several days after the first, signaling the beginning of the prodromal phase
Prodromal Phase (2 to 4 days):
Characterized by the appearance of symptoms such as fever, malaise, and anorexia, followed by conjunctivitis, coryza, and cough
Koplik spots may develop around 48 hours before the exanthem. These are 1 to 3 mm whitish, grayish, or bluish elevations with an erythematous base and are pathognomonic for measles.
Koplik spots typically slough off once the exanthem appears.
Exanthem Phase (6 to 7 days):
The rash typically arises approximately two to four days after the onset of fever
It is described as an erythematous, maculopapular, blanching rash that begins on the face and spreads to the neck, upper trunk, lower trunk, and extremities
The rash becomes non-blanching in later stages and may include petechiae, which can be hemorrhagic
The rash darkens after 3 to 4 days before fading
Other findings include lymphadenopathy, high fever, and worsening respiratory signs
Resolution:
Viremia (viruses present in the bloodstream) and the presence of the virus in tissues and organs cease by days 15 to 17, corresponding to the appearance of antibodies.
Clinical Features:
Prodromal Stage (4-7 days):
Coryza, cough, and conjunctivitis
Fever and malaise
Koplik spots on the buccal mucosa, appearing as tiny white or bluish-gray spots on an irregular erythematous background.
Exanthem Stage (7 days):
High fever and generalized lymphadenopathy
Erythematous maculopapular, blanching, partially confluent rash that begins behind the ears along the hairline before spreading to the rest of the body, including the feet.
Investigations:
Blood Tests:
Measles serology for IgM and IgG antibodies.
Full blood count (FBC) to assess leukocyte and platelet levels
Serum PCR for viral detection
Other Tests:
Lymph node biopsy if indicated.
Management:
Supportive Care:
Implement airborne precautions and isolation.
Administer antipyretics for fever
Vitamin A Supplementation:
Considered in severe cases to improve outcomes.
Prevention:
Measles can be prevented with a live attenuated vaccine, typically given as part of the MMR (measles, mumps, rubella) vaccination schedule
Rubella
Epidemiology:
Australia was declared free of rubella in 2018, but the disease is still prevalent in regions with low vaccination rates.
Rubella primarily affects unvaccinated children and can lead to congenital rubella syndrome in infants born to infected mothers.
Cause:
Pathogen: Rubella virus
Route of Transmission: Respiratory droplets and transplacental transmission
Incubation Period: 14 to 21 days (average 14 days)
Pathophysiology:
Transmission:
Rubella is transmitted from human to human via direct or droplet contact with infected body fluids, most commonly nasopharyngeal secretions.
Patients may shed the infectious virus from 7 to 30 days after infection, which includes the period from one week before to two weeks after the onset of the rash.
Infants with congenital rubella syndrome may be contagious for more than one year.
Replication and Spread:
After inhalation of infectious aerosols, the rubella virus initially replicates in the nasopharyngeal cells and regional lymph nodes.
Viremia occurs 5 to 7 days after inoculation, spreading the virus hematogenously throughout the body.
Infected individuals are potentially contagious for 1 to 2 weeks before the infection becomes clinically apparent.
Clinical Manifestations:
Prodromal Phase (1-5 days):
Symptoms may include low-grade fever, post-auricular and suboccipital lymphadenopathy, mild sore throat, conjunctivitis, headache, and joint pain
Forchheimer spots (enanthem of the soft palate) may appear
Exanthem Phase (2-3 days):
A fine, non-confluent, pink maculopapular rash begins on the face, particularly behind the ears, and spreads caudally to the trunk and extremities, sparing the palms and soles. The rash typically becomes generalized within 24 hours.
The rash is similar in distribution to measles but is less intensely red and spreads more rapidly without darkening.
Immune Response and Viremia:
Systemic symptoms are primarily due to viral infection, but some manifestations (rash, thrombocytopenia, arthritis) have an immunological basis.
The viraemia and presence of the virus in tissues and organs cease by days 15 to 17, corresponding to the appearance of antibodies.
Congenital Rubella Syndrome:
Congenitally infected infants may transmit rubella for months after birth.
Can cause severe birth defects including heart abnormalities, cataracts, and developmental delays.
Clinical Features:
Asymptomatic Cases: Approximately 50% of rubella infections are asymptomatic.
Symptomatic Cases:
Prodromal symptoms include fever, malaise, lymphadenopathy, and Forchheimer spots.
Rash begins on the face and spreads to the body, typically appearing 14 to 17 days after exposure.
Polyarthritis can occur, especially in adolescents and adults.
Investigations:
Blood Tests:
Rubella serology for the detection of IgM antibodies or a four-fold increase in IgG antibodies.
Full blood count (FBC) may show leukopenia, relative lymphocytosis, and increased plasma cells.
Management:
Supportive Care:
Antipyretics for fever
Antihistamines for severe pruritus
Rest and NSAIDs for severe polyarthritis
Prevention:
Vaccination:
MMR (measles, mumps, rubella) vaccine at 12 months of age
MMRV (measles, mumps, rubella, varicella) vaccine at 18 months of age.
Roseola
Epidemiology:
Most common viral exanthem in children younger than 3 years
Peak incidence occurs between 6 months and 2 years of age
Cause:
Pathogen: Primarily caused by Human Herpesvirus 6 (HHV-6), with rare cases caused by Human Herpesvirus 7 (HHV-7). Other potential causative agents include enteroviruses, adenoviruses, and parainfluenza virus type 1.
Route of Transmission: Spread through respiratory secretions from asymptomatic carriers
Incubation Period: 5 to 15 days
Pathophysiology:
Viral Characteristics:
HHV-6 and HHV-7 are double-stranded DNA viruses
These viruses are trophic for CD4+ T lymphocytes, but HHV-6B can also infect other cell types
HHV-6B down-regulates the expression of CD3 on T cells, acting as a potential immunosuppressant and a powerful inducer of TNF-alpha and interleukin-1beta
After primary infection, HHV-6B can remain latent in various tissues and can reactivate, especially during periods of immunosuppression.
Clinical Course:
Febrile Phase (3-5 days):
Fever: Sudden onset of high fever, which can exceed 40ºC (104ºF) in some cases.
Lymphadenopathy: Cervical, postauricular, and/or occipital lymphadenopathy.
Nagayama Spots: Papular enanthem on the uvula and soft palate, sometimes observed during the febrile phase.
Exanthem Phase (1-3 days):
Rash Development: After the fever subsides abruptly, a rash appears. The exanthem is characterized by a blanching macular or maculopapular rash that starts on the neck and trunk and spreads to the face and extremities.
Rash Characteristics: The rash is typically rose-pink in color, non-pruritic, and may sometimes be vesicular. It generally lasts for 3 to 5 days and does not darken like measles rash.
Additional Features:
Symptom Presentation: Some children may present with irritability, mild diarrhea, or a mild cough
Asymptomatic Shedding: HHV-6 and HHV-7 DNA can be found in saliva for extended periods following primary infection, contributing to asymptomatic shedding and transmission
Investigations:
Clinical Diagnosis: Roseola is primarily diagnosed based on clinical presentation
Laboratory Tests: Detection of HHV-6 IgM antibodies and PCR can be used to confirm the diagnosis if necessary.
Management:
Supportive Care:
Fluids: Ensure adequate hydration.
Antipyretics: Administer medications like acetaminophen or ibuprofen to reduce fever.
Prevention:
Hygiene: Encourage good hygiene practices to reduce the spread of the virus.
Varicella
Epidemiology:
Primarily affects children aged 2 to 8 years.
Before widespread vaccination, 90% of children were infected by age 15.
Epidemics occurred in winter and early spring in 3-4 year cycles.
In immunocompetent children, the infection is usually mild; however, it can be severe in adults and immunocompromised children.
Cause:
Pathogen: Varicella zoster virus (VZV), a human herpesvirus type 3.
Route of Transmission: Airborne droplets, direct contact with VZV-infected vesicle fluid, and transplacental transmission
Incubation Period: 10 to 21 days, typically around 14 days
Pathophysiology:
Transmission and Initial Infection:
VZV is transmitted through contact with aerosolized droplets from nasopharyngeal secretions of an infected individual or by direct cutaneous contact with vesicle fluid from skin lesions.
The virus initially replicates in the nasopharyngeal cells and regional lymph nodes.
Viremia and Spread:
Primary Viraemia: Occurs 4 to 6 days after infection, spreading the virus to the liver, spleen, and other reticuloendothelial system cells.
Secondary Viraemia: Occurs around day 9, where mononuclear cells transport the virus to the skin and mucous membranes, leading to the characteristic vesicular rash.
VZV causes vasculitis of small blood vessels and degeneration of epithelial cells, forming fluid-filled vesicles with high levels of the virus.
Clinical Course:
Prodrome (1-2 days): Symptoms include malaise, low-grade fever, cough, coryza, anorexia, sore throat, and headache.
Rash Development: The skin eruption begins on the trunk and spreads to the face (including mucous membranes) and extremities, sparing the palms and soles. Lesions evolve from macules to papules to vesicles, occurring in crops and presenting at various stages simultaneously. Central necrosis and early crusting may also be visible.
Contagious Period: Patients are contagious from 48 hours before the rash onset until all skin lesions have fully crusted.
Clinical Features:
Rash: Widespread, starting on the trunk and spreading to the face, scalp, and extremities.
Various stages of rash occur simultaneously: erythematous macules → papules → vesicles filled with clear fluid on an erythematous base → eruption of vesicles → crusted papules → hypopigmentation of healed lesions
Investigations:
Clinical Diagnosis: Based on characteristic rash and symptoms.
Laboratory Tests: Vesicular swab for VZV PCR or Tzanck smear may be helpful in neonates or immunocompromised children to confirm the diagnosis.
Management:
Supportive Care:
Topical applications (e.g., calamine lotion) to soothe the skin.
Antihistamines for severe pruritus.
Maintain hydration and comfort.
Medical Therapy:
Indications: Immunocompromised individuals, primary infection in adults, unvaccinated adolescents ≥ 13 years, individuals on long-term salicylate therapy, and immunocompetent children with significant pre-existing skin conditions.
Antiviral Medication: Acyclovir can be considered, especially for severe cases or those at higher risk of complications.
Prevention:
Vaccination: Part of the national immunization schedule.
MMRV (measles, mumps, rubella, varicella) vaccine at 18 months
Varicella vaccine at 10-13 years for those who haven't been vaccinated previously
Complications:
Bacterial Superinfection: Including impetigo, cellulitis, necrotizing fasciitis
Reactivation: Latent VZV can reactivate later in life, leading to shingles (herpes zoster)
Other Complications:
Scarring from severe lesions.
Pneumonia, particularly in adults and immunocompromised individuals.
Neurological complications like acute cerebellar ataxia and encephalitis.
Reye Syndrome: Associated with viral infections and salicylate use.
Congenital Varicella Syndrome: If the infection occurs during pregnancy, it can lead to severe birth defects.
Hand food Mouth
Epidemiology:
Primarily affects children under 5 to 7 years of age
Most common during late summer and autumn months
Cause:
Pathogen: Most commonly caused by Coxsackie A virus and Enterovirus A71
Route of Transmission: Airborne droplets, fecal-oral route, direct contact with vesicle fluid, or respiratory secretions.
Incubation Period: Typically 4 to 7 days.
Pathophysiology:
Transmission and Initial Infection:
Infection occurs after oral ingestion of fecal material, oral secretions, vesicle fluid, or respiratory secretions from an infected individual.
The virus is highly contagious and can persist in fecal material for up to 1 month.
Viremia and Spread:
The virus initially replicates in submucosal lymphoid tissues of the lower intestine and pharynx
It then spreads to regional lymph nodes, causing a minor viremia that disseminates the virus throughout the body
This results in the infection of reticuloendothelial tissues and multiple organs, leading to a major viremia
Clinical Course:
Prodrome (3-4 days): Brief period characterized by low-grade fever, malaise, anorexia, and odynophagia.
Oral Lesions: Begin as small red macules that evolve into vesicles measuring 2 to 20 mm. These vesicles rupture, leaving intensely painful erosions, causing children to refuse to eat or drink.
Hand and Feet Lesions: Start as macules and papules that evolve into flat-topped, elliptical vesicles with an erythematous base. These lesions may occur without oral lesions.
Clinical Features:
Oral Lesions: Small red macules that evolve into vesicles, typically found on the tongue, gums, and inside of the cheeks. These vesicles rupture to form painful erosions.
Hand and Feet Lesions: Vesicular rash on the hands and feet, starting as macules and papules and evolving into vesicles. These lesions are often elliptical with a red base.
Systemic Symptoms: Low-grade fever, malaise, anorexia, and sore throat.
Contagious Period:
Individuals are contagious from 2 days before the onset of the rash until 2 days after the eruption.
The disease typically resolves within 10 days.
Treatment:
Supportive Care:
Maintain hydration and provide pain relief with analgesics or antipyretics.
Encourage oral intake with soft, cool foods and fluids to ease pain from oral lesions.
Topical anesthetics may help reduce pain from mouth sores.
Hygiene:
Good hand hygiene is crucial to prevent the spread of the virus.
Clean and disinfect surfaces and objects that may be contaminated with the virus.
No Specific Antiviral Therapy:
There is no specific antiviral treatment available for HFMD. The management focuses on symptomatic relief.
Erythema infectiosum
Epidemiology:
Primarily affects children aged 5 to 15 years.
Peak incidence occurs in late winter and early spring.
Approximately 25% of infections are asymptomatic.
Cause:
Pathogen: Parvovirus B19.
Route of Transmission: Respiratory droplets, percutaneous exposure to blood or blood products, and transplacental transmission.
Incubation Period: Typically 4 to 14 days, but can range up to 21 days.
Pathophysiology:
Transmission and Initial Infection:
Parvovirus B19 is transmitted via respiratory droplets and can also spread through blood products or from mother to fetus.
The virus infects erythrocyte progenitor cells in the bone marrow and blood, using the erythrocyte P antigen (globoside) as its receptor.
Individuals lacking the P antigen are not susceptible to the disease.
Viral Replication and Cytotoxicity:
The virus initially replicates in the submucosal lymphoid tissues of the lower intestine and pharynx.
It then spreads to regional lymph nodes, causing a minor viremia that disseminates the virus throughout the body.
The virus replicates in erythroid progenitor cells, leading to cellular invasion and destruction. This replication results in the transient cessation of erythropoiesis and a drop in hematocrit.
Viremia occurs 4 to 14 days after infection, followed by the appearance of anti-B19 IgM antibodies, with IgG antibodies appearing approximately one week later.
The pathogenesis of the rash and arthropathy is not completely understood but coincides with measurable serum antibody production.
Clinical Manifestations and Immune Response:
In healthy individuals, RBC production returns to normal within 10 to 14 days with minimal anemia.
In individuals with increased RBC turnover (e.g., those with hemolytic anemias), parvovirus B19 can cause a transient aplastic crisis (temporary condition where the bone marrow abruptly stops producing red blood cells)
In fetuses, the virus can cause severe anemia, hydrops fetalis, and intrauterine fetal death due to hemolysis and decreased red-cell survival time.
In immunocompromised individuals, chronic or reactivated infections can lead to severe anemia due to hypoplasia or aplasia of erythroid cells and their precursors.
Clinical Features:
Incubation Period:
Typically 1 to 3 weeks from exposure to the appearance of the rash.
Prodromal Phase (1-3 days):
Mild cold-like symptoms including fever, coryza, headache, nausea, and diarrhea.
Exanthem Phase (2-5 days after prodrome):
Initial Rash: Characteristic "slapped cheek" appearance with bright red erythema on the cheeks, often with perioral sparing.
Subsequent Rash: A lacy, reticulated, or lacelike rash may appear on the trunk and extremities several days after the facial rash. This rash is often pruritic.
Additional Symptoms:
Some children may present with arthropathy (joint pain), particularly in older children and adults.
The rash may reappear or worsen with exposure to sunlight, heat, stress, or exercise.
Investigations:
Clinical Diagnosis: Based on characteristic rash and symptoms.
Laboratory Tests:
Serology for detection of Parvovirus B19-specific IgM and IgG antibodies.
PCR for Parvovirus B19 DNA in blood may be used in immunocompromised patients or in cases of fetal infection.
Complete Blood Count (CBC): May show anemia or reticulocytopenia in severe cases.
Management:
Supportive Care:
Analgesics and antipyretics (e.g., acetaminophen, NSAIDs) for fever and joint pain
Ensure adequate hydration and rest
For Immunocompromised Patients:
May require intravenous immunoglobulin (IVIG) therapy to control the infection and support erythropoiesis.
Complications:
Transient Aplastic Crisis: Particularly in patients with chronic hemolytic anemias (e.g., sickle cell disease).
Chronic Pure Red Cell Aplasia: Can occur in immunocompromised individuals, leading to chronic anemia.
Hydrops Fetalis: Severe anemia in the fetus, potentially leading to fetal death, when infection occurs during pregnancy.
Other Complications:
Hepatitis, myocarditis, and encephalitis, though these are rare.
Parvovirus B19 is considered a TORCH infection, capable of causing congenital infections
Briefly describe the pathology of non- infectious causes of fever and rash
Kawasaki’s disease
Overview:
Kawasaki disease, also known as mucocutaneous lymph node syndrome, is an acute, necrotizing vasculitis of unknown etiology.
Primarily affects children under 5 years old, with a higher incidence in boys
It has a peak incidence in late winter and spring
Cause:
The exact cause is unknown
Potential factors include:
Infectious Agents: The disease may be triggered by an unknown infectious agent
Genetic Factors: There may be a genetic predisposition to the disease
Autoimmune Components: The immune system appears to attack blood vessels, but the precise mechanisms are not well understood
Pathophysiology:
Vasculitis: Kawasaki disease primarily affects the coronary arteries but can also involve other large and medium-sized arteries
Endothelial Damage: The disease leads to endothelial damage, exposing collagen and tissue factor in the tunica media, resulting in:
Clot Formation: Increased risk of clots that can block blood flow in the coronary arteries, leading to ischemia and potential myocardial infarction (MI)
Fibrin Deposition: This makes the arteries stiffer and less elastic, weakening the artery walls and leading to the formation of aneurysms. These aneurysms have a risk of rupturing, causing ischemia and potential MI
Fibrosis without Aneurysms: In cases where fibrosis does not lead to aneurysm formation, the artery walls thicken, reducing the lumen diameter and causing ischemia to the myocardium
Acute Phase:
Characterized by the development of edema and neutrophil infiltration in the coronary arterial wall, with a rapid transition to mononuclear cell infiltration
This is followed by local production of matrix metalloproteinases, causing destruction of the internal elastic lamina and media
Chronic Phase:
Progression to fibrous connective tissue replacement of the intima and media, leading to aneurysm formation, scarring, and stenosis
Clinical course divided into the following stages
Clinical Features:
CRASH AND BURN
Fever: Persistent fever for at least 5 days.
CRASH Symptoms: At least four of the following, or fewer if there is coronary artery involvement:
Conjunctivitis: Bilateral, non-purulent.
Rash: Maculopapular, typically widespread.
Adenopathy: Cervical lymphadenopathy.
Strawberry Tongue: Red, swollen tongue with prominent papillae.
Hand and Foot Changes: Swelling, redness, and desquamation (peeling) of the skin on the palms and soles.
Other Features:
Lymphadenopathy: Especially in the neck.
Mucous Membrane Changes: Red, cracked lips, and red oral mucosa.
Complications:
Cardiac Complications: Without treatment, there is a 20-25% risk of developing heart complications, including:
Coronary Artery Aneurysms: Risk of rupture and MI.
Myocardial Infarction: Due to ischemia from clots or aneurysms.
Long-term Heart Issues: Including ischemic heart disease (IHD) and sudden death.
Investigations:
Inflammatory Markers: Elevated ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein).
Blood Tests: Leukocytosis and thrombocytosis.
Echocardiography: To evaluate for coronary artery aneurysms and monitor heart function.
Management:
IV Immunoglobulins (IVIG):
Neutralizes circulating antibodies through anti-idiotypic antibodies.
Downregulates inflammatory events by modulating Fc receptor function, interfering with complement activation, regulating cell growth, and affecting T and B cell function.
High-Dose Oral Aspirin:
Reduces inflammation and decreases platelet aggregation to prevent clot formation.
IV Glucocorticoids:
Used in severe cases or if IVIG is not effective.
Supportive Care:
Hydration, monitoring for heart complications, and symptomatic treatment for fever and rash.
Henoch-Schonlein purpura
Overview:
Henoch-Schonlein Purpura (HSP), also known as IgA vasculitis, is an acute, immune complex-mediated small vessel vasculitis
It is the most common vasculitis in children, typically affecting those between 2 and 8 years of age
Epidemiology:
More common in children, particularly those aged 2 to 8 years.
Incidence peaks in the spring and fall.
Slightly more common in boys than girls.
Cause:
Unknown Etiology: The exact cause of HSP is unknown, but it is believed to involve an abnormal immune response.
Triggers: Often preceded by an upper respiratory tract infection (URTI), especially Group A streptococcal infections. Other triggers can include viral infections, certain medications (e.g., antibiotics, antiarrhythmics), vaccinations, and environmental factors
Genetic Predisposition: A genetic predisposition may also play a role.
Pathophysiology:
Antigen Exposure:
Exposure to an antigen (e.g., infection, drugs) stimulates the production of IgA.
This IgA may abnormally target host endothelial cells.
Immune Complex Formation:
IgA forms immune complexes that deposit in the vascular walls of various tissues, including the skin, gastrointestinal (GI) tract, joints, and kidneys.
Complement Activation:
The deposition of IgA immune complexes activates the complement system, leading to vascular inflammation and damage.
Vascular Inflammation:
Skin Biopsies: Lesions show predominantly neutrophils and monocytes. Fluorescence microscopy reveals deposits of IgA, C3, and fibrin in the small vessels.
Similar to IgA Nephropathy: The pathogenesis of HSP is similar to that of IgA nephropathy, involving immune complex deposition and complement activation.
Clinical Features:
Incubation Period: Symptoms typically appear 1 to 3 weeks after the triggering event (e.g., infection).
Classic Tetrad of Symptoms:
Palpable Purpura:
Non-blanching, palpable purpuric rash, primarily on the lower extremities and buttocks.
Rash is palpable due to underlying inflammation and fibrosis.
Arthritis/Arthralgia:
Joint pain and swelling, most commonly affecting the knees and ankles
Gastrointestinal Symptoms:
Abdominal pain, which can be colicky and severe.
GI bleeding, manifested as bloody stools or melena.
Renal Involvement:
Hematuria (blood in urine) and proteinuria.
IgA nephropathy can develop, potentially leading to renal insufficiency.
Complications:
Renal Complications:
Renal involvement can be asymptomatic or present as hematuria, proteinuria, and hypertension.
In severe cases, it can progress to nephrotic syndrome or chronic kidney disease.
Gastrointestinal Complications:
Intussusception, bowel infarction, or perforation.
Other Complications:
Rarely, pulmonary or neurological involvement, which can be life-threatening.
Investigations:
Clinical Diagnosis: Based on characteristic symptoms and physical examination findings.
Laboratory Tests:
Urinalysis: To detect hematuria and proteinuria.
Blood Tests:
Full blood count (FBC) may show thrombocytosis, leukocytosis, and anemia.
Elevated serum IgA levels.
Decreased complement levels.
Elevated ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein) indicating inflammation.
UEC (urea and electrolytes) to assess renal function (elevated creatinine and BUN).
Biopsy:
Skin or kidney biopsy can confirm the diagnosis by showing IgA deposition in the vessel walls.
Imaging:
Abdominal ultrasound or CT scan if there are severe GI symptoms or complications.
Management:
Supportive Care:
Ensuring adequate hydration and nutrition.
Pain management with NSAIDs for mild cases.
Medical Therapy:
NSAIDs: For joint pain and inflammation, if there are no contraindications.
Systemic Glucocorticoids: For severe cases, particularly with significant GI or renal involvement.
Prednisone is commonly used.
Monitoring and Follow-Up:
Close follow-up is essential to monitor for renal involvement and other complications.
Regular urinalysis and renal function tests.
Monitoring blood pressure.
Prognosis:
A first episode of HSP, in the absence of significant renal disease, usually resolves within 4 weeks → the rash is usually the last symptom to remit
Joint pain usually resolves spontaneously within 72h
Uncomplicated abdominal pain usually resolves spontaneously within 24-48h
In 25-35% of patients, HSP recurs at least once, usually within 4 months of the initial presentation → subsequent episodes are usually milder and shorter in duration
90% of those who develop renal complications do so within 2 months of the onset, and 97% within 6 months
Learning Points: Clinical Practice
Professional skills; Newborn or Child with acute illness
Demonstrate appropriate newborn examination and the 6-week check
Newborn Examination
Attending midwife:
Ask if there are any concerns or problems
Mother:
Check patient notes for relevant details of the maternal medical history, family history, antenatal and obstetric history, and social history
Ask about feeding and whether the baby has passed meconium/urine
Baby:
When the baby is quiet (if needed, use calming techniques like pacifiers (ที่ดูด), sucking a clean finger, or examination after a feed) note:
General posture and movements, weight, vital signs
Skin colour:
Vernix: Normal ‘cheesy’ white substance on skin at birth
Peripheral cyanosis: Normal in the first few days after birth
Post-mature skin: Dry peeling skin, prone to cracking, common in post-mature babies; resolves, but topical emollients are often beneficial
Jaundice: Usually unconjugated; appears after 24 hours, peaks around 3-4 days, resolves by 14 days; due to immaturity of hepatic bilirubin conjugation; poor feeding can also contribute.
Listen to the heart and lungs:
Murmurs: Detected in 1-2% of all newborns, but only about 1/12 will represent congenital heart disease.
If a murmur is heard, evaluate in the context of other clinical findings (cyanosis, signs of heart failure, peripheral pulses).
An innocent heart murmur is likely if:
Murmur is grade 1-2/6, systolic, not harsh, loudest at the left sternal edge.
Remaining cardiovascular examination is normal.
Good evidence exists to support the use of pre and post-ductal saturation readings (right arm = pre, foot = post) as part of the assessment of a pathological murmur.
ECG and 4-limb BP should also be performed.
Echocardiography should be obtained in infants where there is clinical concern.
If the murmur persists in an otherwise well infant, in whom no echocardiography has been performed, then arrange for repeat examination in a few days to weeks and consider referral for cardiac assessment.
Examine the eyes for size, strabismus:
Blocked lacrimal duct: Leads to recurrent sticky eye; responds to regular eye toilet until ducts open; may persist for months, but only consider surgery if >12 months
If purulent, secondary bacterial conjunctivitis is likely.
Take swab for MCS (including swab for chlamydia); treat with antibiotic eye drops.
Subconjunctival haemorrhage: Associated with precipitate deliveries or cord around the neck; harmless and resolves within a few weeks.
Using an ophthalmoscope: Examine the eyes for bilateral red reflexes to exclude cataract or retinoblastoma.
The baby should be completely undressed for examination in head to toe order:
Cranium:
Measure maximum occipital-frontal circumference (normal 33-37cm at term).
Assess skull shape, fontanelle positions, tension, and size (anterior may be up to 4cmx4cm, posterior 1cm).
Skull moulding: Overriding skull bones with palpable ridges are part of moulding and are harmless; resolves within 2-3 days.
Caput succedaneum: Oedema of the presenting scalp; can be particularly large following ventouse delivery (chignon); rapidly resolves.
Cephalhaematoma: Common fluctuant swelling(s) due to subperiosteal bleed(s); most often occur over parietal bones; swelling limited by suture lines; resolves over weeks.
Face:
Assess any dysmorphism, nose, chin size; inspect mouth; visualize and palpate palate for possible clefts
Epstein’s pearls: Self-resolving white inclusion cysts on palate/gums.
Tongue-tie: Shortened tongue frenulum.
Ranula: Self-resolving bluish mouth floor swelling (mucus retention cyst).
Oral candidiasis (thrush): Mucosal white flecks and erythema; treat with oral antifungal, e.g., nystatin suspension 1mL 6-hourly.
Ears:
Assess position, size, shape, and external meatus patency.
Pre-auricular pits, skin tags, or accessory auricles: Usually isolated, but can be associated with hearing loss or other abnormalities.
Test hearing and consider surgical referral for cosmetic reasons.
Neck: Inspect and assess movements; palpate clavicles.
Chest:
Assess shape, symmetry, nipple position, respiratory rate (normal 40-60/min), pattern, and effort.
Palpate precordium and apex beat.
Breast swelling: Almost always due to maternal hormones and may lactate; spontaneously resolves over several weeks; if does not resolve, then endocrinology investigation is warranted.
Abdomen:
Inspect shape and umbilical stump; check for inguinal hernias; palpate for masses, liver (normally palpable up to 2cm below costal margin), spleen (normally palpable up to 1cm), kidneys (normally palpable), bladder.
Umbilical hernia: Protuberant swelling involving the umbilicus; rarely strangulates and almost all spontaneously resolve within 12 months.
Single umbilical artery: Usually isolated and of no significance, but can be associated with several syndromes and intrauterine growth restriction (IUGR).
Genitalia:
Females:
Inspect (note that the clitoris and labia are normally large).
Vaginal mucoid or bloody discharge: Due to maternal oestrogen withdrawal; almost always spontaneously resolves.
Vaginal/hymenal skin tags: Spontaneously shrink.
Males:
Assess size, shape, position of urinary meatus; palpate for descended testes (retractile testes are normal).
Undescended testes: Differentiate from retractile testes (can be ‘persuaded’ into the scrotum); if still undescended at 1 year, refer to a surgeon.
Hydrocele: Common and most resolve by a year; if persists, refer to a surgeon.
Inguinal hernias: Can rarely be present from birth; refer to a surgeon (there is a relatively high likelihood of strangulation/incarceration).
Palpate the femoral pulses: Absence or weakness may indicate aortic arch abnormalities.
Anus: Assess position and patency.
Spine: Inspect for deformity and sacral naevi/dimple/pit/hair patch/lipoma/pigmentation (may indicate underlying abnormality).
Sacral coccygeal pits: Require no action if within natal cleft.
Higher pits: Require spinal imaging.
Limbs:
Assess symmetry, shape, passive and active movements, digit number and shape; assess palmar creases; examine hips for DDH.
Single palmar crease: Found in approximately 2% of normal babies; may be associated with chromosomal abnormalities, e.g., trisomy 21.
Polydactyly: Can be isolated or associated with other abnormalities; refer to a surgeon (pre vs post axial).
Syndactyly: Most common between the second and third toes; often familial; if toes only are affected, requires no treatment.
Postural deformities: Common, especially after oligohydramnios (little amniotic fluid ) or the baby was in an unusual position before birth, like being breech (bottom-first).
Positional talipes is usually equinovarus or calcaneovalgus.
Positional talipes: This is when the baby's foot is turned inward (equinovarus) or outward (calcaneovalgus)
If affected joint can easily be massaged back to normal neutral position, deformity will rapidly resolve.
If fixed (structural), refer to an orthopedic surgeon/physiotherapist.
These children are also at increased risk of DDH.
CNS:
Assess tone during handling, pulling baby to sitting position by holding wrists, and ventral suspension (baby should be able to hold head almost horizontally).
Check Moro reflex (symmetrical?).
Palmar grasp reflex: When an object is placed in the infant’s hand and strokes their palm, the fingers will close, and they will grasp it with a palmar grasp.
Sucking reflex: Causes the child to instinctively suck anything that touches the roof of their mouth.
Rooting reflex: Present at birth and disappears around four months of age, as it gradually comes under voluntary control; a newborn infant will turn its head toward anything that strokes its cheek or mouth to aid breastfeeding.
Stepping reflex: When the soles of their feet touch a flat surface, they will appear to walk by placing one foot in front of the other.
Moro reflex: Support the infant’s upper back with one hand, then drop back once or twice into your other hand.
The legs and head extend while the arms jerk up with the fingers extended.
The arms are then brought together, and the hands clench into fists, and the infant cries.
Asymmetry may be due to hemiparesis, brachial plexus injury, or fractured clavicle.
Check that urine and meconium were passed within the first 24 hours.
6-Week Check
General examination: Height, weight, head circumference; chart.
Explore with parents: How they are coping
Initial observations:
Does this baby have a syndrome (e.g., Trisomy 21)?
Does this baby engage with the examiner’s gaze and face in a socially responsive way?
Are all limbs moving appropriately?
Is the baby pink? Is the baby jaundiced?
Is there evidence of respiratory distress?
Do the baby’s eyes follow the examiner’s face as it moves from side to side?
Do the reflections of the ceiling light remain symmetrical in each eye as the direction of gaze changes?
Is nystagmus present?
The eyes: Abnormal morphology, nystagmus, and strabismus (as above); check the red reflexes (i.e., retinoblastoma, congenital cataracts).
The mouth: Check for cleft palate; a bifid uvula might herald a submucous cleft.
Heart and lungs:
CCF: Check the baby is pink in color (central cyanosis is always an emergency), not in respiratory distress (i.e., no chest recession), and with a normal liver edge
A large ventriculoseptal defect or patent ductus arteriosus may present with congestive cardiac failure at this age.
Feeding can be a useful symptom when considering shortness of breath in relationship to congenital cardiac issues.
Babies with heart issues often have trouble feeding because they get tired easily or have difficulty breathing while eating.
Assess for systolic murmur.
Respiratory causes of increased work of breathing may be congenital (e.g., an emphysematous lobe) or acquired (e.g., chest infection).
Feel for femoral pulses: Which are absent in coarctation of the aorta.
The abdomen:
Exclude organomegaly, looking for congestive cardiac failure, congenital metabolic or storage disease.
It is normal to occasionally feel the tip of the spleen.
A sharp liver edge can be felt in most babies about three or four finger widths below the right costal margin.
Check for descended testes and genital abnormality.
Determine if the hips are stable:
Enquire about the risk factors for developmental hip dysplasia:
Female gender.
Family history of hip dysplasia in a first-degree relative.
Breech position at birth.
Intrauterine Problems (refer to issues or complications that occur within the uterus during pregnancy)
Packaging:
Plagiocephaly: This is when a baby’s head is flattened on one side, often due to lying in one position for too long.
Torticollis: This is a condition where a baby’s neck muscles are tight on one side, causing their head to tilt to one side and making it difficult to turn their head.
Hyperextended knees: This is when a baby’s knees bend backward more than normal. It can happen if the baby was cramped in the womb.
Foot deformities: These are abnormalities in the shape or position of a baby’s feet, such as clubfoot, where the foot is twisted out of shape or position.
Reduction in uterine volume:
Examples include first pregnancy, oligohydramnios, and multiple pregnancy.
Wrapping the baby while the legs are straight.
Hip Dysplasia Tests
Barlow Test:
Detects if a normally positioned head of the femur can be dislocated out of a shallow acetabulum.
With one hand, fix the pelvis while the other holds the infant's leg of the side being examined with the hip in 90° flexion.
With the knee in full flexion, place your fourth and fifth fingers over the head of the greater trochanter.
Apply gentle pressure down toward the couch while feeling if the femoral head drops out over a shallow acetabular edge.
Ortolani Test:
Designed to see if an already dislocated head of the femur can be relocated.
Using your fourth and fifth fingers, gently lift toward the roof while abducting the infant's leg.
Feel for a clunk as a dislocated head of the femur is slipped over the acetabular edge and into the acetabulum.
Procedure:
This process is carried out on both sides and then both hips are gently abducted simultaneously (it is reassuring to find symmetrical abduction).
Examination of the hips should not cause the baby any distress.
If after the examination there is still doubt about dysplasia, an ultrasound of the hips is the investigation of choice (before 6 months, the head of the femur is not calcified and so an x-ray is inappropriate).
Neurological Examination
Social responsiveness: Check that the baby is spontaneously moving all limbs in an age-appropriate way.
The development of one side predominant ‘handedness’ before 18 months is a red flag for neuromuscular compromise on the less active side.
This means that if a child starts to show a strong preference for using one hand over the other before they are 18 months old, it could be a warning sign.
Red flag for neuromuscular compromise: It suggests there might be a problem with the muscles or nerves on the side that is less active.
Typically, children develop a preference for using one hand (handedness) later, around 2-3 years old. Showing a strong preference too early might indicate an underlying issue that needs to be checked by a doctor.
Complete the examination by holding the baby in ventral suspension, permitting inspection of the spine and an assessment of tone (the head should be held in line with the torso at 6 weeks).
If the tone is increased or decreased, cerebral palsy and its differential diagnoses should be considered.
Eliciting the primitive reflexes complicates the issue and adds little to the information already gained.
Demonstrate accurate, problem-oriented, tactful and organised history, plus succinct presentation this information for children with acute illness
Demonstrate appropriate history and examination assessment of a febrile infant, as per a typical presentation to the Emergency Department
History Taking
Parental Concerns and Perception:
Take parental concerns seriously, as they are often accurate in identifying fever.
Assess their perception of the severity of the fever and any changes in their child's behavior.
Presenting Complaint:
Duration of fever: When did it start?
Degree of fever: How high has the temperature been?
Response to antipyretics: Have any fever-reducing medications been given, and if so, how frequently and at what doses?
Associated symptoms:
Poor appetite
Irritability or increased fussiness
Lethargy or decreased activity level
Changes in crying (e.g., high-pitched, weak, or continuous)
Vomiting or diarrhea
Cough, nasal congestion, or runny nose
Difficulty breathing or rapid breathing
Favoring or refusing to use a limb (suggestive of pain or discomfort)
Foul-smelling or strong urine (suggestive of urinary tract infection)
Systems Review:
Upper Respiratory Tract:
Runny nose and congestion (common in viral URTIs)
Ear pain or tugging at ears (otitis media)
Headache (consider sinusitis or meningitis)
Lower Respiratory Tract:
Cough or wheezing (consider pneumonia or bronchiolitis)
Gastrointestinal:
Abdominal pain (gastroenteritis, UTI, or pneumonia)
Diarrhea and vomiting (gastroenteritis or systemic infection)
Genitourinary:
Foul-smelling urine or back pain (suggestive of pyelonephritis or UTI)
Musculoskeletal:
Joint swelling or redness (consider Lyme disease or osteomyelitis)
Neurological:
Irritability or lethargy (could indicate meningitis or encephalitis)
Chronic Illness Symptoms:
Repeated infections (potential immunodeficiency)
Poor weight gain or weight loss (consider TB or malignancy)
Endocrine:
Palpitations, sweating, or heat intolerance (suggestive of hyperthyroidism)
Pattern of Symptoms:
Cyclic or recurrent symptoms (consider inflammatory conditions or hereditary syndromes)
Medical History:
Recent travel history (risk of travel-related infections)
Exposure to sick contacts (assessing contagious illnesses)
Immunization history (especially crucial for infants under 6 months or those with incomplete vaccinations)
Medication history, including prior antibiotic use (which can mask symptoms)
Identify high-risk groups:
Premature infants
Immunocompromised children
Those with chronic illnesses like chronic lung disease or congenital heart disease
Previous invasive bacterial infections
Aboriginal and Torres Strait Islander populations
Examination
General Observations:
Appearance: Well or unwell looking?
Level of alertness and responsiveness
Behavior: Consolability, irritability, or lethargy
Vital Signs:
Temperature: Document fever and look for patterns.
Heart rate: Tachycardia could indicate fever, dehydration, or sepsis.
Respiratory rate: Tachypnea may suggest respiratory distress or sepsis.
Capillary refill time: Prolonged refill may indicate poor perfusion.
Systemic Examination:
Skin:
Look for rashes, petechiae, or purpura (signs of serious bacterial infections like meningococcemia).
Head, Eyes, Ears, Nose, Throat (HEENT):
Inspect for signs of upper respiratory infections, otitis media, or sinusitis.
Respiratory:
Auscultate for crackles, wheezing, or decreased breath sounds
Observe for signs of respiratory distress (retractions, nasal flaring)
Cardiovascular:
Check for murmurs, gallops, or signs of heart failure.
Abdomen:
Palpate for tenderness, distension, or masses.
Genitourinary:
Examine for signs of infection or discomfort.
Musculoskeletal:
Check for joint swelling, redness, or warmth.
Neurological:
Assess tone, reflexes, and level of consciousness.
Red Flags:
Age less than 1 month
Lethargy or decreased level of consciousness
Signs of respiratory distress
Petechiae or purpura (urgent consideration for sepsis or meningitis)
Inconsolability or severe irritability
ABCDE assessment
Describe the approach to management of a febrile infant
Initial Assessment and Stabilization
Emergency Care:
In hypoxic children or those in shock, follow emergency guidelines:
Provide oxygen if required.
Initiate fluid resuscitation for shock.
Monitor vital signs continuously.
Investigations Based on Age and Clinical Presentation
Under 28 Days:
Investigations:
Blood Tests: Full Blood Count (FBC), C-Reactive Protein (CRP), Blood Cultures.
Imaging: Chest X-ray (CXR) if respiratory symptoms are present.
Other:
Urine Microscopy, Culture, and Sensitivity (MCS) via suprapubic aspirate (SPA).
Lumbar Puncture (LP) to rule out meningitis.
Management:
Start empirical antibiotics immediately.
Common antibiotics: third-generation cephalosporins (e.g., cefotaxime or ceftriaxone) and ampicillin to cover Listeria.
29 Days to 3 Months:
If the infant shows unwell features or signs of septic shock:
Investigations:
Blood Sugar Level (BSL), Urine MCS, FBC, CRP, Lactate, Blood Cultures, CXR, LP.
Management:
Admit to the hospital.
Administer empirical antibiotics: flucloxacillin + ceftriaxone (or gentamicin if meningitis is excluded).
If the infant does not show unwell features:
Investigations:
Urine MCS (via SPA or catheter), FBC, CRP, Blood Cultures.
Management:
Treat the underlying cause if identified.
If no cause is identified, discharge with close follow-up in 12-24 hours.
Over 3 Months:
If the infant shows unwell features or signs of septic shock:
Investigations:
BSL, Urine MCS, FBC, CRP, Lactate, Blood Cultures, CXR, LP.
Management:
Admit to the hospital.
Consider empirical antibiotics: flucloxacillin + ceftriaxone (or gentamicin if meningitis is excluded).
If the infant does not show unwell features:
If fever is less than 24 hours: Consider no investigations.
If there is a history of previous UTI or the infant is under 12 months and fever persists for more than 24 hours: Consider urine MCS.
If fever persists for more than 48 hours: Consider urine MCS.
General Investigations for Febrile Infants with No Apparent Source of Infection
Blood Tests:
FBC, CRP, Urea, Electrolytes, and Creatinine (UEC), Blood Cultures.
Urine Tests:
Urine MCS to rule out UTI.
Lumbar Puncture:
Consider if clinical assessment indicates and no contraindications exist.
Chest X-ray:
Consider if high white cell count (WCC) or respiratory symptoms are present.
Management Strategies
Antibiotics:
Immediate Treatment:
Administer maximum dose third-generation cephalosporins (cefotaxime or ceftriaxone) for febrile infants with:
Signs of shock or coma.
Signs of meningococcal disease.
Specific Scenarios:
Consider high-dose IV acyclovir if herpes simplex encephalitis or disseminated neonatal disease is suspected.
Consider IV corticosteroids if bacterial meningitis is confirmed (not in infants younger than 3 months).
Adjust antibiotics based on suspected pathogens (e.g., Neisseria meningitidis, Streptococcus pneumoniae, Escherichia coli, Staphylococcus aureus, Haemophilus influenzae type b).
Add antibiotics against Listeria (e.g., ampicillin) for infants under 3 months.
Use parenteral antibiotics for infants with a decreased level of consciousness.
Follow local guidelines for antibiotic resistance.
Antipyretics:
Do not use tepid sponging.
Avoid over- or underdressing the child
Use paracetamol or ibuprofen only if the child is distressed due to fever:
Paracetamol: 15 mg/kg per dose, up to 4 times a day (maximum 4 doses in 24 hours)
Ibuprofen (not recommended for children under 6 months): 10 mg/kg per dose, up to 4 times a day (maximum 4 doses in 24 hours)
Temperature Measurement
Under 3 months: Measure axillary temperature.
Over 3 months: Measure tympanic temperature.
Describe the assessment and management of children with suspected meningitis including
Overall
Assessment
History and Examination:
Common Symptoms:
Fever
Severe headache
Neck stiffness
Photophobia
Altered mental status
Vomiting
Seizures
Infant-Specific Symptoms:
Irritability
Lethargy
Drowsiness
Poor feeding
Vomiting
Rash (e.g., meningococcal purpura)
Seizures
Neck stiffness and pain; bulging fontanelle
Recent overseas travel
Classical Triad:
Fever, photophobia, and neck stiffness are present in less than 50% of cases in older children and adolescents, making a lumbar puncture crucial for definitive diagnosis.
Investigations:
Culture: Blood, urine, infected sites, and cerebrospinal fluid (CSF) for bacteria and viruses.
Acute-Phase Reactants: Such as CRP and ESR.
Rapid Bacterial Antigen/Polymerase Chain Reaction (PCR) Tests: For organisms.
Lumbar Puncture
Procedure:
Patient Counselling: Explain the procedure and its purpose to the patient and guardians.
Positioning:
Lateral Recumbent Position: Commonly used, with knees tucked to the chest to increase interspinous distance.
Sitting Position: Consider if there is potential for respiratory compromise due to neck hyperflexion, though it does not allow accurate manometry.
Preparation:
Identify and mark the interspace (L3-L4 or L4-L5); use ultrasound guidance if available
Ensure a sterile environment and technique
Provide analgesia or sedation as needed
Continuous cardiorespiratory monitoring and pulse oximetry are recommended for young infants
Procedure Steps:
Position and advance the spinal needle midline through the spinous ligaments
For lateral recumbent position, aim for 45 degrees from perpendicular in infants under 12 months and 30 degrees for older children.
Remove the stylet, and once CSF returns, attach a manometer to measure opening pressure.
Collect CSF samples in sterile tubes for analysis.
Interpretation of Results:
Normal CSF:
Clear appearance
White Blood Cell (WBC) count: 0-5 cells/µL
Protein: 15-45 mg/dL
Glucose: 40-80 mg/dL (or two-thirds of blood glucose level)
Bacterial Meningitis:
Cloudy appearance
WBC count: Elevated (often >1000 cells/µL, predominantly neutrophils)
Protein: Elevated (usually >100 mg/dL)
Glucose: Low (often <40 mg/dL)
Positive Gram stain and culture
Viral Meningitis:
Clear or slightly cloudy appearance
WBC count: Elevated (10-200 cells/µL, predominantly lymphocytes)
Protein: Mildly elevated (50-100 mg/dL)
Glucose: Normal
Other Indicators:
Positive PCR for specific viruses or bacteria.
Complications:
Common:
Failure to obtain a specimen or traumatic bloody tap.
Less Common:
Post-dural puncture headache (5-15%).
Transient or persistent paraesthesia or numbness.
Rare:
Respiratory arrest from positioning.
Infection introduced by the needle causing meningitis, epidural abscess, or osteomyelitis.
Spinal haematoma, especially in patients with uncorrected bleeding disorders.
Brain herniation in patients with increased intracranial pressure (ICP).
Epidermoid tumor (extremely rare).
Contraindications:
Absolute:
Increased ICP
Glasgow Coma Scale (GCS) < 8 or deteriorating/fluctuating level of consciousness
Relative:
Septic shock or haemodynamic compromise
Significant respiratory compromise
New focal neurological signs or seizures
Seizures within the previous 30 minutes or normal consciousness not returned from seizure
Coagulopathy (INR > 1.5 or platelets < 50,000) or patient on anticoagulant medication
Management
Antibiotics:
Early Administration:
Start empirical antibiotics and dexamethasone as soon as possible, ideally within 60 minutes of presentation.
Neonates (Early-Onset Sepsis within 72 hours of birth):
Cefotaxime: 50 mg/kg IV every 8 hours
Benzylpenicillin: 90 mg/kg IV every 8 hours
Neonates (Late-Onset Sepsis more than 72 hours after birth):
Cefotaxime: 50 mg/kg IV
Amoxicillin: 100 mg/kg IV (timing based on age)
Infants (1 month to under 2 months):
Ceftriaxone: 50 mg/kg IV every 12 hours
Amoxicillin: 50 mg/kg IV every 6 hours
Children (2 months or older):
Ceftriaxone: 50 mg/kg (up to 2g) IV every 12 hours
Dexamethasone: 0.15 mg/kg (up to 10 mg) IV every 6 hours for 4 days
Corticosteroids:
Indication:
Consider in all suspected bacterial meningitis cases over three months of age.
Administration:
Ideally before or immediately following the first antibiotic dose.
Dexamethasone: 10 mg (child: 0.15 mg/kg up to 10 mg) IV, then every 6 hours for 4 days.
Not indicated for neonates and only for specific viral pathogens.
Fluid Therapy:
Initial Resuscitation:
Sodium chloride 0.9% administered in 20 mL/kg bolus. Repeat as clinically indicated.
SIADH Management:
For those with signs of Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH), moderate fluid restriction is advised.
Isotonic Fluids:
Administer isotonic fluids for those without signs of SIADH.
Complications and Sequelae
SIADH:
Mechanism:
Unclear, but bacterial meningitis can cause increased ADH secretion, contributing to hyponatremia and cerebral edema.
Cerebral Edema:
Mechanisms:
Vasogenic Edema: Increased permeability of the blood-brain barrier.
Cytotoxic Edema: Factors from neutrophils, microglia, and astrocytes can produce edema.
Obstructive Edema: Inflammation can impede normal absorption of CSF from the subarachnoid space via the arachnoid villi
Hearing Loss:
Type: Sensorineural hearing loss (transient or permanent).
Cause: Damage to the eighth cranial nerve, cochlea, or labyrinth from bacterial invasion or inflammatory response.
Contact Tracing:
Notification:
Probable and confirmed cases of invasive meningococcal disease are notifiable.
Period of Interest:
From 7 days prior to symptom onset until 24 hours of appropriate antibiotic treatment completion.
Public Health Actions:
Immediate commencement upon notification.
Other Complications:
Seizures
Circulatory shock
Cerebrovascular complications
Motor deficits
Subdural effusion
Intellectual disability
Behavioral problems
Lumbar puncture (Procedure, Interpretation of results, Complications, Contraindications)
Procedure
Equipment Needed:
Sterile gloves and surgical mask
Lumbar puncture kit including:
Manometer
Dressing pack
Aperture drape
3-way tap
2mL syringe
25G needle
22G spinal needle with stylet
CSF tubes
Adhesive dressing
Appropriate size lumbar puncture needle:
25Gx25mm for neonates/newborns
Needle length correlated with height of the child (~0.03xheight in cm)
Needle Size and Child’s Height/Age:
2cm: <50cm (Pre-term neonates)
3cm: 50-80cm (<2 years old)
4cm: 80-120cm (2-5 years old)
5cm: 120-150cm (5-12 years old)
6cm: 150-180cm (>12 years old)
Injectable local anaesthetic: Lignocaine 1% [50mg/5mL], max dose 4.5mg/kg/dose
Alcoholic chlorhexidine 0.5% in 70% alcohol (or aqueous chlorhexidine for neonates)
Topical anaesthetic cream (e.g., LMX 4 or Emla, applied at least 30 minutes prior)
Clear occlusive dressing
Sedation/analgesia as determined by Medical Officer
Patient Preparation:
Apply topical anaesthetic cream to the LP region between the 3rd and 5th lumbar vertebrae half an hour prior to the procedure if time permits.
Assistant washes hands for one minute and prepares trolley and equipment.
Medical officer wears surgical mask, washes hands for three minutes, and wears gloves in approved manner.
Assistant removes the occlusive dressing and wipes away the residual topical anaesthetic cream.
Medical officer prepares the skin at the site with alcoholic chlorhexidine 0.5%.
Positioning the Patient:
Infants:
Avoid over flexing the neck to prevent respiratory compromise.
Avoid pushing down on the back of the head to prevent the baby from arching backwards.
Minimize the risk of trauma to the site or spine if the baby moves during the procedure.
Children:
Position in the lateral recumbent position with hips and knees flexed towards the chin and head flexed towards the knees.
Gentle assistance is required to restrain the child’s arms.
Performing the Procedure:
Local Anaesthetic Injection:
Ensure the correct dosage is administered to the skin at the site.
Remove antiseptic solution from set-up before preparing medication for injection into the spine.
Needle Insertion:
Identify the correct site at L3-L4 or L4-L5.
Ensure the child is correctly positioned and local anaesthetic has taken effect.
Select appropriate lumbar puncture needle size.
Grasp spinal needle with bevel facing upwards; ensure patient’s back is perpendicular to the bed.
Insert the needle slowly through the skin into the subarachnoid space, aiming towards the umbilicus.
Leave the stylet in situ while traversing epidermis and subcutaneous fat.
For infants, gently remove the stylet before it passes through the dura; for older children, continue advancing the needle until decreased resistance or half its length is reached.
Remove the stylet gently; the presence of CSF indicates correct placement.
Measuring CSF Pressure:
Measure CSF pressure with the manometer.
Temporarily relax the flexed position by extending the child’s legs to accurately measure CSF pressure.
Ensure the distal end of the manometer is open to the atmosphere.
Note that nitrous oxide administration can increase intracranial pressure.
CSF Collection:
Hold the collection tube(s) under the needle until sufficient CSF is collected (0.5-1.0mL).
Collect a paired blood glucose level if needed.
Label the specimen, place it in a biohazard bag, and send it to pathology immediately.
Reintroduce the stylet before withdrawing the needle to minimize post-LP headache.
Withdraw the needle quickly and apply pressure to the site for at least one minute, then apply an adhesive dressing.
Discontinue nitrous oxide if used.
Remove the drape and dispose of equipment appropriately.
Document the procedure in the patient’s health care record, noting any equipment problems or incidents.
Post-Procedure Care
No bed rest required post-procedure; the child may mobilize as desired.
Post-LP Headache:
Manage with mild analgesia and rest as indicated by the degree of discomfort.
If the headache becomes severe or persists, seek medical review.
CSF Leakage:
Manage by lying the child down and applying pressure to the site with a sterile piece of gauze.
If leakage persists, seek medical review.
Infection:
Monitor for signs of infection, such as fever or the child becoming unwell.
Seek medical review if infection is suspected.
Site Tenderness or Nerve Root Irritation:
Manage with mild analgesia and rest as needed.
Troubleshooting
Encountering Bone:
If there is firm resistance to needle advancement, bone may have been encountered.
Review landmarks and consider partially withdrawing the needle and re-advancing in a more cranial or caudal direction.
Ensure the needle is inserted in the midline perpendicular to the plane of the back.
Poor CSF Flow:
Gently rotate the lumbar puncture needle to improve CSF flow.
Traumatic/Bloody Tap:
If blood is obtained (not blood-stained CSF), withdraw the needle and prepare for another attempt with a new needle.
Blood-stained CSF is still useful for culture/PCR.
Consider a subarachnoid haemorrhage if clinically appropriate.
Confirm with the presence of xanthochromia after CSF centrifugation.
Means to verify a diagnosis by checking for a yellowish discoloration in the cerebrospinal fluid (CSF) after it has been spun in a centrifuge. This yellow color indicates the presence of old blood, often confirming conditions like a subarachnoid hemorrhage.
Interpretation of Results
CSF Analysis:
Cell Count and Differential:
Elevated white blood cells indicate infection.
Neutrophils predominate in bacterial meningitis.
Lymphocytes predominate in viral meningitis, but bacterial meningitis cannot be excluded.
Glucose Level:
Low CSF glucose relative to blood glucose suggests bacterial infection.
Protein Level:
Elevated protein levels can indicate bacterial or viral meningitis.
Gram Stain and Culture:
Identifies specific pathogens causing the infection.
PCR Tests:
Detect specific pathogens like Neisseria meningitidis, Streptococcus pneumoniae, herpes simplex virus, enterovirus, and parechovirus.
Additional Notes:
Gram stain may be negative in up to 60% of bacterial meningitis cases, even without prior antibiotics.
A predominance of lymphocytes does not exclude bacterial meningitis.
Neutrophils may predominate in viral meningitis, even after the first 24 hours.
If the CSF is abnormal, the safest course is to treat for bacterial meningitis.
Complications
Common:
Failure to obtain a specimen
Need to repeat LP
Traumatic tap (presence of blood in CSF)
Post-dural puncture headache (up to 5-15%)
Uncommon to Rare:
Transient or persistent paraesthesiae or numbness
Respiratory arrest from local anaesthetic toxicity
Spinal haematoma or abscess
Tonsillar herniation (extremely rare in the absence of contraindications)
Contraindications
Absolute:
Unstable patient or reduced level of consciousness
Skin infection at the LP site
Suspicion of space-occupying lesion or raised intracranial pressure (ICP)
Coagulopathy or thrombocytopenia
Relative (delay LP if present):
Coma (absent or non-purposeful response to painful stimulus)
Signs of raised ICP (e.g., drowsiness, diplopia, abnormal pupillary responses, motor posturing, or papilloedema)
Cardiovascular or respiratory compromise
Focal neurological signs or recent seizures
The febrile child with purpura where meningococcal infection is suspected
Management (Antibiotics, Corticosteroids, Fluid therapy)
Antibiotics and Corticosteroids
Neonates and Children <2 Months
Common Pathogens:
Streptococcus agalactiae (group B streptococcus)
Enteric Gram-negative bacilli
Listeria monocytogenes (rare, generally in children up to 1 month old)
Treatment:
Treat as for sepsis or septic shock using regimens for infants where meningitis has not been excluded.
For Neonates:
Empirical therapy choice depends on the time since birth and whether the infant has been in the community.
For Infants Aged 1 to 2 Months:
Treat as for community-acquired sepsis or septic shock using empirical regimens for infants 1 month to younger than 2 months.
Complications:
Ventriculitis or abscess formation during therapy is not infrequent.
Corticosteroids:
Dexamethasone is not indicated in neonates (up to 1 month of age) due to insufficient evidence supporting its use.
Adults and Children ≥2 Months
Antibiotic Regimens:
Ceftriaxone 2g (child: 50mg/kg up to 2g) IV, 12-hourly
OR Cefotaxime 2g (child: 50mg/kg up to 2g) IV, 6-hourly
Corticosteroids:
Dexamethasone 10mg (child: 0.15mg/kg up to 10mg) IV, preferably starting before or with the first dose of antibiotic, then 6-hourly for 4 days.
Fluid Therapy
Hyponatraemia
Occurs in about one-third of children with meningitis
Causes:
Increased ADH secretion
Increased urine sodium losses
Excessive electrolyte-free water intake or administration
Monitoring and Management:
Careful and regular monitoring of clinical signs of hydration state, including:
Signs of overhydration
Serum sodium levels
Laboratory markers of hypovolaemia
Under most circumstances, IV fluids given to a child with meningitis should be isonatraemic (e.g., 0.9% sodium chloride (normal saline) with additional glucose).
Hyponatraemic solutions (e.g., 4% dextrose and one-fifth normal saline), which deliver excess free water, may worsen hyponatraemia and increase the risk of cerebral oedema, and should be avoided.
Immediate Resuscitation (if required):
Clinical signs of shock or hypovolaemia:
Hypotension
Poor peripheral perfusion
Cool pale extremities
Tachycardia with low volume pulses
High blood lactate or large base deficit
Children with more than one of these signs should be given 10-20mL/kg of normal saline as a bolus.
Dehydration Status and Management:
Mild (0-5%) Dehydration:
Weight loss: 5% in infants and 3% in children
Skin turgor: May be decreased
Mucous membranes: Dry
Urine output: May be low
Heart rate: Increased
Blood pressure: Normal
Perfusion: Normal
Skin color: Pale
Consciousness: Irritable
Moderate (5-10%) Dehydration:
Weight loss: 10% in infants and 6% in children
Skin turgor: Decreased
Mucous membranes: Very dry
Urine output: Oliguric
Heart rate: Increased
Blood pressure: May be normal
Perfusion: Prolonged capillary refill time (CRT)
Skin color: Grey
Consciousness: Lethargic
Severe (10-15%) Dehydration:
Weight loss: 15% in infants and 9% in children
Skin turgor: Poor with tenting
Mucous membranes: Parched
Urine output: Anuric
Heart rate: Increased
Blood pressure: Decreased
Perfusion: Prolonged CRT
Skin color: Mottled; blue or white
Consciousness: Comatose
Fluid Management for Severely Ill Children:
Ensure normal blood pressure and adequate circulating volume.
Clinical signs of hydration, including weight, serum sodium, acid-base status, and neurological state, should be assessed every 6-12 hours for the first 48 hours.
Adjust total fluid intake accordingly based on assessments.
Complications and sequelae (SIADH, Cerebral oedema, Hearing loss, Contact tracing)
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
Mechanism:
The exact mechanism is not fully understood.
It is widely accepted that meningitis (especially bacterial) leads to increased secretion of antidiuretic hormone (ADH), which contributes to hyponatraemia and cerebral oedema.
Cerebral Oedema
Pathophysiology:
An increase in the intercellular fluid volume of the brain leads to a rise in intracranial pressure (ICP).
Vasogenic Cerebral Oedema: Results from increased permeability of the blood-brain barrier (BBB), especially in the choroid plexus endothelium and the cerebral microvasculature endothelium.
Cytotoxic Factors: Released from neutrophils and bacteria, which can directly produce cerebral oedema.
Impaired CSF Absorption: Inflammation from infection can impede normal absorption of cerebrospinal fluid (CSF) from the subarachnoid space via the arachnoid villi.
Cerebral Perfusion Pressure: Normally maintained by an autoregulatory mechanism but becomes dependent on peripheral blood pressure during meningitis as autoregulation is impaired.
Increased ICP: Cerebral oedema itself can increase ICP and secondarily reduce cerebral blood flow.
Management:
Contraindication for Lumbar Puncture: Avoid LP in patients with suspected elevated ICP.
Supportive Care:
Intubate and ventilate patients to maintain adequate oxygenation and normocarbia.
Position patients with heads elevated at 30° and in a midline position.
Reduce stimuli by sedation and minimal handling.
Pharmacologic Interventions:
Mannitol, furosemide, dexamethasone, and short periods of hyperventilation may be indicated for the acute treatment of severely elevated ICP.
Hearing Loss
Types and Incidence:
Sensorineural Hearing Loss:
Occurs in 25-35% of patients after pneumococcal meningitis.
Occurs in 5-10% of patients after Haemophilus influenzae type b meningitis.
Hearing loss may be subtle or inapparent during the early phases of infection.
Transient or Permanent Hearing Loss:
Transient hearing loss is usually secondary to a conductive disturbance.
Permanent hearing loss can result from damage to CNVIII, the cochlea, or the labyrinth induced by direct bacterial invasion and/or the inflammatory response elicited by the infection.
Screening and Management:
Hearing should be tested in all children who have had bacterial meningitis before discharge from the hospital or within 4 weeks of discharge.
For severe to profound hearing loss, a cochlear implant may be necessary and should be placed as soon as the child has recovered from the acute stage of meningitis.
Contact Tracing
Definition of Contacts:
Household or Household-like Contacts:
Individuals who lived in the same house or dormitory-type room or had an equivalent degree of contact with the case in the 7 days prior to the onset of symptoms until the case has completed 24 hours of appropriate antibiotic treatment.
Intimate Kissing and Sexual Contacts:
In the 7 days prior to the onset of symptoms until the case has completed 24 hours of appropriate antibiotic treatment.
Child-care Contacts:
Higher-risk contact includes children and staff in childcare who had an equivalent degree of contact with the case as a household contact.
As a guide, two full days (6-8 hours each) of attendance in the same care group or a cumulative of around 20 hours in the same care group in the 7 days prior to the onset of symptoms should be considered higher-risk contact.
Other childcare contact is considered lower-risk. Child-care settings include kindergartens and pre-schools.
Passengers:
Seated immediately adjacent to the case during long-distance travel (>8 hours) by aeroplane, train, bus, or other vehicle.
Healthcare Workers:
Those who had unprotected close exposure of their airway to large particle respiratory droplets of a case during airway management (e.g., suctioning, intubation) or mouth-to-mouth resuscitation up until the case has had 24 hours of appropriate antibiotic treatment.
Actions:
Probable and confirmed cases of invasive meningococcal disease are notifiable.
Public health action should commence immediately.
The period of interest is from 7 days prior to the onset of symptoms in the case to the time the case has completed 24 hours of appropriate antibiotic treatment.
Other Complications and Sequelae
Shock: Can occur due to severe infection leading to systemic inflammatory response and hemodynamic instability.
Raised Intracranial Pressure (ICP): Due to cerebral oedema or other complications.
Seizures: Resulting from inflammation, high fever, or electrolyte imbalances.
Hydrocephalus: Can develop due to impaired CSF flow or absorption.
Cognitive, Academic, and Behavioral Problems: Long-term sequelae can include difficulties with cognitive function, academic performance, and behavior.
Subdural Effusion: Accumulation of fluid in the subdural space, which may require surgical intervention.
Acute Life Support
Apply knowledge of pathology of shock to explain the management principles of shock in children
Pathophysiology of Shock
Shock is characterized by decreased tissue oxygenation and blood pressure, often resulting from systemic inflammation triggered by infectious agents.
This systemic response can lead to multiple organ dysfunction due to inadequate tissue perfusion and oxygenation.
Key Pathophysiological Points:
Inflammatory Response:
White blood cells (WBCs) encounter pathogens, leading to the recruitment of other WBCs and the release of nitric oxide (NO), causing vasodilation and increased vascular permeability.
Systemic vasodilation leads to a drop in systemic vascular resistance (SVR), causing hypotension and decreased tissue perfusion.
Cardiovascular Implications:
Blood Pressure (BP) Determinants:
Cardiac Output (CO) and Systemic Vascular Resistance (SVR):
BP = CO×SVR
CO = HR×SV (HR = Heart Rate, SV = Stroke Volume)
Stroke Volume Factors:
Preload: Volume of blood in the ventricles at the end of diastole.
Myocardial Contractility: The strength of heart muscle contractions.
Afterload: Resistance the heart must overcome to eject blood.
Decreased SVR leads to a drop in BP and tissue perfusion.
Fluid buildup in tissues decreases oxygen delivery to cells, causing cellular hypoxia.
Cellular and Systemic Effects:
Cellular Hypoxia: Leads to cell membrane ion pump dysfunction, intracellular edema, leakage of intracellular contents, and inadequate pH regulation.
Systemic Acidosis and Endothelial Dysfunction: Progression of cellular hypoxia results in systemic acidosis and endothelial damage, further exacerbating the inflammatory response.
Disseminated Intravascular Coagulation (DIC):
Blood vessel damage activates coagulation factors, leading to clot formation and consumption of these factors. This results in bleeding and clot formation within the bloodstream.
Acute Respiratory Distress Syndrome (ARDS):
Damaged blood vessels in the lungs impair oxygen absorption, causing respiratory distress.
Clinical Signs:
Compensatory Mechanisms: Initially, cardiac output (CO) increases to compensate for decreased SVR. As shock progresses, cardiac function may become impaired, further decreasing BP
Skin Changes: Initially, warm skin due to vasodilation. As shock progresses and the sympathetic nervous system attempts to maintain BP by vasoconstriction, skin may become cool.
Symptoms: Respiratory distress, altered mental status, decreased urine output.
Management Principles
Resuscitation and Stabilization (First Hour):
Primary Goals:
Restore or maintain airway, oxygenation, and ventilation.
Ensure adequate circulation.
Maintain threshold heart rate for adequate cardiac output.
Initial Actions:
Obtain Vascular Access: IV or intraosseous (IO) access within 5 minutes
Fluid Resuscitation: Administer appropriate fluids within 30 minutes
Antibiotics: Begin broad-spectrum antibiotics within 60 minutes
Inotropic Support: For fluid-refractory shock, initiate peripheral or central inotropic infusion within 60 minutes
Ongoing Management:
Infection Control:
Identify the optimal antimicrobial therapy based on culture results.
Ensure the source of infection is controlled.
Respiratory Support:
Monitor respiratory status and provide optimal support.
Perfusion Monitoring:
Assess capillary refill time, heart rate, pulses, urine output, and mental status.
Monitor blood pressure and other indicators of tissue perfusion.
Correcting Derangements:
Address electrolyte and metabolic abnormalities, such as hypoglycemia, hypocalcemia, and elevated lactate levels.
Additional Considerations:
Fluid Management:
Use isotonic fluids (e.g., 0.9% sodium chloride) to manage fluid status and avoid hyponatremia.
Carefully monitor for signs of fluid overload and adjust fluid therapy accordingly.
Pharmacologic Interventions:
Use vasoactive medications to support blood pressure and cardiac function as needed.
Consider agents like mannitol, furosemide, dexamethasone, and short periods of hyperventilation for managing elevated ICP
Describe the sepsis pathway in the paediatric clinical practice guidelines and identify Red flags for sepsis
Overview
Sepsis is a medical emergency: Early recognition and treatment are critical for survival.
High-risk groups: Include very young children and children of Aboriginal, Torres Strait Islander, Pacific Islander, and Maori origin.
Diagnosis: Based on clinical judgement supported by laboratory findings.
Management: Includes rapid fluid resuscitation, early consideration of inotropes, and administration of appropriate antibiotics ideally within 15 minutes of presentation.
Critical care involvement: Early involvement of paediatric critical care is essential.
Sepsis Presentation by Age
Infants and Neonates: Often present with non-specific symptoms such as feeding difficulties and/or apnoea.
Older Children: May present with a focus of infection and/or features like fever or hypothermia, vomiting, inappropriate tachycardia, altered mental state, and reduced peripheral perfusion.
Vital Signs Trends: Deviations from pre-existing trends in vital signs can be a red flag.
General Toxic Features
Altered mental state
Tachypnoea: Increased work of breathing, grunting, weak cry
Marked/persistent tachycardia
Moderate to severe dehydration
Red Flags for Sepsis
Mottled, blue, or pale skin
Very lethargic or difficult to wake
Abnormally cold to touch
Fast breathing
Non-blanching rash
Fits or convulsions
Yellow Flags for Sepsis
Babies <3 months with temperature >38°C
Children 3-6 months with temperature >39°C
High temperature for >5 days
Temperature <36°C checked 3 times in 10 minutes
Difficulty breathing:
Grunting noises with each breath
Unable to say more than a few words at once (abnormal for them)
Breathing pauses
Dehydration:
Not drunk for >8 hours while awake
No urination in 12 hours
Sunken eyes
<1 month old with no interest in feeding
Green, bloody, or black vomitus
Lack of interest in surroundings
Not responding, floppy, or irritable
Bulging fontanelle
Weak, whining, or continuous crying
Confusion or stiff neck (older children)
Management Principles
First Hour of Resuscitation Goals:
Restore or maintain airway, oxygenation, and ventilation.
Ensure adequate circulation.
Maintain threshold heart rate (neither too low nor too high to ensure adequate cardiac output).
Initial Actions:
Obtain vascular access (IV or IO) within 5 minutes.
Start appropriate fluid resuscitation within 30 minutes.
Begin broad-spectrum antibiotics within 60 minutes.
Initiate peripheral or central inotropic infusion within 60 minutes for fluid-refractory shock.
Ongoing Management:
Manage infection with optimal antimicrobial therapy based on culture results and ensure the source of infection is controlled.
Monitor respiratory status and provide optimal support.
Monitor tissue perfusion (capillary refill time, heart rate, pulses, urine output, and mental status) and blood pressure.
Correct electrolyte and metabolic derangements (e.g., hypoglycaemia, hypocalcaemia, and elevated lactate levels).
Describe the immediate management of septic shock
First 5 Minutes: Immediate Actions
Call for Senior Help:
Immediate involvement of senior clinical staff for expert guidance and support.
Attach Cardiorespiratory Monitoring:
Continuous monitoring of heart rate, respiratory rate, blood pressure, oxygen saturation, and temperature.
Address Airway and Breathing Compromise:
Positioning:
In shock, elevate the legs to improve venous return (elevate the head in congestive heart failure).
Non-invasive Ventilation:
For patients with normal conscious state, consider High-Flow Nasal Cannula (HFNC), Continuous Positive Airway Pressure (CPAP), or Bilevel Positive Airway Pressure (BiPAP).
Intubation:
For patients with altered conscious state, consider intubation and involve local ICU and anaesthetic services.
Note the high risk of cardiac arrest with the use of induction agents in children with septic shock.
Administer Oxygen:
Provide supplemental oxygen, FiO2 100%. Intubate if required.
First 15 Minutes: Establish Vascular Access
Insert IO Cannula:
If IV access is not promptly established, insert an intraosseous (IO) cannula.
Take Bloods:
Priority Labs:
Blood culture
Venous blood gas (VBG) with lactate and glucose
Measure blood lactate concentration. If initial lactate concentration is >2mmol/L, measure again within 2-4 hours.
Additional Labs:
Full blood count (FBC)
C-reactive protein (CRP)
Urea, electrolytes, and creatinine (UEC)
Liver function tests (LFTs)
Coagulation profile
Group and hold (G&H)
Urinalysis and Lumbar Puncture (LP):
Consider once the child is stabilized.
Administer Antibiotics:
Administer via IV push; consider intramuscular (IM) if delays in IV/IO access.
First 30 Minutes: IV Fluid Administration with NaCl 0.9%
Fluid Resuscitation:
Begin rapid administration of IV fluids to manage hypotension or blood lactate concentration >2mmol/L.
Bolus:
20mL/kg (10mL/kg in neonates) bolus as a push, then reassess.
If needed, give an additional bolus (10mL/kg) and repeat as necessary to a maximum total volume of 40mL/kg.
Children requiring 40mL/kg of fluid resuscitation should be managed in a critical care environment.
Repeated Assessment:
Monitor fluid status, perfusion (heart rate, capillary refill time, urine output), clinical condition, and signs of fluid overload.
Stop Resuscitation:
When clinical improvement is achieved.
If clinical signs of improvement fail to appear.
If there are signs of volume overload (hepatosplenomegaly, JVP distension, gallop rhythm, wheeze, and crackles)
Manage Volume Overload:
Diuresis may be required.
Expected urine volume: 1mL/kg/hr.
Use furosemide 0.5-1mg/kg IV or mannitol 0.5-1g/kg IV for oliguria or anuria.
First 60 Minutes: Inotropes/Vasopressors
Inotropes and Vasopressors:
Inotropes: Agents that alter myocardial contractility (e.g., dobutamine, dopamine, milrinone).
Vasopressors: Sympathomimetic drugs that mimic the effects of the sympathetic nervous system (e.g., adrenaline, noradrenaline, vasopressin).
Administration:
If hypotensive during or after fluid resuscitation, administer a vasopressor to maintain a mean arterial pressure of at least 65mmHg.
For persisting circulatory failure after 40mL/kg fluid resuscitation, administer adrenaline 0.05-0.2μg/kg/min via peripheral access (IV or IO) while awaiting transfer to PICU.
Push Dose Inotropes:
Can be used by experienced clinicians:
Dopamine: 1-20μg/kg/min (start at 5μg/kg/min).
Dobutamine: 2-20μg/kg/min (start at 5μg/kg/min), can use peripheral IV.
Summary of Immediate Management Steps
Early Recognition and Seeking Senior Help:
Any red zone observation indicates severe sepsis or septic shock until proven otherwise.
Obtain senior clinical review within 30 minutes for suspected sepsis.
ABCDE Primary Survey:
A (Airway): Assess and maintain a patent airway.
B (Breathing): Assess and provide supplemental oxygen if required.
C (Circulation): Establish IV access, obtain blood samples, and monitor blood glucose levels.
D (Disability): Assess the level of consciousness.
E (Exposure): Obtain history and re-examine the patient for the source of sepsis.
F (Fluids): Monitor fluid input and output; consider insertion of an indwelling catheter (IDC).
Empiric Antibiotic Therapy:
Neonates: Benzylpenicillin + cefotaxime (or gentamicin if meningitis is excluded).
1-2 Months: Amoxicillin + cefotaxime/ceftriaxone (or gentamicin if meningitis is excluded).
2 Months: Gentamicin + cefotaxime/ceftriaxone + vancomycin.
Fluid Resuscitation:
Initial 20mL/kg 0.9% sodium chloride bolus.
Repeat as necessary if no improvement.
Early Initiation of Inotropes:
For persistent circulatory failure after 40mL/kg fluid resuscitation, use vasopressors such as adrenaline 0.05-0.2μg/kg/min.
Frequent Reassessment:
Monitor observations every 30 minutes for 2 hours, then hourly for 4 hours.
Watch for signs of deterioration and escalate care if needed:
Tachypnoea
Persistent tachycardia, slow capillary refill, and hypotension
Pale color and mottling
Drowsiness or decreased level of consciousness
Urine output <1mL/kg/hour
Acidosis, increasing serum lactate, or procalcitonin
Hypoglycaemia, leukopenia, or abnormal coagulation
Source Control:
Investigate and treat the underlying cause of sepsis.
Demonstrate the critical steps of acute life support in neonate, infant and child
Demonstrations/Technique:
A: Establish an Airway
Provide Oxygen:
Use fractional inspired oxygen (FiO2) 100%; use the optimum method for patient size and monitor.
Neonates, Infants: Head-box oxygen with in-situ FiO2 monitor
Infants, Toddlers: Nasal cannulae (NC). The ideal estimate of FiO2 from tidal volume (7mL/kg) and NC flow rate:
Example: A 6kg infant on 0.25L/min NC oxygen (tidal volume = 42mL; NC flow = 250mL/min, 4mL/s; inspiratory time = 1s).
FiO2 value: 4mL × 1.0 = 4mL oxygen, plus 38mL × 0.21 = 8mL oxygen.
FiO2 = (4 + 8)/42 = 0.29.
Toddlers, Pre-school: NC, face mask
School-age Child: Non-rebreathing mask
Maintain Airway and Air Movement:
Support airway with jaw lift, suction nasopharynx and mouth as needed.
Provide oral or nasopharyngeal airway.
Maintain the patient in an upright position; do not force a distressed patient to lie down and minimize discomfort.
B: Use Respiratory Support for Breathing
Identify the Level of Respiratory Involvement:
Treat specific problems appropriately (e.g., bronchodilators).
Assist Work of Breathing with Non-Invasive Support:
This can be achieved with nasopharyngeal continuous positive airway pressure (CPAP) (bronchiolitis) or negative pressure ventilation.
Intubation and Mechanical Ventilation:
Consider intubation and mechanical ventilation if necessary.
C: Assess Circulation; Establish IV Access
Start Pulse Oximetry and Cardiac Monitoring:
Continuous monitoring of heart rate, respiratory rate, blood pressure, oxygen saturation, and temperature.
Provide IV Fluids:
When circulation is good, limit fluid intake to an amount ranging from restricted to just below maintenance.
Detailed Steps in Life Support for Neonates, Infants, and Children
Airway:
Opening Maneuvers:
Infant’s airway is optimized at the neutral position.
Child airways are optimized at the "sniffing position" (mild extension of head on neck).
Use head tilt with chin lift or jaw thrust.
Airway Clearance:
Use a tongue depressor or laryngoscopy to clear any secretions, vomit, or blood with a suction device.
Airway Adjuncts:
Oropharyngeal Airway: Measured as the distance from the center of the mouth to the angle of the mandible.
Nasopharyngeal Airway: Measured as the distance from the top of the nose to the tragus of the ear.
Facemasks:
Correctly fitted, iat should extend from the bridge of the nose to between the lower lip and point of the chin.
Breathing:
Options Include:
Mouth-to-mouth ventilations.
Bag-valve-mask (BVM) ventilation.
Supraglottic airway (SGA).
Endotracheal tube (ETT).
For Neonates:
Supplemental oxygen is reserved for when the newborn’s saturations do not meet the lower end of the target despite respiratory effort.
If initial airway and breathing methods are unsuccessful, tracheal intubation and ventilation may be performed.
Circulation:
Compressions:
Commence chest compressions if the infant/child is unresponsive and not breathing normally, or a pulse is not palpable within 10 seconds or the pulse rate is <60 bpm accompanied by signs of poor circulation.
Compression Method:
Infant: Two-thumb or two-finger method.
Child: Use the heel of one hand or the two-handed technique.
Compression Ratio: 15:2 at a rate of 100-120 bpm.
Vascular Access:
Options include peripheral venous access, intraosseous (IO) injection and infusion, or central venous cannulation.
Use a bone marrow injection gun/drill to insert IO needle perpendicular to the bone surface. Confirm correct position by aspirating bone marrow or injecting normal saline to avoid compartment syndrome.
Fluids:
If hypovolemia is suspected, use IV or IO crystalloid for resuscitation.
Initial Bolus: 20mL/kg 0.9% sodium chloride.
Repeat if no improvement in heart rate, capillary refill time, or color.
Medications:
Calculate doses based on the child’s weight. Use a body length tape with pre-calculated doses if weight is unknown.
Flush IV and IO medications with small boluses of 0.9% NaCl or 5% glucose (for amiodarone) to ensure medications enter circulation.
Defibrillation:
Use pediatric defibrillation guidelines, adjusting energy doses based on the child’s weight and size.
Neonatal Specific Steps:
Assessment:
Initial assessment addresses tone, breathing, heart rate, color, and pulse oximetry.
Tone: Normally moving limbs and flexed posture. If responses are absent or weak, gently but briskly dry the newborn with a warmed towel to stimulate breathing.
Breathing: Includes crying.
Heart Rate: Should be >100 bpm within 2 minutes of birth.
Color: Normal newborns are blue but go pink soon after the onset of breathing.
Pulse Oximetry: Used to assess heart rate and oxygenation.
Airway Positioning:
On their back with the head in a neutral or slightly extended position ("sniffing position").
Mouth and Pharyngeal Suction:
To remove obstructions such as meconium or blood clots.
Tactile Stimulation:
To stimulate breathing. If not breathing within 1 minute of birth, commence CPAP or positive pressure ventilation.
Positive Pressure Ventilation:
Using a T-piece resuscitation device, self-inflating bag, flow-inflating bag, CPAP, mouth-to-mouth, or mouth-to-mask ventilation.
Chest Compressions:
If HR <60 despite assisted ventilation for 30 seconds, chest compressions are indicated.
Method: Two-thumb technique.
Compression Ratio: 3:1.
Medications and Fluids:
If HR <60 despite adequate assisted ventilations and chest compressions, administer adrenaline via the umbilical vein.
Consider volume expansion with fluids if necessary.
Summary of Immediate Management Steps
Early Recognition and Seeking Senior Help:
Recognize signs of severe distress and call for senior help immediately.
Any red zone observation = severe sepsis or septic shock until proven otherwise.
Obtain senior clinical review within 30 minutes for suspected sepsis.
ABCDE Primary Survey:
A (Airway): Assess and maintain a patent airway.
B (Breathing): Support as necessary, including supplemental oxygen and ventilation.
C (Circulation): Establish IV/IO access, monitor vital signs, and provide fluids and medications as needed.
D (Disability): Assess the level of consciousness.
E (Exposure): Look for signs of infection or other causes.
F (Fluids): Monitor fluid input and output; consider insertion of an indwelling catheter (IDC).
Administer Oxygen and Support Breathing:
Ensure adequate oxygenation and ventilation using appropriate methods for the age and condition of the child.
Establish Vascular Access and Administer Fluids:
Promptly obtain IV/IO access and start fluid resuscitation as needed.
Monitor and Reassess Continuously:
Frequently reassess the child’s condition and response to interventions.
Monitor observations every 30 minutes for 2 hours, then hourly for 4 hours.
Watch for signs of deterioration and escalate care if needed:
Tachypnoea
Persistent tachycardia, slow capillary refill, and hypotension
Pale color and mottling
Drowsiness or decreased level of consciousness
Urine output <1mL/kg/hour
Acidosis, increasing serum lactate, or procalcitonin
Hypoglycaemia, leukopenia, or abnormal coagulation
Source Control:
Investigate and treat the underlying cause of sepsis.
Describe an evidence-based approach to clinical pharmacology for the management of sepsis (Antibiotic prescribing guidelines)
Major Pathogens in Sepsis by Age Group
Infants <2 Months:
Escherichia coli
Group B Streptococcus
Listeria monocytogenes (uncommon)
Herpes Simplex Virus (HSV) infection should be considered in the differential diagnosis of sepsis.
Older Children:
Neisseria meningitidis
Streptococcus pneumoniae
Staphylococcus aureus (Methicillin-Sensitive Staphylococcus Aureus - MSSA, or Methicillin-Resistant Staphylococcus Aureus - MRSA)
Group A Streptococcus (GAS)
Antibiotic Regimens by Age Group
Neonates (≤7 Days):
Benzylpenicillin: 60mg/kg IV 12-hourly
Cefotaxime: 50mg/kg IV 12-hourly
Neonates (>7-28 Days):
Benzylpenicillin: 60mg/kg IV 6-8-hourly
Cefotaxime: 50mg/kg IV 6-8-hourly
Infants (1-≤2 Months):
Benzylpenicillin: 60mg/kg IV 4-6-hourly
Cefotaxime: 50mg/kg IV 4-6-hourly
Children (>2 Months):
Ceftriaxone: 100mg/kg (max 4g) IV daily or
Cefotaxime: 50mg/kg (max 2g) IV 6-hourly and
Flucloxacillin: 50mg/kg (max 2g) IV 6-hourly
Special Considerations
Oncology Patients:
Piperacillin/Tazobactam: 100mg/kg (max 4g) IV 6-hourly
Severely Unwell/High Risk:
Add Amikacin: 22.5mg/kg (18mg/kg if >10 years old) (max 1.5g) IV daily
Add Vancomycin: 15mg/kg (max 750mg) IV 6-hourly
Non-Oncology Patients with Central Venous Access:
Vancomycin: 15mg/kg (max 750mg) IV 6-hourly and
Ceftriaxone: 100mg/kg (max 4g) IV daily or
Cefotaxime: 50mg/kg (max 2g) IV 6-hourly
HSV Suspected (<3 months):
Add Acyclovir: 20mg/kg IV 8-hourly (indications: skin lesions, seizures, hepatitis)
Suspected MRSA:
Add Vancomycin based on local epidemiology and risk factors.
Suspected Toxin-Mediated Disease:
Consider adding Clindamycin: 15mg/kg (max 900mg) IV 8-hourly and
IV Immunoglobulin (Ig)
Alternatives and Special Cases
If IV Access Unavailable:
IM Ceftriaxone: 100mg/kg (max 4g) daily (can also be used in infants ≤2 months).
Previous Antibiotic Anaphylaxis:
Seek specialist advice for alternative antibiotic regimens.
Describe the special considerations for the management of sepsis for Aboriginal children
Higher Risk and Early Intervention
Higher Risk: Aboriginal children are at a higher risk of developing sepsis compared to non-Aboriginal children.
Early Intervention: Prompt recognition and early intervention are crucial to prevent poorer outcomes and reduce the risk of severe complications.
Epidemiological Data
ICU Admissions: Between 2002-2013, there was a gradual increase in the proportion of children admitted to intensive care units (ICUs) who were Indigenous Australians.
Invasive Infections: Among these admissions, one-quarter were due to invasive infections.
Sepsis and Septic Shock: Approximately one-tenth of the invasive infection cases involved sepsis or septic shock.
Specific Management Considerations
Cultural Sensitivity and Family Engagement:
Provide culturally sensitive care, understanding and respecting cultural practices and beliefs.
Engage with families and communities to build trust and ensure adherence to treatment plans.
Consider the role of extended family in the care and decision-making processes for Aboriginal children.
Access to Care:
Address potential barriers to accessing healthcare, such as geographical isolation, socio-economic factors, and lack of transportation.
Ensure timely access to medical facilities equipped to handle sepsis management, including transport to tertiary centers if necessary.
Health Education and Prevention:
Implement community-based education programs to raise awareness about the signs and symptoms of sepsis and the importance of early medical intervention.
Promote preventive measures such as vaccination and early treatment of infections to reduce the incidence of sepsis.
Tailored Antibiotic Regimens:
Use evidence-based antibiotic prescribing guidelines, considering the higher risk of severe infections and resistance patterns that may be more prevalent in Indigenous communities.
Ensure appropriate antibiotic stewardship to minimize the risk of resistance.
Comprehensive Care Approach:
Address underlying health disparities and comorbidities that may contribute to an increased risk of sepsis, such as malnutrition, chronic diseases, and poor living conditions.
Provide holistic care that includes social, emotional, and mental health support for the child and family.
Learning Points: Health society and environment
List Vaccine preventable infections and the immunisation schedule and briefly describe the evidence-based approach of vaccination
Vaccine-preventable infections
Cholera
Diphtheria
Haemophilus influenza type b (Hib)
Hepatitis A
Hepatitis B
Human papillomavirus (HPV)
Influenza
Japanese encephalitis
Measles
Meningococcal disease
Mumps
Pertussis (whooping cough)
Pneumococcal disease
Poliomyelitis
Q fever
Rabies and other lyssaviruses
Rotavirus
Rubella
Tetanus
Tuberculosis
Typhoid fever
Varicella (chicken pox)
Yellow fever
Zoster (herpes zoster)
Briefly describe the public health strategies employed to encourage vaccination and discourage the anti-vaccination movement
National Immunisation Program
Accessibility and Affordability:
Focus on making vaccines accessible and affordable to encourage national immunisation coverage.
Comprehensive strategies to ensure vaccines are available to all segments of the population.
Misinformation Correction
Public Health Organisations:
Actively work to correct misinformation that fuels the anti-vaccination movement.
Provide accurate information about vaccines and debunk common myths to build public trust.
Key Strategies
Improve Immunisation Coverage:
Enhance national immunisation efforts to increase vaccine uptake.
Implement targeted strategies to reach underserved populations.
Effective Governance:
Ensure robust management and oversight of the National Immunisation Program.
Implement policies that support vaccine distribution and monitoring.
Vaccine Supply and Efficiency:
Secure a reliable supply of vaccines.
Promote efficient use of vaccines to prevent shortages and ensure timely immunisation.
Vaccine Safety Monitoring:
Continuously enhance systems for monitoring vaccine safety.
Address safety concerns promptly to maintain public confidence.
Community Confidence:
Use effective communication strategies to build and maintain community trust in vaccines.
Engage with the public through transparent and consistent messaging.
Monitoring and Evaluation:
Strengthen the monitoring and evaluation of the immunisation program.
Use data from immunisation registers and disease surveillance to inform strategies.
Skilled Workforce:
Ensure an adequately trained immunisation workforce.
Promote effective training programs for healthcare providers.
Regional Contribution:
Maintain strong contributions to regional vaccination efforts.
Support international vaccination programs to control the spread of diseases globally.
Community Engagement Strategies
Increase Knowledge and Awareness:
Implement patient reminder/recalls and provider reminders.
Conduct public and provider education campaigns.
Integrate vaccination status checks into routine health assessments.
Use mass media for targeted promotion campaigns.
Reduce Costs and Increase Convenience:
Develop catch-up plans for those overdue for vaccination.
Implement accelerated vaccination schedules for diseases like hepatitis B.
Conduct home visits for routine childhood vaccination, especially for Aboriginal and Torres Strait Islander children.
Expand access to vaccination in hospitals and public clinics.
Establish Guidelines and Policies:
Fund vaccines under the National Immunisation Program (NIP).
Implement school-based vaccination programs.
Offer national parental incentives and maternity immunisation allowances.
Link vaccination to childcare benefits.
Mandate vaccination policies for healthcare workers.
Describe the public health principles for notifiable infectious illnesses, and how these are applied when caring for children
Principles of Notifiable Infectious Illnesses
Prompt Notification:
Healthcare providers must notify public health authorities within 24 hours of diagnosing a notifiable disease.
Notification is essential for immediate public health response and containment measures.
Mandatory Reporting by Various Entities:
Medical Practitioners and Hospital Chief Executives: Must report cases of notifiable diseases.
Pathology Laboratories: Required to notify relevant authorities upon confirmation of a notifiable infectious disease.
Primary and Secondary Schools and Child Care Centres: Principals and directors must report cases or suspicions of notifiable diseases.
Proactive Notification for Suspected Risk:
Not only diagnosed cases but also suspected cases that may pose a significant risk to public health must be reported.
This includes situations where children are reasonably suspected to have come into contact with a person who has a notifiable disease and the child’s immunization status is unknown or incomplete.
Outbreak Management:
School principals and child care directors are encouraged to seek advice and notify local public health units when they suspect an outbreak of infectious disease, such as gastrointestinal or respiratory illnesses.
Application in Caring for Children
Notification Requirements for Schools and Child Care Centres:
Principals and child care directors should notify their local public health unit (PHU) as soon as they are aware that a child has a notifiable vaccine-preventable disease or has been in contact with such a disease without proof of immunization.
Diseases to be notified include:
Diphtheria
Mumps
Poliomyelitis
Haemophilus influenzae Type b (Hib)
Meningococcal disease
Rubella ("German measles")
Measles
Pertussis ("whooping cough")
Tetanus
Health Practitioners’ Role:
Health practitioners must ensure hospital CEOs are aware of notifiable diseases among patients.
They have a duty to act on reasonable clinical suspicion and report accordingly.
Case Notification Timing:
Notifications should be made within 24 hours of diagnosis to enable rapid public health interventions.
Public Health Response:
Rapid notification allows public health units to implement control measures, conduct contact tracing, and provide guidance to prevent further spread of the disease.
This includes informing parents and guardians, managing quarantine or exclusion periods, and providing vaccination campaigns if necessary.
Preventive Measures:
Schools and child care centres are advised to maintain accurate immunization records for enrolled children.
Proactive communication and education about vaccination and disease prevention are critical to reducing the incidence of vaccine-preventable diseases.
List the factors that influence infectious disease in Aboriginal & Torres Strait Islander children
Overcrowding:
Increased risk of transmission of infectious diseases due to close living conditions.
Lack of Parental Supervision:
Children may be at greater risk of exposure to infectious agents without adequate supervision.
Poor Nutrition:
Malnutrition weakens the immune system, making children more susceptible to infections.
Wariness of the Healthcare System:
Distrust or fear of healthcare institutions may lead to delayed or avoided medical care.
Rural and Remote Locations:
Limited access to healthcare facilities and services, leading to delayed diagnosis and treatment.
Transport Issues:
Difficulty accessing healthcare services due to lack of transportation options.
Lack of Culturally Appropriate Health Services:
Healthcare services that do not respect or incorporate cultural practices may discourage Indigenous families from seeking care.
Intergenerational Trauma:
Historical and ongoing trauma can impact health behaviors and access to healthcare services.
Parental Factors:
Poor Mental Health: Parents with mental health issues may struggle to provide adequate care and supervision.
Substance Abuse: Drug and alcohol abuse can impair parenting capacity and lead to neglect.
Family Violence: Exposure to violence can disrupt family stability and access to healthcare.
Imprisonment: Parental incarceration can lead to unstable living conditions and reduced supervision.
Maternal Factors:
Low Birth Weight: Associated with increased vulnerability to infections.
Intrauterine Growth Restriction: Can lead to compromised immune function in infants.
Substance Use in Pregnancy: Increases the risk of neonatal infections and poor health outcomes.
Communal Living:
Shared living spaces can facilitate the spread of infectious diseases.
Lower Socioeconomic Status (SES):
Limited resources for healthcare, nutrition, and sanitation contribute to higher infection rates.
Lower Health Literacy:
Lack of understanding about disease prevention and treatment can hinder effective healthcare practices.
Access to Treatment:
Institutional barriers and limited availability of healthcare services can delay treatment.
Remote Communities Susceptible to Water Contamination:
Poor water quality and sanitation can lead to waterborne diseases.
Describe the support services available for Aboriginal children and their families
Aboriginal medical service
Aboriginal Liaison Officers (in hospital)
Aboriginal Maternal and Infant Health Services
The Aboriginal Maternal and Infant Health Service (AMIHS) was implemented in 2001 to improve the health of Aboriginal women during pregnancy and decrease perinatal morbidity and mortality for Aboriginal babies.
The service is delivered through a continuity-of-care model, where midwives and Aboriginal Health Workers collaborate to provide a high-quality maternity service that is culturally safe, women-centred, based on primary healthcare principles and provided in partnership with Aboriginal people.
AMIHS midwives and Aboriginal Health Workers provide antenatal and postnatal care, from as early as possible after conception up to eight weeks postpartum. The care is provided in the community but is linked into mainstream maternity services to ensure that risk management and education are available to AMIHS teams.
Services provided by AMIHS include:
Comprehensive and regular antenatal health checks
Booking into maternity hospitals
Smoking cessation programs
Referral and support to access other services
Health promotion and community development activities
Postnatal checks and support
Information on infant feeding and nutrition.
Building Strong Foundations for Aboriginal Children, Families and Communities
Building Strong Foundations (BSF) for Aboriginal Children, Families and Communities services provide a free, culturally safe and appropriate early childhood health service for Aboriginal children from birth to school entry age and their families. The service is provided by teams of Aboriginal health workers and child and family health nurses. In some locations, the core team is supported by other allied health therapists including social workers. The BSF service works with families, parents, carers, and the local community, to support the health, growth and development of Aboriginal children, so they are able to fully engage in life and learning.
The BSF service includes:
Developmental surveillance and health monitoring
Health promotion, including primary prevention, health education, anticipatory guidance and support for parents and carers and community development
Early identification of child and family needs
Responding to identified need, with information, brief interventions and appropriate referrals.
Families can get assistance and information on topics including:
Breastfeeding
Other feeding issues
Their child’s sleep and settling issues
Their child’s immunisations
Childhood safety
Their child’s growth and development
Parenting issues.
Aboriginal Community Controlled Health Services
An Aboriginal Community Controlled Health Service (ACCHS) is an incorporated Aboriginal organisation initiated by and based in a local Aboriginal community. They deliver a holistic and culturally appropriate health service to the community.
Aboriginal & Torres Strait Islander Health
What percentage of the total “Burden of Disease” for Aboriginal and Torres Strait Islander populations was due to the Burden of Disease in children aged 0-4?
Infants and Children Aged 0-4:
Population Representation:
Children aged 0-4 years comprised 12% of the Indigenous population in 2011.
Burden of Disease:
This age group accounted for 9% of the total burden of disease among Indigenous Australians
Significant contributors to the burden in this age group included:
Pre-term and low birthweight complications
Sudden Infant Death Syndrome (SIDS)
Other disorders of infancy
Birth trauma and asphyxia
Other Age Groups:
Children Aged 5-14:
Population Representation:
This age group comprised 24% of the total Indigenous population.
Burden of Disease:
Accounted for only 6% of the total burden of disease.
Main causes of health loss included:
Asthma
Anxiety disorders
Depressive disorders
Conduct disorders (estimates should be interpreted with caution due to lower accuracy)
Adolescents and Adults Aged 15-24:
Population Representation:
Made up about 20% of the Indigenous population.
Burden of Disease:
Accounted for 13% of the total burden.
Main contributors included:
Injuries
Mental and substance use disorders
Leading causes of burden in males:
Suicide and self-inflicted injuries
Alcohol use disorders
Motor vehicle traffic accidents
Leading causes of burden in females:
Anxiety disorders
Suicide and self-inflicted injuries
Depressive disorders
What were the three most common “diseases” contributing to the Burden of Disease in Aboriginal and Torres Strait Islander children in the 0-4 age group?
Preterm/Low Birth Weight Complications (20%)
Sudden Infant Death Syndrome (SIDS) (11%)
Birth Trauma/Asphyxia (7.7%)
How do Immunisation schedules differ between Aboriginal non-Aboriginal children?
Routine Vaccination
Aboriginal and Torres Strait Islander Children:
Aboriginal and Torres Strait Islander children aged 5 years or under should receive all routine vaccines under the National Immunisation Program (NIP).
Additional Vaccines for Aboriginal and Torres Strait Islander Children
In addition to routine childhood vaccines, the following additional vaccines are recommended for Aboriginal and Torres Strait Islander children aged 5 years or under:
Meningococcal B Vaccine:
Schedule:
Administered at 2, 4, and 12 months of age.
An extra dose at 6 months is required for infants with certain medical risk conditions for invasive meningococcal disease.
Eligibility:
Recommended and free under the NIP for Aboriginal and Torres Strait Islander children.
Children who missed out can still receive their meningococcal B vaccines for free under the NIP until they turn 2 years of age.
Pneumococcal Disease Vaccine:
Eligibility:
Aboriginal and Torres Strait Islander children living in Queensland (QLD), Northern Territory (NT), Western Australia (WA), and South Australia (SA).
Schedule:
An additional dose at 6 months.
Further doses at 4 years and at least 5 years later.
The type of vaccine and dosage schedule depend on age and any conditions that increase the risk of pneumococcal disease.
Hepatitis A Vaccine:
Eligibility:
Aboriginal and Torres Strait Islander children living in QLD, NT, WA, and SA.
Schedule:
Two doses at 18 months and 4 years of age.
Free under the NIP.
Influenza Vaccine:
Eligibility:
Free for all Aboriginal and Torres Strait Islander people aged 6 months and over through the NIP.
Catch-Up Vaccines:
Eligibility:
Aboriginal and Torres Strait Islander children aged 5 years and under should receive any missed routine childhood vaccinations.
Free under the NIP.
Resources
Impact and causes of illness and death in Aboriginal and Torres Strait Islander people
Immunisation for Aboriginal and Torres Strait Islander people https://beta.health.gov.au/health-topics/immunisation/immunisation-throughout-life/immunisation-for-aboriginal-and-torres-strait-islander-people
Learning Points: Professional Development
Aboriginal & Torres Strait Islander Health
Demonstrate engagement with Aboriginal Liaison Officers and Aboriginal Medical Services
NSW Health - Aboriginal Maternal and Infant Health Services. Located on this page are links for local AMIHS at Clinical sites
https://www.health.nsw.gov.au/kidsfamilies/MCFhealth/priority/Pages/amihs.aspx
Services provided by AMIHS include:
Comprehensive and regular antenatal health checks
Booking into maternity hospitals
Smoking cessation programs
Referral and support to access other services
Health promotion and community development activities
Postnatal checks and support
Information on infant feeding and nutrition.
Clinical Forum
Describe the role of the different health care professions involved in newborn care, including from the parent perspective
Maternal and Child Health Nurse (MCH Nurse)
Monitoring Growth and Development:
Works with families and healthcare professionals to monitor the growth and development of children from birth until about three and a half years old.
Focus Areas:
Prevention, promotion, early detection, and intervention of health and wellbeing concerns for young children and their families.
Services Provided:
Regular check-ups and developmental screenings.
Health education and support for parents.
Referral to specialists if any health concerns are identified.
Midwife
Post-Birth Care:
Newborn Screening Tests: Set up and explain the importance of newborn screening tests.
Feeding Support: Discuss feeding choices and refer to a lactation consultant if necessary.
Home Visits: Offer and arrange home visits for postnatal care for both mother and baby.
Life at Home: Provide guidance on adapting to life at home with a new baby.
Referrals: Organize referrals to specialists such as paediatricians if needed.
General Practitioner (GP)
Immunisations:
Administer the 6-week immunizations and monitor for any reactions.
Regular Reviews:
Conduct regular reviews at 5–10 days and six weeks postpartum.
Monitor and manage common neonatal concerns and maternal health issues.
Provide comprehensive care and support for the mother and family members.
Collaboration:
Work effectively with other health providers such as MCH nurses, midwives, lactation consultants, paediatricians, and obstetricians.
Ongoing Management:
Manage medical conditions that may have developed during pregnancy, such as hypertension, diabetes, and anemia.
Provide preventive health and lifestyle recommendations.
Paediatrician
Immediate Post-Birth Care:
Examine and treat babies immediately after birth.
Assess and resuscitate newborns if necessary.
Specialized Treatment:
Treat a wide range of illnesses, injuries, and conditions.
Manage the treatment of premature babies and infants with complex health issues.
Conditions Treated:
Cancer, genetic disorders (e.g., cystic fibrosis, Down syndrome), disabilities (e.g., cerebral palsy), developmental delays, chronic diseases (e.g., diabetes), infectious diseases (e.g., meningitis), asthma, allergies, and autism spectrum disorder.
Lactation Consultant
Breastfeeding Support:
Help mothers find the best way to breastfeed for both mom and baby to increase chances of success.
Issues Addressed:
Poor milk supply, breast pain and sore nipples, trouble latching, finding a comfortable nursing position, refusal to feed, poor infant weight gain, falling asleep at the breast, problems pumping breastmilk, and engorgement.
Parent Perspective
From a parent's perspective, these healthcare professionals provide a comprehensive support system to ensure the health and wellbeing of both the newborn and the mother. This multidisciplinary approach helps to:
Ensure Timely and Appropriate Care: By having access to various specialists, parents can be confident that their child's health needs are being met comprehensively and promptly.
Receive Guidance and Education: Parents receive valuable information on child development, feeding, and general care, which empowers them to make informed decisions.
Feel Supported: The involvement of multiple healthcare professionals ensures that parents are not alone in their journey and can rely on expert advice and support whenever needed.
Address Health Concerns Early: Early detection and intervention of health issues can prevent more serious problems down the line, ensuring better long-term health outcomes for the child.
Describe the ethical issues unique to decisions to resuscitate (or not) in cases of extreme prematurity
Threshold of Viability:
Generally considered between 23 to 25+6 weeks’ gestation.
Decisions to resuscitate are complicated by the fact that life-sustaining interventions are not normally recommended before 24 weeks’ gestation due to low survival rates and high risks of severe disability.
Ethical Considerations:
Best Interests of the Child:
The primary ethical consideration is whether resuscitation is in the best interests of the child.
Weighing the potential for survival against the likelihood of severe disability or suffering is crucial.
Each day of gestation after 24 weeks increases the chances of survival by 3-6%, so this incremental improvement must be considered.
Quality of Life:
Potential outcomes include severe disabilities, chronic health issues, and significant developmental delays.
Ethical dilemmas arise when considering if a life with severe disabilities would be in the child's best interest.
Parental Wishes and Autonomy:
Parents’ values, beliefs, and wishes should be respected and play a significant role in decision-making.
However, parents might be under emotional distress or lack the medical knowledge to fully understand the implications, raising questions about how much weight should be given to their wishes.
Medical Uncertainty:
Prognostic uncertainty at the threshold of viability makes decision-making challenging.
Variability in survival rates and outcomes based on gestational age, birth weight, and sex of the infant (e.g., male preterm infants have higher mortality rates and are more likely to have adverse outcomes).
Resource Allocation:
Intensive care for extremely preterm infants requires significant medical resources.
Ethical considerations involve whether the allocation of such resources is justified given the high risk of poor outcomes.
Informed Consent:
Ensuring parents are fully informed about the risks, benefits, and possible outcomes of resuscitation is crucial.
Ethical issues arise if there is a lack of clear, honest communication from the healthcare team.
Non-Maleficence and Beneficence:
The principle of non-maleficence (do no harm) requires careful consideration of the potential harms of resuscitation versus non-resuscitation.
The principle of beneficence (do good) requires that actions taken should benefit the child, but in cases of extreme prematurity, the potential for benefit is often uncertain.
Legal and Policy Frameworks:
Ethical decisions are influenced by legal standards and hospital policies regarding the resuscitation of extremely preterm infants.
Policies may vary, leading to different standards of care and ethical dilemmas about consistency in treatment decisions.
Long-Term Implications:
Consideration of the long-term implications for both the child and the family, including emotional, psychological, and financial burdens.
Additional (From CBL)
Impetigo
Description: Highly contagious skin infection of the upper layers of the epidermis.
Epidemiology: Most common skin infection in children, particularly affects those aged 2-6 years. Can occur in epidemics in preschools or schools.
Cause & Pathophysiology:
Caused by Staphylococcus aureus (80%), Streptococcus pyogenes (GAS) (10%), or co-infection (10%).
Risk Factors: Warm, humid climate; crowded, unsanitary living conditions; poor personal hygiene; pre-existing skin lesions; diabetes mellitus; immunodeficiency.
Clinical Features:
Nonbullous Impetigo: Papules that evolve into vesicles/pustules, rupture to form honey-colored crusts. Most often on the face around the nose and mouth.
Bullous Impetigo: Large, flaccid bullae that rupture to form thin, brown crusts. Most often on the trunk and upper extremities.
Pruritus and negative Nikolsky sign.
Investigations: Primarily clinical diagnosis; lesion swab for MCS to detect causative pathogen.
Management:
Non-endemic settings: Mupirocin 2% ointment or cream for localized sores; oral dicloxacillin + flucloxacillin for multiple sores or recurrent infection.
Endemic settings (e.g., remote communities): IM benzylpenicillin.
Cellulitis
Description: Local infection of the deep dermis and subcutaneous tissue.
Cause: Streptococcus pyogenes (Group A strep) and Staphylococcus aureus
Clinical Features: Erythema, oedema, warmth, tenderness, poorly defined lesion with induration. Possible systemic features (e.g., fever, tachycardia)
Investigations: Swab for MCS; consider imaging if abscess, deep infection, or foreign body is suspected.
Management:
Manage sepsis if present.
Manage source (e.g., remove foreign body, drain abscess).
Antibiotics:
Without systemic features: Oral phenoxymethylpenicillin
With systemic features: IV benzylpenicillin
Staphylococcal Scalded Skin Syndrome (SSSS)
Description: Blistering skin disorder induced by the exfoliative toxins of Staphylococcus aureus
Epidemiology: Typically affects children < 6 years
Cause & Pathophysiology: Spread of exfoliative toxins from a local infection (e.g., skin, mouth, nose, throat, impetigo).
Clinical Features:
Initially: Fever, malaise, irritability, skin tenderness, erythema (often starts periorally)
After 24-48 hours: Flaccid, easily ruptured blisters; widespread sloughing of epidermal skin; positive Nikolsky sign; no mucosal involvement
Investigations: WCC, ESR, cultures of the site of preceding infection, biopsy
Management: Close observation, IV fluid resuscitation, pain relief, empirical antibiotics
Scarlet Fever
Description: Syndrome caused by infection with a toxin-producing group A streptococci
Epidemiology: Peak incidence in children aged 5-15 years, often associated with streptococcal tonsillopharyngitis.
Cause & Pathophysiology: Aerosol transmission of GAS producing erythrogenic exotoxins leading to a delayed type IV hypersensitivity reaction and rash.
Clinical Features:
Initial Phase (Acute Tonsillitis): Fever, malaise, sore throat, difficulty swallowing, tonsillar exudates, white coating on the tongue.
Exanthem Phase: Fine, erythematous, blanching rash with a sandpaper-like texture; Pastia lines in flexural surfaces; begins on the neck and spreads to the trunk and extremities.
Desquamation Phase: 7-10 days after rash resolution, peeling of the skin on the face, trunk, hands, fingers, and toes.
Investigations: Throat culture, urinalysis (for post-strep glomerulonephritis), FBC, LFTs, CRP/ESR, elevated antistreptolysin O.
Management:
Supportive: Analgesia, antipyretics, maintenance fluids.
Medical: Oral benzylpenicillin for high risk of acute rheumatic fever.
Complications: Post-streptococcal glomerulonephritis, acute rheumatic fever, Sydenham chorea, Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS)
Stevens-Johnson Syndrome (SJS)
Description: Rare, life-threatening, immune-mediated skin reaction causing blistering and extensive epidermal detachment, usually precipitated by medications or infections.
Epidemiology: Affects all ages, more common in females.
Cause:
Drugs (80%): Antibiotics, corticosteroids, antiretrovirals, antiepileptics, allopurinol, sulfasalazine.
Infections: Mycoplasma pneumoniae, CMV, herpes.
Pathophysiology: Delayed type IV hypersensitivity reaction leading to cytotoxic T cell activation and granulysin release causing keratinocyte damage.
Clinical Features:
Prodromal Phase: High fever, malaise, sore throat, myalgia, arthralgia.
Mucocutaneous Lesions: Painful erythematous macules (target appearance) evolving to bullae/vesicles, full-thickness epidermal necrosis, and sloughing; severe involvement of mucous membranes.
Investigations: Clinical diagnosis.
Management: Discontinue offending drug, supportive care (fluids, wound management, antibiotics if septic).
Learning Points: Science & Scholarship
Describe the pathogenesis of Fever
Definition and Temperature Thresholds:
Fever is typically defined as a body temperature exceeding 38°C (100.4°F)
In neonates (0-28 to 30 days old) and young infants (1-3 months), fever is concerning at a rectal temperature ≥38.0°C.
In children aged 3-36 months, fever is defined by rectal temperatures ranging from ≥38.0-39.0°C and concerning at ≥39.0°C without an infection focus.
In older children and adults, fever is defined by oral temperatures ranging from ≥37.8-39.4°C and concerning at ≥39.5°C.
Mechanism:
Pyrogen Entry and Prostaglandin Synthesis:
Fever is initiated by pyrogens (substances that cause fever) entering the bloodstream.
These pyrogens travel to the hypothalamus and induce the synthesis of prostaglandin E2 (PGE2).
Pyrogens can be:
Exogenous: Usually microbes (viruses, bacteria) or their products (endotoxins).
Endogenous: Cytokines such as IL-1, TNF-alpha, IL-6, and others produced by the body.
Hypothalamic Set Point Adjustment:
The induction of PGE2 raises the hypothalamic set point for body temperature.
The hypothalamus then recognizes the current body temperature as too low and initiates processes to raise it to the new set point.
Body's Response to Raise Temperature:
Peripheral Vasoconstriction: Reduces heat loss by shunting blood from the skin to the core.
Increased Muscle Tone and Activity: Shivering and increased metabolic rate generate more heat.
Decreased Heat Loss: Reduced perfusion of the skin conserves heat.
Equilibrium at New Set Point:
The body temperature rises until it reaches the new equilibrium at the elevated set point.
Fever rarely exceeds 41°C unless there is a component of hyperthermia.
Role of Cytokines:
Endogenous pyrogenic cytokines (IL-1, IL-6, TNF, IF-alpha) released by phagocytic cells induce PGE2 synthesis in the hypothalamus.
These cytokines also cause systemic effects:
Acute-Phase Response: Increased synthesis of acute-phase proteins by the liver.
Decreased Serum Iron and Zinc: Inhibits bacterial growth.
Leucocytosis: Increased white blood cell count.
Muscle Proteolysis: Breakdown of muscle proteins.
Slow-Wave Sleep: IL-1 induces slow-wave sleep, explaining the somnolence frequently associated with febrile illnesses.
Myalgias and Arthralgias: Increased peripheral PGE2 may account for the muscle and joint pains that often accompany fever.
Increased Heart Rate: A normal physiological response to fever.
Clinical Effects and Benefits vs. Harms:
Benefits of Fever:
Retards Growth and Reproduction of Some Bacteria and Viruses
Retards Growth and Reproduction: Higher body temperatures can slow down or inhibit the growth and reproduction of certain bacteria and viruses. These pathogens often have optimal temperature ranges for their survival and replication. A fever creates an environment less conducive to their growth.
Decreased Serum Iron: Fever can also lead to a reduction in serum iron levels. Many bacteria require iron to grow and reproduce. When serum iron is decreased, it limits the availability of this essential nutrient to the pathogens, further inhibiting their ability to thrive.
Enhances Immunologic Function at Moderately Elevated Temperatures
Enhances Immunologic Function: Moderate fever can boost various aspects of the immune system. This includes:
Increased Production of White Blood Cells (WBCs): White blood cells are crucial for fighting infections. Fever can stimulate the production of WBCs, including lymphocytes, which are involved in the adaptive immune response.
Enhanced Activity of Immune Cells: Immune cells, such as neutrophils and macrophages, can become more active and efficient at engulfing and destroying pathogens at elevated temperatures.
Improved Function of Cytokines: Cytokines are signaling molecules that help regulate the immune response. Fever can enhance the effectiveness of cytokines, improving communication and coordination within the immune system.
Temperature Limitations: However, these benefits are seen at moderately elevated temperatures. When body temperatures approach 40°C (104°F), some of the positive effects can be reversed. Extremely high fevers can be harmful, leading to cellular damage and impairing the function of proteins and enzymes essential for normal body functions.
Harms of Fever:
Discomfort for the patient.
Associated with increased metabolic rate, oxygen consumption, carbon dioxide production, and demands on the cardiovascular and pulmonary systems → demands may offset any immunologic benefit for the child in shock
Hyperthermia vs. Fever:
Hyperthermia: Abnormal elevation of body temperature without a change in the hypothalamic set point.
Failure of normal homeostasis → heat production that exceeds the body’s capacity for dissipation
Body temperature does not respond to antipyretic agents
Characteristic clinical features
History of environmental heat exposure or use of drugs that interfere with normal thermoregulation (e.g. anticholinergics)
Hot, dry skin
CNS dysfunction (e.g. delirium, convulsions, coma)
Can be rapidly fatal
Adverse physiologic effects begin to occur at temperatures >41C
Describe the pathogenesis of Rash
Categories of Childhood Rashes:
Maculopapular: Flat, red area covered with small confluent bumps.
Pustular: Pus-filled lesions.
Vesiculobullous: Fluid-filled lesions.
Diffuse/Erythematous: Generalized redness.
Petechial/Purpureal: Small <2mm red/purple spots caused by hemorrhage from small blood vessels.
Hypersensitivity Reactions:
Type 1: Immediate hypersensitivity (e.g., urticaria)
Mediated by IgE.
Binding of allergen to IgE on cell surface causes cross-linking and mast-cell activation, releasing histamine.
Occurs within 2-30 minutes.
Examples include allergic rhinitis, allergic asthma, atopic eczema, systemic anaphylaxis, and some drug allergies.
Type 2: Humoral cytotoxic reactions (e.g., blistering, vesicles)
Mediated by IgG and/or IgM.
Cell- or matrix-associated antigen: binding of IgG to allergen → complement activation, FcR+ (monocyte) cells → opsonisation and phagocytosis OR cell lysis (NK cells) (e.g. some drug allergies (e.g. penicillin), blood transfusion rejection)
Cell-surface receptor: binding of IgG to antigen on cell-surface receptors → alters signalling → antibody dependent cell-mediated cytotoxicity (ADCC) OR antibody interference with cell surface receptor → chronic stimulation OR impairment (e.g. chronic urticaria (antibody against FC€RI alpha chain))
Occurs within 5-8 hours.
Examples include some drug allergies, blood transfusion rejection, and chronic urticaria.
Type 3: Immune complex mediated (e.g., vasculitis, petechiae, purpura)
Mediated by IgG and/or IgM.
Humoral IgG binds to blood-borne allergen → insoluble complex → complement and phagocyte activation → tissue damage in vasculature, and locations of complex deposition (e.g. lung, skin, kidneys, joints)
Occurs within 2-8 hours.
Examples include serum sickness and arthus reaction.
Type 4: Cell mediated immune reactions (e.g., macules, papules)
Th1 cells e.g. allergic contact dermatitis, tuberculin reaction
Soluble antigen
1st exposure → CD4+ T cells and MHC-II → differentiate to Th1 cells → cytokine release (IL12, IFNg, IL-2, lymphotoxin) and immune cell (e.g. macrophage) activation → cell damage
Th2 cells e.g. chronic asthma, chronic allergic rhinitis
Soluble antigen
1st exposure → CD4+ T cells and MHC-II → differentiate to Th2 cells → IgE production, eosinophil activation, mastocytosis
CTL e.g. graft rejection, allergic contact dermatitis to poison ivy
Cell-associated antigen
CD8+ T cell recognition of allergen on cell-surface receptor → cytotoxicity
24-72 hours
Pathogenesis:
Viral Infection:
Caused by either an immune response to the virus or damage to skin cells from factors released by the virus.
Common viral rashes include:
Measles: Caused by an RNA paramyxoviridae virus
Rubella (German Measles): Caused by an RNA togavirus
Erythema Infectiosum (Slapped Cheek): Caused by parvovirus B19
Roseola Infantum: Caused by HHV6 and 7
Varicella-Zoster: Almost all cases occur in children under 10 years old.
EBV (Epstein-Barr Virus): Around 15-35% will have a cutaneous eruption, which increases with ingestion of ampicillin or amoxicillin.
CMV (Cytomegalovirus): Primary infection often asymptomatic except in immunocompromised individuals.
HIV: 10-12% will develop an acute seroconversion syndrome with a morbilliform cutaneous eruption.
Hand-Foot-and-Mouth Disease: Most typically caused by coxsackie virus type A16 or enterovirus 71.
Cutaneous Herpes Simplex (HSV-1/2): Causes oral, genital, and ocular ulcers during initial infection.
Molluscum Contagiosum: Lesions appear as pearl-like, smooth papules caused by skin-to-skin or fomite contact.
Inflammatory Dermatoses:
Atopic Dermatitis (Eczema): Type 1 hypersensitivity reaction.
Seborrheic dermatitis: infants and adolescents (in adolescents, sebaceous secretions are altered by the normal skin flora → induces dermatitis)
Irritant contact dermatitis
Allergic contact dermatitis: involves a true allergy (most common precipitating agents are species of Toxicodendron, i.e. poison ivy, poison oak, or poison sumac, and the metal nickel)
Psoriasis: exacerbated by stress, local trauma, infections, some medications
Pityriasis rosea: self-limited papulosquamous disorder (?infectious aetiology)
Mastocytosis: heterogenous group of disorders, characterised by clonal mast cell proliferation and accumulation within various organs → in the skin, urticaria, vesicle and bulla formation may be seen
Local Bacterial/Fungal Infection:
Damage to cells from infection and the body’s inflammatory response.
Examples include:
Impetigo: Superficial skin infection caused by Staphylococcus aureus or group A beta-hemolytic streptococci.
Folliculitis: Pyoderma located within a hair follicle, secondary to follicular occlusion by keratin, over-hydration, or infection → bacterial causes include S. aureus and Pseudomonas
Tinea corporis (ringworm): dermatophytic infection of the skin on the body caused by Trichophyton (most commonly) and Microsporum fungal species
Scabies: an infestation with Sarcoptes scabiei organisms
Cutaneous candidiasis: primary or secondary fungal infection caused by members of the genus Candida → typically involves fold areas with an erythematous patch centrally and surrounding smaller satellite lesions, occasionally has whitish discharge centrally
Drug Eruptions:
Caused by delayed immunological hypersensitivity (type 4 hypersensitivity) to the drug or its metabolite.
Drugs can act as haptens, forming complexes with carrier proteins and eliciting an immune response.
Both humoral and cell-mediated mechanisms are involved.
Commonly implicated drugs include antibiotics (sulfonamides, aminopenicillins) and anticonvulsants.
More severe reactions include Stevens-Johnson syndrome/toxic epidermal necrolysis, erythema multiforme, and systemic hypersensitivity syndrome.
Haematological Disorders:
Often due to hemorrhage from small blood vessels.
Conditions include:
Acute Leukemia: Associated with signs and symptoms of underlying cytopenias.
Immune Thrombocytopenia: Diagnosis of exclusion with no systemic upset or organomegaly.
Petechial Rash with Ecchymosis: May be a presenting feature of thrombocytopenia.
Vasculitic/Rheumatological Diseases:
Involves inflamed or damaged cutaneous vessels.
Examples include:
Kawasaki Disease
Henoch-Schonlein Purpura
Systemic Lupus Erythematous
Juvenile Arthritis
Rheumatic Fever
Sarcoidosis
Systemic bacterial infections
Meningococcal disease: generalised purpuric (non-blanching) rash may be a presenting sign of meningococcal septicaemia (Neisseria meningitidis infection)
Syphilis: caused by the spirochete Treponema pallidum → transmitted by sexual contact or vertical transmission → secondary syphilis lesions result from the haematogenous dissemination of treponemes from a syphilitic chancre → manifests primarily as mucocutaneous rash in association with vague constitutional symptoms, diffuse lymphadenopathy, and highly infectious skin lesions
Gonorrhoea infection: caused by Neisseria gonorrhoeae → disseminated gonococcal infection develops as a consequence of untreated primary infection → commonly causes skin papules that progress into haemorrhagic pustules, bullae, petechiae, or necrotic lesions on the extremities
Bacterial endocarditis: rare skin manifestations are Janeway lesions (painless maculopapular lesions on palms and soles) and Osler nodes (painful nodules on tips of fingers → bacterial aetiologies include S. aureus, Enterococcus, Streptococcus bovis, Streptococcus viridans, and HACEK (Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella species) organisms
Toxin-mediated infections:
Staphylococcal scalded skin syndrome: uncommon manifestation of S.aureus toxin-producing strains → toxin targets the granular layer and cause blister formation
Scarlet fever: caused by an erythrogenic toxin produced by group A beta-haemolytic streptococci → manifests as pharyngitis and an accompanying cutaneous eruption (appears in all areas at the same time without a particular pattern of development)
Toxic shock syndrome (TSS): caused by TSS toxin 1, staphylococcal enterotoxins, streptococcal toxins, or other toxins → consists of a complex of symptoms, including fever, low BP, and a diffuse, erythematous rash on the trunk, palms, and soles of the feet that may be desquamative
Anaphylactic/ hypersensitivity reactions
Urticaria
Consists of transient localised wheals (hives), found anywhere on the body
Most commonly in response to either a drug/food allergy or an bite/sting
Cutaneous findings occur due to histamine release in the skin and increased permeability of blood vessels
Each urticarial lesion lasts for 24-48h, although the eruption itself may last longer due to recurrent crops of lesions
Classic Rashes of Childhood:
First Disease: Measles
Second Disease: Scarlet Fever
Third Disease: Rubella
Fourth Disease: Duke’s Disease (etiology unknown)
Fifth Disease: Erythema Infectiosum
Sixth Disease: Roseola
List and briefly describe the mechanisms for underlying factors that predispose children to particular sites of infection and pathogens
Maternal History:
Maternal Health and Illness:
Maternal infections such as HIV, CMV, and HSV can increase the risk of fetal illness and resultant immunodeficiency.
Risky behaviors during pregnancy, including alcohol (ETOH) consumption, smoking, and exposure to toxins, further elevate the risk of fetal immunodeficiency.
HIV can be transmitted from mother to child during pregnancy, childbirth, or breastfeeding, leading to congenital or perinatally acquired HIV infection.
CMV (Cytomegalovirus) can cause congenital CMV infection, leading to developmental delays, hearing loss, and other health issues.
HSV (Herpes Simplex Virus) can cause neonatal herpes, which can be severe and affect multiple organs.
Birth History:
Length of Gestation:
Premature birth (low length of gestation) is associated with an underdeveloped immune system, increasing susceptibility to infections.
Birth Weight:
Low birth weight is linked to immunodeficiency and higher susceptibility to infections.
Mode of Delivery:
Vaginal delivery exposes the newborn to the maternal birth canal flora, which is vital for initiating the development of the immune system.
Non-vaginal deliveries (e.g., cesarean section) are associated with an increased risk of lower respiratory tract infections (LRTI) and allergies, possibly due to the lack of exposure to beneficial maternal flora during birth.
Social History:
Day Care Attendance:
Increased exposure and transmission of pathogens due to close contact with other children, leading to a higher risk of respiratory infections and other communicable diseases.
Pets and Farm Animals:
Animals can be sources of zoonotic infections (infections transmitted from animals to humans) and other pathogens.
Exposure to Solvents, Smoke, and Toxins:
Environmental exposure to these substances at home or day care can increase the risk of respiratory conditions such as asthma.
Growth and Development:
Growth metrics like weight and height, along with underlying chronic conditions, can predispose children to infections.
Feeding History:
Increased duration of breastfeeding provides protective antibodies and enhances immune function, reducing the risk of infections.
Immunization History:
Poor vaccine adherence or incomplete vaccination schedules leave children vulnerable to vaccine-preventable diseases.
Medications:
Immunosuppressants:
Use of medications that suppress the immune system (e.g., corticosteroids, chemotherapy agents) increases vulnerability to infections by reducing the body’s ability to fight off pathogens.
Family History:
Autoimmune Conditions:
A family history of autoimmune conditions or recurrent infections may increase the likelihood of children developing similar conditions due to genetic predispositions and shared environmental factors.
Exposure to family members with contagious diseases increases the risk of transmission and subsequent infection in children.
Common Sites of Infection and Predisposing Factors:
Tonsillitis:
Red, enlarged tonsils +/- purulent exudate
Some children have large tonsils, inflammation needs to be present to make a diagnosis of tonsillitis
Most commonly caused by rhinovirus → coronavirus → adenovirus
If associated with infectious mononucleosis → EBV
If bacterial (10-30%), most commonly group A beta-haemolytic streptococci
Local inflammatory pathways → oropharyngeal swelling, oedema, erythema and pain
Predisposition: frequent contact with pathogens (childcare, etc.), anatomically primarily accessible site by pathogens
Otitis Media:
Purulent effusion (bulging ear drum) + inflammation (redness of ear drum)
Often over-called, a pink eardrum is not otitis media
Respiratory viruses account for most cases and are self-limiting
Co-infections of the middle ear with a virus and a bacterium → development of acute, suppurative otitis media or pus drum
Most common bacteria: Streptococcus pneumoniae (~40%), non-typable Haemophilus influenzae (25-30%) and Moraxella catarrhalis (10-15%)
Under normal conditions the mucociliary action and ventilatory function of the eustachian tube clear the nasopharyngeal flora that enter the middle ear
Upper respiratory viruses can infect the nasal passages, eustachian tube, and middle ear, causing inflammation and impairing these processes
Short length of eustachian tube in children increases risk for infection
List the causes of early and late onset neonatal sepsis
Early Onset Neonatal Sepsis (EOS):
Definition:
Occurs within the first 72 hours to 7 days of life, with some definitions using 72 hours as the cutoff for both term and preterm infants.
Symptoms often appear within the first 6 hours of birth.
Pathophysiology:
Vertical transmission or perinatal transmission from mother to infant.
Pathogens are typically acquired intrapartum, meaning during the delivery process.
Common Causative Pathogens:
Group B Streptococcus (Streptococcus agalactiae):
Most common in industrialized countries.
Universal screening and intrapartum antibiotic prophylaxis have significantly decreased the rate of early onset Group B Streptococcus sepsis.
Escherichia coli:
A gram-negative enteric organism, significant cause of EOS.
Listeria monocytogenes:
Less common but can occur in clusters.
Other Gram-Negative Enteric Bacilli:
Includes Klebsiella species.
Gram-Positive Bacteria:
Includes Enterococcus faecalis, Group D streptococci, alpha-hemolytic streptococci, and staphylococci.
Less Common Pathogens:
Streptococcus pneumoniae
Haemophilus influenzae (Type A and B)
Neisseria meningitidis
Neisseria gonorrhoeae
Viral Infections Mimicking Bacterial Sepsis:
Neonatal infection with herpes simplex virus (HSV) and enterovirus may present similarly to bacterial sepsis
Late Onset Neonatal Sepsis (LOS):
Definition:
Occurs after the first 72 hours to 7 days of life, extending to one month of age
Typically, for preterm infants, LOS is defined as occurring >72 hours after birth, and for term infants, it is ≥7 days
Pathophysiology:
Infections are usually acquired from the environment, which includes hospital (nosocomial) settings or home environments
Pathogens are acquired at delivery but invade later or are acquired postnatally.
Common Causative Pathogens:
Coagulase-Negative Staphylococci (CONS):
The most common cause of LOS due to high incidence in vascular catheter-associated infections in hospitalized neonatal patients.
Gram-Negative Bacilli:
Includes various enteric bacteria.
Streptococci and Anaerobes:
Includes different species of streptococci and anaerobic bacteria.
Staphylococcus aureus:
Significant pathogen in LOS.
Chlamydia trachomatis:
Can cause late onset neonatal sepsis.
Genital Mycoplasmas:
Includes Mycoplasma species associated with genital infections.
E. coli:
Becoming more recognized as a significant cause of LOS, especially in low birth weight infants.
Less Common Pathogens:
Pseudomonas aeruginosa
Enterobacter cloacae
Candida albicans:
Particularly causative in low birth weight infants and immunocompromised neonates.
Viral Infections:
Disseminated infections with HSV, enterovirus, adenovirus, and respiratory syncytial virus (RSV) may manifest as early or late onset sepsis.
Serious bacterial infections:
Briefly describe the pathophysiology of serious bacterial infections in infants and children
UTI
Overview:
Urinary Tract Infections (UTIs) are among the most common serious bacterial infections in children. They can involve the lower urinary tract (cystitis), the upper urinary tract (pyelonephritis), or both.
Pathophysiology:
Colonization:
UTIs begin with the colonization of the periurethral mucosa by genitourinary bacteria. This initial step is crucial for the development of an infection.
Ascending Infection:
Cystitis:
The infection ascends from the urethra into the bladder
In the bladder, bacteria can multiply and cause inflammation of the bladder mucosa
Pyelonephritis:
If vesicoureteral reflux (VUR) is present, bacteria can ascend further into the upper urinary tract, reaching the kidneys and causing pyelonephritis.
Pyelonephritis involves infection of the renal parenchyma and can lead to renal damage and scarring.
Predisposing Factors:
Anatomical Abnormalities:
Conditions such as neurogenic bladder, obstructive uropathy, and vesicoureteral reflux increase the risk of UTIs.
These conditions can lead to incomplete bladder emptying, which facilitates bacterial growth.
Functional Abnormalities:
Functional issues like chronic constipation can lead to incomplete elimination of urine, allowing bacteria to remain in the bladder and grow
Indwelling Foreign Bodies:
Presence of catheters or other foreign bodies can act as a nidus for bacterial colonization and infection
Virulence Factors:
E. coli isolates from UTIs often express virulence factors that enhance their ability to adhere to the uroepithelial cells and grow
These factors include adhesins that mediate attachment to uroepithelial receptors and aerobactin, which enhances bacterial growth
Epidemiology:
UTIs are the most common serious bacterial infections in children without a focal infection.
Prevalence:
8% of girls and 2% of boys will have had a UTI by age 7.
Higher incidence in uncircumcised male infants.
Risk Factors:
Female Sex:
Females have a shorter urethra, which facilitates the ascent of bacteria into the bladder.
Uncircumcised Infants:
Higher prevalence of UTIs due to potential for increased bacterial colonization around the foreskin.
Urogenital Anomalies:
Congenital anomalies such as vesicoureteral reflux and urinary obstruction increase the risk of UTIs
Functional Anomalies:
Conditions such as chronic constipation and withholding behavior, which lead to incomplete bladder emptying and bacterial retention.
Causative Organisms:
Neonates:
Escherichia coli (E. coli): The most common pathogen.
Other less common pathogens include Citrobacter, Enterobacter, and Klebsiella species.
Older Children:
E. coli: The predominant pathogen.
Other less common pathogens include Klebsiella, Enterobacter, and Enterococcus species.
Clinical Features:
General Symptoms:
Fever, abdominal or loin pain, dysuria (painful urination), and frequency (increased need to urinate).
Young Infants:
Non-specific symptoms such as jaundice, failure to thrive, poor feeding, vomiting, irritability, and strong-smelling urine.
Diagnosis:
Urine Dipstick:
Can guide initial management but should be followed by a urine culture and sensitivity (MCS) before starting antibiotics
Urine Collection:
Older Children:
Midstream urine collection is preferred.
Pre-Continent Children ( those who are not yet able to consistently control their urination and bowel movements. This usually includes infants and toddlers):
Not Seriously Unwell:
Clean catch method, which involves stimulating urination by rubbing the lower abdomen.
Seriously Unwell:
Suprapubic aspirate or in/out catheter is used to collect urine directly from the bladder.
Management:
Empirical Antibiotics:
Uncomplicated UTI:
Oral cefalexin is commonly used.
Complicated Cases or Infants <3 months:
Intravenous antibiotics are administered. Common regimens include:
Gentamicin: Administered intravenously over 3-5 minutes.
Dosing:
Child <10 years: 7.5 mg/kg up to 320 mg
Child ≥10 years with septic shock or requiring intensive care: 7 mg/kg
Child ≥10 years without septic shock and not requiring intensive care: 6 mg/kg up to 560 mg
Amoxicillin or Ampicillin: 50 mg/kg up to 2 g IV, 6-hourly
If gentamicin is contraindicated:
Cefotaxime: 50 mg/kg up to 1 g IV, 8-hourly. For children with septic shock or requiring intensive care, 50 mg/kg up to 2 g IV, 8-hourly.
Ceftriaxone (child ≥1 month): 50 mg/kg up to 1 g IV, daily. For children with septic shock or requiring intensive care, 50 mg/kg up to 1 g IV, 12-hourly.
Adjustment Based on Culture and Sensitivity:
Antibiotic regimen should be adjusted according to the results of urine culture and sensitivity testing to target the specific pathogens causing the infection.
Viral Infections Mimicking UTIs:
Disseminated viral infections such as herpes simplex virus (HSV), enterovirus, adenovirus, and respiratory syncytial virus (RSV) can present with similar symptoms to bacterial sepsis.
Bacteraemia
Definition:
Bacteraemia: The presence of bacteria in the blood, which may or may not be symptomatic.
Septicaemia: A clinical condition involving a systemic inflammatory response to infection, typically referring to sepsis.
Pathophysiology:
Recognition and Immune Activation:
Innate Immune Response:
Innate immune cells recognize invading pathogens through pattern recognition receptors (PRRs)
Activation of immune cells leads to the secretion of pro-inflammatory cytokines.
This triggers the migration of polymorphonuclear leukocytes to the site of infection.
Cytokine Release and Systemic Inflammatory Response Syndrome (SIRS):
Pro-inflammatory cytokines induce vasodilation and increase vascular permeability.
Symptoms of SIRS include elevated temperature, accelerated pulse and breathing, and leucocytosis (increased white blood cells).
Sepsis: Suspected or proven infection plus SIRS.
Severe Sepsis: Sepsis with organ dysfunction (e.g., hypotension, hypoxemia, oliguria, metabolic acidosis, thrombocytopenia, confusion).
Septic Shock: Severe sepsis with hypotension unresponsive to fluid resuscitation.
Pathological Processes:
Endothelial Dysfunction: Damage to the endothelial lining of blood vessels.
Cell Death: Apoptosis and necrosis of cells due to severe infection and immune response.
Bio-energetic Derangement: Disruption of cellular energy metabolism.
Immunoparalysis: A state of immune system suppression following an initial hyper-inflammatory phase.
Early-Onset Neonatal Sepsis (EOS):
Timing: Occurs within the first 72 hours of life.
Common Pathogens:
Group B Streptococcus (GBS)
Gram-negative bacilli (e.g., E. coli)
Late-Onset Neonatal Sepsis (LOS):
Timing: Occurs after 72 hours to 1 month of life
Common Pathogens:
Coagulase-Negative Staphylococci (CONS): Most common due to high incidence in vascular catheter-associated infections in hospitalized neonates.
Other EOS Pathogens: Can also cause LOS.
Infants and Young Children:
Common Pathogens:
Streptococcus pneumoniae: Major cause of invasive bacterial infections in childhood.
Neisseria meningitidis: Affects young children and adolescents, less common since vaccination.
Staphylococcus aureus: Can cause severe sepsis in previously healthy children.
Group A Streptococci: Also a cause of severe sepsis.
Epidemiology:
The introduction of the pneumococcal vaccine has reduced the rate of occult bacteraemia to less than 1% in healthy, immunized infants.
Clinical Features:
General Symptoms:
Fever, lethargy, poor perfusion, cyanosis, marked hypo/hyperventilation.
Apparent Focal Disease:
Pneumonia: Cough, dyspnea, pulmonary crackles.
Cellulitis: Skin erythema.
Septic Arthritis: Joint pain and swelling.
Investigations:
Bedside Tests:
Urinalysis, urine microscopy culture and sensitivity (MCS), stool MCS, viral respiratory panel
Blood Tests:
Blood cultures, full blood count (FBC), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), procalcitonin
Imaging:
Chest X-ray (CXR) if pneumonia is suspected.
Other Tests:
Lumbar puncture (LP) if meningitis is suspected.
Management:
Empirical Antibiotics:
Neonates:
Early Onset Sepsis: Benzylpenicillin plus cefotaxime (if meningitis possible) or gentamicin (if meningitis excluded).
Late Onset Sepsis: Amoxicillin/amoxicillin plus cefotaxime (if meningitis possible) or gentamicin (if meningitis excluded)
Infants 1-2 Months:
Amoxicillin/amoxicillin plus cefotaxime/ceftriaxone (if meningitis possible) or gentamicin (if meningitis excluded).
Children >2 Months:
Gentamicin plus cefotaxime/ceftriaxone plus vancomycin
Adjustment After Culture Results:
Adjust antibiotic regimen based on culture and susceptibility results
Risk Factors for Infection with MRSA:
Residence in areas with high prevalence of MRSA
Previous colonization or infection with MRSA, especially if recent or related to the current episode of care.
Frequent or prolonged hospital stays, especially with recent antibiotic exposure or surgery
Management Protocols for MRSA Risk:
Empirical Regimen:
Gentamicin IV:
Children 2 months to <10 years: 7.5 mg/kg up to 320 mg for the first dose.
Children ≥10 years with septic shock or requiring intensive care support: 7 mg/kg for the first dose.
Children ≥10 years without septic shock and not requiring intensive care support: 6 mg/kg up to 560 mg for the first dose.
Plus either:
Cefotaxime 50 mg/kg up to 2 g IV, 6-hourly.
OR ceftriaxone 50 mg/kg up to 2 g IV, 12-hourly.
Plus vancomycin IV if the child has septic shock or is at increased risk of MRSA infection, considering a 25-30 mg/kg loading dose.
Meningitis
Overview:
Meningitis is an inflammation of the protective membranes covering the brain and spinal cord, known as the meninges.
It can be caused by bacterial, viral, or fungal infections.
Types of Meningitis:
Viral Meningitis:
Most common cause of aseptic meningitis (meningitis that is not caused by bacteria)
Causative Agents: Human enteroviruses (most common), herpes simplex virus (HSV), mumps, arboviruses (e.g., West Nile virus), HIV, and rarely, influenza.
Typically self-limiting without serious sequelae
Bacterial Meningitis:
Less common but more serious than viral meningitis.
Causative Agents: Streptococcus pneumoniae, Haemophilus influenzae type b (Hib), and Neisseria meningitidis are the predominant pathogens in both adults and children.
Fungal Meningitis:
Progressive, life-threatening, chronic, or subacute meningitis.
Causative Agent: Cryptococcus species
Often seen in immunosuppressed patients, including infants and neonates.
Pathophysiology:
Colonization and Invasion:
Nasopharyngeal Colonization: Pathogens colonize the nasopharyngeal epithelium.
Common pathogens include
Streptococcus pneumoniae
Neisseria meningitidis
Haemophilus influenzae type b.
The introduction of routine immunization has significantly decreased infections caused by H. influenzae and meningococcal group C.
Tuberculous meningitis should also be considered.
Bloodstream Invasion:
Pathogens invade the bloodstream, allowing them to disseminate and reach the meninges
Attachment and Invasion of the Meninges:
Bacteria attach to and invade the meninges, leading to inflammation
This process involves the release of pro-inflammatory cytokines, leading to increased permeability of the blood-brain barrier and the infiltration of immune cells.
Inflammation and Cerebral Edema:
Inflammation leads to the leakage of proteins and other substances into the brain tissue, causing cerebral edema.
This can alter cerebral blood flow and metabolism, contributing to cerebral vasculitis and further brain damage.
Clinical Features:
Neonates:
Early Symptoms: Lethargy, muscle hypotonia, irritability, poor appetite, vomiting, hyperthermia or hypothermia, dyspnea, and abnormal breathing patterns
Late Symptoms: Bulging fontanelle, high-pitched crying, seizures.
Children:
Classic Triad: Fever, headache, neck stiffness
Other symptoms include altered mental status, photophobia, nausea, vomiting, malaise, seizures.
N. meningitidis (Meningococcal): Myalgia, petechial or purpuric rash.
Investigation:
Blood Tests:
Full blood count (FBC), urea, electrolytes, creatinine (UEC), liver function tests (LFT), C-reactive protein (CRP), venous blood gas (VBG), serum glucose, and blood cultures.
Imaging:
Head CT scan may be required, especially if there are indications of increased intracranial pressure (e.g., focal neurological deficits, altered mental status).
Lumbar Puncture and CSF Analysis:
Perform lumbar puncture (LP) to obtain cerebrospinal fluid (CSF) for analysis.
Procedure: Position patient in the lateral recumbent position, identify the interspace (L3-L4 or L4-L5), and use sterile technique. Obtain CSF for pressure measurement and analysis.
Complications
Failure to obtain a specimen/traumatic bloody tap (common)
Post-dural puncture headache (uncommon) 5-15%
Transient/persistent paraesthesia/numbness (very uncommon)
Respiratory arrest from positioning (rare)
Infection introduced by needle → meningitis, epidural abscess, osteomyelitis (very rare)
Spinal haematoma (very rare)
Brain herniation (extremely rare in the absence of contraindications above)
Contraindications
Absolute contraindications: GCS < 8 or deteriorating LOC, ↑ ICP (but bulging fontanelles without other signs of ↑ ICP is not a contraindication)
Relative contraindications: septic shock, hemodynamic comprise, significant respiratory distress, new focal neurological signs or seizures, seizure within previous 30 minutes, bleeding predisposition (e.g. INR > 1.5, platelets < 50 or child on anticoagulant)
Management:
Supportive Therapy:
Fluid Therapy:
Normal: 3 mL/kg/hour of Plasma-Lyte 148 or normal saline plus 5% glucose.
Hyponatremia: 2 mL/kg/hour Plasma-Lyte 148 or normal saline plus 5% glucose.
Raised ICP or Generalized Edema: 1-2 mL/kg/hour Plasma-Lyte 148 or normal saline plus 5% glucose.
Shock or Hypovolemia: Fluid resuscitation with 10-20 mL/kg normal saline bolus.
Supplemental Oxygen: Administer as needed.
Medical Therapy:
Empirical Antibiotics:
<2 Months:
Treat as sepsis or septic shock
Early Onset Sepsis: Benzylpenicillin plus cefotaxime
Late Onset Sepsis: Amoxicillin/amoxicillin plus cefotaxime
1-2 Months: Amoxicillin/amoxicillin plus cefotaxime/ceftriaxone
2 Months: Ceftriaxone/cefotaxime plus dexamethasone.
Pathogen-Specific Antibiotics:
N. meningitidis: Benzylpenicillin
S. pneumoniae (Penicillin-sensitive): Benzylpenicillin
S. pneumoniae (Penicillin-resistant): Vancomycin
Hib: Ceftriaxone/cefotaxime.
Gram-negative Bacteria: Ceftriaxone/cefotaxime
GBS, Listeria: Benzylpenicillin
HSV: Aciclovir
Antiviral Therapy: For confirmed viral infections like HSV or varicella-zoster, aciclovir or valaciclovir is recommended.
Complications and Sequelae:
SIADH: Syndrome of inappropriate antidiuretic hormone secretion, affecting about 1/3 of children with meningitis.
Cerebral Edema: Increased permeability of the blood-brain barrier leads to vasogenic cerebral edema.
Sensorineural Hearing Loss: Direct bacterial invasion or inflammatory response damages the 8th cranial nerve, cochlea, or labyrinth.
Other Complications: Seizures, circulatory shock, cerebrovascular complications, motor deficits, subdural effusion, intellectual disability, and behavioral problems.
Contact Tracing:
Probable and confirmed cases of invasive meningococcal disease are notifiable.
Close contacts should be traced and monitored for symptoms.
Pneumonia
Risk Factors:
Neonates and Infants:
Prolonged rupture of membranes (PROM), maternal fever, maternal Group B Streptococcus (GBS) colonization, congenital lung cysts, chronic lung disease, immunodeficiency, cystic fibrosis, sickle cell disease, and presence of a tracheostomy
Prolonged rupture of membranes (PROM) refers to the rupture of the amniotic sac and the leakage of amniotic fluid before the onset of labor, lasting more than 18 hours before delivery.
Children:
Chronic lung disease (e.g., asthma), immunodeficiency, cystic fibrosis, and congenital lung abnormalities.
Cause & Pathophysiology:
Neonates (< 2 months):
Common pathogens include
Group B Streptococcus (Streptococcus agalactiae)
Escherichia coli
Klebsiella species
Staphylococcus aureus
Haemophilus influenzae
Pathogenesis involves infection of the lower respiratory tract and lung parenchyma leading to consolidation.
Infants and Children (> 2 months):
Viral Causes (70%): Influenza A, respiratory syncytial virus (RSV), parainfluenza virus, human metapneumovirus (hMPV), and adenovirus
Bacterial Causes: Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydia trachomatis, Staphylococcus aureus.
Viruses are the most common cause of community-acquired pneumonia (CAP) in children older than 2 months.
Clinical Features:
Non-specific symptoms in neonates (temperature instability, poor feeding, irritability).
In older children: cough, fever, tachypnea, retractions, hypoxemia, congestion, irritability, poor feeding
Investigation:
Bedside Tests: Sputum culture, influenza testing (via nasal swab, PCR)
Blood Tests: Full blood count (FBC) to check for leukocytosis, and urea, electrolytes, and creatinine (UEC) for children receiving IV fluids.
Imaging: Chest X-ray (CXR) showing hazy lungs and distinct infiltrates, which may be challenging to differentiate from transient tachypnea of the newborn (TTN) and respiratory distress syndrome (RDS).
Delayed clearance of fetal lung fluid: Normally, fetal lung fluid is absorbed shortly before or during birth. In TTN, this process is delayed, leading to fluid retention in the lungs.
Surfactant deficiency: Surfactant reduces surface tension in the lungs, preventing alveolar collapse. A deficiency leads to widespread atelectasis and impaired gas exchange.
Complications:
Lung abscess
Parapneumonic effusion
Empyema
Management:
Neonates (< 2 months):
Early-Onset CAP (within 72 hours of birth): Benzylpenicillin (60 mg/kg IV) plus gentamicin IV. Modify treatment based on susceptibility testing.
Late-Onset CAP (≥ 72 hours after birth): Ampicillin (50 mg/kg IV) or amoxicillin (50 mg/kg IV) plus gentamicin IV.
Children (≥ 2 months):
Low Severity: Oral amoxicillin (25 mg/kg up to 1g PO, 8-hourly for 3 days).
Moderate Severity: Oral amoxicillin or IV benzylpenicillin (50 mg/kg IV, 6-hourly) for 5-7 days
High Severity: IV cefotaxime (50 mg/kg up to 2g IV, 8-hourly) or IV ceftriaxone (50 mg/kg up to 2g IV, daily). In case of severe penicillin allergy, ciprofloxacin plus vancomycin IV, or moxifloxacin IV.
Supportive Therapies:
Antipyretics for fever.
IV fluids for dehydration.
Supplemental oxygen to maintain SpO2 > 92%.
Chest drain for empyema.
Connective tissue
Pathophysiology:
Infection Sites:
Infections often occur in the metaphyseal region of bones due to the rich blood supply.
Infection spreads hematogenously from a primary site of entry (e.g., respiratory tract, gastrointestinal tract, ENT, skin).
Direct inoculation can occur from open fractures or penetrating wounds.
Local extension from adjacent infected sites is also possible.
Spread of Infection:
In infants, transphyseal vessels allow infection to spread to adjacent joints, leading to septic arthritis.
In adolescents, infections tend to spread through the medullary canal of the bone.
Common Pathogens:
Age <12 months: Staphylococcus aureus, Group B Streptococcus, Gram-negative bacilli, Candida albicans.
Age 1-5 years: Staphylococcus aureus, Haemophilus influenzae (rare in immunized children), Group A Streptococcus (pyogenes), Streptococcus pneumoniae, Kingella kingae, Neisseria gonorrhoeae (consider child abuse).
Age 5-12 years: Staphylococcus aureus, Group A Streptococcus.
Age 12-18 years: Staphylococcus aureus, Neisseria gonorrhoeae (sexually active).
Commonly Affected Joints:
75% of cases affect the lower limb (knee > hip > ankle).
25% of cases affect the upper limbs.
Complications:
Systemic: Septicemia.
Local: Pathological fractures, sequestration, growth disturbances.
Management Approach:
Medical:
Medical: IV antibiotics for a minimum of 2wks, followed by oral antibiotics for 4 weeks → early liaison with microbiologist required
Treat as sepsis or septic shock with an unknown source (as for bacteraemia above)
Empirical regimens target Staphylococcus aureus as well as other potential pathogens (e.g. beta-haemolytic streptococci, Enterobacteriaceae, Pseudomonas aeruginosa)
Give antibiotics within 1h of the patient presenting to medical care or, for a ward-based patient, developing sepsis or septic shock; antibiotics should be given immediately after appropriate samples are taken for culture
Blood samples should always be taken before antibiotic administration
Other relevant samples (e.g. joint aspirate, pus aspirate, bone biopsy) should be collected as soon as possible but should not delay antibiotic administration
Surgical:
Drainage and debridement are necessary if there is frank pus on aspiration, a sequestered abscess, or a collection not accessible to antibiotics.
Other Connective Tissue Disorders in Children
Chondromalacia Patellae:
Pathophysiology: Softening of the cartilage underneath the patella leads to generalized knee pain, especially when climbing stairs, playing sports with an axial load on the knee, or sitting for long periods.
Management: Physiotherapy, ice, analgesia, and arthroscopic smoothing of the patella undersurface.
Cutis Laxa:
Pathophysiology: Inherited or acquired mutation leads to abnormal elastin metabolism, resulting in reduced skin elasticity. This manifests as loose skin that hangs in folds, gastrointestinal hernias or diverticula, pulmonary emphysema, bronchiectasis, heart failure, and aortic aneurysms.
Management: No specific treatment; physical therapy can help increase skin tone. Sometimes plastic surgery is needed.
Ehlers-Danlos Syndrome:
Pathophysiology: Autosomal dominant mutation in genes that encode collagen affects the amount, structure, or assembly of different collagens, leading to articular hypermobility, dermal hyperelasticity, widespread tissue fragility, and bleeding tendencies.
Types: Classic, hypermobility, vascular, kyphoscoliosis, arthrochalasis, dermatosparaxis.
Complications: Bleeding, synovial effusions, sprains, dislocations, spinal kyphoscoliosis, thoracic deformity, pes planus, hernias, diverticula, gastrointestinal hemorrhage, GI perforation, dissecting aortic aneurysm, valve prolapse.
Investigations: Genetic testing, skin biopsy, echocardiography, vascular imaging.
Management: Supportive care such as protective clothing, padding, meticulous hemostasis during surgeries.
Infrapatellar Tendinitis:
Epidemiology: More common in figure skaters, basketball or volleyball players, ages 10-23 years.
Pathophysiology: Overuse injury to the patella tendon at the attachment of the lower pole of the patella leads to microvascular fractures, causing knee pain, especially when straightening the knee against force (e.g., climbing stairs, jumping).
Management: Activity modification, physical therapy, analgesia, and surgical repair if necessary.
Juvenile Idiopathic Arthritis:
Epidemiology: Uncommon, onset before 16 years, females more affected than males.
Pathophysiology: Autoimmune and/or autoinflammatory disease leads to chronic synovial inflammation, joint capsule hyperplasia, pannus formation, and invasion of the articular surface, resulting in loss of joint function.
Clinical Features: Arthritis, fever, rash, adenopathy, splenomegaly, iridocyclitis.
Investigations: FBC (leukocytosis, anemia, thrombocytosis), increased CRP/ESR, positive ANA, RF usually absent, ultrasound, X-ray, slit lamp examination.
Management: Physiotherapy, NSAIDs (first line), DMARDs (second line), surgery if necessary.
Marfan Syndrome:
Pathophysiology: Autosomal dominant mutation of the fibrillin-1 gene on chromosome 15 leads to defective fibrillin, affecting connective tissue microfibrils and elastin.
Clinical Features: Mitral valve prolapse, aortic dissection/aneurysm/regurgitation, retinal detachment, fibrillin-1 mutation, arm span greater than height, near-sightedness, nasal voice (high arched palate), scoliosis, subluxated lens.
Management: Beta-blockers to prevent cardiac complications, symptom management.
Nail-Patella Syndrome:
Pathophysiology: Autosomal dominant mutation in a gene for a transcription factor involved in limb and kidney development results in abnormal bones, joints, fingernails, toenails, and kidneys.
Management: ACE inhibitors for proteinuria and hypertension, kidney transplantation in severe cases.
Osteochondrodysplasias:
Pathophysiology: Mutations in genes encoding proteins involved in the growth and development of connective tissue, bone, or cartilage lead to skeletal maldevelopment and short-limbed dwarfism.
Management: Surgical limb-lengthening, surgical correction of leg bowing, or joint replacement as needed.
Osteogenesis Imperfecta:
Pathophysiology: Mutations in genes encoding for a type of collagen result in diffuse abnormal fragility of bones and sometimes sensorineural hearing loss, blue sclerae, dentinogenesis imperfecta, and joint hypermobility.
Management: Supportive measures such as walking aids and wheelchairs, bisphosphonates, and surgery to improve mobility and correct skeletal defects.
Pseudoxanthoma Elasticum:
Pathophysiology: Gene mutation in a protein involved in cellular detoxification leads to calcification of elastic fibers in the skin, retina, and cardiovascular system. Manifestations include small yellowish papules on the neck, axillae, and flexural surfaces (cutaneous), angled streaks of the retina and retinal hemorrhages leading to gradual vision loss (ocular), and premature atherosclerosis with intermittent claudication, hypertension, angina, and myocardial infarction (cardiovascular).
Management: Symptomatic management and prevention of complications.
Meningococcal sepsis
Epidemiology:
Primarily affects children under 5 years of age and adolescents.
Approximately 50% of cases occur in children under 2 years old, with 25% in individuals over 30 years old.
Cause:
Caused by Neisseria meningitidis, an aerobic gram-negative diplococcus found exclusively in the human nasopharynx.
There are 13 serogroups of Neisseria meningitidis, with the most common being A, B, C, W, and Y.
Pathophysiology:
Transmission and Initial Infection:
Spread by respiratory droplets.
Bacteria colonize the nasopharynx and can invade the bloodstream.
Bacterial Factors and Immune Response:
Bacterial lipo-oligosaccharide stimulates a pro-inflammatory cytokine response.
Endotoxins released by the bacteria trigger a widespread inflammatory response, leading to endothelial necrosis, intraluminal thrombosis, and perivascular hemorrhage.
Systemic Effects:
Vascular Permeability and Hypotension:
Increased vascular permeability and dysregulation of vascular tone result in hypotension.
Myocarditis and myocardial depression may further impair tissue perfusion.
Disseminated Intravascular Coagulation (DIC):
Activation of the coagulation cascade and downregulation of anticoagulant and fibrinolytic pathways.
DIC is characterized by acquired deficiencies of protein C, protein S, and antithrombin III, increased plasminogen activator inhibitor, and thrombin-activatable fibrinolysis inhibitor.
Small-vessel thrombosis and skin necrosis cause purpura fulminans.
Thrombosis of larger blood vessels leads to ischemia or infarction of digits or extremities.
Meningitis and Neurological Complications:
Local inflammatory responses in the brain cause cerebral edema, raised intracranial pressure (ICP), and vascular thrombosis.
Waterhouse-Friderichsen Syndrome:
Bilateral adrenal hemorrhage and necrosis lead to acute adrenal insufficiency.
Clinical Features:
Early Signs (within 12 hours):
Fever, headache, loss of appetite, nausea, vomiting, sore throat, coryza.
Limb pain, myalgia, refusal to walk, cold hands and feet.
Red rash progressing to petechiae and then purpura.
Signs of Sepsis:
Pallor or mottling, cool peripheries, prolonged capillary refill, tachypnea, hypoxia, grunting.
Late Signs (after 12 hours):
Altered level of consciousness, neck stiffness, headache, photophobia, bulging fontanelles, positive Kernig or Brudzinski signs.
Non-blanching rash (purpuric or petechial lesions).
Increased heart rate, respiratory rate, and capillary refill time ≥2 seconds.
Investigations:
Blood Tests:
Blood culture, serum PCR, full blood count (FBC), urea and electrolytes (UEC), liver function tests (LFT), C-reactive protein (CRP), venous blood gas (VBG), serum glucose.
Imaging:
Head CT scan if there are indications of increased intracranial pressure or other neurological signs.
Other Tests:
Lumbar puncture and synovial fluid analysis.
Management:
Management of Sepsis:
Immediate administration of broad-spectrum IV antibiotics within one hour of presentation or upon developing sepsis or septic shock.
Empirical antibiotics should target Neisseria meningitidis and other potential pathogens.
Specific Management of Meningococcal Infection:
Antibiotics:
Initial Therapy: IV ceftriaxone (50 mg/kg up to 2 g, 12-hourly for 5 days) or IV cefotaxime (50 mg/kg up to 2 g, 6-hourly for 5 days).
De-escalation: If susceptibility to benzylpenicillin is confirmed and the patient is not hypersensitive to penicillin, switch to IV benzylpenicillin (60 mg/kg up to 2.4 g, 4-hourly for 5 days).
Penicillin Allergy: For severe hypersensitivity to penicillins, use IV ciprofloxacin (10 mg/kg up to 400 mg, 8-hourly for 5 days).
Supportive Therapy: Consider antipyretics for fever, IV fluids for dehydration, supplemental oxygen, and chest drain if necessary.
Infection Control:
Isolation and droplet precautions for at least 24 hours after antibiotic administration.
Notify the local public health unit and initiate contact tracing. Provide clearance antibiotics for close contacts.
Complications:
Meningitis:
Complications include cerebral edema, raised ICP, hydrocephalus, and long-term neurological deficits.
Sepsis:
Systemic complications such as septic shock, multi-organ failure, and disseminated intravascular coagulation (DIC).
Local complications include tissue necrosis, limb ischemia, and amputations.
Waterhouse-Friderichsen Syndrome:
Acute adrenal insufficiency due to adrenal hemorrhage and necrosis, leading to hypotension, shock, and metabolic disturbances.
Symptoms include salt craving, weight loss, anorexia, fatigue, lethargy, gastrointestinal complaints, orthostatic hypotension, and signs of meningococcal meningitis.
Management involves treating the underlying cause and supportive care.
Prognosis:
Mortality rate is approximately 8%, with a higher rate for sepsis (15-20%) compared to meningitis alone (5%).
Most deaths occur within the first 24 hours of illness onset.
Describe the management approach to serious bacterial infections in infants and children
Initial Stabilization:
Stabilize Airway, Breathing, and Circulation (ABCs):
Ensure the airway is clear and provide oxygen if necessary.
Support breathing with ventilation if required.
Maintain circulation with intravenous fluids and medications to support blood pressure.
Transfer to Pediatric Intensive Care Unit (PICU) if in Septic Shock:
Continuous monitoring and advanced supportive care are essential in the PICU.
Urgent Investigations (Septic Screen):
Full Blood Count (FBC): To check for leukocytosis or leukopenia.
Blood Culture: To identify the causative pathogen.
C-reactive Protein (CRP): To assess inflammation levels.
Urine Microscopy, Culture, and Sensitivity (MCS): To check for urinary tract infections.
Cerebrospinal Fluid (CSF) MCS: To diagnose meningitis if indicated.
Chest X-ray (CXR): To identify pneumonia or other thoracic infections.
Immediate Antibiotic Administration:
Antibiotic choice depends on the age of the child and the suspected or confirmed pathogen. Empirical antibiotic therapy should be initiated promptly.
Empiric Antimicrobial Regimens:
For febrile infants younger than 90 days without focal infections:
<1 Month with Fever but Well Appearing: Empiric antibiotics such as ampicillin and gentamicin or cefotaxime.
1-2 Months Well Appearing with One Risk Factor (e.g., risk factor, abnormal WCC, elevated CRP, CXR findings): Empiric antibiotics.
Additional Considerations:
Acyclovir: Add when indicated (e.g., mucocutaneous vesicles, seizures, CSF pleocytosis (increased number of white blood cells (WBCs) in the cerebrospinal fluid.)) for possible herpes simplex virus infection.
Gentamicin: Add for broader Gram-negative pathogen coverage.
Vancomycin: Add for MRSA coverage if suspected.
Fluid Resuscitation:
Administer intravenous fluids to maintain adequate perfusion and blood pressure.
Fluid boluses of isotonic saline or lactated Ringer's solution, typically 20 mL/kg, may be given and repeated as necessary.
Circulatory Support:
Inotropes (e.g., dopamine, epinephrine): If fluids alone are insufficient to maintain blood pressure and perfusion.
Management of Disseminated Intravascular Coagulation (DIC)
Fresh Frozen Plasma (FFP) and Platelets: Administer to correct coagulopathy and manage bleeding.
No evidence supports the routine use of steroids in septic shock.
Monitoring and Supportive Care:
Continuous monitoring of vital signs, urine output, and other clinical parameters.
Supportive therapies may include antipyretics for fever, supplemental oxygen, and mechanical ventilation if required.
Ensure adequate nutrition and hydration.
Viral Infections
Briefly describe the pathophysiology of viral infections in children
Measles
Epidemiology:
Typically occurs in regions with low vaccination rates and in resource-limited countries
Peak incidence is in children under 12 months of age, especially before routine vaccination
Cause:
Pathogen: Measles virus, an RNA virus of the Morbillivirus genus belonging to the Paramyxoviridae family
Route of Transmission: Direct contact with or inhalation of virus-containing droplets
Incubation Period: Approximately 2 weeks
Pathophysiology:
Incubation (6 to 21 days):
Virus enters the body via respiratory mucosa or conjunctivae
It replicates locally and then spreads to regional lymphatic tissues
Disseminates to other reticuloendothelial sites via the bloodstream (first viremia).
Initial Infection: The virus enters your body, for example, through your nose or mouth.
Local Replication: It starts to multiply where it first entered.
First Viremia: The virus gets into your blood for the first time.
Dissemination: From the blood, the virus spreads to other parts of your body, like the liver and spleen
Secondary Sites of Infection: The virus multiplies in these new areas, possibly entering the blood again and spreading even more
Contagiousness is estimated from five days before the appearance of the rash to four days afterward
A second viremia occurs several days after the first, signaling the beginning of the prodromal phase
Prodromal Phase (2 to 4 days):
Characterized by the appearance of symptoms such as fever, malaise, and anorexia, followed by conjunctivitis, coryza, and cough
Koplik spots may develop around 48 hours before the exanthem. These are 1 to 3 mm whitish, grayish, or bluish elevations with an erythematous base and are pathognomonic for measles.
Koplik spots typically slough off once the exanthem appears.
Exanthem Phase (6 to 7 days):
The rash typically arises approximately two to four days after the onset of fever
It is described as an erythematous, maculopapular, blanching rash that begins on the face and spreads to the neck, upper trunk, lower trunk, and extremities
The rash becomes non-blanching in later stages and may include petechiae, which can be hemorrhagic
The rash darkens after 3 to 4 days before fading
Other findings include lymphadenopathy, high fever, and worsening respiratory signs
Resolution:
Viremia (viruses present in the bloodstream) and the presence of the virus in tissues and organs cease by days 15 to 17, corresponding to the appearance of antibodies.
Clinical Features:
Prodromal Stage (4-7 days):
Coryza, cough, and conjunctivitis
Fever and malaise
Koplik spots on the buccal mucosa, appearing as tiny white or bluish-gray spots on an irregular erythematous background.
Exanthem Stage (7 days):
High fever and generalized lymphadenopathy
Erythematous maculopapular, blanching, partially confluent rash that begins behind the ears along the hairline before spreading to the rest of the body, including the feet.
Investigations:
Blood Tests:
Measles serology for IgM and IgG antibodies.
Full blood count (FBC) to assess leukocyte and platelet levels
Serum PCR for viral detection
Other Tests:
Lymph node biopsy if indicated.
Management:
Supportive Care:
Implement airborne precautions and isolation.
Administer antipyretics for fever
Vitamin A Supplementation:
Considered in severe cases to improve outcomes.
Prevention:
Measles can be prevented with a live attenuated vaccine, typically given as part of the MMR (measles, mumps, rubella) vaccination schedule
Rubella
Epidemiology:
Australia was declared free of rubella in 2018, but the disease is still prevalent in regions with low vaccination rates.
Rubella primarily affects unvaccinated children and can lead to congenital rubella syndrome in infants born to infected mothers.
Cause:
Pathogen: Rubella virus
Route of Transmission: Respiratory droplets and transplacental transmission
Incubation Period: 14 to 21 days (average 14 days)
Pathophysiology:
Transmission:
Rubella is transmitted from human to human via direct or droplet contact with infected body fluids, most commonly nasopharyngeal secretions.
Patients may shed the infectious virus from 7 to 30 days after infection, which includes the period from one week before to two weeks after the onset of the rash.
Infants with congenital rubella syndrome may be contagious for more than one year.
Replication and Spread:
After inhalation of infectious aerosols, the rubella virus initially replicates in the nasopharyngeal cells and regional lymph nodes.
Viremia occurs 5 to 7 days after inoculation, spreading the virus hematogenously throughout the body.
Infected individuals are potentially contagious for 1 to 2 weeks before the infection becomes clinically apparent.
Clinical Manifestations:
Prodromal Phase (1-5 days):
Symptoms may include low-grade fever, post-auricular and suboccipital lymphadenopathy, mild sore throat, conjunctivitis, headache, and joint pain
Forchheimer spots (enanthem of the soft palate) may appear
Exanthem Phase (2-3 days):
A fine, non-confluent, pink maculopapular rash begins on the face, particularly behind the ears, and spreads caudally to the trunk and extremities, sparing the palms and soles. The rash typically becomes generalized within 24 hours.
The rash is similar in distribution to measles but is less intensely red and spreads more rapidly without darkening.
Immune Response and Viremia:
Systemic symptoms are primarily due to viral infection, but some manifestations (rash, thrombocytopenia, arthritis) have an immunological basis.
The viraemia and presence of the virus in tissues and organs cease by days 15 to 17, corresponding to the appearance of antibodies.
Congenital Rubella Syndrome:
Congenitally infected infants may transmit rubella for months after birth.
Can cause severe birth defects including heart abnormalities, cataracts, and developmental delays.
Clinical Features:
Asymptomatic Cases: Approximately 50% of rubella infections are asymptomatic.
Symptomatic Cases:
Prodromal symptoms include fever, malaise, lymphadenopathy, and Forchheimer spots.
Rash begins on the face and spreads to the body, typically appearing 14 to 17 days after exposure.
Polyarthritis can occur, especially in adolescents and adults.
Investigations:
Blood Tests:
Rubella serology for the detection of IgM antibodies or a four-fold increase in IgG antibodies.
Full blood count (FBC) may show leukopenia, relative lymphocytosis, and increased plasma cells.
Management:
Supportive Care:
Antipyretics for fever
Antihistamines for severe pruritus
Rest and NSAIDs for severe polyarthritis
Prevention:
Vaccination:
MMR (measles, mumps, rubella) vaccine at 12 months of age
MMRV (measles, mumps, rubella, varicella) vaccine at 18 months of age.
Roseola
Epidemiology:
Most common viral exanthem in children younger than 3 years
Peak incidence occurs between 6 months and 2 years of age
Cause:
Pathogen: Primarily caused by Human Herpesvirus 6 (HHV-6), with rare cases caused by Human Herpesvirus 7 (HHV-7). Other potential causative agents include enteroviruses, adenoviruses, and parainfluenza virus type 1.
Route of Transmission: Spread through respiratory secretions from asymptomatic carriers
Incubation Period: 5 to 15 days
Pathophysiology:
Viral Characteristics:
HHV-6 and HHV-7 are double-stranded DNA viruses
These viruses are trophic for CD4+ T lymphocytes, but HHV-6B can also infect other cell types
HHV-6B down-regulates the expression of CD3 on T cells, acting as a potential immunosuppressant and a powerful inducer of TNF-alpha and interleukin-1beta
After primary infection, HHV-6B can remain latent in various tissues and can reactivate, especially during periods of immunosuppression.
Clinical Course:
Febrile Phase (3-5 days):
Fever: Sudden onset of high fever, which can exceed 40ºC (104ºF) in some cases.
Lymphadenopathy: Cervical, postauricular, and/or occipital lymphadenopathy.
Nagayama Spots: Papular enanthem on the uvula and soft palate, sometimes observed during the febrile phase.
Exanthem Phase (1-3 days):
Rash Development: After the fever subsides abruptly, a rash appears. The exanthem is characterized by a blanching macular or maculopapular rash that starts on the neck and trunk and spreads to the face and extremities.
Rash Characteristics: The rash is typically rose-pink in color, non-pruritic, and may sometimes be vesicular. It generally lasts for 3 to 5 days and does not darken like measles rash.
Additional Features:
Symptom Presentation: Some children may present with irritability, mild diarrhea, or a mild cough
Asymptomatic Shedding: HHV-6 and HHV-7 DNA can be found in saliva for extended periods following primary infection, contributing to asymptomatic shedding and transmission
Investigations:
Clinical Diagnosis: Roseola is primarily diagnosed based on clinical presentation
Laboratory Tests: Detection of HHV-6 IgM antibodies and PCR can be used to confirm the diagnosis if necessary.
Management:
Supportive Care:
Fluids: Ensure adequate hydration.
Antipyretics: Administer medications like acetaminophen or ibuprofen to reduce fever.
Prevention:
Hygiene: Encourage good hygiene practices to reduce the spread of the virus.
Varicella
Epidemiology:
Primarily affects children aged 2 to 8 years.
Before widespread vaccination, 90% of children were infected by age 15.
Epidemics occurred in winter and early spring in 3-4 year cycles.
In immunocompetent children, the infection is usually mild; however, it can be severe in adults and immunocompromised children.
Cause:
Pathogen: Varicella zoster virus (VZV), a human herpesvirus type 3.
Route of Transmission: Airborne droplets, direct contact with VZV-infected vesicle fluid, and transplacental transmission
Incubation Period: 10 to 21 days, typically around 14 days
Pathophysiology:
Transmission and Initial Infection:
VZV is transmitted through contact with aerosolized droplets from nasopharyngeal secretions of an infected individual or by direct cutaneous contact with vesicle fluid from skin lesions.
The virus initially replicates in the nasopharyngeal cells and regional lymph nodes.
Viremia and Spread:
Primary Viraemia: Occurs 4 to 6 days after infection, spreading the virus to the liver, spleen, and other reticuloendothelial system cells.
Secondary Viraemia: Occurs around day 9, where mononuclear cells transport the virus to the skin and mucous membranes, leading to the characteristic vesicular rash.
VZV causes vasculitis of small blood vessels and degeneration of epithelial cells, forming fluid-filled vesicles with high levels of the virus.
Clinical Course:
Prodrome (1-2 days): Symptoms include malaise, low-grade fever, cough, coryza, anorexia, sore throat, and headache.
Rash Development: The skin eruption begins on the trunk and spreads to the face (including mucous membranes) and extremities, sparing the palms and soles. Lesions evolve from macules to papules to vesicles, occurring in crops and presenting at various stages simultaneously. Central necrosis and early crusting may also be visible.
Contagious Period: Patients are contagious from 48 hours before the rash onset until all skin lesions have fully crusted.
Clinical Features:
Rash: Widespread, starting on the trunk and spreading to the face, scalp, and extremities.
Various stages of rash occur simultaneously: erythematous macules → papules → vesicles filled with clear fluid on an erythematous base → eruption of vesicles → crusted papules → hypopigmentation of healed lesions
Investigations:
Clinical Diagnosis: Based on characteristic rash and symptoms.
Laboratory Tests: Vesicular swab for VZV PCR or Tzanck smear may be helpful in neonates or immunocompromised children to confirm the diagnosis.
Management:
Supportive Care:
Topical applications (e.g., calamine lotion) to soothe the skin.
Antihistamines for severe pruritus.
Maintain hydration and comfort.
Medical Therapy:
Indications: Immunocompromised individuals, primary infection in adults, unvaccinated adolescents ≥ 13 years, individuals on long-term salicylate therapy, and immunocompetent children with significant pre-existing skin conditions.
Antiviral Medication: Acyclovir can be considered, especially for severe cases or those at higher risk of complications.
Prevention:
Vaccination: Part of the national immunization schedule.
MMRV (measles, mumps, rubella, varicella) vaccine at 18 months
Varicella vaccine at 10-13 years for those who haven't been vaccinated previously
Complications:
Bacterial Superinfection: Including impetigo, cellulitis, necrotizing fasciitis
Reactivation: Latent VZV can reactivate later in life, leading to shingles (herpes zoster)
Other Complications:
Scarring from severe lesions.
Pneumonia, particularly in adults and immunocompromised individuals.
Neurological complications like acute cerebellar ataxia and encephalitis.
Reye Syndrome: Associated with viral infections and salicylate use.
Congenital Varicella Syndrome: If the infection occurs during pregnancy, it can lead to severe birth defects.
Hand food Mouth
Epidemiology:
Primarily affects children under 5 to 7 years of age
Most common during late summer and autumn months
Cause:
Pathogen: Most commonly caused by Coxsackie A virus and Enterovirus A71
Route of Transmission: Airborne droplets, fecal-oral route, direct contact with vesicle fluid, or respiratory secretions.
Incubation Period: Typically 4 to 7 days.
Pathophysiology:
Transmission and Initial Infection:
Infection occurs after oral ingestion of fecal material, oral secretions, vesicle fluid, or respiratory secretions from an infected individual.
The virus is highly contagious and can persist in fecal material for up to 1 month.
Viremia and Spread:
The virus initially replicates in submucosal lymphoid tissues of the lower intestine and pharynx
It then spreads to regional lymph nodes, causing a minor viremia that disseminates the virus throughout the body
This results in the infection of reticuloendothelial tissues and multiple organs, leading to a major viremia
Clinical Course:
Prodrome (3-4 days): Brief period characterized by low-grade fever, malaise, anorexia, and odynophagia.
Oral Lesions: Begin as small red macules that evolve into vesicles measuring 2 to 20 mm. These vesicles rupture, leaving intensely painful erosions, causing children to refuse to eat or drink.
Hand and Feet Lesions: Start as macules and papules that evolve into flat-topped, elliptical vesicles with an erythematous base. These lesions may occur without oral lesions.
Clinical Features:
Oral Lesions: Small red macules that evolve into vesicles, typically found on the tongue, gums, and inside of the cheeks. These vesicles rupture to form painful erosions.
Hand and Feet Lesions: Vesicular rash on the hands and feet, starting as macules and papules and evolving into vesicles. These lesions are often elliptical with a red base.
Systemic Symptoms: Low-grade fever, malaise, anorexia, and sore throat.
Contagious Period:
Individuals are contagious from 2 days before the onset of the rash until 2 days after the eruption.
The disease typically resolves within 10 days.
Treatment:
Supportive Care:
Maintain hydration and provide pain relief with analgesics or antipyretics.
Encourage oral intake with soft, cool foods and fluids to ease pain from oral lesions.
Topical anesthetics may help reduce pain from mouth sores.
Hygiene:
Good hand hygiene is crucial to prevent the spread of the virus.
Clean and disinfect surfaces and objects that may be contaminated with the virus.
No Specific Antiviral Therapy:
There is no specific antiviral treatment available for HFMD. The management focuses on symptomatic relief.
Erythema infectiosum
Epidemiology:
Primarily affects children aged 5 to 15 years.
Peak incidence occurs in late winter and early spring.
Approximately 25% of infections are asymptomatic.
Cause:
Pathogen: Parvovirus B19.
Route of Transmission: Respiratory droplets, percutaneous exposure to blood or blood products, and transplacental transmission.
Incubation Period: Typically 4 to 14 days, but can range up to 21 days.
Pathophysiology:
Transmission and Initial Infection:
Parvovirus B19 is transmitted via respiratory droplets and can also spread through blood products or from mother to fetus.
The virus infects erythrocyte progenitor cells in the bone marrow and blood, using the erythrocyte P antigen (globoside) as its receptor.
Individuals lacking the P antigen are not susceptible to the disease.
Viral Replication and Cytotoxicity:
The virus initially replicates in the submucosal lymphoid tissues of the lower intestine and pharynx.
It then spreads to regional lymph nodes, causing a minor viremia that disseminates the virus throughout the body.
The virus replicates in erythroid progenitor cells, leading to cellular invasion and destruction. This replication results in the transient cessation of erythropoiesis and a drop in hematocrit.
Viremia occurs 4 to 14 days after infection, followed by the appearance of anti-B19 IgM antibodies, with IgG antibodies appearing approximately one week later.
The pathogenesis of the rash and arthropathy is not completely understood but coincides with measurable serum antibody production.
Clinical Manifestations and Immune Response:
In healthy individuals, RBC production returns to normal within 10 to 14 days with minimal anemia.
In individuals with increased RBC turnover (e.g., those with hemolytic anemias), parvovirus B19 can cause a transient aplastic crisis (temporary condition where the bone marrow abruptly stops producing red blood cells)
In fetuses, the virus can cause severe anemia, hydrops fetalis, and intrauterine fetal death due to hemolysis and decreased red-cell survival time.
In immunocompromised individuals, chronic or reactivated infections can lead to severe anemia due to hypoplasia or aplasia of erythroid cells and their precursors.
Clinical Features:
Incubation Period:
Typically 1 to 3 weeks from exposure to the appearance of the rash.
Prodromal Phase (1-3 days):
Mild cold-like symptoms including fever, coryza, headache, nausea, and diarrhea.
Exanthem Phase (2-5 days after prodrome):
Initial Rash: Characteristic "slapped cheek" appearance with bright red erythema on the cheeks, often with perioral sparing.
Subsequent Rash: A lacy, reticulated, or lacelike rash may appear on the trunk and extremities several days after the facial rash. This rash is often pruritic.
Additional Symptoms:
Some children may present with arthropathy (joint pain), particularly in older children and adults.
The rash may reappear or worsen with exposure to sunlight, heat, stress, or exercise.
Investigations:
Clinical Diagnosis: Based on characteristic rash and symptoms.
Laboratory Tests:
Serology for detection of Parvovirus B19-specific IgM and IgG antibodies.
PCR for Parvovirus B19 DNA in blood may be used in immunocompromised patients or in cases of fetal infection.
Complete Blood Count (CBC): May show anemia or reticulocytopenia in severe cases.
Management:
Supportive Care:
Analgesics and antipyretics (e.g., acetaminophen, NSAIDs) for fever and joint pain
Ensure adequate hydration and rest
For Immunocompromised Patients:
May require intravenous immunoglobulin (IVIG) therapy to control the infection and support erythropoiesis.
Complications:
Transient Aplastic Crisis: Particularly in patients with chronic hemolytic anemias (e.g., sickle cell disease).
Chronic Pure Red Cell Aplasia: Can occur in immunocompromised individuals, leading to chronic anemia.
Hydrops Fetalis: Severe anemia in the fetus, potentially leading to fetal death, when infection occurs during pregnancy.
Other Complications:
Hepatitis, myocarditis, and encephalitis, though these are rare.
Parvovirus B19 is considered a TORCH infection, capable of causing congenital infections
Briefly describe the pathology of non- infectious causes of fever and rash
Kawasaki’s disease
Overview:
Kawasaki disease, also known as mucocutaneous lymph node syndrome, is an acute, necrotizing vasculitis of unknown etiology.
Primarily affects children under 5 years old, with a higher incidence in boys
It has a peak incidence in late winter and spring
Cause:
The exact cause is unknown
Potential factors include:
Infectious Agents: The disease may be triggered by an unknown infectious agent
Genetic Factors: There may be a genetic predisposition to the disease
Autoimmune Components: The immune system appears to attack blood vessels, but the precise mechanisms are not well understood
Pathophysiology:
Vasculitis: Kawasaki disease primarily affects the coronary arteries but can also involve other large and medium-sized arteries
Endothelial Damage: The disease leads to endothelial damage, exposing collagen and tissue factor in the tunica media, resulting in:
Clot Formation: Increased risk of clots that can block blood flow in the coronary arteries, leading to ischemia and potential myocardial infarction (MI)
Fibrin Deposition: This makes the arteries stiffer and less elastic, weakening the artery walls and leading to the formation of aneurysms. These aneurysms have a risk of rupturing, causing ischemia and potential MI
Fibrosis without Aneurysms: In cases where fibrosis does not lead to aneurysm formation, the artery walls thicken, reducing the lumen diameter and causing ischemia to the myocardium
Acute Phase:
Characterized by the development of edema and neutrophil infiltration in the coronary arterial wall, with a rapid transition to mononuclear cell infiltration
This is followed by local production of matrix metalloproteinases, causing destruction of the internal elastic lamina and media
Chronic Phase:
Progression to fibrous connective tissue replacement of the intima and media, leading to aneurysm formation, scarring, and stenosis
Clinical course divided into the following stages
Clinical Features:
CRASH AND BURN
Fever: Persistent fever for at least 5 days.
CRASH Symptoms: At least four of the following, or fewer if there is coronary artery involvement:
Conjunctivitis: Bilateral, non-purulent.
Rash: Maculopapular, typically widespread.
Adenopathy: Cervical lymphadenopathy.
Strawberry Tongue: Red, swollen tongue with prominent papillae.
Hand and Foot Changes: Swelling, redness, and desquamation (peeling) of the skin on the palms and soles.
Other Features:
Lymphadenopathy: Especially in the neck.
Mucous Membrane Changes: Red, cracked lips, and red oral mucosa.
Complications:
Cardiac Complications: Without treatment, there is a 20-25% risk of developing heart complications, including:
Coronary Artery Aneurysms: Risk of rupture and MI.
Myocardial Infarction: Due to ischemia from clots or aneurysms.
Long-term Heart Issues: Including ischemic heart disease (IHD) and sudden death.
Investigations:
Inflammatory Markers: Elevated ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein).
Blood Tests: Leukocytosis and thrombocytosis.
Echocardiography: To evaluate for coronary artery aneurysms and monitor heart function.
Management:
IV Immunoglobulins (IVIG):
Neutralizes circulating antibodies through anti-idiotypic antibodies.
Downregulates inflammatory events by modulating Fc receptor function, interfering with complement activation, regulating cell growth, and affecting T and B cell function.
High-Dose Oral Aspirin:
Reduces inflammation and decreases platelet aggregation to prevent clot formation.
IV Glucocorticoids:
Used in severe cases or if IVIG is not effective.
Supportive Care:
Hydration, monitoring for heart complications, and symptomatic treatment for fever and rash.
Henoch-Schonlein purpura
Overview:
Henoch-Schonlein Purpura (HSP), also known as IgA vasculitis, is an acute, immune complex-mediated small vessel vasculitis
It is the most common vasculitis in children, typically affecting those between 2 and 8 years of age
Epidemiology:
More common in children, particularly those aged 2 to 8 years.
Incidence peaks in the spring and fall.
Slightly more common in boys than girls.
Cause:
Unknown Etiology: The exact cause of HSP is unknown, but it is believed to involve an abnormal immune response.
Triggers: Often preceded by an upper respiratory tract infection (URTI), especially Group A streptococcal infections. Other triggers can include viral infections, certain medications (e.g., antibiotics, antiarrhythmics), vaccinations, and environmental factors
Genetic Predisposition: A genetic predisposition may also play a role.
Pathophysiology:
Antigen Exposure:
Exposure to an antigen (e.g., infection, drugs) stimulates the production of IgA.
This IgA may abnormally target host endothelial cells.
Immune Complex Formation:
IgA forms immune complexes that deposit in the vascular walls of various tissues, including the skin, gastrointestinal (GI) tract, joints, and kidneys.
Complement Activation:
The deposition of IgA immune complexes activates the complement system, leading to vascular inflammation and damage.
Vascular Inflammation:
Skin Biopsies: Lesions show predominantly neutrophils and monocytes. Fluorescence microscopy reveals deposits of IgA, C3, and fibrin in the small vessels.
Similar to IgA Nephropathy: The pathogenesis of HSP is similar to that of IgA nephropathy, involving immune complex deposition and complement activation.
Clinical Features:
Incubation Period: Symptoms typically appear 1 to 3 weeks after the triggering event (e.g., infection).
Classic Tetrad of Symptoms:
Palpable Purpura:
Non-blanching, palpable purpuric rash, primarily on the lower extremities and buttocks.
Rash is palpable due to underlying inflammation and fibrosis.
Arthritis/Arthralgia:
Joint pain and swelling, most commonly affecting the knees and ankles
Gastrointestinal Symptoms:
Abdominal pain, which can be colicky and severe.
GI bleeding, manifested as bloody stools or melena.
Renal Involvement:
Hematuria (blood in urine) and proteinuria.
IgA nephropathy can develop, potentially leading to renal insufficiency.
Complications:
Renal Complications:
Renal involvement can be asymptomatic or present as hematuria, proteinuria, and hypertension.
In severe cases, it can progress to nephrotic syndrome or chronic kidney disease.
Gastrointestinal Complications:
Intussusception, bowel infarction, or perforation.
Other Complications:
Rarely, pulmonary or neurological involvement, which can be life-threatening.
Investigations:
Clinical Diagnosis: Based on characteristic symptoms and physical examination findings.
Laboratory Tests:
Urinalysis: To detect hematuria and proteinuria.
Blood Tests:
Full blood count (FBC) may show thrombocytosis, leukocytosis, and anemia.
Elevated serum IgA levels.
Decreased complement levels.
Elevated ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein) indicating inflammation.
UEC (urea and electrolytes) to assess renal function (elevated creatinine and BUN).
Biopsy:
Skin or kidney biopsy can confirm the diagnosis by showing IgA deposition in the vessel walls.
Imaging:
Abdominal ultrasound or CT scan if there are severe GI symptoms or complications.
Management:
Supportive Care:
Ensuring adequate hydration and nutrition.
Pain management with NSAIDs for mild cases.
Medical Therapy:
NSAIDs: For joint pain and inflammation, if there are no contraindications.
Systemic Glucocorticoids: For severe cases, particularly with significant GI or renal involvement.
Prednisone is commonly used.
Monitoring and Follow-Up:
Close follow-up is essential to monitor for renal involvement and other complications.
Regular urinalysis and renal function tests.
Monitoring blood pressure.
Prognosis:
A first episode of HSP, in the absence of significant renal disease, usually resolves within 4 weeks → the rash is usually the last symptom to remit
Joint pain usually resolves spontaneously within 72h
Uncomplicated abdominal pain usually resolves spontaneously within 24-48h
In 25-35% of patients, HSP recurs at least once, usually within 4 months of the initial presentation → subsequent episodes are usually milder and shorter in duration
90% of those who develop renal complications do so within 2 months of the onset, and 97% within 6 months
Learning Points: Clinical Practice
Professional skills; Newborn or Child with acute illness
Demonstrate appropriate newborn examination and the 6-week check
Newborn Examination
Attending midwife:
Ask if there are any concerns or problems
Mother:
Check patient notes for relevant details of the maternal medical history, family history, antenatal and obstetric history, and social history
Ask about feeding and whether the baby has passed meconium/urine
Baby:
When the baby is quiet (if needed, use calming techniques like pacifiers (ที่ดูด), sucking a clean finger, or examination after a feed) note:
General posture and movements, weight, vital signs
Skin colour:
Vernix: Normal ‘cheesy’ white substance on skin at birth
Peripheral cyanosis: Normal in the first few days after birth
Post-mature skin: Dry peeling skin, prone to cracking, common in post-mature babies; resolves, but topical emollients are often beneficial
Jaundice: Usually unconjugated; appears after 24 hours, peaks around 3-4 days, resolves by 14 days; due to immaturity of hepatic bilirubin conjugation; poor feeding can also contribute.
Listen to the heart and lungs:
Murmurs: Detected in 1-2% of all newborns, but only about 1/12 will represent congenital heart disease.
If a murmur is heard, evaluate in the context of other clinical findings (cyanosis, signs of heart failure, peripheral pulses).
An innocent heart murmur is likely if:
Murmur is grade 1-2/6, systolic, not harsh, loudest at the left sternal edge.
Remaining cardiovascular examination is normal.
Good evidence exists to support the use of pre and post-ductal saturation readings (right arm = pre, foot = post) as part of the assessment of a pathological murmur.
ECG and 4-limb BP should also be performed.
Echocardiography should be obtained in infants where there is clinical concern.
If the murmur persists in an otherwise well infant, in whom no echocardiography has been performed, then arrange for repeat examination in a few days to weeks and consider referral for cardiac assessment.
Examine the eyes for size, strabismus:
Blocked lacrimal duct: Leads to recurrent sticky eye; responds to regular eye toilet until ducts open; may persist for months, but only consider surgery if >12 months
If purulent, secondary bacterial conjunctivitis is likely.
Take swab for MCS (including swab for chlamydia); treat with antibiotic eye drops.
Subconjunctival haemorrhage: Associated with precipitate deliveries or cord around the neck; harmless and resolves within a few weeks.
Using an ophthalmoscope: Examine the eyes for bilateral red reflexes to exclude cataract or retinoblastoma.
The baby should be completely undressed for examination in head to toe order:
Cranium:
Measure maximum occipital-frontal circumference (normal 33-37cm at term).
Assess skull shape, fontanelle positions, tension, and size (anterior may be up to 4cmx4cm, posterior 1cm).
Skull moulding: Overriding skull bones with palpable ridges are part of moulding and are harmless; resolves within 2-3 days.
Caput succedaneum: Oedema of the presenting scalp; can be particularly large following ventouse delivery (chignon); rapidly resolves.
Cephalhaematoma: Common fluctuant swelling(s) due to subperiosteal bleed(s); most often occur over parietal bones; swelling limited by suture lines; resolves over weeks.
Face:
Assess any dysmorphism, nose, chin size; inspect mouth; visualize and palpate palate for possible clefts
Epstein’s pearls: Self-resolving white inclusion cysts on palate/gums.
Tongue-tie: Shortened tongue frenulum.
Ranula: Self-resolving bluish mouth floor swelling (mucus retention cyst).
Oral candidiasis (thrush): Mucosal white flecks and erythema; treat with oral antifungal, e.g., nystatin suspension 1mL 6-hourly.
Ears:
Assess position, size, shape, and external meatus patency.
Pre-auricular pits, skin tags, or accessory auricles: Usually isolated, but can be associated with hearing loss or other abnormalities.
Test hearing and consider surgical referral for cosmetic reasons.
Neck: Inspect and assess movements; palpate clavicles.
Chest:
Assess shape, symmetry, nipple position, respiratory rate (normal 40-60/min), pattern, and effort.
Palpate precordium and apex beat.
Breast swelling: Almost always due to maternal hormones and may lactate; spontaneously resolves over several weeks; if does not resolve, then endocrinology investigation is warranted.
Abdomen:
Inspect shape and umbilical stump; check for inguinal hernias; palpate for masses, liver (normally palpable up to 2cm below costal margin), spleen (normally palpable up to 1cm), kidneys (normally palpable), bladder.
Umbilical hernia: Protuberant swelling involving the umbilicus; rarely strangulates and almost all spontaneously resolve within 12 months.
Single umbilical artery: Usually isolated and of no significance, but can be associated with several syndromes and intrauterine growth restriction (IUGR).
Genitalia:
Females:
Inspect (note that the clitoris and labia are normally large).
Vaginal mucoid or bloody discharge: Due to maternal oestrogen withdrawal; almost always spontaneously resolves.
Vaginal/hymenal skin tags: Spontaneously shrink.
Males:
Assess size, shape, position of urinary meatus; palpate for descended testes (retractile testes are normal).
Undescended testes: Differentiate from retractile testes (can be ‘persuaded’ into the scrotum); if still undescended at 1 year, refer to a surgeon.
Hydrocele: Common and most resolve by a year; if persists, refer to a surgeon.
Inguinal hernias: Can rarely be present from birth; refer to a surgeon (there is a relatively high likelihood of strangulation/incarceration).
Palpate the femoral pulses: Absence or weakness may indicate aortic arch abnormalities.
Anus: Assess position and patency.
Spine: Inspect for deformity and sacral naevi/dimple/pit/hair patch/lipoma/pigmentation (may indicate underlying abnormality).
Sacral coccygeal pits: Require no action if within natal cleft.
Higher pits: Require spinal imaging.
Limbs:
Assess symmetry, shape, passive and active movements, digit number and shape; assess palmar creases; examine hips for DDH.
Single palmar crease: Found in approximately 2% of normal babies; may be associated with chromosomal abnormalities, e.g., trisomy 21.
Polydactyly: Can be isolated or associated with other abnormalities; refer to a surgeon (pre vs post axial).
Syndactyly: Most common between the second and third toes; often familial; if toes only are affected, requires no treatment.
Postural deformities: Common, especially after oligohydramnios (little amniotic fluid ) or the baby was in an unusual position before birth, like being breech (bottom-first).
Positional talipes is usually equinovarus or calcaneovalgus.
Positional talipes: This is when the baby's foot is turned inward (equinovarus) or outward (calcaneovalgus)
If affected joint can easily be massaged back to normal neutral position, deformity will rapidly resolve.
If fixed (structural), refer to an orthopedic surgeon/physiotherapist.
These children are also at increased risk of DDH.
CNS:
Assess tone during handling, pulling baby to sitting position by holding wrists, and ventral suspension (baby should be able to hold head almost horizontally).
Check Moro reflex (symmetrical?).
Palmar grasp reflex: When an object is placed in the infant’s hand and strokes their palm, the fingers will close, and they will grasp it with a palmar grasp.
Sucking reflex: Causes the child to instinctively suck anything that touches the roof of their mouth.
Rooting reflex: Present at birth and disappears around four months of age, as it gradually comes under voluntary control; a newborn infant will turn its head toward anything that strokes its cheek or mouth to aid breastfeeding.
Stepping reflex: When the soles of their feet touch a flat surface, they will appear to walk by placing one foot in front of the other.
Moro reflex: Support the infant’s upper back with one hand, then drop back once or twice into your other hand.
The legs and head extend while the arms jerk up with the fingers extended.
The arms are then brought together, and the hands clench into fists, and the infant cries.
Asymmetry may be due to hemiparesis, brachial plexus injury, or fractured clavicle.
Check that urine and meconium were passed within the first 24 hours.
6-Week Check
General examination: Height, weight, head circumference; chart.
Explore with parents: How they are coping
Initial observations:
Does this baby have a syndrome (e.g., Trisomy 21)?
Does this baby engage with the examiner’s gaze and face in a socially responsive way?
Are all limbs moving appropriately?
Is the baby pink? Is the baby jaundiced?
Is there evidence of respiratory distress?
Do the baby’s eyes follow the examiner’s face as it moves from side to side?
Do the reflections of the ceiling light remain symmetrical in each eye as the direction of gaze changes?
Is nystagmus present?
The eyes: Abnormal morphology, nystagmus, and strabismus (as above); check the red reflexes (i.e., retinoblastoma, congenital cataracts).
The mouth: Check for cleft palate; a bifid uvula might herald a submucous cleft.
Heart and lungs:
CCF: Check the baby is pink in color (central cyanosis is always an emergency), not in respiratory distress (i.e., no chest recession), and with a normal liver edge
A large ventriculoseptal defect or patent ductus arteriosus may present with congestive cardiac failure at this age.
Feeding can be a useful symptom when considering shortness of breath in relationship to congenital cardiac issues.
Babies with heart issues often have trouble feeding because they get tired easily or have difficulty breathing while eating.
Assess for systolic murmur.
Respiratory causes of increased work of breathing may be congenital (e.g., an emphysematous lobe) or acquired (e.g., chest infection).
Feel for femoral pulses: Which are absent in coarctation of the aorta.
The abdomen:
Exclude organomegaly, looking for congestive cardiac failure, congenital metabolic or storage disease.
It is normal to occasionally feel the tip of the spleen.
A sharp liver edge can be felt in most babies about three or four finger widths below the right costal margin.
Check for descended testes and genital abnormality.
Determine if the hips are stable:
Enquire about the risk factors for developmental hip dysplasia:
Female gender.
Family history of hip dysplasia in a first-degree relative.
Breech position at birth.
Intrauterine Problems (refer to issues or complications that occur within the uterus during pregnancy)
Packaging:
Plagiocephaly: This is when a baby’s head is flattened on one side, often due to lying in one position for too long.
Torticollis: This is a condition where a baby’s neck muscles are tight on one side, causing their head to tilt to one side and making it difficult to turn their head.
Hyperextended knees: This is when a baby’s knees bend backward more than normal. It can happen if the baby was cramped in the womb.
Foot deformities: These are abnormalities in the shape or position of a baby’s feet, such as clubfoot, where the foot is twisted out of shape or position.
Reduction in uterine volume:
Examples include first pregnancy, oligohydramnios, and multiple pregnancy.
Wrapping the baby while the legs are straight.
Hip Dysplasia Tests
Barlow Test:
Detects if a normally positioned head of the femur can be dislocated out of a shallow acetabulum.
With one hand, fix the pelvis while the other holds the infant's leg of the side being examined with the hip in 90° flexion.
With the knee in full flexion, place your fourth and fifth fingers over the head of the greater trochanter.
Apply gentle pressure down toward the couch while feeling if the femoral head drops out over a shallow acetabular edge.
Ortolani Test:
Designed to see if an already dislocated head of the femur can be relocated.
Using your fourth and fifth fingers, gently lift toward the roof while abducting the infant's leg.
Feel for a clunk as a dislocated head of the femur is slipped over the acetabular edge and into the acetabulum.
Procedure:
This process is carried out on both sides and then both hips are gently abducted simultaneously (it is reassuring to find symmetrical abduction).
Examination of the hips should not cause the baby any distress.
If after the examination there is still doubt about dysplasia, an ultrasound of the hips is the investigation of choice (before 6 months, the head of the femur is not calcified and so an x-ray is inappropriate).
Neurological Examination
Social responsiveness: Check that the baby is spontaneously moving all limbs in an age-appropriate way.
The development of one side predominant ‘handedness’ before 18 months is a red flag for neuromuscular compromise on the less active side.
This means that if a child starts to show a strong preference for using one hand over the other before they are 18 months old, it could be a warning sign.
Red flag for neuromuscular compromise: It suggests there might be a problem with the muscles or nerves on the side that is less active.
Typically, children develop a preference for using one hand (handedness) later, around 2-3 years old. Showing a strong preference too early might indicate an underlying issue that needs to be checked by a doctor.
Complete the examination by holding the baby in ventral suspension, permitting inspection of the spine and an assessment of tone (the head should be held in line with the torso at 6 weeks).
If the tone is increased or decreased, cerebral palsy and its differential diagnoses should be considered.
Eliciting the primitive reflexes complicates the issue and adds little to the information already gained.
Demonstrate accurate, problem-oriented, tactful and organised history, plus succinct presentation this information for children with acute illness
Demonstrate appropriate history and examination assessment of a febrile infant, as per a typical presentation to the Emergency Department
History Taking
Parental Concerns and Perception:
Take parental concerns seriously, as they are often accurate in identifying fever.
Assess their perception of the severity of the fever and any changes in their child's behavior.
Presenting Complaint:
Duration of fever: When did it start?
Degree of fever: How high has the temperature been?
Response to antipyretics: Have any fever-reducing medications been given, and if so, how frequently and at what doses?
Associated symptoms:
Poor appetite
Irritability or increased fussiness
Lethargy or decreased activity level
Changes in crying (e.g., high-pitched, weak, or continuous)
Vomiting or diarrhea
Cough, nasal congestion, or runny nose
Difficulty breathing or rapid breathing
Favoring or refusing to use a limb (suggestive of pain or discomfort)
Foul-smelling or strong urine (suggestive of urinary tract infection)
Systems Review:
Upper Respiratory Tract:
Runny nose and congestion (common in viral URTIs)
Ear pain or tugging at ears (otitis media)
Headache (consider sinusitis or meningitis)
Lower Respiratory Tract:
Cough or wheezing (consider pneumonia or bronchiolitis)
Gastrointestinal:
Abdominal pain (gastroenteritis, UTI, or pneumonia)
Diarrhea and vomiting (gastroenteritis or systemic infection)
Genitourinary:
Foul-smelling urine or back pain (suggestive of pyelonephritis or UTI)
Musculoskeletal:
Joint swelling or redness (consider Lyme disease or osteomyelitis)
Neurological:
Irritability or lethargy (could indicate meningitis or encephalitis)
Chronic Illness Symptoms:
Repeated infections (potential immunodeficiency)
Poor weight gain or weight loss (consider TB or malignancy)
Endocrine:
Palpitations, sweating, or heat intolerance (suggestive of hyperthyroidism)
Pattern of Symptoms:
Cyclic or recurrent symptoms (consider inflammatory conditions or hereditary syndromes)
Medical History:
Recent travel history (risk of travel-related infections)
Exposure to sick contacts (assessing contagious illnesses)
Immunization history (especially crucial for infants under 6 months or those with incomplete vaccinations)
Medication history, including prior antibiotic use (which can mask symptoms)
Identify high-risk groups:
Premature infants
Immunocompromised children
Those with chronic illnesses like chronic lung disease or congenital heart disease
Previous invasive bacterial infections
Aboriginal and Torres Strait Islander populations
Examination
General Observations:
Appearance: Well or unwell looking?
Level of alertness and responsiveness
Behavior: Consolability, irritability, or lethargy
Vital Signs:
Temperature: Document fever and look for patterns.
Heart rate: Tachycardia could indicate fever, dehydration, or sepsis.
Respiratory rate: Tachypnea may suggest respiratory distress or sepsis.
Capillary refill time: Prolonged refill may indicate poor perfusion.
Systemic Examination:
Skin:
Look for rashes, petechiae, or purpura (signs of serious bacterial infections like meningococcemia).
Head, Eyes, Ears, Nose, Throat (HEENT):
Inspect for signs of upper respiratory infections, otitis media, or sinusitis.
Respiratory:
Auscultate for crackles, wheezing, or decreased breath sounds
Observe for signs of respiratory distress (retractions, nasal flaring)
Cardiovascular:
Check for murmurs, gallops, or signs of heart failure.
Abdomen:
Palpate for tenderness, distension, or masses.
Genitourinary:
Examine for signs of infection or discomfort.
Musculoskeletal:
Check for joint swelling, redness, or warmth.
Neurological:
Assess tone, reflexes, and level of consciousness.
Red Flags:
Age less than 1 month
Lethargy or decreased level of consciousness
Signs of respiratory distress
Petechiae or purpura (urgent consideration for sepsis or meningitis)
Inconsolability or severe irritability
ABCDE assessment
Describe the approach to management of a febrile infant
Initial Assessment and Stabilization
Emergency Care:
In hypoxic children or those in shock, follow emergency guidelines:
Provide oxygen if required.
Initiate fluid resuscitation for shock.
Monitor vital signs continuously.
Investigations Based on Age and Clinical Presentation
Under 28 Days:
Investigations:
Blood Tests: Full Blood Count (FBC), C-Reactive Protein (CRP), Blood Cultures.
Imaging: Chest X-ray (CXR) if respiratory symptoms are present.
Other:
Urine Microscopy, Culture, and Sensitivity (MCS) via suprapubic aspirate (SPA).
Lumbar Puncture (LP) to rule out meningitis.
Management:
Start empirical antibiotics immediately.
Common antibiotics: third-generation cephalosporins (e.g., cefotaxime or ceftriaxone) and ampicillin to cover Listeria.
29 Days to 3 Months:
If the infant shows unwell features or signs of septic shock:
Investigations:
Blood Sugar Level (BSL), Urine MCS, FBC, CRP, Lactate, Blood Cultures, CXR, LP.
Management:
Admit to the hospital.
Administer empirical antibiotics: flucloxacillin + ceftriaxone (or gentamicin if meningitis is excluded).
If the infant does not show unwell features:
Investigations:
Urine MCS (via SPA or catheter), FBC, CRP, Blood Cultures.
Management:
Treat the underlying cause if identified.
If no cause is identified, discharge with close follow-up in 12-24 hours.
Over 3 Months:
If the infant shows unwell features or signs of septic shock:
Investigations:
BSL, Urine MCS, FBC, CRP, Lactate, Blood Cultures, CXR, LP.
Management:
Admit to the hospital.
Consider empirical antibiotics: flucloxacillin + ceftriaxone (or gentamicin if meningitis is excluded).
If the infant does not show unwell features:
If fever is less than 24 hours: Consider no investigations.
If there is a history of previous UTI or the infant is under 12 months and fever persists for more than 24 hours: Consider urine MCS.
If fever persists for more than 48 hours: Consider urine MCS.
General Investigations for Febrile Infants with No Apparent Source of Infection
Blood Tests:
FBC, CRP, Urea, Electrolytes, and Creatinine (UEC), Blood Cultures.
Urine Tests:
Urine MCS to rule out UTI.
Lumbar Puncture:
Consider if clinical assessment indicates and no contraindications exist.
Chest X-ray:
Consider if high white cell count (WCC) or respiratory symptoms are present.
Management Strategies
Antibiotics:
Immediate Treatment:
Administer maximum dose third-generation cephalosporins (cefotaxime or ceftriaxone) for febrile infants with:
Signs of shock or coma.
Signs of meningococcal disease.
Specific Scenarios:
Consider high-dose IV acyclovir if herpes simplex encephalitis or disseminated neonatal disease is suspected.
Consider IV corticosteroids if bacterial meningitis is confirmed (not in infants younger than 3 months).
Adjust antibiotics based on suspected pathogens (e.g., Neisseria meningitidis, Streptococcus pneumoniae, Escherichia coli, Staphylococcus aureus, Haemophilus influenzae type b).
Add antibiotics against Listeria (e.g., ampicillin) for infants under 3 months.
Use parenteral antibiotics for infants with a decreased level of consciousness.
Follow local guidelines for antibiotic resistance.
Antipyretics:
Do not use tepid sponging.
Avoid over- or underdressing the child
Use paracetamol or ibuprofen only if the child is distressed due to fever:
Paracetamol: 15 mg/kg per dose, up to 4 times a day (maximum 4 doses in 24 hours)
Ibuprofen (not recommended for children under 6 months): 10 mg/kg per dose, up to 4 times a day (maximum 4 doses in 24 hours)
Temperature Measurement
Under 3 months: Measure axillary temperature.
Over 3 months: Measure tympanic temperature.
Describe the assessment and management of children with suspected meningitis including
Overall
Assessment
History and Examination:
Common Symptoms:
Fever
Severe headache
Neck stiffness
Photophobia
Altered mental status
Vomiting
Seizures
Infant-Specific Symptoms:
Irritability
Lethargy
Drowsiness
Poor feeding
Vomiting
Rash (e.g., meningococcal purpura)
Seizures
Neck stiffness and pain; bulging fontanelle
Recent overseas travel
Classical Triad:
Fever, photophobia, and neck stiffness are present in less than 50% of cases in older children and adolescents, making a lumbar puncture crucial for definitive diagnosis.
Investigations:
Culture: Blood, urine, infected sites, and cerebrospinal fluid (CSF) for bacteria and viruses.
Acute-Phase Reactants: Such as CRP and ESR.
Rapid Bacterial Antigen/Polymerase Chain Reaction (PCR) Tests: For organisms.
Lumbar Puncture
Procedure:
Patient Counselling: Explain the procedure and its purpose to the patient and guardians.
Positioning:
Lateral Recumbent Position: Commonly used, with knees tucked to the chest to increase interspinous distance.
Sitting Position: Consider if there is potential for respiratory compromise due to neck hyperflexion, though it does not allow accurate manometry.
Preparation:
Identify and mark the interspace (L3-L4 or L4-L5); use ultrasound guidance if available
Ensure a sterile environment and technique
Provide analgesia or sedation as needed
Continuous cardiorespiratory monitoring and pulse oximetry are recommended for young infants
Procedure Steps:
Position and advance the spinal needle midline through the spinous ligaments
For lateral recumbent position, aim for 45 degrees from perpendicular in infants under 12 months and 30 degrees for older children.
Remove the stylet, and once CSF returns, attach a manometer to measure opening pressure.
Collect CSF samples in sterile tubes for analysis.
Interpretation of Results:
Normal CSF:
Clear appearance
White Blood Cell (WBC) count: 0-5 cells/µL
Protein: 15-45 mg/dL
Glucose: 40-80 mg/dL (or two-thirds of blood glucose level)
Bacterial Meningitis:
Cloudy appearance
WBC count: Elevated (often >1000 cells/µL, predominantly neutrophils)
Protein: Elevated (usually >100 mg/dL)
Glucose: Low (often <40 mg/dL)
Positive Gram stain and culture
Viral Meningitis:
Clear or slightly cloudy appearance
WBC count: Elevated (10-200 cells/µL, predominantly lymphocytes)
Protein: Mildly elevated (50-100 mg/dL)
Glucose: Normal
Other Indicators:
Positive PCR for specific viruses or bacteria.
Complications:
Common:
Failure to obtain a specimen or traumatic bloody tap.
Less Common:
Post-dural puncture headache (5-15%).
Transient or persistent paraesthesia or numbness.
Rare:
Respiratory arrest from positioning.
Infection introduced by the needle causing meningitis, epidural abscess, or osteomyelitis.
Spinal haematoma, especially in patients with uncorrected bleeding disorders.
Brain herniation in patients with increased intracranial pressure (ICP).
Epidermoid tumor (extremely rare).
Contraindications:
Absolute:
Increased ICP
Glasgow Coma Scale (GCS) < 8 or deteriorating/fluctuating level of consciousness
Relative:
Septic shock or haemodynamic compromise
Significant respiratory compromise
New focal neurological signs or seizures
Seizures within the previous 30 minutes or normal consciousness not returned from seizure
Coagulopathy (INR > 1.5 or platelets < 50,000) or patient on anticoagulant medication
Management
Antibiotics:
Early Administration:
Start empirical antibiotics and dexamethasone as soon as possible, ideally within 60 minutes of presentation.
Neonates (Early-Onset Sepsis within 72 hours of birth):
Cefotaxime: 50 mg/kg IV every 8 hours
Benzylpenicillin: 90 mg/kg IV every 8 hours
Neonates (Late-Onset Sepsis more than 72 hours after birth):
Cefotaxime: 50 mg/kg IV
Amoxicillin: 100 mg/kg IV (timing based on age)
Infants (1 month to under 2 months):
Ceftriaxone: 50 mg/kg IV every 12 hours
Amoxicillin: 50 mg/kg IV every 6 hours
Children (2 months or older):
Ceftriaxone: 50 mg/kg (up to 2g) IV every 12 hours
Dexamethasone: 0.15 mg/kg (up to 10 mg) IV every 6 hours for 4 days
Corticosteroids:
Indication:
Consider in all suspected bacterial meningitis cases over three months of age.
Administration:
Ideally before or immediately following the first antibiotic dose.
Dexamethasone: 10 mg (child: 0.15 mg/kg up to 10 mg) IV, then every 6 hours for 4 days.
Not indicated for neonates and only for specific viral pathogens.
Fluid Therapy:
Initial Resuscitation:
Sodium chloride 0.9% administered in 20 mL/kg bolus. Repeat as clinically indicated.
SIADH Management:
For those with signs of Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH), moderate fluid restriction is advised.
Isotonic Fluids:
Administer isotonic fluids for those without signs of SIADH.
Complications and Sequelae
SIADH:
Mechanism:
Unclear, but bacterial meningitis can cause increased ADH secretion, contributing to hyponatremia and cerebral edema.
Cerebral Edema:
Mechanisms:
Vasogenic Edema: Increased permeability of the blood-brain barrier.
Cytotoxic Edema: Factors from neutrophils, microglia, and astrocytes can produce edema.
Obstructive Edema: Inflammation can impede normal absorption of CSF from the subarachnoid space via the arachnoid villi
Hearing Loss:
Type: Sensorineural hearing loss (transient or permanent).
Cause: Damage to the eighth cranial nerve, cochlea, or labyrinth from bacterial invasion or inflammatory response.
Contact Tracing:
Notification:
Probable and confirmed cases of invasive meningococcal disease are notifiable.
Period of Interest:
From 7 days prior to symptom onset until 24 hours of appropriate antibiotic treatment completion.
Public Health Actions:
Immediate commencement upon notification.
Other Complications:
Seizures
Circulatory shock
Cerebrovascular complications
Motor deficits
Subdural effusion
Intellectual disability
Behavioral problems
Lumbar puncture (Procedure, Interpretation of results, Complications, Contraindications)
Procedure
Equipment Needed:
Sterile gloves and surgical mask
Lumbar puncture kit including:
Manometer
Dressing pack
Aperture drape
3-way tap
2mL syringe
25G needle
22G spinal needle with stylet
CSF tubes
Adhesive dressing
Appropriate size lumbar puncture needle:
25Gx25mm for neonates/newborns
Needle length correlated with height of the child (~0.03xheight in cm)
Needle Size and Child’s Height/Age:
2cm: <50cm (Pre-term neonates)
3cm: 50-80cm (<2 years old)
4cm: 80-120cm (2-5 years old)
5cm: 120-150cm (5-12 years old)
6cm: 150-180cm (>12 years old)
Injectable local anaesthetic: Lignocaine 1% [50mg/5mL], max dose 4.5mg/kg/dose
Alcoholic chlorhexidine 0.5% in 70% alcohol (or aqueous chlorhexidine for neonates)
Topical anaesthetic cream (e.g., LMX 4 or Emla, applied at least 30 minutes prior)
Clear occlusive dressing
Sedation/analgesia as determined by Medical Officer
Patient Preparation:
Apply topical anaesthetic cream to the LP region between the 3rd and 5th lumbar vertebrae half an hour prior to the procedure if time permits.
Assistant washes hands for one minute and prepares trolley and equipment.
Medical officer wears surgical mask, washes hands for three minutes, and wears gloves in approved manner.
Assistant removes the occlusive dressing and wipes away the residual topical anaesthetic cream.
Medical officer prepares the skin at the site with alcoholic chlorhexidine 0.5%.
Positioning the Patient:
Infants:
Avoid over flexing the neck to prevent respiratory compromise.
Avoid pushing down on the back of the head to prevent the baby from arching backwards.
Minimize the risk of trauma to the site or spine if the baby moves during the procedure.
Children:
Position in the lateral recumbent position with hips and knees flexed towards the chin and head flexed towards the knees.
Gentle assistance is required to restrain the child’s arms.
Performing the Procedure:
Local Anaesthetic Injection:
Ensure the correct dosage is administered to the skin at the site.
Remove antiseptic solution from set-up before preparing medication for injection into the spine.
Needle Insertion:
Identify the correct site at L3-L4 or L4-L5.
Ensure the child is correctly positioned and local anaesthetic has taken effect.
Select appropriate lumbar puncture needle size.
Grasp spinal needle with bevel facing upwards; ensure patient’s back is perpendicular to the bed.
Insert the needle slowly through the skin into the subarachnoid space, aiming towards the umbilicus.
Leave the stylet in situ while traversing epidermis and subcutaneous fat.
For infants, gently remove the stylet before it passes through the dura; for older children, continue advancing the needle until decreased resistance or half its length is reached.
Remove the stylet gently; the presence of CSF indicates correct placement.
Measuring CSF Pressure:
Measure CSF pressure with the manometer.
Temporarily relax the flexed position by extending the child’s legs to accurately measure CSF pressure.
Ensure the distal end of the manometer is open to the atmosphere.
Note that nitrous oxide administration can increase intracranial pressure.
CSF Collection:
Hold the collection tube(s) under the needle until sufficient CSF is collected (0.5-1.0mL).
Collect a paired blood glucose level if needed.
Label the specimen, place it in a biohazard bag, and send it to pathology immediately.
Reintroduce the stylet before withdrawing the needle to minimize post-LP headache.
Withdraw the needle quickly and apply pressure to the site for at least one minute, then apply an adhesive dressing.
Discontinue nitrous oxide if used.
Remove the drape and dispose of equipment appropriately.
Document the procedure in the patient’s health care record, noting any equipment problems or incidents.
Post-Procedure Care
No bed rest required post-procedure; the child may mobilize as desired.
Post-LP Headache:
Manage with mild analgesia and rest as indicated by the degree of discomfort.
If the headache becomes severe or persists, seek medical review.
CSF Leakage:
Manage by lying the child down and applying pressure to the site with a sterile piece of gauze.
If leakage persists, seek medical review.
Infection:
Monitor for signs of infection, such as fever or the child becoming unwell.
Seek medical review if infection is suspected.
Site Tenderness or Nerve Root Irritation:
Manage with mild analgesia and rest as needed.
Troubleshooting
Encountering Bone:
If there is firm resistance to needle advancement, bone may have been encountered.
Review landmarks and consider partially withdrawing the needle and re-advancing in a more cranial or caudal direction.
Ensure the needle is inserted in the midline perpendicular to the plane of the back.
Poor CSF Flow:
Gently rotate the lumbar puncture needle to improve CSF flow.
Traumatic/Bloody Tap:
If blood is obtained (not blood-stained CSF), withdraw the needle and prepare for another attempt with a new needle.
Blood-stained CSF is still useful for culture/PCR.
Consider a subarachnoid haemorrhage if clinically appropriate.
Confirm with the presence of xanthochromia after CSF centrifugation.
Means to verify a diagnosis by checking for a yellowish discoloration in the cerebrospinal fluid (CSF) after it has been spun in a centrifuge. This yellow color indicates the presence of old blood, often confirming conditions like a subarachnoid hemorrhage.
Interpretation of Results
CSF Analysis:
Cell Count and Differential:
Elevated white blood cells indicate infection.
Neutrophils predominate in bacterial meningitis.
Lymphocytes predominate in viral meningitis, but bacterial meningitis cannot be excluded.
Glucose Level:
Low CSF glucose relative to blood glucose suggests bacterial infection.
Protein Level:
Elevated protein levels can indicate bacterial or viral meningitis.
Gram Stain and Culture:
Identifies specific pathogens causing the infection.
PCR Tests:
Detect specific pathogens like Neisseria meningitidis, Streptococcus pneumoniae, herpes simplex virus, enterovirus, and parechovirus.
Additional Notes:
Gram stain may be negative in up to 60% of bacterial meningitis cases, even without prior antibiotics.
A predominance of lymphocytes does not exclude bacterial meningitis.
Neutrophils may predominate in viral meningitis, even after the first 24 hours.
If the CSF is abnormal, the safest course is to treat for bacterial meningitis.
Complications
Common:
Failure to obtain a specimen
Need to repeat LP
Traumatic tap (presence of blood in CSF)
Post-dural puncture headache (up to 5-15%)
Uncommon to Rare:
Transient or persistent paraesthesiae or numbness
Respiratory arrest from local anaesthetic toxicity
Spinal haematoma or abscess
Tonsillar herniation (extremely rare in the absence of contraindications)
Contraindications
Absolute:
Unstable patient or reduced level of consciousness
Skin infection at the LP site
Suspicion of space-occupying lesion or raised intracranial pressure (ICP)
Coagulopathy or thrombocytopenia
Relative (delay LP if present):
Coma (absent or non-purposeful response to painful stimulus)
Signs of raised ICP (e.g., drowsiness, diplopia, abnormal pupillary responses, motor posturing, or papilloedema)
Cardiovascular or respiratory compromise
Focal neurological signs or recent seizures
The febrile child with purpura where meningococcal infection is suspected
Management (Antibiotics, Corticosteroids, Fluid therapy)
Antibiotics and Corticosteroids
Neonates and Children <2 Months
Common Pathogens:
Streptococcus agalactiae (group B streptococcus)
Enteric Gram-negative bacilli
Listeria monocytogenes (rare, generally in children up to 1 month old)
Treatment:
Treat as for sepsis or septic shock using regimens for infants where meningitis has not been excluded.
For Neonates:
Empirical therapy choice depends on the time since birth and whether the infant has been in the community.
For Infants Aged 1 to 2 Months:
Treat as for community-acquired sepsis or septic shock using empirical regimens for infants 1 month to younger than 2 months.
Complications:
Ventriculitis or abscess formation during therapy is not infrequent.
Corticosteroids:
Dexamethasone is not indicated in neonates (up to 1 month of age) due to insufficient evidence supporting its use.
Adults and Children ≥2 Months
Antibiotic Regimens:
Ceftriaxone 2g (child: 50mg/kg up to 2g) IV, 12-hourly
OR Cefotaxime 2g (child: 50mg/kg up to 2g) IV, 6-hourly
Corticosteroids:
Dexamethasone 10mg (child: 0.15mg/kg up to 10mg) IV, preferably starting before or with the first dose of antibiotic, then 6-hourly for 4 days.
Fluid Therapy
Hyponatraemia
Occurs in about one-third of children with meningitis
Causes:
Increased ADH secretion
Increased urine sodium losses
Excessive electrolyte-free water intake or administration
Monitoring and Management:
Careful and regular monitoring of clinical signs of hydration state, including:
Signs of overhydration
Serum sodium levels
Laboratory markers of hypovolaemia
Under most circumstances, IV fluids given to a child with meningitis should be isonatraemic (e.g., 0.9% sodium chloride (normal saline) with additional glucose).
Hyponatraemic solutions (e.g., 4% dextrose and one-fifth normal saline), which deliver excess free water, may worsen hyponatraemia and increase the risk of cerebral oedema, and should be avoided.
Immediate Resuscitation (if required):
Clinical signs of shock or hypovolaemia:
Hypotension
Poor peripheral perfusion
Cool pale extremities
Tachycardia with low volume pulses
High blood lactate or large base deficit
Children with more than one of these signs should be given 10-20mL/kg of normal saline as a bolus.
Dehydration Status and Management:
Mild (0-5%) Dehydration:
Weight loss: 5% in infants and 3% in children
Skin turgor: May be decreased
Mucous membranes: Dry
Urine output: May be low
Heart rate: Increased
Blood pressure: Normal
Perfusion: Normal
Skin color: Pale
Consciousness: Irritable
Moderate (5-10%) Dehydration:
Weight loss: 10% in infants and 6% in children
Skin turgor: Decreased
Mucous membranes: Very dry
Urine output: Oliguric
Heart rate: Increased
Blood pressure: May be normal
Perfusion: Prolonged capillary refill time (CRT)
Skin color: Grey
Consciousness: Lethargic
Severe (10-15%) Dehydration:
Weight loss: 15% in infants and 9% in children
Skin turgor: Poor with tenting
Mucous membranes: Parched
Urine output: Anuric
Heart rate: Increased
Blood pressure: Decreased
Perfusion: Prolonged CRT
Skin color: Mottled; blue or white
Consciousness: Comatose
Fluid Management for Severely Ill Children:
Ensure normal blood pressure and adequate circulating volume.
Clinical signs of hydration, including weight, serum sodium, acid-base status, and neurological state, should be assessed every 6-12 hours for the first 48 hours.
Adjust total fluid intake accordingly based on assessments.
Complications and sequelae (SIADH, Cerebral oedema, Hearing loss, Contact tracing)
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
Mechanism:
The exact mechanism is not fully understood.
It is widely accepted that meningitis (especially bacterial) leads to increased secretion of antidiuretic hormone (ADH), which contributes to hyponatraemia and cerebral oedema.
Cerebral Oedema
Pathophysiology:
An increase in the intercellular fluid volume of the brain leads to a rise in intracranial pressure (ICP).
Vasogenic Cerebral Oedema: Results from increased permeability of the blood-brain barrier (BBB), especially in the choroid plexus endothelium and the cerebral microvasculature endothelium.
Cytotoxic Factors: Released from neutrophils and bacteria, which can directly produce cerebral oedema.
Impaired CSF Absorption: Inflammation from infection can impede normal absorption of cerebrospinal fluid (CSF) from the subarachnoid space via the arachnoid villi.
Cerebral Perfusion Pressure: Normally maintained by an autoregulatory mechanism but becomes dependent on peripheral blood pressure during meningitis as autoregulation is impaired.
Increased ICP: Cerebral oedema itself can increase ICP and secondarily reduce cerebral blood flow.
Management:
Contraindication for Lumbar Puncture: Avoid LP in patients with suspected elevated ICP.
Supportive Care:
Intubate and ventilate patients to maintain adequate oxygenation and normocarbia.
Position patients with heads elevated at 30° and in a midline position.
Reduce stimuli by sedation and minimal handling.
Pharmacologic Interventions:
Mannitol, furosemide, dexamethasone, and short periods of hyperventilation may be indicated for the acute treatment of severely elevated ICP.
Hearing Loss
Types and Incidence:
Sensorineural Hearing Loss:
Occurs in 25-35% of patients after pneumococcal meningitis.
Occurs in 5-10% of patients after Haemophilus influenzae type b meningitis.
Hearing loss may be subtle or inapparent during the early phases of infection.
Transient or Permanent Hearing Loss:
Transient hearing loss is usually secondary to a conductive disturbance.
Permanent hearing loss can result from damage to CNVIII, the cochlea, or the labyrinth induced by direct bacterial invasion and/or the inflammatory response elicited by the infection.
Screening and Management:
Hearing should be tested in all children who have had bacterial meningitis before discharge from the hospital or within 4 weeks of discharge.
For severe to profound hearing loss, a cochlear implant may be necessary and should be placed as soon as the child has recovered from the acute stage of meningitis.
Contact Tracing
Definition of Contacts:
Household or Household-like Contacts:
Individuals who lived in the same house or dormitory-type room or had an equivalent degree of contact with the case in the 7 days prior to the onset of symptoms until the case has completed 24 hours of appropriate antibiotic treatment.
Intimate Kissing and Sexual Contacts:
In the 7 days prior to the onset of symptoms until the case has completed 24 hours of appropriate antibiotic treatment.
Child-care Contacts:
Higher-risk contact includes children and staff in childcare who had an equivalent degree of contact with the case as a household contact.
As a guide, two full days (6-8 hours each) of attendance in the same care group or a cumulative of around 20 hours in the same care group in the 7 days prior to the onset of symptoms should be considered higher-risk contact.
Other childcare contact is considered lower-risk. Child-care settings include kindergartens and pre-schools.
Passengers:
Seated immediately adjacent to the case during long-distance travel (>8 hours) by aeroplane, train, bus, or other vehicle.
Healthcare Workers:
Those who had unprotected close exposure of their airway to large particle respiratory droplets of a case during airway management (e.g., suctioning, intubation) or mouth-to-mouth resuscitation up until the case has had 24 hours of appropriate antibiotic treatment.
Actions:
Probable and confirmed cases of invasive meningococcal disease are notifiable.
Public health action should commence immediately.
The period of interest is from 7 days prior to the onset of symptoms in the case to the time the case has completed 24 hours of appropriate antibiotic treatment.
Other Complications and Sequelae
Shock: Can occur due to severe infection leading to systemic inflammatory response and hemodynamic instability.
Raised Intracranial Pressure (ICP): Due to cerebral oedema or other complications.
Seizures: Resulting from inflammation, high fever, or electrolyte imbalances.
Hydrocephalus: Can develop due to impaired CSF flow or absorption.
Cognitive, Academic, and Behavioral Problems: Long-term sequelae can include difficulties with cognitive function, academic performance, and behavior.
Subdural Effusion: Accumulation of fluid in the subdural space, which may require surgical intervention.
Acute Life Support
Apply knowledge of pathology of shock to explain the management principles of shock in children
Pathophysiology of Shock
Shock is characterized by decreased tissue oxygenation and blood pressure, often resulting from systemic inflammation triggered by infectious agents.
This systemic response can lead to multiple organ dysfunction due to inadequate tissue perfusion and oxygenation.
Key Pathophysiological Points:
Inflammatory Response:
White blood cells (WBCs) encounter pathogens, leading to the recruitment of other WBCs and the release of nitric oxide (NO), causing vasodilation and increased vascular permeability.
Systemic vasodilation leads to a drop in systemic vascular resistance (SVR), causing hypotension and decreased tissue perfusion.
Cardiovascular Implications:
Blood Pressure (BP) Determinants:
Cardiac Output (CO) and Systemic Vascular Resistance (SVR):
BP = CO×SVR
CO = HR×SV (HR = Heart Rate, SV = Stroke Volume)
Stroke Volume Factors:
Preload: Volume of blood in the ventricles at the end of diastole.
Myocardial Contractility: The strength of heart muscle contractions.
Afterload: Resistance the heart must overcome to eject blood.
Decreased SVR leads to a drop in BP and tissue perfusion.
Fluid buildup in tissues decreases oxygen delivery to cells, causing cellular hypoxia.
Cellular and Systemic Effects:
Cellular Hypoxia: Leads to cell membrane ion pump dysfunction, intracellular edema, leakage of intracellular contents, and inadequate pH regulation.
Systemic Acidosis and Endothelial Dysfunction: Progression of cellular hypoxia results in systemic acidosis and endothelial damage, further exacerbating the inflammatory response.
Disseminated Intravascular Coagulation (DIC):
Blood vessel damage activates coagulation factors, leading to clot formation and consumption of these factors. This results in bleeding and clot formation within the bloodstream.
Acute Respiratory Distress Syndrome (ARDS):
Damaged blood vessels in the lungs impair oxygen absorption, causing respiratory distress.
Clinical Signs:
Compensatory Mechanisms: Initially, cardiac output (CO) increases to compensate for decreased SVR. As shock progresses, cardiac function may become impaired, further decreasing BP
Skin Changes: Initially, warm skin due to vasodilation. As shock progresses and the sympathetic nervous system attempts to maintain BP by vasoconstriction, skin may become cool.
Symptoms: Respiratory distress, altered mental status, decreased urine output.
Management Principles
Resuscitation and Stabilization (First Hour):
Primary Goals:
Restore or maintain airway, oxygenation, and ventilation.
Ensure adequate circulation.
Maintain threshold heart rate for adequate cardiac output.
Initial Actions:
Obtain Vascular Access: IV or intraosseous (IO) access within 5 minutes
Fluid Resuscitation: Administer appropriate fluids within 30 minutes
Antibiotics: Begin broad-spectrum antibiotics within 60 minutes
Inotropic Support: For fluid-refractory shock, initiate peripheral or central inotropic infusion within 60 minutes
Ongoing Management:
Infection Control:
Identify the optimal antimicrobial therapy based on culture results.
Ensure the source of infection is controlled.
Respiratory Support:
Monitor respiratory status and provide optimal support.
Perfusion Monitoring:
Assess capillary refill time, heart rate, pulses, urine output, and mental status.
Monitor blood pressure and other indicators of tissue perfusion.
Correcting Derangements:
Address electrolyte and metabolic abnormalities, such as hypoglycemia, hypocalcemia, and elevated lactate levels.
Additional Considerations:
Fluid Management:
Use isotonic fluids (e.g., 0.9% sodium chloride) to manage fluid status and avoid hyponatremia.
Carefully monitor for signs of fluid overload and adjust fluid therapy accordingly.
Pharmacologic Interventions:
Use vasoactive medications to support blood pressure and cardiac function as needed.
Consider agents like mannitol, furosemide, dexamethasone, and short periods of hyperventilation for managing elevated ICP
Describe the sepsis pathway in the paediatric clinical practice guidelines and identify Red flags for sepsis
Overview
Sepsis is a medical emergency: Early recognition and treatment are critical for survival.
High-risk groups: Include very young children and children of Aboriginal, Torres Strait Islander, Pacific Islander, and Maori origin.
Diagnosis: Based on clinical judgement supported by laboratory findings.
Management: Includes rapid fluid resuscitation, early consideration of inotropes, and administration of appropriate antibiotics ideally within 15 minutes of presentation.
Critical care involvement: Early involvement of paediatric critical care is essential.
Sepsis Presentation by Age
Infants and Neonates: Often present with non-specific symptoms such as feeding difficulties and/or apnoea.
Older Children: May present with a focus of infection and/or features like fever or hypothermia, vomiting, inappropriate tachycardia, altered mental state, and reduced peripheral perfusion.
Vital Signs Trends: Deviations from pre-existing trends in vital signs can be a red flag.
General Toxic Features
Altered mental state
Tachypnoea: Increased work of breathing, grunting, weak cry
Marked/persistent tachycardia
Moderate to severe dehydration
Red Flags for Sepsis
Mottled, blue, or pale skin
Very lethargic or difficult to wake
Abnormally cold to touch
Fast breathing
Non-blanching rash
Fits or convulsions
Yellow Flags for Sepsis
Babies <3 months with temperature >38°C
Children 3-6 months with temperature >39°C
High temperature for >5 days
Temperature <36°C checked 3 times in 10 minutes
Difficulty breathing:
Grunting noises with each breath
Unable to say more than a few words at once (abnormal for them)
Breathing pauses
Dehydration:
Not drunk for >8 hours while awake
No urination in 12 hours
Sunken eyes
<1 month old with no interest in feeding
Green, bloody, or black vomitus
Lack of interest in surroundings
Not responding, floppy, or irritable
Bulging fontanelle
Weak, whining, or continuous crying
Confusion or stiff neck (older children)
Management Principles
First Hour of Resuscitation Goals:
Restore or maintain airway, oxygenation, and ventilation.
Ensure adequate circulation.
Maintain threshold heart rate (neither too low nor too high to ensure adequate cardiac output).
Initial Actions:
Obtain vascular access (IV or IO) within 5 minutes.
Start appropriate fluid resuscitation within 30 minutes.
Begin broad-spectrum antibiotics within 60 minutes.
Initiate peripheral or central inotropic infusion within 60 minutes for fluid-refractory shock.
Ongoing Management:
Manage infection with optimal antimicrobial therapy based on culture results and ensure the source of infection is controlled.
Monitor respiratory status and provide optimal support.
Monitor tissue perfusion (capillary refill time, heart rate, pulses, urine output, and mental status) and blood pressure.
Correct electrolyte and metabolic derangements (e.g., hypoglycaemia, hypocalcaemia, and elevated lactate levels).
Describe the immediate management of septic shock
First 5 Minutes: Immediate Actions
Call for Senior Help:
Immediate involvement of senior clinical staff for expert guidance and support.
Attach Cardiorespiratory Monitoring:
Continuous monitoring of heart rate, respiratory rate, blood pressure, oxygen saturation, and temperature.
Address Airway and Breathing Compromise:
Positioning:
In shock, elevate the legs to improve venous return (elevate the head in congestive heart failure).
Non-invasive Ventilation:
For patients with normal conscious state, consider High-Flow Nasal Cannula (HFNC), Continuous Positive Airway Pressure (CPAP), or Bilevel Positive Airway Pressure (BiPAP).
Intubation:
For patients with altered conscious state, consider intubation and involve local ICU and anaesthetic services.
Note the high risk of cardiac arrest with the use of induction agents in children with septic shock.
Administer Oxygen:
Provide supplemental oxygen, FiO2 100%. Intubate if required.
First 15 Minutes: Establish Vascular Access
Insert IO Cannula:
If IV access is not promptly established, insert an intraosseous (IO) cannula.
Take Bloods:
Priority Labs:
Blood culture
Venous blood gas (VBG) with lactate and glucose
Measure blood lactate concentration. If initial lactate concentration is >2mmol/L, measure again within 2-4 hours.
Additional Labs:
Full blood count (FBC)
C-reactive protein (CRP)
Urea, electrolytes, and creatinine (UEC)
Liver function tests (LFTs)
Coagulation profile
Group and hold (G&H)
Urinalysis and Lumbar Puncture (LP):
Consider once the child is stabilized.
Administer Antibiotics:
Administer via IV push; consider intramuscular (IM) if delays in IV/IO access.
First 30 Minutes: IV Fluid Administration with NaCl 0.9%
Fluid Resuscitation:
Begin rapid administration of IV fluids to manage hypotension or blood lactate concentration >2mmol/L.
Bolus:
20mL/kg (10mL/kg in neonates) bolus as a push, then reassess.
If needed, give an additional bolus (10mL/kg) and repeat as necessary to a maximum total volume of 40mL/kg.
Children requiring 40mL/kg of fluid resuscitation should be managed in a critical care environment.
Repeated Assessment:
Monitor fluid status, perfusion (heart rate, capillary refill time, urine output), clinical condition, and signs of fluid overload.
Stop Resuscitation:
When clinical improvement is achieved.
If clinical signs of improvement fail to appear.
If there are signs of volume overload (hepatosplenomegaly, JVP distension, gallop rhythm, wheeze, and crackles)
Manage Volume Overload:
Diuresis may be required.
Expected urine volume: 1mL/kg/hr.
Use furosemide 0.5-1mg/kg IV or mannitol 0.5-1g/kg IV for oliguria or anuria.
First 60 Minutes: Inotropes/Vasopressors
Inotropes and Vasopressors:
Inotropes: Agents that alter myocardial contractility (e.g., dobutamine, dopamine, milrinone).
Vasopressors: Sympathomimetic drugs that mimic the effects of the sympathetic nervous system (e.g., adrenaline, noradrenaline, vasopressin).
Administration:
If hypotensive during or after fluid resuscitation, administer a vasopressor to maintain a mean arterial pressure of at least 65mmHg.
For persisting circulatory failure after 40mL/kg fluid resuscitation, administer adrenaline 0.05-0.2μg/kg/min via peripheral access (IV or IO) while awaiting transfer to PICU.
Push Dose Inotropes:
Can be used by experienced clinicians:
Dopamine: 1-20μg/kg/min (start at 5μg/kg/min).
Dobutamine: 2-20μg/kg/min (start at 5μg/kg/min), can use peripheral IV.
Summary of Immediate Management Steps
Early Recognition and Seeking Senior Help:
Any red zone observation indicates severe sepsis or septic shock until proven otherwise.
Obtain senior clinical review within 30 minutes for suspected sepsis.
ABCDE Primary Survey:
A (Airway): Assess and maintain a patent airway.
B (Breathing): Assess and provide supplemental oxygen if required.
C (Circulation): Establish IV access, obtain blood samples, and monitor blood glucose levels.
D (Disability): Assess the level of consciousness.
E (Exposure): Obtain history and re-examine the patient for the source of sepsis.
F (Fluids): Monitor fluid input and output; consider insertion of an indwelling catheter (IDC).
Empiric Antibiotic Therapy:
Neonates: Benzylpenicillin + cefotaxime (or gentamicin if meningitis is excluded).
1-2 Months: Amoxicillin + cefotaxime/ceftriaxone (or gentamicin if meningitis is excluded).
2 Months: Gentamicin + cefotaxime/ceftriaxone + vancomycin.
Fluid Resuscitation:
Initial 20mL/kg 0.9% sodium chloride bolus.
Repeat as necessary if no improvement.
Early Initiation of Inotropes:
For persistent circulatory failure after 40mL/kg fluid resuscitation, use vasopressors such as adrenaline 0.05-0.2μg/kg/min.
Frequent Reassessment:
Monitor observations every 30 minutes for 2 hours, then hourly for 4 hours.
Watch for signs of deterioration and escalate care if needed:
Tachypnoea
Persistent tachycardia, slow capillary refill, and hypotension
Pale color and mottling
Drowsiness or decreased level of consciousness
Urine output <1mL/kg/hour
Acidosis, increasing serum lactate, or procalcitonin
Hypoglycaemia, leukopenia, or abnormal coagulation
Source Control:
Investigate and treat the underlying cause of sepsis.
Demonstrate the critical steps of acute life support in neonate, infant and child
Demonstrations/Technique:
A: Establish an Airway
Provide Oxygen:
Use fractional inspired oxygen (FiO2) 100%; use the optimum method for patient size and monitor.
Neonates, Infants: Head-box oxygen with in-situ FiO2 monitor
Infants, Toddlers: Nasal cannulae (NC). The ideal estimate of FiO2 from tidal volume (7mL/kg) and NC flow rate:
Example: A 6kg infant on 0.25L/min NC oxygen (tidal volume = 42mL; NC flow = 250mL/min, 4mL/s; inspiratory time = 1s).
FiO2 value: 4mL × 1.0 = 4mL oxygen, plus 38mL × 0.21 = 8mL oxygen.
FiO2 = (4 + 8)/42 = 0.29.
Toddlers, Pre-school: NC, face mask
School-age Child: Non-rebreathing mask
Maintain Airway and Air Movement:
Support airway with jaw lift, suction nasopharynx and mouth as needed.
Provide oral or nasopharyngeal airway.
Maintain the patient in an upright position; do not force a distressed patient to lie down and minimize discomfort.
B: Use Respiratory Support for Breathing
Identify the Level of Respiratory Involvement:
Treat specific problems appropriately (e.g., bronchodilators).
Assist Work of Breathing with Non-Invasive Support:
This can be achieved with nasopharyngeal continuous positive airway pressure (CPAP) (bronchiolitis) or negative pressure ventilation.
Intubation and Mechanical Ventilation:
Consider intubation and mechanical ventilation if necessary.
C: Assess Circulation; Establish IV Access
Start Pulse Oximetry and Cardiac Monitoring:
Continuous monitoring of heart rate, respiratory rate, blood pressure, oxygen saturation, and temperature.
Provide IV Fluids:
When circulation is good, limit fluid intake to an amount ranging from restricted to just below maintenance.
Detailed Steps in Life Support for Neonates, Infants, and Children
Airway:
Opening Maneuvers:
Infant’s airway is optimized at the neutral position.
Child airways are optimized at the "sniffing position" (mild extension of head on neck).
Use head tilt with chin lift or jaw thrust.
Airway Clearance:
Use a tongue depressor or laryngoscopy to clear any secretions, vomit, or blood with a suction device.
Airway Adjuncts:
Oropharyngeal Airway: Measured as the distance from the center of the mouth to the angle of the mandible.
Nasopharyngeal Airway: Measured as the distance from the top of the nose to the tragus of the ear.
Facemasks:
Correctly fitted, iat should extend from the bridge of the nose to between the lower lip and point of the chin.
Breathing:
Options Include:
Mouth-to-mouth ventilations.
Bag-valve-mask (BVM) ventilation.
Supraglottic airway (SGA).
Endotracheal tube (ETT).
For Neonates:
Supplemental oxygen is reserved for when the newborn’s saturations do not meet the lower end of the target despite respiratory effort.
If initial airway and breathing methods are unsuccessful, tracheal intubation and ventilation may be performed.
Circulation:
Compressions:
Commence chest compressions if the infant/child is unresponsive and not breathing normally, or a pulse is not palpable within 10 seconds or the pulse rate is <60 bpm accompanied by signs of poor circulation.
Compression Method:
Infant: Two-thumb or two-finger method.
Child: Use the heel of one hand or the two-handed technique.
Compression Ratio: 15:2 at a rate of 100-120 bpm.
Vascular Access:
Options include peripheral venous access, intraosseous (IO) injection and infusion, or central venous cannulation.
Use a bone marrow injection gun/drill to insert IO needle perpendicular to the bone surface. Confirm correct position by aspirating bone marrow or injecting normal saline to avoid compartment syndrome.
Fluids:
If hypovolemia is suspected, use IV or IO crystalloid for resuscitation.
Initial Bolus: 20mL/kg 0.9% sodium chloride.
Repeat if no improvement in heart rate, capillary refill time, or color.
Medications:
Calculate doses based on the child’s weight. Use a body length tape with pre-calculated doses if weight is unknown.
Flush IV and IO medications with small boluses of 0.9% NaCl or 5% glucose (for amiodarone) to ensure medications enter circulation.
Defibrillation:
Use pediatric defibrillation guidelines, adjusting energy doses based on the child’s weight and size.
Neonatal Specific Steps:
Assessment:
Initial assessment addresses tone, breathing, heart rate, color, and pulse oximetry.
Tone: Normally moving limbs and flexed posture. If responses are absent or weak, gently but briskly dry the newborn with a warmed towel to stimulate breathing.
Breathing: Includes crying.
Heart Rate: Should be >100 bpm within 2 minutes of birth.
Color: Normal newborns are blue but go pink soon after the onset of breathing.
Pulse Oximetry: Used to assess heart rate and oxygenation.
Airway Positioning:
On their back with the head in a neutral or slightly extended position ("sniffing position").
Mouth and Pharyngeal Suction:
To remove obstructions such as meconium or blood clots.
Tactile Stimulation:
To stimulate breathing. If not breathing within 1 minute of birth, commence CPAP or positive pressure ventilation.
Positive Pressure Ventilation:
Using a T-piece resuscitation device, self-inflating bag, flow-inflating bag, CPAP, mouth-to-mouth, or mouth-to-mask ventilation.
Chest Compressions:
If HR <60 despite assisted ventilation for 30 seconds, chest compressions are indicated.
Method: Two-thumb technique.
Compression Ratio: 3:1.
Medications and Fluids:
If HR <60 despite adequate assisted ventilations and chest compressions, administer adrenaline via the umbilical vein.
Consider volume expansion with fluids if necessary.
Summary of Immediate Management Steps
Early Recognition and Seeking Senior Help:
Recognize signs of severe distress and call for senior help immediately.
Any red zone observation = severe sepsis or septic shock until proven otherwise.
Obtain senior clinical review within 30 minutes for suspected sepsis.
ABCDE Primary Survey:
A (Airway): Assess and maintain a patent airway.
B (Breathing): Support as necessary, including supplemental oxygen and ventilation.
C (Circulation): Establish IV/IO access, monitor vital signs, and provide fluids and medications as needed.
D (Disability): Assess the level of consciousness.
E (Exposure): Look for signs of infection or other causes.
F (Fluids): Monitor fluid input and output; consider insertion of an indwelling catheter (IDC).
Administer Oxygen and Support Breathing:
Ensure adequate oxygenation and ventilation using appropriate methods for the age and condition of the child.
Establish Vascular Access and Administer Fluids:
Promptly obtain IV/IO access and start fluid resuscitation as needed.
Monitor and Reassess Continuously:
Frequently reassess the child’s condition and response to interventions.
Monitor observations every 30 minutes for 2 hours, then hourly for 4 hours.
Watch for signs of deterioration and escalate care if needed:
Tachypnoea
Persistent tachycardia, slow capillary refill, and hypotension
Pale color and mottling
Drowsiness or decreased level of consciousness
Urine output <1mL/kg/hour
Acidosis, increasing serum lactate, or procalcitonin
Hypoglycaemia, leukopenia, or abnormal coagulation
Source Control:
Investigate and treat the underlying cause of sepsis.
Describe an evidence-based approach to clinical pharmacology for the management of sepsis (Antibiotic prescribing guidelines)
Major Pathogens in Sepsis by Age Group
Infants <2 Months:
Escherichia coli
Group B Streptococcus
Listeria monocytogenes (uncommon)
Herpes Simplex Virus (HSV) infection should be considered in the differential diagnosis of sepsis.
Older Children:
Neisseria meningitidis
Streptococcus pneumoniae
Staphylococcus aureus (Methicillin-Sensitive Staphylococcus Aureus - MSSA, or Methicillin-Resistant Staphylococcus Aureus - MRSA)
Group A Streptococcus (GAS)
Antibiotic Regimens by Age Group
Neonates (≤7 Days):
Benzylpenicillin: 60mg/kg IV 12-hourly
Cefotaxime: 50mg/kg IV 12-hourly
Neonates (>7-28 Days):
Benzylpenicillin: 60mg/kg IV 6-8-hourly
Cefotaxime: 50mg/kg IV 6-8-hourly
Infants (1-≤2 Months):
Benzylpenicillin: 60mg/kg IV 4-6-hourly
Cefotaxime: 50mg/kg IV 4-6-hourly
Children (>2 Months):
Ceftriaxone: 100mg/kg (max 4g) IV daily or
Cefotaxime: 50mg/kg (max 2g) IV 6-hourly and
Flucloxacillin: 50mg/kg (max 2g) IV 6-hourly
Special Considerations
Oncology Patients:
Piperacillin/Tazobactam: 100mg/kg (max 4g) IV 6-hourly
Severely Unwell/High Risk:
Add Amikacin: 22.5mg/kg (18mg/kg if >10 years old) (max 1.5g) IV daily
Add Vancomycin: 15mg/kg (max 750mg) IV 6-hourly
Non-Oncology Patients with Central Venous Access:
Vancomycin: 15mg/kg (max 750mg) IV 6-hourly and
Ceftriaxone: 100mg/kg (max 4g) IV daily or
Cefotaxime: 50mg/kg (max 2g) IV 6-hourly
HSV Suspected (<3 months):
Add Acyclovir: 20mg/kg IV 8-hourly (indications: skin lesions, seizures, hepatitis)
Suspected MRSA:
Add Vancomycin based on local epidemiology and risk factors.
Suspected Toxin-Mediated Disease:
Consider adding Clindamycin: 15mg/kg (max 900mg) IV 8-hourly and
IV Immunoglobulin (Ig)
Alternatives and Special Cases
If IV Access Unavailable:
IM Ceftriaxone: 100mg/kg (max 4g) daily (can also be used in infants ≤2 months).
Previous Antibiotic Anaphylaxis:
Seek specialist advice for alternative antibiotic regimens.
Describe the special considerations for the management of sepsis for Aboriginal children
Higher Risk and Early Intervention
Higher Risk: Aboriginal children are at a higher risk of developing sepsis compared to non-Aboriginal children.
Early Intervention: Prompt recognition and early intervention are crucial to prevent poorer outcomes and reduce the risk of severe complications.
Epidemiological Data
ICU Admissions: Between 2002-2013, there was a gradual increase in the proportion of children admitted to intensive care units (ICUs) who were Indigenous Australians.
Invasive Infections: Among these admissions, one-quarter were due to invasive infections.
Sepsis and Septic Shock: Approximately one-tenth of the invasive infection cases involved sepsis or septic shock.
Specific Management Considerations
Cultural Sensitivity and Family Engagement:
Provide culturally sensitive care, understanding and respecting cultural practices and beliefs.
Engage with families and communities to build trust and ensure adherence to treatment plans.
Consider the role of extended family in the care and decision-making processes for Aboriginal children.
Access to Care:
Address potential barriers to accessing healthcare, such as geographical isolation, socio-economic factors, and lack of transportation.
Ensure timely access to medical facilities equipped to handle sepsis management, including transport to tertiary centers if necessary.
Health Education and Prevention:
Implement community-based education programs to raise awareness about the signs and symptoms of sepsis and the importance of early medical intervention.
Promote preventive measures such as vaccination and early treatment of infections to reduce the incidence of sepsis.
Tailored Antibiotic Regimens:
Use evidence-based antibiotic prescribing guidelines, considering the higher risk of severe infections and resistance patterns that may be more prevalent in Indigenous communities.
Ensure appropriate antibiotic stewardship to minimize the risk of resistance.
Comprehensive Care Approach:
Address underlying health disparities and comorbidities that may contribute to an increased risk of sepsis, such as malnutrition, chronic diseases, and poor living conditions.
Provide holistic care that includes social, emotional, and mental health support for the child and family.
Learning Points: Health society and environment
List Vaccine preventable infections and the immunisation schedule and briefly describe the evidence-based approach of vaccination
Vaccine-preventable infections
Cholera
Diphtheria
Haemophilus influenza type b (Hib)
Hepatitis A
Hepatitis B
Human papillomavirus (HPV)
Influenza
Japanese encephalitis
Measles
Meningococcal disease
Mumps
Pertussis (whooping cough)
Pneumococcal disease
Poliomyelitis
Q fever
Rabies and other lyssaviruses
Rotavirus
Rubella
Tetanus
Tuberculosis
Typhoid fever
Varicella (chicken pox)
Yellow fever
Zoster (herpes zoster)
Briefly describe the public health strategies employed to encourage vaccination and discourage the anti-vaccination movement
National Immunisation Program
Accessibility and Affordability:
Focus on making vaccines accessible and affordable to encourage national immunisation coverage.
Comprehensive strategies to ensure vaccines are available to all segments of the population.
Misinformation Correction
Public Health Organisations:
Actively work to correct misinformation that fuels the anti-vaccination movement.
Provide accurate information about vaccines and debunk common myths to build public trust.
Key Strategies
Improve Immunisation Coverage:
Enhance national immunisation efforts to increase vaccine uptake.
Implement targeted strategies to reach underserved populations.
Effective Governance:
Ensure robust management and oversight of the National Immunisation Program.
Implement policies that support vaccine distribution and monitoring.
Vaccine Supply and Efficiency:
Secure a reliable supply of vaccines.
Promote efficient use of vaccines to prevent shortages and ensure timely immunisation.
Vaccine Safety Monitoring:
Continuously enhance systems for monitoring vaccine safety.
Address safety concerns promptly to maintain public confidence.
Community Confidence:
Use effective communication strategies to build and maintain community trust in vaccines.
Engage with the public through transparent and consistent messaging.
Monitoring and Evaluation:
Strengthen the monitoring and evaluation of the immunisation program.
Use data from immunisation registers and disease surveillance to inform strategies.
Skilled Workforce:
Ensure an adequately trained immunisation workforce.
Promote effective training programs for healthcare providers.
Regional Contribution:
Maintain strong contributions to regional vaccination efforts.
Support international vaccination programs to control the spread of diseases globally.
Community Engagement Strategies
Increase Knowledge and Awareness:
Implement patient reminder/recalls and provider reminders.
Conduct public and provider education campaigns.
Integrate vaccination status checks into routine health assessments.
Use mass media for targeted promotion campaigns.
Reduce Costs and Increase Convenience:
Develop catch-up plans for those overdue for vaccination.
Implement accelerated vaccination schedules for diseases like hepatitis B.
Conduct home visits for routine childhood vaccination, especially for Aboriginal and Torres Strait Islander children.
Expand access to vaccination in hospitals and public clinics.
Establish Guidelines and Policies:
Fund vaccines under the National Immunisation Program (NIP).
Implement school-based vaccination programs.
Offer national parental incentives and maternity immunisation allowances.
Link vaccination to childcare benefits.
Mandate vaccination policies for healthcare workers.
Describe the public health principles for notifiable infectious illnesses, and how these are applied when caring for children
Principles of Notifiable Infectious Illnesses
Prompt Notification:
Healthcare providers must notify public health authorities within 24 hours of diagnosing a notifiable disease.
Notification is essential for immediate public health response and containment measures.
Mandatory Reporting by Various Entities:
Medical Practitioners and Hospital Chief Executives: Must report cases of notifiable diseases.
Pathology Laboratories: Required to notify relevant authorities upon confirmation of a notifiable infectious disease.
Primary and Secondary Schools and Child Care Centres: Principals and directors must report cases or suspicions of notifiable diseases.
Proactive Notification for Suspected Risk:
Not only diagnosed cases but also suspected cases that may pose a significant risk to public health must be reported.
This includes situations where children are reasonably suspected to have come into contact with a person who has a notifiable disease and the child’s immunization status is unknown or incomplete.
Outbreak Management:
School principals and child care directors are encouraged to seek advice and notify local public health units when they suspect an outbreak of infectious disease, such as gastrointestinal or respiratory illnesses.
Application in Caring for Children
Notification Requirements for Schools and Child Care Centres:
Principals and child care directors should notify their local public health unit (PHU) as soon as they are aware that a child has a notifiable vaccine-preventable disease or has been in contact with such a disease without proof of immunization.
Diseases to be notified include:
Diphtheria
Mumps
Poliomyelitis
Haemophilus influenzae Type b (Hib)
Meningococcal disease
Rubella ("German measles")
Measles
Pertussis ("whooping cough")
Tetanus
Health Practitioners’ Role:
Health practitioners must ensure hospital CEOs are aware of notifiable diseases among patients.
They have a duty to act on reasonable clinical suspicion and report accordingly.
Case Notification Timing:
Notifications should be made within 24 hours of diagnosis to enable rapid public health interventions.
Public Health Response:
Rapid notification allows public health units to implement control measures, conduct contact tracing, and provide guidance to prevent further spread of the disease.
This includes informing parents and guardians, managing quarantine or exclusion periods, and providing vaccination campaigns if necessary.
Preventive Measures:
Schools and child care centres are advised to maintain accurate immunization records for enrolled children.
Proactive communication and education about vaccination and disease prevention are critical to reducing the incidence of vaccine-preventable diseases.
List the factors that influence infectious disease in Aboriginal & Torres Strait Islander children
Overcrowding:
Increased risk of transmission of infectious diseases due to close living conditions.
Lack of Parental Supervision:
Children may be at greater risk of exposure to infectious agents without adequate supervision.
Poor Nutrition:
Malnutrition weakens the immune system, making children more susceptible to infections.
Wariness of the Healthcare System:
Distrust or fear of healthcare institutions may lead to delayed or avoided medical care.
Rural and Remote Locations:
Limited access to healthcare facilities and services, leading to delayed diagnosis and treatment.
Transport Issues:
Difficulty accessing healthcare services due to lack of transportation options.
Lack of Culturally Appropriate Health Services:
Healthcare services that do not respect or incorporate cultural practices may discourage Indigenous families from seeking care.
Intergenerational Trauma:
Historical and ongoing trauma can impact health behaviors and access to healthcare services.
Parental Factors:
Poor Mental Health: Parents with mental health issues may struggle to provide adequate care and supervision.
Substance Abuse: Drug and alcohol abuse can impair parenting capacity and lead to neglect.
Family Violence: Exposure to violence can disrupt family stability and access to healthcare.
Imprisonment: Parental incarceration can lead to unstable living conditions and reduced supervision.
Maternal Factors:
Low Birth Weight: Associated with increased vulnerability to infections.
Intrauterine Growth Restriction: Can lead to compromised immune function in infants.
Substance Use in Pregnancy: Increases the risk of neonatal infections and poor health outcomes.
Communal Living:
Shared living spaces can facilitate the spread of infectious diseases.
Lower Socioeconomic Status (SES):
Limited resources for healthcare, nutrition, and sanitation contribute to higher infection rates.
Lower Health Literacy:
Lack of understanding about disease prevention and treatment can hinder effective healthcare practices.
Access to Treatment:
Institutional barriers and limited availability of healthcare services can delay treatment.
Remote Communities Susceptible to Water Contamination:
Poor water quality and sanitation can lead to waterborne diseases.
Describe the support services available for Aboriginal children and their families
Aboriginal medical service
Aboriginal Liaison Officers (in hospital)
Aboriginal Maternal and Infant Health Services
The Aboriginal Maternal and Infant Health Service (AMIHS) was implemented in 2001 to improve the health of Aboriginal women during pregnancy and decrease perinatal morbidity and mortality for Aboriginal babies.
The service is delivered through a continuity-of-care model, where midwives and Aboriginal Health Workers collaborate to provide a high-quality maternity service that is culturally safe, women-centred, based on primary healthcare principles and provided in partnership with Aboriginal people.
AMIHS midwives and Aboriginal Health Workers provide antenatal and postnatal care, from as early as possible after conception up to eight weeks postpartum. The care is provided in the community but is linked into mainstream maternity services to ensure that risk management and education are available to AMIHS teams.
Services provided by AMIHS include:
Comprehensive and regular antenatal health checks
Booking into maternity hospitals
Smoking cessation programs
Referral and support to access other services
Health promotion and community development activities
Postnatal checks and support
Information on infant feeding and nutrition.
Building Strong Foundations for Aboriginal Children, Families and Communities
Building Strong Foundations (BSF) for Aboriginal Children, Families and Communities services provide a free, culturally safe and appropriate early childhood health service for Aboriginal children from birth to school entry age and their families. The service is provided by teams of Aboriginal health workers and child and family health nurses. In some locations, the core team is supported by other allied health therapists including social workers. The BSF service works with families, parents, carers, and the local community, to support the health, growth and development of Aboriginal children, so they are able to fully engage in life and learning.
The BSF service includes:
Developmental surveillance and health monitoring
Health promotion, including primary prevention, health education, anticipatory guidance and support for parents and carers and community development
Early identification of child and family needs
Responding to identified need, with information, brief interventions and appropriate referrals.
Families can get assistance and information on topics including:
Breastfeeding
Other feeding issues
Their child’s sleep and settling issues
Their child’s immunisations
Childhood safety
Their child’s growth and development
Parenting issues.
Aboriginal Community Controlled Health Services
An Aboriginal Community Controlled Health Service (ACCHS) is an incorporated Aboriginal organisation initiated by and based in a local Aboriginal community. They deliver a holistic and culturally appropriate health service to the community.
Aboriginal & Torres Strait Islander Health
What percentage of the total “Burden of Disease” for Aboriginal and Torres Strait Islander populations was due to the Burden of Disease in children aged 0-4?
Infants and Children Aged 0-4:
Population Representation:
Children aged 0-4 years comprised 12% of the Indigenous population in 2011.
Burden of Disease:
This age group accounted for 9% of the total burden of disease among Indigenous Australians
Significant contributors to the burden in this age group included:
Pre-term and low birthweight complications
Sudden Infant Death Syndrome (SIDS)
Other disorders of infancy
Birth trauma and asphyxia
Other Age Groups:
Children Aged 5-14:
Population Representation:
This age group comprised 24% of the total Indigenous population.
Burden of Disease:
Accounted for only 6% of the total burden of disease.
Main causes of health loss included:
Asthma
Anxiety disorders
Depressive disorders
Conduct disorders (estimates should be interpreted with caution due to lower accuracy)
Adolescents and Adults Aged 15-24:
Population Representation:
Made up about 20% of the Indigenous population.
Burden of Disease:
Accounted for 13% of the total burden.
Main contributors included:
Injuries
Mental and substance use disorders
Leading causes of burden in males:
Suicide and self-inflicted injuries
Alcohol use disorders
Motor vehicle traffic accidents
Leading causes of burden in females:
Anxiety disorders
Suicide and self-inflicted injuries
Depressive disorders
What were the three most common “diseases” contributing to the Burden of Disease in Aboriginal and Torres Strait Islander children in the 0-4 age group?
Preterm/Low Birth Weight Complications (20%)
Sudden Infant Death Syndrome (SIDS) (11%)
Birth Trauma/Asphyxia (7.7%)
How do Immunisation schedules differ between Aboriginal non-Aboriginal children?
Routine Vaccination
Aboriginal and Torres Strait Islander Children:
Aboriginal and Torres Strait Islander children aged 5 years or under should receive all routine vaccines under the National Immunisation Program (NIP).
Additional Vaccines for Aboriginal and Torres Strait Islander Children
In addition to routine childhood vaccines, the following additional vaccines are recommended for Aboriginal and Torres Strait Islander children aged 5 years or under:
Meningococcal B Vaccine:
Schedule:
Administered at 2, 4, and 12 months of age.
An extra dose at 6 months is required for infants with certain medical risk conditions for invasive meningococcal disease.
Eligibility:
Recommended and free under the NIP for Aboriginal and Torres Strait Islander children.
Children who missed out can still receive their meningococcal B vaccines for free under the NIP until they turn 2 years of age.
Pneumococcal Disease Vaccine:
Eligibility:
Aboriginal and Torres Strait Islander children living in Queensland (QLD), Northern Territory (NT), Western Australia (WA), and South Australia (SA).
Schedule:
An additional dose at 6 months.
Further doses at 4 years and at least 5 years later.
The type of vaccine and dosage schedule depend on age and any conditions that increase the risk of pneumococcal disease.
Hepatitis A Vaccine:
Eligibility:
Aboriginal and Torres Strait Islander children living in QLD, NT, WA, and SA.
Schedule:
Two doses at 18 months and 4 years of age.
Free under the NIP.
Influenza Vaccine:
Eligibility:
Free for all Aboriginal and Torres Strait Islander people aged 6 months and over through the NIP.
Catch-Up Vaccines:
Eligibility:
Aboriginal and Torres Strait Islander children aged 5 years and under should receive any missed routine childhood vaccinations.
Free under the NIP.
Resources
Impact and causes of illness and death in Aboriginal and Torres Strait Islander people
Immunisation for Aboriginal and Torres Strait Islander people https://beta.health.gov.au/health-topics/immunisation/immunisation-throughout-life/immunisation-for-aboriginal-and-torres-strait-islander-people
Learning Points: Professional Development
Aboriginal & Torres Strait Islander Health
Demonstrate engagement with Aboriginal Liaison Officers and Aboriginal Medical Services
NSW Health - Aboriginal Maternal and Infant Health Services. Located on this page are links for local AMIHS at Clinical sites
https://www.health.nsw.gov.au/kidsfamilies/MCFhealth/priority/Pages/amihs.aspx
Services provided by AMIHS include:
Comprehensive and regular antenatal health checks
Booking into maternity hospitals
Smoking cessation programs
Referral and support to access other services
Health promotion and community development activities
Postnatal checks and support
Information on infant feeding and nutrition.
Clinical Forum
Describe the role of the different health care professions involved in newborn care, including from the parent perspective
Maternal and Child Health Nurse (MCH Nurse)
Monitoring Growth and Development:
Works with families and healthcare professionals to monitor the growth and development of children from birth until about three and a half years old.
Focus Areas:
Prevention, promotion, early detection, and intervention of health and wellbeing concerns for young children and their families.
Services Provided:
Regular check-ups and developmental screenings.
Health education and support for parents.
Referral to specialists if any health concerns are identified.
Midwife
Post-Birth Care:
Newborn Screening Tests: Set up and explain the importance of newborn screening tests.
Feeding Support: Discuss feeding choices and refer to a lactation consultant if necessary.
Home Visits: Offer and arrange home visits for postnatal care for both mother and baby.
Life at Home: Provide guidance on adapting to life at home with a new baby.
Referrals: Organize referrals to specialists such as paediatricians if needed.
General Practitioner (GP)
Immunisations:
Administer the 6-week immunizations and monitor for any reactions.
Regular Reviews:
Conduct regular reviews at 5–10 days and six weeks postpartum.
Monitor and manage common neonatal concerns and maternal health issues.
Provide comprehensive care and support for the mother and family members.
Collaboration:
Work effectively with other health providers such as MCH nurses, midwives, lactation consultants, paediatricians, and obstetricians.
Ongoing Management:
Manage medical conditions that may have developed during pregnancy, such as hypertension, diabetes, and anemia.
Provide preventive health and lifestyle recommendations.
Paediatrician
Immediate Post-Birth Care:
Examine and treat babies immediately after birth.
Assess and resuscitate newborns if necessary.
Specialized Treatment:
Treat a wide range of illnesses, injuries, and conditions.
Manage the treatment of premature babies and infants with complex health issues.
Conditions Treated:
Cancer, genetic disorders (e.g., cystic fibrosis, Down syndrome), disabilities (e.g., cerebral palsy), developmental delays, chronic diseases (e.g., diabetes), infectious diseases (e.g., meningitis), asthma, allergies, and autism spectrum disorder.
Lactation Consultant
Breastfeeding Support:
Help mothers find the best way to breastfeed for both mom and baby to increase chances of success.
Issues Addressed:
Poor milk supply, breast pain and sore nipples, trouble latching, finding a comfortable nursing position, refusal to feed, poor infant weight gain, falling asleep at the breast, problems pumping breastmilk, and engorgement.
Parent Perspective
From a parent's perspective, these healthcare professionals provide a comprehensive support system to ensure the health and wellbeing of both the newborn and the mother. This multidisciplinary approach helps to:
Ensure Timely and Appropriate Care: By having access to various specialists, parents can be confident that their child's health needs are being met comprehensively and promptly.
Receive Guidance and Education: Parents receive valuable information on child development, feeding, and general care, which empowers them to make informed decisions.
Feel Supported: The involvement of multiple healthcare professionals ensures that parents are not alone in their journey and can rely on expert advice and support whenever needed.
Address Health Concerns Early: Early detection and intervention of health issues can prevent more serious problems down the line, ensuring better long-term health outcomes for the child.
Describe the ethical issues unique to decisions to resuscitate (or not) in cases of extreme prematurity
Threshold of Viability:
Generally considered between 23 to 25+6 weeks’ gestation.
Decisions to resuscitate are complicated by the fact that life-sustaining interventions are not normally recommended before 24 weeks’ gestation due to low survival rates and high risks of severe disability.
Ethical Considerations:
Best Interests of the Child:
The primary ethical consideration is whether resuscitation is in the best interests of the child.
Weighing the potential for survival against the likelihood of severe disability or suffering is crucial.
Each day of gestation after 24 weeks increases the chances of survival by 3-6%, so this incremental improvement must be considered.
Quality of Life:
Potential outcomes include severe disabilities, chronic health issues, and significant developmental delays.
Ethical dilemmas arise when considering if a life with severe disabilities would be in the child's best interest.
Parental Wishes and Autonomy:
Parents’ values, beliefs, and wishes should be respected and play a significant role in decision-making.
However, parents might be under emotional distress or lack the medical knowledge to fully understand the implications, raising questions about how much weight should be given to their wishes.
Medical Uncertainty:
Prognostic uncertainty at the threshold of viability makes decision-making challenging.
Variability in survival rates and outcomes based on gestational age, birth weight, and sex of the infant (e.g., male preterm infants have higher mortality rates and are more likely to have adverse outcomes).
Resource Allocation:
Intensive care for extremely preterm infants requires significant medical resources.
Ethical considerations involve whether the allocation of such resources is justified given the high risk of poor outcomes.
Informed Consent:
Ensuring parents are fully informed about the risks, benefits, and possible outcomes of resuscitation is crucial.
Ethical issues arise if there is a lack of clear, honest communication from the healthcare team.
Non-Maleficence and Beneficence:
The principle of non-maleficence (do no harm) requires careful consideration of the potential harms of resuscitation versus non-resuscitation.
The principle of beneficence (do good) requires that actions taken should benefit the child, but in cases of extreme prematurity, the potential for benefit is often uncertain.
Legal and Policy Frameworks:
Ethical decisions are influenced by legal standards and hospital policies regarding the resuscitation of extremely preterm infants.
Policies may vary, leading to different standards of care and ethical dilemmas about consistency in treatment decisions.
Long-Term Implications:
Consideration of the long-term implications for both the child and the family, including emotional, psychological, and financial burdens.
Additional (From CBL)
Impetigo
Description: Highly contagious skin infection of the upper layers of the epidermis.
Epidemiology: Most common skin infection in children, particularly affects those aged 2-6 years. Can occur in epidemics in preschools or schools.
Cause & Pathophysiology:
Caused by Staphylococcus aureus (80%), Streptococcus pyogenes (GAS) (10%), or co-infection (10%).
Risk Factors: Warm, humid climate; crowded, unsanitary living conditions; poor personal hygiene; pre-existing skin lesions; diabetes mellitus; immunodeficiency.
Clinical Features:
Nonbullous Impetigo: Papules that evolve into vesicles/pustules, rupture to form honey-colored crusts. Most often on the face around the nose and mouth.
Bullous Impetigo: Large, flaccid bullae that rupture to form thin, brown crusts. Most often on the trunk and upper extremities.
Pruritus and negative Nikolsky sign.
Investigations: Primarily clinical diagnosis; lesion swab for MCS to detect causative pathogen.
Management:
Non-endemic settings: Mupirocin 2% ointment or cream for localized sores; oral dicloxacillin + flucloxacillin for multiple sores or recurrent infection.
Endemic settings (e.g., remote communities): IM benzylpenicillin.
Cellulitis
Description: Local infection of the deep dermis and subcutaneous tissue.
Cause: Streptococcus pyogenes (Group A strep) and Staphylococcus aureus
Clinical Features: Erythema, oedema, warmth, tenderness, poorly defined lesion with induration. Possible systemic features (e.g., fever, tachycardia)
Investigations: Swab for MCS; consider imaging if abscess, deep infection, or foreign body is suspected.
Management:
Manage sepsis if present.
Manage source (e.g., remove foreign body, drain abscess).
Antibiotics:
Without systemic features: Oral phenoxymethylpenicillin
With systemic features: IV benzylpenicillin
Staphylococcal Scalded Skin Syndrome (SSSS)
Description: Blistering skin disorder induced by the exfoliative toxins of Staphylococcus aureus
Epidemiology: Typically affects children < 6 years
Cause & Pathophysiology: Spread of exfoliative toxins from a local infection (e.g., skin, mouth, nose, throat, impetigo).
Clinical Features:
Initially: Fever, malaise, irritability, skin tenderness, erythema (often starts periorally)
After 24-48 hours: Flaccid, easily ruptured blisters; widespread sloughing of epidermal skin; positive Nikolsky sign; no mucosal involvement
Investigations: WCC, ESR, cultures of the site of preceding infection, biopsy
Management: Close observation, IV fluid resuscitation, pain relief, empirical antibiotics
Scarlet Fever
Description: Syndrome caused by infection with a toxin-producing group A streptococci
Epidemiology: Peak incidence in children aged 5-15 years, often associated with streptococcal tonsillopharyngitis.
Cause & Pathophysiology: Aerosol transmission of GAS producing erythrogenic exotoxins leading to a delayed type IV hypersensitivity reaction and rash.
Clinical Features:
Initial Phase (Acute Tonsillitis): Fever, malaise, sore throat, difficulty swallowing, tonsillar exudates, white coating on the tongue.
Exanthem Phase: Fine, erythematous, blanching rash with a sandpaper-like texture; Pastia lines in flexural surfaces; begins on the neck and spreads to the trunk and extremities.
Desquamation Phase: 7-10 days after rash resolution, peeling of the skin on the face, trunk, hands, fingers, and toes.
Investigations: Throat culture, urinalysis (for post-strep glomerulonephritis), FBC, LFTs, CRP/ESR, elevated antistreptolysin O.
Management:
Supportive: Analgesia, antipyretics, maintenance fluids.
Medical: Oral benzylpenicillin for high risk of acute rheumatic fever.
Complications: Post-streptococcal glomerulonephritis, acute rheumatic fever, Sydenham chorea, Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS)
Stevens-Johnson Syndrome (SJS)
Description: Rare, life-threatening, immune-mediated skin reaction causing blistering and extensive epidermal detachment, usually precipitated by medications or infections.
Epidemiology: Affects all ages, more common in females.
Cause:
Drugs (80%): Antibiotics, corticosteroids, antiretrovirals, antiepileptics, allopurinol, sulfasalazine.
Infections: Mycoplasma pneumoniae, CMV, herpes.
Pathophysiology: Delayed type IV hypersensitivity reaction leading to cytotoxic T cell activation and granulysin release causing keratinocyte damage.
Clinical Features:
Prodromal Phase: High fever, malaise, sore throat, myalgia, arthralgia.
Mucocutaneous Lesions: Painful erythematous macules (target appearance) evolving to bullae/vesicles, full-thickness epidermal necrosis, and sloughing; severe involvement of mucous membranes.
Investigations: Clinical diagnosis.
Management: Discontinue offending drug, supportive care (fluids, wound management, antibiotics if septic).
