Growth and gastrointestinal problems
Learning Points: Science & Scholarship
Describe the pathophysiological basis of vomiting
Vomiting, or emesis, is a complex protective reflex designed to expel harmful substances from the stomach and upper intestine.
This reflex involves multiple components and pathways, integrating signals from the central nervous system, gastrointestinal tract, and other areas. Here’s a detailed explanation of the pathophysiology of vomiting:
Central Nervous System Components
Vomiting Center:
Location: Medulla oblongata
Function: The primary control center that initiates the vomiting reflex
Receptors: Muscarinic receptors
Input: Receives signals from various sources, including the chemoreceptor trigger zone, labyrinth of the inner ear, higher brain centers, and the gastrointestinal tract.
Chemoreceptor Trigger Zone (CTZ):
Location: Area postrema, outside the blood-brain barrier, in the floor of the fourth ventricle.
Receptors: Dopamine and serotonin receptors
Function: Detects blood-borne toxins and chemicals (e.g., chemotherapy agents) and activates the vomiting center through muscarinic receptors
Labyrinth of the Inner Ear:
Function: Involved in motion sickness.
Pathway: Movements activate the vestibulocochlear nerve, which sends signals to the vestibular nuclei in the pons. This activates histamine and muscarinic receptors, relays to the CTZ, and finally to the vomiting center.
Higher Brain Centers:
Function: Emotional and sensory inputs (e.g., pain, repulsive sights or smells) can trigger vomiting.
Pathway: These inputs directly stimulate the vomiting center.
Gastrointestinal Tract
Mechanoreceptors and Chemoreceptors:
Location: Throughout the gastrointestinal tract.
Function: Detect irritation, distension, and chemical stimuli.
Pathway: Signals from the vagal afferent nerves synapse in the nucleus tractus solitarius (NTS) in the medulla. Some neurons extend to the area postrema and other brain regions, contributing to the sensation of nausea.
Vomiting Reflex Mechanism
Initiation:
The vomiting center sends efferent signals via cranial nerves V, VII, IX, X, and XII.
Physiological Responses:
Tachycardia: Increased heart rate.
Increased Saliva Production: Protects the teeth and mucosa from stomach acid.
Closure of Epiglottis: Prevents aspiration of vomitus.
Diaphragm Contraction: Creates negative thoracic pressure aiding in the expulsion of gastric contents
Relaxation of Lower Esophageal Sphincter: Allows contents to move from the stomach into the esophagus.
Contraction of Abdominal Muscles: Increases intra-abdominal pressure.
Anti-peristalsis: Reversal of normal peristaltic movement to push contents upwards.
Ejection Phase:
Gastric and Lower Esophageal Sphincter Relaxation: Facilitates the movement of stomach contents.
Retching: Preceding phase where the glottis closes, and respiratory muscles counteract abdominal contraction, preventing expulsion.
Final Expulsion: Chyme is forced upwards and expelled through the mouth.
Neurotransmitters Involved
Muscarinic M1 Receptors: Involved in the activation of the vomiting reflex
Dopamine D2 Receptors: Triggered by toxins and drugs in the CTZ
Histamine H1 Receptors: Play a role in motion sickness
5-Hydroxytryptamine (5-HT)3 Receptors: Activated by serotonin in the gastrointestinal tract
Neurokinin 1 (NK1) Receptors: Substance P acts on these receptors in the vomiting center
List the common causes of vomiting in infants and children including surgical and other causes
Infancy
Gastroenteritis
Symptoms: Diarrhea (fluid stools), vomiting.
Cause: Viral or bacterial infection.
Acute Infections
Examples:
Tonsillitis
Otitis media
Pneumonia
Meningitis
Urinary Tract Infection (UTI)
Lesions of the GI Tract
Examples:
Duodenal obstruction from volvulus complicating malrotation
Strangulated inguinal hernia
Intussusception
Gastroesophageal Reflux Disease (GORD)
Symptoms: Recurrent fussiness during or after feedings, poor weight gain, recurrent respiratory symptoms (e.g., cough, stridor, wheezing).
Pyloric Stenosis
Symptoms: Recurrent projectile vomiting immediately after feeding in neonates aged 2–12 weeks, infrequent stools.
Infants may be emaciated (extremely thin or dehydrated) and dehydrated. Sometimes a palpable "olive" in the right upper quadrant.
Significance: Sudden onset of forceful, projectile vomiting, infants remain hungry/keen to feed, may contain blood, thickened pylorus felt.
Malabsorption
Examples: Coeliac disease (not common).
Intestinal Obstruction
Examples:
Meconium ileum
Meconium ileus is a condition in newborns where the meconium, which is the first stool passed by an infant, is abnormally thick and sticky, causing a blockage in the ileum, the final part of the small intestine
Volvulus
Intestinal malrotation
Intestinal malrotation refers to an abnormal rotation of the intestine during fetal development. This condition can lead to improper positioning of the intestines within the abdomen
Intestinal atresia
Intestinal atresia is a congenital condition where a portion of the intestine is absent, leading to a complete obstruction.
Increased Intracranial Pressure (ICP)
Examples: Space-occupying lesion (e.g., trauma, tumor).
Cyclical Vomiting Syndrome
Characteristics: Severe, discrete attacks of vomiting or nausea at varying intervals, with normal health between episodes and no demonstrable structural abnormalities.
Children
Infections
Examples:
Respiratory tract infections
Gastrointestinal tract infections
Acute Appendicitis and Peritonitis
Symptoms: Guarding, sometimes diarrhea.
Poisoning
Examples: Ingestion of toxic substances.
Migraine
Symptoms: Severe paroxysmal frontal headache with pallor, positive family history common.
Intracranial Neoplasm
Symptoms: Signs of increased ICP, vomiting in the morning before breakfast.
Psychological/Psychogenic Causes
Examples: Stress or anxiety-related vomiting.
Cyclical Vomiting Syndrome
Characteristics: Exclusion diagnosis, periodic severe vomiting.
Surgical and Other Causes
Intussusception
Symptoms: Colicky abdominal pain, inconsolable crying, lethargy, drawing of legs up to chest, later bloody ("currant jelly") stool. Typically ages 3–36 months but can be outside this range.
Malrotation with Volvulus
Symptoms: In neonates, bilious emesis, abdominal distention, and pain, bloody stool.
Sepsis
Symptoms: Fever, lethargy, tachycardia, tachypnea, widened pulse pressure, hypotension.
Food Intolerance
Symptoms: Abdominal pain, diarrhea, possibly eczematous rash or urticaria.
Other Medical Causes
Examples:
Urinary tract infection (UTI)
Meningitis
Raised intracranial pressure (ICP)
Metabolic disorders
Surgical Causes
Examples:
Appendicitis
Surgical obstruction (e.g., adhesions)
Meckel’s diverticulum
Vomiting Clinical Scenarios
Acute Vomiting
Description: Discrete episode of moderate to high intensity, most common, usually associated with an acute illness.
Investigations:
Full Blood Count (FBC)
Urea & Electrolytes (U&E)
Creatinine
Stool for culture and virology
Abdominal X-ray (AXR)
Surgical opinion if obstruction or acute abdomen possible
Exclude systemic disease
Causes: GI infection, non-GI infection (e.g., UTI), GI obstruction (congenital or acquired), adverse food reaction, poisoning, raised intracranial pressure, endocrine/metabolic disease (e.g., diabetic ketoacidosis).
Chronic Vomiting
Description: Low-grade daily pattern, frequently with mild illness.
Investigations:
FBC
Erythrocyte Sedimentation Rate (ESR)/C-Reactive Protein (CRP)
U&E
Liver Function Tests (LFT)
Helicobacter pylori serology
Urinalysis
Abdominal ultrasound
Small bowel enema
Sinus X-rays
Test feed or abdominal ultrasound for pyloric stenosis
Brain imaging (CNS tumor)
Consider urine pregnancy testing in teenage girls
Upper GI endoscopy
Causes: Peptic ulcer disease, gastroesophageal reflux, chronic infection, gastritis, gastroparesis, food allergy, psychogenic, bulimia, pregnancy.
Cyclic Vomiting
Description: Severe, discrete episodes associated with pallor, lethargy, +/- abdominal pain. The child is well between episodes. Often a family history of migraine or vomiting.
Investigations:
As for chronic vomiting, plus:
Serum amylase
Serum lipase
Blood glucose
Serum ammonia
Causes: Usually non-GI cause, idiopathic, CNS disease, abdominal migraine, endocrine (e.g., Addison’s disease), metabolic (e.g., acute intermittent porphyria), intermittent GI obstruction, fabricated illness.
More information
Distinguishing Features and Important Points for Vomiting in Infants and Children
Nature of Vomiting
Bilious Vomiting
Indicates: Gastrointestinal (GIT) obstruction until proven otherwise.
Action: Requires urgent surgical referral.
Blood in Vomit
Swallowed Blood:
Causes: Epistaxis (nosebleed), maternal blood due to delivery, or nipple trauma.
Action: Investigate source of blood.
Upper GI Hemorrhage:
Causes: Potential source if blood is present.
Action: Requires endoscopic evaluation.
Projectile Vomiting
Indicates: Pyloric stenosis.
Action: Requires investigation and often surgical management.
Early Morning Vomiting
Indicates: Raised intracranial pressure (ICP).
Action: Requires urgent evaluation for possible space-occupying lesion
Associated Signs and Symptoms
Evidence of Diarrhea
Indicates: Gastroenteritis
Fever or Systemic Illness
Indicates: Infection or sepsis
Action: Requires full sepsis workup and treatment
Abdominal Distension and Tenderness
Indicates: GIT obstruction
Additional Clues: “Tinkling” or absent bowel sounds
Headache
Indicates: Possible migraine, raised ICP, or infection
Action: Requires neurological evaluation
Rectal Bleeding
Indicates: Gastroenteritis, colitis, intussusception, Meckel’s diverticulum.
Bulging Fontanelle in Infants
Indicates: Raised ICP.
Action: Requires immediate investigation.
Specific Conditions
Meconium Ileus
Definition: Failure to pass the first stool in neonates (usually within the first 24-48 hours).
Cause: Cystic fibrosis (90% of cases)
Clinical Features: Signs of small bowel obstruction (bilious vomiting, abdominal distention, no passing of meconium)
Investigations: Abdominal X-ray (dilated small bowel loops, microcolon, Neuhauser signs - soap bubble appearance).
Management: Enema with a contrast agent, surgery in complicated cases.
Intestinal Malrotation
Definition: Abnormal or incomplete rotation of the gastrointestinal tract during fetal development.
Pathophysiology: Arrest in normal gut rotation leading to abnormal orientation of the bowel and mesentery.
Clinical Features: Mostly asymptomatic unless complicated by volvulus.
Associated Congenital Anomalies: Congenital diaphragmatic hernia, congenital heart defects, omphalocele (a birth defect in which the infant's intestine or other abdominal organs protrude through a hole in the belly button area and are covered with a membrane), Meckel’s diverticulum, esophageal atresia, biliary atresia.
Investigations: Upper GI series, barium enema, abdominal ultrasound, abdominal X-ray.
Management: Elective surgery (Ladd procedure).
Volvulus
Definition: Twisting of a loop of bowel on its mesentery.
Pathophysiology: Torsion of a malrotated gut leading to mechanical bowel obstruction.
Clinical Features:
Midgut Volvulus: Bilious vomiting, abdominal distention, signs of bowel ischemia (hematochezia, hematemesis, hypotension, tachycardia).
Gastric Volvulus: Severe abdominal pain, retching, inability to pass an NG tube.
Duodenal Obstruction: Bilious vomiting without abdominal distention.
Investigations: Upper GI series (duodenal obstruction, corkscrew duodenum), barium enema (Bird’s peak sign at the site of the twist), abdominal ultrasound (whirlpool sign), abdominal X-ray.
Management:
Initial: NPO, NGT insertion, IV fluids, broad-spectrum antibiotics.
Emergency Surgery (Ladd Procedure): Reduce/untwist the volvulus and remove Ladd bands.
Duodenal Atresia
Definition: Complete occlusion or absence of the duodenal lumen.
Epidemiology: Associated with chromosomal abnormalities, especially Down syndrome.
Pathophysiology: Failed or partial reuniting of the duodenum during the embryonic period.
Clinical Features:
Intrauterine: Polyhydramnios (excessive accumulation of amniotic fluid — the protective liquid contained within the amniotic sac of a pregnant woman)
Postpartum: Vomiting (bilious if stenosis is distal to the major duodenal papilla), distended upper abdomen, scaphoid lower abdomen, delayed meconium passage.
Investigations:
Prenatal: Ultrasound (double bubble sign).
Postnatal: Abdominal X-ray (gasless distal bowel).
Management:
Initial Management: IV fluids, NGT for gastric decompression.
Surgical Management: Bypass of the atresia or stenosis.
List the common causes of abdominal pain in infants and children; Including surgical causes
Infants and Children
Gastrointestinal Causes
Gastroenteritis
Appendicitis
Mesenteric Lymphadenitis
Constipation
Abdominal Trauma
Intestinal Obstruction
Peritonitis
Food Poisoning
Peptic Ulcer
Meckel's Diverticulum
Inflammatory Bowel Disease (IBD)
Lactose Intolerance
Hepatitis
Cholecystitis
Cholelithiasis
Choledocholithiasis
Splenic Infarction
Splenic Rupture
Pancreatitis
Genitourinary Causes
Urinary Tract Infection (UTI)
Urinary Calculi
Dysmenorrhea
Mittelschmerz
Pelvic Inflammatory Disease (PID)
Threatened Abortion
Ectopic Pregnancy
Ovarian/Testicular Torsion
Endometriosis
Metabolic Disorders
Diabetic Ketoacidosis (DKA)
Hypoglycemia
Porphyria
Acute Adrenal Insufficiency
Hematologic Disorders
Sickle Cell Anemia
Henoch-Schonlein Purpura
Hemolytic Uremic Syndrome
Miscellaneous Causes
Drugs and Toxins
Erythromycin
Salicylates
Lead Poisoning
Venoms
Pulmonary Causes
Pneumonia
Diaphragmatic Hernia
Pleurisy
Time-Critical Causes of Abdominal Pain by Age
Neonates
Hirschsprung Enterocolitis
Hirschsprung enterocolitis is an inflammatory condition of the bowel that occurs in patients with Hirschsprung disease. It involves inflammation of the colon and can lead to severe complications such as sepsis and bowel perforation.
Etiology (Causes)
Hirschsprung Disease:
The primary underlying cause is Hirschsprung disease, where a segment of the colon lacks nerve cells (ganglion cells), leading to chronic obstruction and stasis of intestinal contents.
Bacterial Overgrowth:
Stasis of intestinal contents can promote bacterial overgrowth and translocation, contributing to the development of enterocolitis.
Mucosal Barrier Dysfunction:
The absence of ganglion cells can impair mucosal barrier function, making the bowel more susceptible to inflammation and infection.
Incarcerated Hernia
Intussusception
Necrotizing Enterocolitis
Volvulus
Infants and Children
Abdominal Trauma
Appendicitis
Constipation
Gastroenteritis
Incarcerated Hernia
Intussusception
Meckel's Diverticulum
Mesenteric Adenitis
Ovarian Torsion
Pyloric Stenosis
Testicular Torsion
Volvulus
Adolescents
Appendicitis
Abdominal Trauma
Cholecystitis/Cholelithiasis
Constipation
Ectopic Pregnancy
Gastroenteritis
Inflammatory Bowel Disease (IBD)
Ovarian Cyst – Torsion/Rupture
Pancreatitis
Pelvic Inflammatory Disease (PID)
Renal Calculi
Testicular Torsion
Important Non-Abdominal Causes of Abdominal Pain
Diabetic Ketoacidosis (DKA)
Headache (Migraine)
Henoch-Schonlein Purpura
Hip Pathology
Pneumonia
Psychological Factors
Sepsis
Sexually Transmitted Infection
Sickle Cell Disease (Vaso-occlusive Crisis)
Toxin Exposure or Overdose
UTI/Pyelonephritis
Detailed Information on Specific Conditions
Hirschsprung Enterocolitis
Characterized by: An aganglionic colon segment (usually rectosigmoid) that fails to relax.
Epidemiology: Affects 1 in 5000 newborns, more common in males (4:1).
Cause: RET gene mutations associated with MEN2 and familial Hirschsprung disease.
Pathophysiology: Genetic mutation → defective migration of parasympathetic neuroblasts → absence of Meissner and Auerbach plexuses → aganglionic colon segment → inability to control intestinal wall muscles → uncoordinated peristalsis + slow motility → stenosis and functional obstruction → megacolon.
Clinical Features:
Early: Delayed passage of meconium, distal intestinal obstruction, tight anal sphincter, explosive stool on DRE.
Late: Chronic constipation, poor feeding, failure to thrive.
Investigations: Abdominal X-ray, barium enema.
Complications: Toxic megacolon, fecal incontinence, urinary dysfunction, erectile dysfunction, bowel perforation.
Management: Initial medical management (fluids, NGT, IV antibiotics), surgical correction.
Intussusception
Characterized by: Invagination of a proximal bowel segment into a distal lumen, most often occurs at the ileocecal valve.
Epidemiology: Most common between 2 months and 2 years, more common in males.
Cause: Idiopathic (90%) or pathological lead points (e.g., Meckel's diverticulum, polyps).
Pathophysiology: Imbalance in bowel wall → invagination (Invagination, in a medical context, refers to the process where a part of the intestine folds into an adjacent section) → venous impairment → ischemia → sloughed bowel wall → necrosis and perforation.
Clinical Features: Cyclic colicky abdominal pain, palpable sausage-shaped mass, red currant jelly stools, vomiting, high pitched bowel sounds, lethargy, pallor.
Investigations: Enema, ultrasound, abdominal X-ray.
Management: IV fluid resuscitation, NPO, analgesia, NGT, IV antibiotics, enema, surgical reduction if necessary.
Necrotizing Enterocolitis
Characterized by: Hemorrhagic necrotizing inflammation of the intestinal wall.
Epidemiology: Most common cause of acute abdomen in premature infants, typically between 2-4 weeks of life.
Cause: Unknown; factors include intestinal wall perfusion and motility disorders, microbial overgrowth, formula feeding, rapid increase in enteral nutrition.
Clinical Features: Lethargy, distended abdomen, gastric retention, vomiting, diarrhea, rectal bleeding, abdominal tenderness.
Investigations: FBC, ESR/CRP, coagulation studies, ABG, blood cultures, abdominal X-ray, portal vein gas.
Management: Supportive care, stop enteral feeding, decompression via NGT, IV antibiotics, radiographic monitoring, surgical intervention if needed.
Meckel's Diverticulum
Characterized by: A true diverticulum located approximately 2 feet proximal to the ileocecal valve.
Epidemiology: Most common congenital GIT abnormality, present in 2% of the population.
Pathophysiology: Persistence of the omphalomesenteric duct.
Clinical Features: Lower GI bleeding, bowel obstruction symptoms, diverticulitis symptoms.
Investigations: Meckel scintigraphy scan, CT angiography.
Management: Surgical resection if symptomatic.
Mesenteric Lymphadenitis
Characterized by: Enlargement and inflammation of mesenteric lymph nodes.
Epidemiology: Common in children under 15.
Cause: Yersinia species, beta-hemolytic streptococcus, E. coli, Strep viridans.
Clinical Features: Abdominal pain, fever, diarrhea, malaise, anorexia, nausea, vomiting.
Investigations: CT abdomen and pelvis.
Management: Supportive care, empirical antibiotics.
Pyloric Stenosis
Characterized by: Hypertrophy and hyperplasia of the pyloric sphincter.
Epidemiology: Most common cause of gastric outlet obstruction in infants, more common in males and firstborn children.
Causes: Environmental factors, genetic factors, macrolide antibiotics.
Clinical Features: Projectile non-bilious vomiting, palpable olive-shaped pylorus, peristaltic wave, "hungry vomiter."
Investigations: Abdominal ultrasound, UEC.
Management: Pyloromyotomy.
Pyloromyotomy involves making an incision in the outer layer of the hypertrophied pyloric muscle to relieve the obstruction.
Describe the main causes and mechanisms for abnormal growth patterns
Abnormal Growth Patterns
Abnormal growth patterns can be divided into:
Failure to thrive
Short stature
Tall stature
Failure to Thrive
Causes
Mechanism | Specific Causes |
---|---|
Inadequate Calorie Intake/Retention | - Inadequate nutrition (breastmilk, formula, and/or food) |
- Breastfeeding difficulties | |
- Error in infant formula preparation | |
- Restricted diet (e.g., restricting food groups, vegan, sensory aversions) | |
- Structural (e.g., cleft palate) | |
- Persistent vomiting | |
- Appetite loss due to chronic disease | |
- Early (<4 months) or delayed (>6 months) introduction of solids | |
Inadequate Absorption | - Cow milk protein allergy |
- Coeliac disease (if having gluten-containing diet) | |
- Pancreatic insufficiency (e.g., cystic fibrosis) | |
- Chronic diarrhea | |
- Chronic liver disease | |
Excessive Caloric Utilization | - Urinary tract infection |
- Chronic illness/inflammation | |
- Chronic respiratory disease (e.g., cystic fibrosis) | |
- Congenital heart disease | |
- Diabetes mellitus | |
- Hyperthyroidism | |
Psychosocial Factors | - Parental mental illness, disability, or chronic illness |
- Poor carer understanding (e.g., language barrier, limited literacy) | |
- Non-secure attachment patterns | |
- Behavioral disorders | |
- Difficulties at meal times | |
- Coercive feeding (including feeding child while asleep) | |
- Food insecurity | |
- Social isolation | |
- Failure to attend appointments | |
- Parental substance abuse | |
- Family violence | |
- Trauma or neglect | |
- Current or past child protection involvement | |
Other Medical Conditions | - Genetic syndromes |
- Inborn errors of metabolism |
Investigations
Bedside: Urinalysis, urine MCS, stool MCS, fat globules, fatty acid crystals, fecal calprotectin.
Bloods: FBC, UEC, LFT, ESR, iron studies, TSH, glucose, coeliac serology and total IgA (if on solid or feeds containing gluten), vitamin B12.
Short Stature
Causes
Mechanism | Specific Causes |
---|---|
Normal Variants of Growth | - Familial short stature |
- Constitutional delay of growth and puberty | |
- SGA (small gestational age) infant with catch-up growth | |
Systemic | - Undernutrition |
- Glucocorticoid therapy | |
- GI disease (especially IBD) | |
- Rheumatological disease (e.g., systemic-onset juvenile idiopathic arthritis) | |
- Renal disease (e.g., CKD, renal tubular acidosis) | |
- Cancer | |
- Pulmonary disease (e.g., cystic fibrosis, severe asthma) | |
- Immunodeficiency | |
Endocrine Diseases | - Hypothyroidism |
- GH deficiency | |
- Precocious puberty | |
- Cushing syndrome | |
- Pseudohypoparathyroidism type 1 | |
Genetic Diseases | - Turner syndrome |
- SHOX mutations | |
Skeletal Dysplasias | - Osteogenesis imperfecta |
- Achondroplasia | |
- Hypochondroplasia |
Investigations
Bedside: Urinalysis
Bloods: FBC, UEC, CMP, CRP/ESR, TSH, cortisol studies, coeliac serology, ANA screening, GH, IGF-1, FSH, LH
Imaging: Bone age (X-ray of the wrist)
Other: GH stimulation test, karyotype analysis
Tall Stature
Causes
In Infancy
Mechanism | Specific Causes |
---|---|
Causes in Infancy | - Infant of a diabetic mother |
- Cerebral gigantism | |
- Beckwith-Wiedemann syndrome |
In Childhood or Adolescence
Mechanism | Specific Causes |
---|---|
Endocrine Disorders | - Familial/constitutional tall stature |
- Precocious puberty | |
- Growth hormone excess | |
- Hyperthyroidism | |
- Sex hormone deficiency or insensitivity | |
- Familial glucocorticoid deficiency/resistance | |
Non-Endocrine Disorders | - Exogenous obesity |
- MC4R mutation | |
- Klinefelter syndrome (47XXY) | |
- 47, XYY | |
- Marfan syndrome |
Investigations
Bloods: TSH, GH, IGF-1, LH, FSH, testosterone levels, serum cortisol, serum prolactin
Imaging: Bone age (X-ray of the wrist)
Other: Karyotype analysis
Detailed Information on Specific Conditions
Cow Milk Protein Allergy
Epidemiology: One of the most common food allergies in children, affects 1-2% of preschool children.
Pathophysiology: IgE antibodies against milk proteins.
Risk Factors: Family history, atopic disease, allergic disease.
Clinical Features:
Mild to Moderate Reactions: Hives, swelling of the lips/face/eyes, tingling of the mouth, abdominal pain, vomiting.
Severe Reactions (Anaphylaxis): Difficulty/noisy breathing, swelling of the tongue, persistent cough, dizziness, collapse.
Investigations: Allergy skin prick test, RAST test.
Management: Diet free of cow’s milk and cow’s milk products.
Prognosis: 90% of children with delayed reactions and 50% with immediate reactions will outgrow their allergy by 3-5 years of age.
Short Stature
Physiological Causes:
Familial short stature
Constitutional delay of growth and puberty
Small for gestational age infant with catch-up growth
Idiopathic short stature
Pathological Causes:
Defects of nutrition, digestion, or absorption
Social and emotional deprivation
Chronic disease (e.g., rheumatologic, CKD, cancer)
Genetic syndromes (e.g., Turner syndrome in girls)
Endocrine (e.g., deficiency of thyroid or growth hormone)
Iatrogenic (e.g., long-term steroid therapy)
Disorders of bone growth (e.g., skeletal dysplasia)
Investigations: Urinalysis, blood tests (FBC, UEC, CMP, etc.), imaging (bone age X-ray), GH stimulation test, karyotype analysis.
Tall Stature
Causes of Overgrowth in Infancy:
Infant of a diabetic mother
Cerebral gigantism
Beckwith-Wiedemann syndrome
Causes of Overgrowth in Childhood or Adolescence:
Familial/constitutional tall stature
Endocrine disorders (e.g., precocious puberty, growth hormone excess, hyperthyroidism)
Non-endocrine disorders (e.g., exogenous obesity, Klinefelter syndrome, Marfan syndrome)
Investigations: TSH, GH, IGF-1, LH, FSH, testosterone levels, serum cortisol, serum prolactin, bone age X-ray, karyotype analysis.
Describe the pathophysiology for the common causes of chronic abdominal pain and or diarrhoea in children (Coeliac disease, IBD)
Coeliac Disease
Coeliac disease is an autoimmune disorder characterized by an abnormal immune response to gluten, a protein found in wheat, rye, and barley.
Genetic Predisposition:
Majority of patients carry one of two major histocompatibility complex class-II molecules: HLA-DQ2 (95%) and HLA-DQ8 (5%).
Immune Response:
Loss of immune tolerance to gluten-derived peptides (gliadin) leads to the activation of an antigen-specific T-cell response.
Gluten peptides are resistant to human proteases and persist intact in the small intestinal lumen.
These peptides access the lamina propria through:
Faulty tight junctions.
Endothelial cell transcytosis.
Dendritic cell sampling of the intestinal lumen.
Passage during the resorption of apoptotic villous enterocytes.
Innate and Adaptive Immune Activation:
In the intestinal submucosa, gluten peptides trigger both innate and adaptive immune activation:
Innate Response:
Gluten peptides stimulate IL-15 production by dendritic cells, macrophages, and intestinal epithelial cells, leading to epithelial damage via intra-epithelial lymphocytes.
Adaptive Response:
In the submucosa, gluten peptides are deamidated by tissue transglutaminase (tTG), allowing high-affinity binding to HLA-DQ2 or DQ8.
This triggers activation of helper T (Th) cells, leading to:
Cell death and tissue remodeling with villous atrophy and crypt hyperplasia.
Th2-mediated plasma cell maturation and production of anti-gliadin and anti-tTG antibodies.
Associated Conditions:
Positive family history, Type 1 diabetes, Down syndrome, and IgA deficiency.
Presentation:
Initial Features:
Pallor, diarrhea, pale bulky floating stools, anorexia, failure to thrive (FTT), irritability.
Later Features:
Apathy, gross motor developmental delay, ascites, peripheral edema, anemia, delayed puberty, arthralgia, hypotonia, muscle wasting, specific nutritional disorders.
Investigations:
Bedside: Urinalysis, stool MCS.
Bloods: IgA tissue transglutaminase antibody (tTG IgA), total IgA, deamidated gliadin peptide, FBC (iron, folate, B12 deficiency anemia), endomysial antibody (EMA), HLA testing.
Other: Upper endoscopy and biopsy (villous atrophy, crypt hyperplasia, intraepithelial lymphocyte infiltration), skin biopsy (if dermatitis herpetiformis).
Management:
Consultation with a dietician.
Education about the disease.
Lifelong adherence to a strict gluten-free diet.
Identification and treatment of nutritional deficiencies (iron, vitamin D, B12, folate).
Continuous long-term follow-up by a multidisciplinary team (serology, FBC, TSH, vitamin D).
Inflammatory Bowel Disease (IBD)
IBD encompasses Crohn's disease and ulcerative colitis, both of which involve chronic relapsing inflammation of the gastrointestinal tract.
Crohn's Disease
Pathology:
Chronic relapsing inflammation with "skip lesions" affecting any part of the GIT.
Involves transmural inflammation (including the serosa), fissured ulceration, "cobblestone" appearance, and granuloma formation.
Commonly involves the ileum (80% of cases) and rectum (25% of cases).
Aetiology:
Genetic: Mutations in CARD15 (NOD2).
Environmental: Cigarette smoking, oral contraceptives, high refined sugar diet, nutritional deficiencies, infectious agents, NSAIDs.
Main Clinical Features:
Persistent or grumbling pain with severe acute attacks.
Diarrhea less prominent (without blood), rectal bleeding less common.
Abdominal mass relatively common, abdominal pain/tenderness.
Extra-intestinal manifestations include arthritis, uveitis, erythema nodosum, pyoderma gangrenosum, primary sclerosing cholangitis, vitamin B12 deficiency.
Complications:
Strictures, fistulae, anal and perianal lesions, massive hemorrhage, incomplete obstruction, toxic megacolon.
Ulcerative Colitis
Pathology:
Recurrent acute inflammation with intervening quiescent phases, continuous involvement of the affected colon.
Confined to the mucosa and submucosa, with widespread superficial ulceration, pseudopolyps.
Aetiology:
Genetic: 10% have a 1st-degree relative affected, higher incidence in Ashkenazi Jews.
Environmental: Higher incidence in developed countries, smoking protective, previous enteric infections increase risk.
Immunologic: Impaired epithelial barrier, reduced dendritic cell numbers, exaggerated Th2 cell response.
Main Clinical Features:
Severe diarrhea with blood, tenesmus, rectal bleeding very common.
Abdominal pain and tenderness.
Extra-intestinal manifestations include arthropathy, eye, skin, and biliary tract disorders, anemia.
Complications:
Strictures rare, fistulae rare, massive hemorrhage, toxic megacolon, high risk of malignant change with severe or longstanding disease.
Pathophysiology Overview
Condition | Pathophysiology |
---|---|
Coeliac Disease | Autoimmune response to gluten, leading to villous atrophy, crypt hyperplasia, and malabsorption due to an immune response triggered by gliadin peptides. |
Crohn's Disease | Immune dysregulation and chronic relapsing inflammation with transmural involvement, skip lesions, granuloma formation, leading to fibrosis, strictures, and fistulae. |
Ulcerative Colitis | Chronic inflammation confined to the mucosa and submucosa with continuous colonic involvement, leading to widespread ulceration, pseudopolyps, and increased risk of colorectal cancer. |
Detailed Descriptions:
Coeliac Disease:
Epidemiology: Females > males, bimodal peak incidence (8-12 months, 30-40s), more common in individuals of northern European descent.
Cause: Genetic predisposition (HLA-DQ2, HLA-DQ8), associated with autoimmune diseases.
Pathophysiology: Consumption of gluten triggers chronic intestinal inflammation due to an autoimmune response, leading to epithelial damage, villous atrophy, crypt hyperplasia, and malabsorption.
Clinical Features:
Gastrointestinal: Chronic or recurring diarrhea (steatorrhea), flatulence, abdominal bloating and pain, nausea, vomiting, lack of appetite.
Extraintestinal: Vitamin deficiency, iron deficiency anemia, fatigue, weight loss, osteoporosis, hypocalcemia, failure to thrive, growth failure, delayed puberty, dermatitis herpetiformis, neuropsychiatric symptoms, reduced fertility or infertility, autoimmune thyroid disease, type 1 diabetes mellitus, Turner syndrome, Down syndrome, rheumatoid arthritis, sarcoidosis, selective IgA deficiency.
Investigations: IgA tissue transglutaminase antibody (tTG IgA), total IgA, deamidated gliadin peptide, FBC, endomysial antibody (EMA), HLA testing, upper endoscopy and biopsy, skin biopsy (if dermatitis herpetiformis).
Management:
Consultation with dietician
Education about disease
Lifelong adherence to strict gluten-free diet - abdominal discomfort lessens within days and diarrhoea within weeks.
Identification and treatment of nutritional deficiencies - iron, vitamin D, B12, folate.
Access to an advocacy group
Continuous long term follow up by a multidisciplinary team
Serology at 6 month intervals until levels normalise, then annually.
Measure FBC, TSH, vitamin D.
Monitor growth of child
IBD (Crohn's Disease and Ulcerative Colitis):
Epidemiology: More common in whites, particularly individuals of Ashkenazi Jewish descent, with 10-20% of IBD cases diagnosed during childhood. Peak age of onset at 15-29 years.
Risk Factors: Genetic predisposition (HLA-B27), smoking, oral contraceptive use, NSAIDs, high refined sugar diet, previous intestinal infection.
Pathophysiology:
Crohn's Disease: Dysregulation of Th17 signaling, immune dysregulation, NOD2 mutations leading to unregulated inflammation, transmural involvement, "skip lesions," granuloma formation.
Ulcerative Colitis: Abnormal host immune response to commensal bacteria, Th2-mediated response, continuous inflammation from the rectum proximally, confined to mucosa and submucosa.
Pattern of involvement
Ulcerative colitis
Inflammation is limited to the mucosa and submucosa.
Ascending inflammation beginning in the rectum and moves retrograde the colon.
In children, the disease is often pancolonic at diagnosis.
Crohn’s disease
Inflammation is transmural (i.e. affects the full thickness of the GI wall)
Most commonly infects the terminal ileum and colon.
Any part of the GIT can be involved, but the rectum is generally spared.
Inflammation is irregular and does not occur continuously throughout the GIT.
In children, upper GI involvement is more common than in adults.
Clinical Features:
Crohn's Disease: Chronic watery diarrhea, perianal fistulas and abscesses, malabsorption, abdominal pain, palpable abdominal mass.
Ulcerative Colitis: Bloody diarrhea with mucus, fecal urgency, abdominal pain and cramps, tenesmus.
Investigations:
Laboratory studies and stool tests
FBC: anaemia
LFT
UEC: electrolyte abnormalities from diarrhoea and dehydration.
↑ ESR + CRP
Stool:
MCS: Microscopy, culture, sensitivities
OCP: Ova, cysts, parasites
Confirm diagnosis: colonoscopy & biopsy
Colonoscopy findings:
Ulcerative colitis: Circumferential inflammation or ulceration that is continuous throughout a section of rectum/ colon. Friable mucosa with bleeding on contact with endoscope.
Crohn’s disease: “Skip lesions” with cobblestone appearance - linear patches of damaged tissue with normal patches of mucosa in between. Usually does not involve the rectum.
Biopsy findings:
Ulcerative colitis: Neutrophil infiltration limited to the mucosa and submucosa. Crypt abscesses (due to aggression of lymphocytes) => crypt atrophy.
Crohn’s disease: Transmural inflammation. Inflammatory cells and non-caseous sarcoid granulomas.
Radiological studies
Plain x ray
Barium enema radiography
Management
Non-pharmacological therapy
Multidisciplinary team involvement - paediatrician, gastroenterologist, GP.
Education
Dietetic assessment
Consider social work, psychological or other allied health services.
Group support
Vaccination - ensure vaccinations are up to date and commence live vaccinations prior to starting immunosuppressive therapy. After therapy begins, NO LIVE vaccinations.
Pharmacological therapy
Ulcerative colitis
Acute flare
Mild to moderate:
Oral 5-aminosalicylate (induction)
If unresponsive, add oral prednisone
Moderate to severe:
IV hydrocortisone or methylprednisolone
If unresponsive, add IV infliximab or ciclosporin
Chronic (i.e. maintenance therapy)
Rectal and/or Oral 5-aminosalicylate
If unresponsive, add oral azathioprine, mercaptopurine or methotrexate
If unresponsive, add IV infliximab
Gastroenteritis in children
Briefly describe common causes, investigations and treatment; antibiotics, fluid management, electrolyte management, antiemetics / antidiarrhoeal agents
Gastroenteritis in Children:
Common Causes
Viral Gastroenteritis:
Transmission: Faecal-oral route, often through contaminated water. Common during winter. Breastfeeding provides some protection. More severe in malnourished children.
Causes:
Rotavirus (most common before vaccination)
Norovirus
Enteric adenovirus
Astrovirus
Cytomegalovirus (CMV in immunocompromised patients)
Bacterial Gastroenteritis:
Sources of Infection: Contaminated water, poor food hygiene (meat, fresh produce, chicken, eggs, previously cooked rice). Most common in children under 2 years old.
Causes:
Salmonella spp.
Campylobacter jejuni
Shigella spp.
Yersinia enterocolitica
Escherichia coli
Clostridium difficile
Bacillus cereus
Vibrio cholerae
Presentation
Viral Gastroenteritis:
Watery diarrhea (rarely bloody)
Vomiting
Cramping abdominal pain
Fever
Dehydration
Electrolyte disturbances
Upper respiratory tract signs common with rotavirus
Vomiting predominates with norovirus
Bacterial Gastroenteritis:
Secretory and inflammatory diarrhea
Symptoms similar to viral gastroenteritis plus:
Malaise
Dysentery (bloody and mucous diarrhea)
Abdominal pain mimicking appendicitis or IBD
Tenesmus
Complications
Viral:
Prominent UGI symptoms (N/V)
Acute, resolves within 24-48h
Possible secondary cases due to person-to-person transmission
Bacterial:
Bacteraemia
Secondary infections (pneumonia, osteomyelitis, meningitis)
Reiter’s syndrome (Shigella, Campylobacter)
Haemolytic-uraemic syndrome (E. coli O157, Shigella)
Guillain-Barré syndrome (Campylobacter)
Reactive arthropathy (Yersinia)
Haemorrhagic colitis
Toxin-mediated:
N/V and abdominal pain prominent
Diarrhoea occurs later
Short incubation period (several hours)
Closely clustered cases
Infections arise from a single point source
Investigations
Assess degree of dehydration: Use weight change, signs, vital signs, pallor (blood loss), abdominal tenderness, signs of associated illness (e.g., petechial rash in HSP).
Calculate fluid deficit
Faecal samples for bacterial culture if significant abdominal pain or blood in faeces.
C. difficile infection: Based on clinical features (diarrhoea, ileus, toxic megacolon) and microbiological evidence or colonoscopy findings.
Stool microbiological investigations: If diarrhea persists beyond 7 days, suspicion of septicaemia, blood/mucus in stool, or immunocompromised child.
Blood tests: For severe dehydration, renal disease, altered conscious state, 'doughy' skin (hypernatraemia), home therapy with hypertonic/hypotonic fluids, profuse losses, ileostomy.
Treatment
Antibiotics:
Most acute diarrhoea is viral and does not require antibiotic therapy
Empirical antibiotics are usually not indicated for community-acquired infectious diarrhoea
In children with bloody diarrhoea without fever or sepsis, empirical antibiotic therapy is not recommended due to the risk of precipitating haemolytic uraemic syndrome (HUS) if the infection is caused by enterohaemorrhagic Escherichia coli
Empirical therapy is indicated or should be considered in some groups.
Empirical antibiotics are indicated for patients with manifestations of severe disease
Consider empirical antibiotics in immunocompromised patients, even if they do not have clinical features suggesting severe disease, as they are at greater risk of rapid deterioration and poor outcomes
There is evidence that empirical antibiotic therapy shortens the duration of illness by 1-3 days in returned travellers with acute diarrhoea
If empirical antibiotic therapy for acute infectious diarrhoea is indicated, obtain samples for faecal testing before starting therapy → use:
Ciprofloxacin 500mg (child: 12.5mg/kg up to 500mg) orally, 12-hourly for 3 days
Norfloxacin 400mg (child: 10mg/kg up to 400mg) orally, 12-hourly for 3 days
If the infection is likely to have been acquired in an area where quinolone resistance is common (e.g. South and East Asia), or an oral suspension is required (e.g. for young children), consider: azithromycin 500mg (child: 10mg/kg up to 500mg) orally, daily for 3 days
If oral therapy is not tolerated or absorption is likely to be impaired, consider: ceftriaxone 2g (child ≥1mth: 50mg/kg up to 2g) IV, daily for 3 days
C. difficile infection:
First episode:
Metronidazole 400mg (child: 10mg/kg up to 400mg) orally or enterally, 8-hourly for 10 days
OR vancomycin 125mg (child: 10mg/kg up to 125mg) orally or enterally, 6-hourly for 10 days
There is evidence that vancomycin has similar efficacy to metronidazole in this setting; however, for antimicrobial stewardship reasons, it is not the preferred drug
First recurrence or refractory disease
Vancomycin 125mg (child: 10mg/kg up to 125mg) orally or enterally, 6-hourly for 10 days
OR fidaxomicin 200mg orally, 12-hourly for 10 days
Second and subsequent recurrences or ongoing refractory disease
Vancomycin 10mg/kg up to 125mg orally or enterally, 6-hourly for 14 days
OR nitazoxanide 100mg (for children 1-3y/o) or 200mg (for children ≥4y/o) orally, 12-hourly for 10 days
Severe infection
Vancomycin 125mg (child: 10mg/kg up to 125mg) orally or enterally, 6-hourly for 10 days
IV vancomycin is not effective against C. difficile infection due to inadequate penetration of the drug into the lumen of the colon
In complicated cases (e.g. hypotension or shock, ileus, megacolon), in addition to oral or enteral vancomycin à use: metronidazole 500mg (child: 12.5mg/kg up to 500 mg) IV, 8-hourly for 10 days
Consider adding intracolonic vancomycin, particularly in the presence of ileus → use: vancomycin 500mg in 100mL sodium chloride 0.9% rectally (via rectal tube), administered as a retention enema, 6-hourly
Early surgical referral is indicated for patients with severe disease, because outcomes are poor after organ dysfunction is established
Patients with severe disease may require a colectomy to survive, particularly if toxic megacolon develops
Faecal microbiota transplantation (FMT) can also be considered
Fluid Management:
Children with minimal or no dehydration should be encouraged to continue eating and drinking as tolerated
Oral rehydration solutions are strongly recommended for patients at risk of dehydration (e.g. infants and toddlers, children having frequent episodes of vomiting or diarrhoea)
Children with mild to moderate dehydration can be adequately rehydrated with an oral rehydration solution
Contain a balanced quantity of sodium and glucose and other electrolytes e.g. potassium and chloride
Sodium concentrations of 45-60mmol/L, glucose concentrations of 80-120mmol/L and total osmolarity of about 240mOsm/L
Nasogastric rehydration (NGTR)
Most children stop vomiting after NGT fluids are started
If vomiting continues, consider ondansetron and slow NG fluids temporarily
Rapid nasogastric rehydration: 25mL/kg/h for 4h
Treatment is divided into the rehydration phase and the maintenance phase
Rehydration phase: replace the fluid deficit à give 50-100mL/kg of fluids (depending on the degree of dehydration) over 4h, then reassess hydration status
Maintenance phase: provide the usual maintenance fluid requirement and replace ongoing losses from diarrhoea or vomiting (10mL/kg body weight for each loose or watery stool, and 2mL/kg for each episode of vomiting)
Maintenance fluid requirements (24h)
100mL/kg: for the first 10kg of weight (4mL/h)
+50mL/kg: for the second 10kg of weight (2mL/h)
+20mL/kg: for the remaining weight above 20kg (1mL/h)
Severe dehydration
Severely dehydrated children should be admitted to hospital for rehydration and close monitoring → IV rehydration is usually necessary
A fluid bolus of sodium chloride 0.9% (20mL/kg) is given, and may be repeated until the child’s mental state and perfusion improves
The child’s hydration status should be reassessed after each fluid bolus to determine ongoing fluid therapy, and serum electrolyte (especially sodium, potassium and bicarbonate) and glucose concentrations should be measured
Lack of response to intravenous rehydration may indicate an underlying condition such as infection, septic shock, or a cardiac or metabolic disorder
Electrolyte Management:
Use Plasma-Lyte 148 and 5% Glucose OR 0.9% sodium chloride (normal saline) and 5% Glucose for rehydration after any required boluses
If serum K <3mmol/L, add KCl 20mmol/L, or give oral supplements
Measure Na, K and glucose at the outset and at least 24-hourly from then on (more frequent testing is indicated for patients with comorbidities or if more unwell)
24-hr electrolyte requirements
Antiemetics/Antidiarrhoeal Agents:
Antiemetics
Ondansetron reduces vomiting, improves intake of oral rehydration solutions, and reduces the need for intravenous fluids and hospitalisation
Well tolerated, non-sedating and does not cause extrapyramidal adverse effects (like dopamine receptor antagonists e.g. metoclopramide)
Ondansetron can worsen diarrhoea (possibly due to retention of fluids and toxins normally eliminated by vomiting)
If ondansetron is considered appropriate, use: ondansetron 0.15mg/kg up to 8mg orally or IV; repeat dose after 8-12h if necessary
Antidiarrhoeals: not recommended for acute diarrhoea in infants and children
Urinary Tract Infection in children
Briefly describe common causes, investigations and treatment; Diagnosis, Investigations, Treatment, Follow up
Common Causes
Bacterial Infections:
Escherichia coli (E. coli): Causes 85-90% of pediatric UTIs.
Proteus mirabilis: Found in 30% of boys with uncomplicated cystitis.
Staphylococcus saprophyticus: Found in adolescents of both sexes with acute UTI.
Staphylococcus aureus: Common cause of renal abscess.
Pseudomonas species, Serratia marcescens, Citrobacter species, Staphylococcus epidermidis: Cause low-virulence infections in patients with urinary tract malformation or dysfunction.
Other Bacteria: Klebsiella aerogenes, Enterococcus species.
Risk Factors:
Younger Children:
Malformations and obstruction of the urinary tract.
Prematurity.
Indwelling urinary catheters.
Lack of circumcision (in males).
High-grade vesicoureteral reflux (VUR).
Older Children:
Diabetes.
Trauma.
Sexual intercourse (in females).
Epidemiology
Bimodal Peak Age Incidence: Infancy, 2-4 years.
Gender Ratio:
First 2 months: males > females.
2 months to 2 years: females > males.
4 years: females > males.
Clinical Presentation
Young Children (Infants and Pre-verbal):
Fever
Vomiting
Poor feeding
Lethargy
Irritability
Older Children:
Dysuria
Urinary frequency
Lower abdominal and loin pain
Diagnosis
Clinical Symptoms: Dysuria, frequency, loin pain.
Positive Urine Culture:
Urine bag: Not recommended due to high contamination rates.
Clean catch: >10^5 organisms/mL with pyuria/bacteriuria.
Catheterisation: 10% contamination rate.
Suprapubic aspiration: Gold standard with 1% contamination rate.
Urine Collection Methods:
Urine Bag: Adhesive plastic bag applied to perineum; used if all else fails.
Clean Catch (CCU or MSU): Stream of urine caught in a specimen jar; used if child can void on request.
Catheterisation (CSU): Mid-stream sample collected using an in/out catheter; used if unable to obtain CCU/MSU.
Suprapubic Aspiration (SPA): Needle inserted into the bladder under US guidance; used if child is unable to void.
Contamination Rates and Suitability:
Urine Bag: 50% contamination, not recommended (false positive rate 88-99%).
Clean Catch: 25% potential contamination.
Catheterisation: 10% potential contamination.
Suprapubic Aspiration: 1% contamination, gold standard.
Investigations
Initial Testing:
Infants and children presenting with unexplained fever of 38°C or higher should have a urine sample tested within 24h
Dipstick test in the urine: ‘leucocytes’ and ‘nitrites’ strongly suggests UTI
Urine should be sent for microscopy, culture, and sensitivity
In infants and children who are suspected to have acute pyelonephritis/upper UTI
In infants and children with a high to intermediate risk of serious illness
In infants <3mths
In infants and children with a positive result for leukocyte esterase or nitrite
In infants and children with recurrent UTI
In infants and children with an infection that does not respond to treatment within 24-48h, if no sample has already been sent
When clinical symptoms and dipstick tests do not correlate
Laboratory tests for localising UTI: CRP alone should not be used to differentiate acute pyelonephritis/upper urinary tract infection from cystitis/lower urinary tract infection
Imaging tests for localising UTI: routine use of imaging is not recommended
In the rare instances when it is clinically important to confirm or exclude acute pyelonephritis/upper urinary tract infection, power Doppler ultrasound is recommended
When this is not available or the diagnosis still cannot be confirmed, a dimercaptosuccinic acid (DMSA) scintigraphy scan is recommended
Treatment
Conservative:
For asymptomatic bacteriuria, improve hygiene, hydration, and bowel habits.
Medical:
Oral Antibiotics:
First Line: Trimethoprim or Trimethoprim-sulfamethoxazole.
Second Line: Cephalexin.
For non-severe UTI in infants >3 months.
IV Antibiotics:
Indicated for severe UTI, sepsis, or infants <3 months.
Antibiotics: Gentamicin with amoxicillin (or ampicillin), switch to oral when improving.
Specific Treatment for UTI:
Non-severe UTI in Infants >3 months:
Trimethoprim or Trimethoprim-sulfamethoxazole.
Cephalexin.
Severe UTI (e.g., sepsis, shock) or Infants <3 months:
Gentamicin with amoxicillin (or ampicillin).
Switch to oral when improving.
Special Considerations:
Circumcision: May lower the risk of UTIs; not routinely recommended but considered if recurrent UTIs.
Assess for Hypospadias: If indicated.
Follow-Up
Repeat Urine Culture: On completion of antibiotics.
Imaging: If <6 months, atypical UTI, or recurrent UTIs.
Specialist Follow-Up: For pyelonephritis, recurrent pyrexial UTIs, or known renal anomalies.
NICE Guidelines on Imaging Tests:
<6 Months:
Uncomplicated: USS as outpatient.
Atypical: Acute USS.
Recurrent: Acute USS, DMSA at 3 to 6 months after infection.
6 Months to 3 Years:
Uncomplicated: No imaging for the first episode.
Atypical: Acute USS.
Recurrent: Routine USS, DMSA at 3 to 6 months after infection.
3 Years:
Uncomplicated: No imaging for the first episode.
Atypical: Acute USS, nothing else if normal.
Recurrent: Routine USS.
CRP Testing:
Not recommended to differentiate acute pyelonephritis/upper UTI from cystitis/lower UTI.
Detailed Treatment Guidelines
Antibiotic Choices for Children
Trimethoprim 4mg/kg BD
Cefradine 25mg/kg BD
Cefalexin 25mg/kg BD
Co-amoxiclav 125/31 (1-6y/o), 5mL TDS
Co-amoxiclav 250/62 (7-12y/o), 5mL TDS
IV cefuroxime 25mg/kg 8-hourly
IV gentamicin 2.5mg/kg/dose 8-hourly
Antibiotic Treatment Duration
Cystitis: Oral antibiotics for 3-7 days.
Pyelonephritis: Oral antibiotics for 7-10 days or IV antibiotics for 2-4 days followed by oral antibiotics for a total duration of 10 days.
Follow-Up Imaging
<6 Months:
USS During Acute Infection: Yes for atypical and recurrent UTI.
USS Within 6 Weeks: Yes for uncomplicated.
DMSA 4-6 Months After Acute Infection: Yes for atypical and recurrent UTI.
Micturating Cystourethrography (MCUG): Yes for atypical and recurrent UTI.
6 Months to 3 Years:
USS During Acute Infection: Yes for atypical and recurrent UTI.
USS Within 6 Weeks: No.
DMSA 4-6 Months After Acute Infection: Yes for atypical and recurrent UTI.
MCUG: Yes for recurrent UTI.
3 Years:
USS During Acute Infection: Yes for atypical UTI.
USS Within 6 Weeks: No.
DMSA 4-6 Months After Acute Infection: No.
MCUG: Yes for recurrent UTI.
Prophylaxis
Oral Antibiotic Prophylaxis: May be needed and continued until investigations are complete.
Trimethoprim: 2mg/kg at night.
Nitrofurantoin: 1mg/kg.
Indications: Vesicoureteric reflux (VUR), recurrent UTIs (more than 2-3 episodes).
Additional Considerations from Uploaded Images
Diagnosis and Investigations:
Diagnosis is based on clinical symptoms and positive urine culture.
Clinical Symptoms: Dysuria, frequency, loin pain.
Positive Urine Culture: Varies depending on the method of collection:
Urine Bag: Adhesive plastic bag applied to perineum; if all else fails.
Clean Catch (CCU or MSU): Stream of urine caught in a specimen jar; child capable of voiding on request.
Catheterisation (CSU): Mid-stream sample collected using an in/out catheter; unable to obtain CCU/MSU sample.
Suprapubic Aspiration (SPA): Needle inserted into the bladder under US guidance; child unable to void on request.
Contamination Rates:
Urine Bag: 50% contamination, not recommended.
Clean Catch: 25% potential contamination from foreskin or reflux of urine into the vagina.
Catheterisation: 10% potential contamination.
Suprapubic Aspiration: 1% contamination, gold standard.
Positive Urine Culture:
Urine Bag: Not suitable due to high contamination rates.
Clean Catch: >10^5 organisms/mL clinically relevant organisms + pyuria/bacteriuria.
Catheterisation: >10^5 organisms/mL clinically relevant organisms + pyuria/bacteriuria.
Suprapubic Aspiration: Any growth of clinically relevant organisms + pyuria/bacteriuria.
DMSA = Technetium-99m-labeled dimercaptosuccinic acid scan of kidneys (for renal scarring from pyelonephritis)
Learning Points: Clinical Practice
Professional skills in growth and GI problems
Demonstrate the accurate measurement and charting of growth
Weighing Children Less Than 2 Years
Equipment:
Use a levelled pan scale, either high-quality electronic digital or beam balance.
Scale should weigh up to 20kg, in 5g (0.005kg) increments.
The tray needs to be large enough to support children up to 2 years of age.
Scales should be located on a stable, non-carpeted surface.
Clean the scales after every use.
Service the scale (including calibration) according to manufacturers’ guidelines.
Preparation:
Place a sheet/paper towel on the scale.
Child is undressed with the nappy removed.
Procedure:
Turn on scale and ‘tare’ to zero.
Place the baby in the center of the scale and ensure that weight is evenly distributed.
Weigh with parent/carer on a platform scale if unable to weigh alone. This can be done either using a scale which can be ‘zeroed’ after the parent/carer stands on them (a ‘taring’ scale) or by subtraction as follows:
Example:
Weigh the parent/carer and record weight = 60kg
Weigh the parent carer with child = 66.5kg
Difference is the weight of the child. e.g. 66.5-60 = 6.5kg
Recording:
Wait until the scales settle at a reading.
Record weight to the nearest 5g (0.005kg).
Make a note if the child is in plaster, harness, or any other item unable to be removed.
Plot the World Health Organization (WHO) weight-for-age growth chart.
Children less than 2 who can stand without assistance may be weighed on either infant or platform scales.
Include measurements and weight status description on relevant clinical documents such as discharge summaries and in the Child Personal Health Record where appropriate.
Weighing Children 2 Years and Over
Equipment:
Scales for weighing children can be either high-quality beam balance with movable weights, or high-quality electronic.
The scale should weigh in 100g (0.1kg) increments and can be ‘locked’ in.
The scale can be easily ‘zeroed’.
Scales should have a stable weighing platform, which is large enough to support the child.
Preparation:
Place the scale on a firm surface (not carpet).
Explain to the child that you are measuring their weight.
Make sure that any outer heavy clothing such as a coat, jacket, or jumper is removed. Light clothing can be worn.
Remove shoes and socks and ensure pockets are empty.
Procedure:
Turn the scales on and wait until they zero.
Ask the child to stand on the middle of the scales, look straight ahead, and stand still.
You may need to move them into the right position.
Check the child is not holding onto a wall or table; and arms are at their side.
Wait until the scales settle at a reading.
Bend down if necessary to read the scale at eye level.
Record weight to the nearest 100g (0.1kg).
Plot weight on the appropriate weight-for-age growth chart.
Include measurements and weight status description on relevant clinical documents such as discharge summaries, and in the Child Personal Health Record where appropriate.
Length Measurement for Children Less Than 2 Years
Equipment:
Length is measured in the recumbent position using an infantometer (infant length board or mat) designed for the purpose.
The measuring board or mat should have a firm, flat, horizontal surface with a fixed measure in 1mm (0.1cm) increments.
The device has a fixed head-board at right angles to the measuring board or mat, and a smoothly-moving foot-board perpendicular to the measuring board or mat.
Preparation:
Ask the child to remove their shoes and socks.
Procedure:
Ask the parent/carer to place the child on the length-board.
The child should be facing vertically upwards with the crown of the head firmly on the headboard.
Ensure the child’s body and pelvis are straight along the measuring device.
Parent holds the child’s head against the immovable headboard.
A second person straightens both of the child’s legs, holds the feet with toes pointing directly up, and moves the foot-board into position against the child’s feet.
Recording:
Record length to the nearest 1mm (0.1cm).
Plot length on the WHO length-for-age chart.
Record whether length or height/stature has been measured because length is greater than height/stature. If measuring length of a child over 2 years, subtract 0.7 centimeters from the length to convert it to height because length measurements are usually larger than height measurements by this amount.
Include measurements and weight status description on relevant clinical documents such as discharge summaries, and in the Child Personal Health Record where appropriate.
Height/Stature Measurement for Children 2 Years and Older
Equipment:
Height is measured in the standing position using a stadiometer (height measurer).
A stadiometer consists of a vertical board with an attached metric ruler with an easily moveable horizontal headboard that can be brought into contact with the most superior part of the head.
The equipment has a wide and stable platform, or firm uncarpeted floor as the base.
Equipment should be accurately and firmly mounted on a wall.
Ensure that fixed position devices have been installed correctly, and re-check after moving or re-location.
Should have an easy-to-read, stable metric ruler or digital readout in 1mm (0.1cm) increments.
Preparation:
Show the child the stadiometer and explain you are going to see how tall they are.
It can be helpful to measure the parent first if the child is hesitant.
Take the child over to the stadiometer and make sure they face away from the equipment.
Remove the child’s shoes and socks.
Procedure:
Position the child facing away from the stadiometer or wall with bare feet close together, legs straight, arms at side, and shoulders relaxed.
Ask the child to look straight ahead and take a big breath in and out to relax.
Double-check their position, making sure their knees are straight, heels on the floor, and head, shoulder blades, bottom, and heels are in contact with the stadiometer (height measurer) or the wall. Check that their arms are by their sides, and shoulders relaxed. Check that a horizontal line can be drawn from the lower border of the eye to the tragus, located over the ear canal.
Bring the measuring device down to rest on the child’s head.
Recording:
Record height to the nearest 1mm (0.1cm).
Plot height on the appropriate height-for-age growth chart.
Record whether height/stature has been measured because length is greater than height/stature.
Include measurements and weight status description on relevant clinical documents such as discharge summaries, and in the Child Personal Health Record where appropriate.
Determining Weight Status in Children
For Children Aged Up to 2 Years Old:
Appropriate interpretation of serial measurements on the weight-for-age and length-for-age growth charts will allow determination of the child’s weight status. For example:
If the percentile recorded on the weight-for-age chart is roughly the same as the
Demonstrate the key steps for evidence-based assessment of hydration status in children
Degree of Dehydration and Corresponding Clinical Features:
Clinical Feature | Mild Dehydration (<5%) | Moderate Dehydration (5-9%) | Shock (≥10%) |
---|---|---|---|
Conscious State | Alert and responsive | Lethargic, irritable | Reduced conscious state |
Heart Rate | Normal | Normal/mild tachycardia | Tachycardia |
Breathing | Normal | Increased respiratory rate | Increased respiratory rate, deep acidotic breathing |
Blood Pressure | Normal | Normal | Hypotension |
Skin Color | Normal | Normal | Pale or mottled |
Extremities | Warm | Warm | Cold |
Peripheral Pulses | Normal | Normal | Weak |
Eyes and Fontanelle | Not sunken | Sunken | Deeply sunken |
Mucous Membranes | Moist | Dry | Dry |
Skin Turgor | Instant recoil | Mildly decreased | Decreased |
Central Capillary Refill Time | Normal | Prolonged | Markedly prolonged |
Additional Clinical Features:
Clinical Feature | Minimal (<3%) | Mild to Moderate (3-9%) | Severe (>9%) |
---|---|---|---|
Mental State | Alert, well | Normal to irritable | Apathetic, lethargic |
Thirst | Normal, may refuse liquids | Thirsty | Drinks poorly |
Pulse | Normal and strong | Tachycardia | Tachycardia, weak |
Respiration | Normal | Tachypnoea | Tachypnoea and deep |
Capillary Refill | Normal (<2s) | Prolonged | Prolonged |
Skin Turgor | Normal | Recoil <2s | Recoil >2s |
Extremities | Warm peripheries | Cool peripheries | Cold, mottled, acrocyanosis |
Eyes and Fontanelle | Normal | Mildly sunken | Deeply sunken |
Oral Mucous Membranes | Moist | Dry | Parched |
Urine Output | Normal to reduced | Reduced | Minimal to anuric |
Measured Weight Loss or Percentage Dehydration:
5% dehydration = loss of 5mL of fluid per 100g body weight, or 50mL/kg or 10 x percent dehydrated/kg.
Deficit Calculation:
Calculated following an estimation of the degree of dehydration expressed as % of body weight.
Example: A 10kg child who is 5% dehydrated has a water deficit of 500mL.
The deficit is replaced over a time period that varies according to the child's condition. The rate of rehydration should be adjusted with ongoing assessment of the child.
Assessment Steps:
History:
Intake: Foods and fluids intake compared to normal.
Output: Urine and stool output compared to normal.
Excessive Loss: Vomiting, polyuria, diarrhea.
Recent Consumption: Intake of hypertonic or hypotonic fluids (e.g., diluted formula, lots of water, fortified feeds).
Risk Factors for Severe Dehydration and Electrolyte Disturbances:
Infants <6 months old.
GI issues (e.g., Hirschsprung, short gut syndrome, ileostomy, colostomy).
Cystic Fibrosis (CF).
Renal impairment.
Diuretic use.
Metabolic disorders.
Dehydration is especially dangerous in children with:
Congenital heart disease (especially if they have cardiac shunts).
Slow weight gain.
Immunocompromised.
Previous organ transplant.
Use of nephrotoxic medications.
Examination:
Vitals: Check vital signs.
Weight: Compare current weight with previous readings from the last two weeks.
Mucous Membranes: Assess for moisture.
Capillary Refill: Check time taken for capillary refill.
Skin Appearance and Turgor: Evaluate skin turgor and general appearance.
Investigations:
UEC: Check urea, electrolytes, and creatinine levels.
Blood Glucose Level: Assess blood glucose levels.
Additional Considerations:
Calculation of hydration status using clinical signs is typically inaccurate. However, a combination of examination findings is often utilized to assess hydration status.
"No single symptom or clinical sign reliably predicts the degree of dehydration" – NSW Health.
Weighing a child bare and comparing with previous readings from within the last two weeks is the most reliable measure, although this is not often available.
The most useful clinical signs are abnormal capillary refill time, abnormal skin turgor, and abnormal respiratory pattern. These can be used to guide a rough percentage loss:
Mild Dehydration (<4%): No clinical signs. May have increased thirst.
Moderate Dehydration (4-6%): Delayed CRT (>2 seconds), increased respiratory rate, and mild decreased tissue turgor.
Severe Dehydration (≥7%): Very delayed CRT (>3 seconds), mottled skin, other signs of shock (tachycardia, irritable or reduced conscious level, hypotension), deep, acidotic breathing, and decreased tissue turgor.
Other 'Signs of Dehydration':
Sunken eyes, lethargy, and dry mucous membranes may be considered in the assessment of dehydration. Although their significance has not been validated in studies, they are less reliable than the signs listed above.
Describe an evidence-based approach to the standards for paediatric IV fluid management (Clinical Practice Guidelines)
IV Fluid Content for Children (Excluding Neonates)
For Resuscitation/Bolus:
Fluid: 0.9% Sodium Chloride
Alternative (only under specialist direction): Other crystalloids (e.g., balanced salt solutions) or colloids may be used.
For Replacement Fluids (Dehydration or Ongoing Losses):
Fluid: 0.9% Sodium Chloride + 5% Glucose +/- Potassium Chloride 20mmol/L
Alternative (only under specialist direction): Plasma-Lyte148 + 5% Glucose
For Maintenance Fluids:
Fluid: 0.9% Sodium Chloride + 5% Glucose +/- Potassium Chloride 20mmol/L
Alternative (only under specialist direction):
0.45% Sodium Chloride + 5% Glucose +/- Potassium Chloride 20mmol/L
Plasma-Lyte148 + 5% Glucose
Note: If electrolytes are outside the normal range, discussion with a specialist is necessary.
IV Fluid Content for Neonates (<1 Month)
For Resuscitation/Bolus:
Fluid: 0.9% Sodium Chloride
For Replacement (Dehydration or Ongoing Losses) or Maintenance:
Special Care Nurseries:
Day 1: 10% Glucose
Day 2 Onwards:
0.225% Sodium Chloride + 10% Glucose +/- Potassium Chloride 10mmol/500mL (Special Care Nurseries)
0.45% Sodium Chloride + 10% Glucose (No Potassium Chloride) (Emergency Departments)
0.45% Sodium Chloride + 10% Glucose +/- Potassium Chloride 10mmol/500mL (Paediatric Wards)
Note: If electrolytes are outside the normal range, discussion with a specialist is necessary.
Detailed Guidelines for Paediatric IV Fluid Management
Resuscitation:
Indication: Shock
Fluid: 0.9% Sodium Chloride (NB: must write this in full)
Amount:
For infants and children (>28 days old): 20mL/kg bolus
For neonates (<28 days old): 10mL/kg bolus
Speed: Over 15-60 minutes
Maintenance:
Indication: Fasting or unable to tolerate oral fluids.
Fluid:
For infants and children (>28 days old): 0.9% Sodium Chloride + 5% Dextrose (+/- 20mmol/L Potassium Chloride).
For neonates (<28 days old):
Day 1: 10% Dextrose
Day 2 Onwards: 0.225% Sodium Chloride + 10% Dextrose (+/- 10mmol/500mL Potassium Chloride).
Amount:
For 1st 10kg: 100mL/kg/day (4mL/kg/hr)
For 2nd 10kg: 50mL/kg/day (2mL/kg/hr)
For every kg above 20kg: 20mL/kg/day (1mL/kg/hr)
Example Calculation:
33kg child:
Total fluid per day = 1000mL + 500mL + 20 * 13mL = 1760mL/day
Hourly rate = 40mL + 20mL + 13mL = 73mL/hour
Rehydration:
Indication: Dehydration
Fluid:
For infants and children (>28 days old): 0.9% Sodium Chloride + 5% Dextrose (+/- 20mmol/L Potassium Chloride).
For neonates (<28 days old):
Day 1: 10% Dextrose
Day 2 Onwards: 0.225% Sodium Chloride + 10% Dextrose (+/- 10mmol/500mL Potassium Chloride).
Amount:
Volume deficit = weight (kg) x deficit (%) x 10
Only replace a max of 5% per 24 hours due to the risk of cerebral or pulmonary edema.
Example: If 10% dehydrated, give 5% replacement per 24 hours over 48 hours.
Example Calculation:
22kg child with estimated 5% dehydration:
Maintenance = 1000mL + 500mL + 40mL = 1540mL/day
Replacement (5%) = 22kg x 5% x 10 = 1100mL/day
Total fluids = 1540 + 1100 = 2640mL/day
Hourly rate = 110mL/hour
Ongoing Losses:
Indication: Additional fluids may be required (i.e., beyond rehydration) if very high stoma/gut or renal losses.
Fluid: 0.9% Sodium Chloride
Amount:
Measure losses over 4-6 hours. Divide by the number of hours to find the hourly losses. Give this amount over the same timeframe in addition to other IV fluids.
Example: Child has stoma losses of 200mL over 4 hours. Give 50mL/hr of additional fluids for the next 4 hours.
Demonstrate communication of appropriate oral rehydration management
Criteria for Oral Rehydration Management:
Suitable for Intervention:
The patient has been assessed and triaged as category 4 or 5, and allocated to the waiting room.
The patient has vomiting, with or without diarrhea.
The child shows signs of dehydration consistent with mild dehydration.
Exclusion Criteria:
Abdominal distension
Bile-stained vomiting
Blood in vomitus or stool
Severe abdominal pain
Moderate to severe headache
Age less than 6 months
Respiratory distress
Moderate tachycardia or hypotension
Oral Rehydration Guidelines:
Appropriate Fluids for Rehydration:
Inappropriate Fluids: Lemonade, homemade oral rehydration solutions (ORS), and sports drinks.
Recommended ORS: Gastrolyte™, HYDRAlyte™, Pedialyte™.
Feeding and Hydration:
Stop any feed fortifications (e.g., extra scoops of formula, Polyjoule).
Encourage parents to use methods to help children drink (e.g., cup, icy pole, syringe), aiming for small amounts of fluid often.
Continue breastfeeding.
Early feeding (as soon as rehydrated) reduces stool output and aids gastrointestinal tract recovery.
Recommend returning to the usual diet once rehydrated.
If diarrhea worsens with formula feeding, consider temporary (2 weeks) use of lactose-free formula.
Trial of Oral Fluids in the Emergency Department:
Most children with mild/no dehydration can be discharged without a trial of fluids after appropriate advice and follow-up.
Aim for 10-20mL/kg fluid over 1 hour of ORS; give frequent small amounts.
Significant ongoing GI losses (frequent vomiting or profuse diarrhea) reduce the chance of successful rehydration at home.
Additional Causes of Vomiting to Consider:
Gastroenteritis: Common cause, but other causes should be ruled out.
Obstruction: Intussusception, volvulus.
Infection: Pneumonia, appendicitis, meningitis, urinary tract infection.
Raised Intracranial Pressure: Brain tumor.
Metabolic Disease: Diabetes.
Demonstrate charting oral rehydration and IV fluids for children
IV Fluids
Total fluid requirement = Maintenance + Replacement of deficit + Replacement of ongoing losses
Calculating fluid deficit
Deficit (mL) = Weight (kg) change (premorbid weight minus current weight) x 1000
g. a 10 kg child who now weighs 9.5 kg has a 500 mL water deficit and is 5% dehydrated
You need to replace the deficit over 24-48 hours
For children with ≤5% dehydration, replace deficit in the first 24 hours
For children with >5% dehydration, replace deficit more slowly. Give 5% in the first 24 hours and the remainder over the following 24 hours
Ongoing losses
Measure any ongoing loss and replace at the same rate it is lost
g. if there is a 200mL loss over 4 hours replace this by delivering 50mL/hr of fluids over the next 4 hours
GI losses are usually replaced with NaCl 0.9% + KCl 20mmol/L
Maintenance fluid rates
The preferred fluid type for IV maintenance is sodium chloride 0.9% with glucose 5%
Demonstrate appropriate history and examination in assessment of pain in children, including acute abdominal pain
History Taking:
General Information:
Age: of the child
SOCRATES: (Site, Onset, Character, Radiation, Associated symptoms, Timing, Exacerbating/relieving factors, Severity) for pain assessment
Recent Trauma: Assess for any recent trauma or injury
Past Medical History: Including immunizations, allergies, previous illnesses, surgeries
Prenatal and Birth History: Complications, Apgar score, NICU admission, term or preterm
Developmental History: Milestones, delays
Growth and Nutrition Status: Weight, height, dietary habits
Sleep Patterns: Normal sleep habits and changes
Gynecological History: (if applicable)
Family History and Social History: Conditions, family dynamics
GI-Specific History:
Stool Color and Character: Diarrhea, constipation, blood in stool
Vomiting: Frequency, color, presence of blood
Hematemesis: Presence of blood in vomit
Jaundice: Yellowing of skin/eyes
Abdominal Pain: Location, intensity, duration, radiation
Colic: Patterns of crying and discomfort
Appetite: Changes in eating habits
GU-Specific History:
Urinary Symptoms: Frequency, dysuria, hematuria, discharge
Abdominal Pain: Related to urination
Quality of Urinary Stream: Changes or difficulties
Polyuria: Increased frequency of urination
Previous Infections: History of UTIs or other infections
Facial Edema: Swelling around the face
Physical Examination:
General Inspection:
Alertness and Activity Level: How alert and active is the child?
Skin Color: Pallor, jaundice, cyanosis
Rash: Presence of any obvious rash
Healthy Weight: Does the child appear to be of a healthy weight?
Signs of Pain: Does the child look in pain?
Overall Appearance: Does the child look well or sick?
Genetic Condition Indicators: Stature, syndromic facial features
Position During Exam:
Parent’s Lap vs. Exam Table: Depending on the child's comfort
Order of Examination:
Least Distressing to Most Distressing: Use distraction as a valuable tool
Pediatric Assessment Triangle (PAT):
Appearance:
Tone, interactiveness, consolability, look/gaze, speech/cry
Work of Breathing:
Abnormal airway sounds, positioning, retractions, flaring
Circulation to Skin:
Pallor, mottling, cyanosis
Hands:
Finger Clubbing: Cystic fibrosis, liver disease, inflammatory bowel disease
Leukonychia: (whitened nail bed) – hypoalbuminaemia
Palmar Erythema: Liver disease, polycythaemia, Kawasaki disease, thyrotoxicosis
Peripheral Edema: Nephrotic syndrome, liver disease
Pulse Assessment: Radial pulse, femoral pulse in babies, assess rate and rhythm
Face:
Oedema: Nephrotic syndrome, liver disease
Pallor: Anemia
Conjunctival Pallor: Anemia
Scleral Icterus: Jaundice (hepatic pathology, hemolysis)
Aniridia: Wilm’s tumor, WAGR syndrome
Kayser-Fleischer Rings: Wilson’s disease
Neuroblastoma: Loss of the eye’s red reflex
Xanthelasma and Corneal Arcus: Hyperlipidaemia
Angular Stomatitis: Inflammation of mouth corners (iron or vitamin B12 deficiency)
Glossitis: Smooth tongue swelling with erythema (iron/B12/folate deficiency)
Aphthous Ulcers: Benign, Crohn’s disease, Bechet’s disease
Dental Caries: Neglect, gastroesophageal reflux disease
Macroglossia: Down’s syndrome, hypothyroidism, mucopolysaccharidoses, Beckwith-Wiedemann syndrome
Pigmentation/Polyps: Peutz-Jeghers syndrome
Lymph Nodes: Palpate cervical and supraclavicular lymph nodes – may indicate infection or malignancy
Abdomen:
Inspection:
Distension, caput medusae, spider naevi, hernia, drains/tubes/access
Palpation:
Tenderness (focal vs. generalized), rebound tenderness, guarding, rigidity, abdominal masses, distension, palpable feces
Percussion and Auscultation:
Assess for bowel sounds and other abnormalities
Special Techniques for Abdominal Exam:
Play Techniques: To elicit subtle guarding
"Can you jump up and down?"
"Blow out your tummy as big as you can, then suck it in as far as you can"
Specific Organ Examination:
Liver Palpation: Right upper quadrant for hepatomegaly or masses
Splenic Palpation: Left upper quadrant for splenomegaly
Kidneys: Bilateral palpation for masses
Ascites: Fluid wave test or shifting dullness
Auscultation: Bowel sounds, bruits
Genital Examination:
Penile and Scrotal Development: Hypospadias, chordee, descended testicles, scrotal swelling
Female Genital Examination: Confirm external genitalia normalcy
Rectal Examination:
Indicated Situations: Confirm anus looks normal and patent, assess for tags, prolapse, staining of underwear
Lower Limbs:
Inspection: Ankle edema (nephrotic syndrome/liver disease)
History of Presenting Complaint:
Site:
RLQ pain suggests appendicitis
Epigastric pain suggests peptic ulcer disease
Diffuse pain may indicate perforation or peritonitis
Onset:
Gastroenteritis lasting >10 days suggests parasitic or non-infectious cause
Recurrent, self-resolving episodes of pain characteristic of biliary colic
Sudden-onset flank pain may indicate nephrolithiasis or pyelonephritis
Character:
Peptic ulcer disease pain is dull, appendicitis is sharp/stabbing
Radiation:
Abdominal pain radiating to the back suggests cholecystitis or pancreatitis
Associated Symptoms:
Fever, nausea, vomiting, diarrhea (gastroenteritis)
Jaundice (viral hepatitis)
Blood in stool (ulcerative colitis)
Blood or bile in vomitus (small bowel obstruction)
Genitourinary symptoms: dysuria, frequency, hematuria (UTI)
Timing:
History of trauma: blunt or penetrating, accidental or non-accidental
Exacerbating or Relieving Factors:
Movement, food, medication
Severity:
Assess using pain scales appropriate for the child's age
Past Medical History:
Previous Conditions:
Operations, medication use, immunizations, allergies, and current comorbidities
Conditions like sickle cell disease, cystic fibrosis, spina bifida, developmental delay, cerebral palsy, splenic infarction, recent or current URTI
Potential Complications Causing Abdominal Pain:
Hirschsprung Disease:
Enterocolitis
Cystic Fibrosis:
Abdominal distension, bloody diarrhea, electrolyte disturbances
Liver Disease/Ascites:
Primary bacterial peritonitis
Nephrotic Syndrome:
Pancreatitis
VP Shunt:
Pancreatitis
Chemotherapy:
Pancreatitis
Immunocompromised:
Toxic megacolon
Sickle Cell Disease:
Vaso-occlusive crisis
Family and Social History:
Family History:
Risk factors for inflammatory bowel disease, nephrolithiasis
Social History:
Travel history to developing countries, dietary habits, family dynamics, social and psychiatric history, sexual history in reproductive-age females
Examination Techniques:
Comprehensive Physical Examination:
Including vital signs, abdominal examination, checking for non-abdominal causes
Observation:
Child's movements, gait, position, level of comfort
Pelvic Examination:
Reserved for sexually active adolescents
Abdominal Examination:
Thorough inspection, palpation, percussion, and auscultation.
Describe the evidence-based approach to managing abdominal pain in children (Clinical Practice Guidelines)
General Management of Abdominal Pain
Fluid Resuscitation: May be required in cases of dehydration or shock.
Analgesia: Provide pain relief based on the severity of the pain (see detailed table below).
NPO (Nil Per Os): Keep the child fasting, especially if surgical intervention is being considered.
Consider NG Tube: If bowel obstruction is suspected.
Early Referral: If surgical or gynecological management may be required.
Analgesic Options Based on Pain Severity
Pain Severity | Analgesic | Route |
---|---|---|
Mild to Moderate Pain | Sucrose | Oral |
Paracetamol | Oral, PR (per rectum), IV | |
Ibuprofen | Oral | |
Moderate to Severe Pain (in addition to the above) | Oxycodone | Oral |
Morphine | IV, subcutaneous | |
Fentanyl | Intranasal | |
Tramadol | Oral, IV |
Assessment and Monitoring
Repeated Examination: To look for persistence or evolution of signs and to evaluate the response to treatment.
Pain Assessment Tools:
Wong-Baker FACES Pain Rating Scale: For children 3 years and older.
FLACC Scale: Face, Legs, Activity, Cry, Consolability for behavioral observation.
Neonatal Infant Pain Scale (NIPS): For infants.
Common and Time-Critical Causes of Abdominal Pain by Age
Age Group | Causes |
---|---|
Neonates | Hirschsprung enterocolitis, Incarcerated hernia, Intussusception, Necrotizing enterocolitis, Volvulus |
Infants/Children | Abdominal trauma, Appendicitis, Constipation, Gastroenteritis, Incarcerated hernia, Intussusception, Meckel diverticulum, Mesenteric adenitis, Ovarian torsion, Pyloric stenosis, Testicular torsion, Volvulus |
Adolescents | Appendicitis, Abdominal trauma, Cholecystitis, Cholelithiasis, Constipation, Ectopic pregnancy, Gastroenteritis, Inflammatory bowel disease, Ovarian cyst - torsion/rupture, Pancreatitis, Pelvic Inflammatory Disease, Renal calculi, Testicular torsion |
Important Non-Abdominal Causes to Consider
Diabetic ketoacidosis (DKA)
Headache (Migraine)
Henoch-Schonlein Purpura
Hip pathology
Pneumonia
Psychological factors
Sepsis
Sexually transmitted infections
Sickle Cell Disease (vaso-occlusive crisis)
Toxin exposure or overdose
Urinary Tract Infection (UTI)/Pyelonephritis
Investigations
Most children need no investigations.
Investigations may include:
Urine analysis: (+/- culture, +/- pregnancy test if indicated)
Electrolytes +/- Liver Function Tests (LFTs)
Lipase: For pancreatitis
Venous blood gas
Blood sugar: For DKA
Imaging:
Abdominal X-Ray (AXR): If obstruction is suspected.
Chest X-Ray (CXR): If pneumonia is suspected.
Ultrasound: After discussion with senior staff, appropriate for suspected ovarian torsion or intussusception.
Treatment
Fluid Resuscitation: May be required.
Analgesia:
Mild Pain (Pain Score 1-3, NIPS Score 1-2): Oral paracetamol and/or ibuprofen.
Moderate Pain (Pain Score 4-6, NIPS Score 3-4): Oral paracetamol or ibuprofen and oral oxycodone.
Severe Pain (Pain Score 7-10, NIPS Score 5-7): Oral paracetamol or ibuprofen and intranasal fentanyl or oral oxycodone or IV morphine.
Opioid and Non-Opioid Analgesia
Non-Opioid Analgesia:
AnGel/EMLA
Paracetamol
NSAIDs (e.g., ibuprofen, ketorolac)
Tramadol
Local anesthesia blocks
Opioid Analgesia:
Oral: Morphine/MS Contin, Oxycodone IR/oxycontin SR
IV: Morphine, Fentanyl, Hydromorphone
Additional Management Considerations
Keep children fasting: Consider enteral or intravenous fluids if assessment or diagnosis is delayed (consult local fasting guidelines).
Early referral: For possible diagnoses requiring surgical or gynecological management.
Consider a nasogastric tube: If bowel obstruction is suspected.
Describe the key features for recognising a presentation of Diabetic Ketoacidosis in children
Overview
Diabetic ketoacidosis (DKA) in children is a critical medical emergency requiring immediate hospital admission.
It primarily occurs in children with type 1 diabetes but can also be seen in type 2 diabetes under stress conditions.
Pathophysiology
Decrease in Effective Circulating Insulin: This is associated with elevations in counter-regulatory hormones (glucagon, catecholamines, cortisol, growth hormone).
Hyperglycemia: Increased glucose production by the liver and kidney and impaired peripheral glucose utilization.
Hyperosmolality: Due to high blood sugar levels.
Lipolysis: Increased fat breakdown leading to the production of ketone bodies (beta-hydroxybutyrate, acetoacetate).
Acidosis: Metabolic acidosis from ketone bodies.
Osmotic Diuresis: Leads to dehydration and electrolyte imbalances.
Ketoacid Accumulation: Causes nausea, vomiting, and exacerbation of dehydration.
Major Complications:
Clinical Features
History: Weight loss, abdominal pain, vomiting, polyuria, and polydipsia.
Examination:
Dehydration
Kussmaul breathing (deep and laboured), chest pain
Altered level of consciousness (due to cerebral oedema - occurs in severe DKA)
Abdominal pain and vomiting
Hx of polyuria and polydipsia
Hx of nocturnal enuresis (bed wetting)
Hx of weight loss
Precipitants
Inadequate Insulin: In known diabetics (e.g., missed doses, pump failure).
First Presentation of Type 1 Diabetes Mellitus.
Illness: Such as infections (e.g., pneumonia, UTI), surgery, or trauma.
Diagnostic Criteria
Serum Glucose > 11 mmol/L
Venous pH < 7.3 or Bicarbonate < 15 mmol/L
Presence of Ketonaemia/Ketonuria
Severity Assessment
Mild: Venous pH < 7.3, Bicarbonate < 15 mmol/L
Moderate: Venous pH < 7.2, Bicarbonate < 10 mmol/L
Severe: Venous pH < 7.1, Bicarbonate < 5 mmol/L
Investigations
Urine Analysis: To check for ketonuria and glucose.
Blood Tests: Serum glucose, electrolytes (UEC), liver function tests (CMP), venous blood gas (VBG), blood ketones, full blood count (FBC), HbA1c, and septic workup if infection is suspected.
Imaging: May include chest X-ray if pneumonia is suspected, abdominal X-ray if bowel obstruction is suspected, and ultrasound if indicated for other conditions.
Management
Goals:
Correct Dehydration
Reverse Ketosis, Correct Acidosis, and Glucose Levels
Monitor for Complications: Cerebral edema, hypoglycemia, hypo/hyperkalemia.
Identify and Treat Precipitating Causes
Supportive Measures and Monitoring:
Nurse Head Up: To prevent aspiration.
Airway Monitoring: Especially in children with reduced consciousness.
NPO (Nil Per Os): Until the child is alert and acidosis resolves.
IV Access: For fluid and insulin administration.
Neurological Observations: To monitor for cerebral edema.
Cardiac Monitoring: For electrolyte disturbances (e.g., hyperkalemia, hypokalemia).
Antibiotics: If febrile, after obtaining cultures.
Urinary Catheterization: For strict fluid balance in unconscious children.
Fluid Resuscitation:
Initial Bolus: 10 mL/kg 0.9% sodium chloride for children with tachycardia and delayed capillary refill.
Potassium Management: Add potassium to fluids if serum potassium < 5.5 mmol/L and child is passing urine.
Glucose Addition: Once blood glucose levels drop to 15 mmol/L, switch to 0.9% sodium chloride with 5% glucose and potassium chloride.
Insulin Therapy:
Infusion: Start with 0.1 units/kg/hour (0.05 units/kg/hour in specific cases).
Transition to Subcutaneous Insulin: Once the child is alert and stable.
Monitoring for Complications:
Cerebral Edema: Symptoms include headache, vomiting, altered consciousness, and rising blood pressure. Managed with mannitol infusion or hypertonic saline.
Hypoglycemia: Managed with glucose infusion.
Electrolyte Imbalances: Managed based on regular monitoring and adjustments.
Timeline of Monitoring and Management:
Demonstrate patient assessment leading to the recognition of serious illness using A-G assessment
A - Airway
Is the airway patent?
Signs of Airway Obstruction: Look for chest and abdomen rising and falling alternately and vigorously.
Skin Color: Is it blue or mottled?
Noises of Obstruction: Listen for snoring, expiratory wheezing, or gurgling.
Additional points for detailed airway assessment:
Facial Fractures: Look for signs.
Contaminants: Check for blood, vomit, or teeth in the mouth/airway.
Epistaxis: Note any nosebleeds.
Examine the Anterior Neck:
Tracheal deviation
Wounds
Subcutaneous emphysema
Laryngeal tenderness/crepitus
Venous distension
Esophageal injury (unlikely if the child can swallow easily)
Carotid hematoma/bruits/swelling
Management of Airway Obstruction:
Positioning: Age-appropriate positioning of the head into a neutral position (use a thoracic elevation device if <8 years old or a towel under the shoulder blades).
Suction: Gentle suction to remove blood/vomit/secretions.
Oxygen: Apply high-flow oxygen.
Jaw Thrust: Avoid head-tilt or chin lift.
Airway Devices: Use an oropharyngeal airway if tolerated, or a nasopharyngeal airway (if head injury is excluded/unlikely).
Intubation: To be performed by an experienced operator.
Cervical Spine Protection: Manual in-line stabilization, followed by the application of a properly fitted hard collar, sandbags, and strap.
B - Breathing
Observation: Look, listen, and feel.
Oxygen Saturation: Measure.
High-Flow Oxygen: Apply to all spontaneously breathing patients (10-15L O2 via a non-rebreather mask).
Work of Breathing: Check for recession, respiratory rate, and accessory muscle use.
Effectiveness of Breathing: Assess oxygen saturation, symmetry and degree of chest expansion, and breath sounds.
Effects of Inadequate Respiration: Check heart rate and mental state.
Signs of Injury: Look for seat belt marks, bruising, and wounds.
Thoracic Cage Assessment: Feel for emphysema/crepitus and clavicle/chest wall tenderness.
CXR: Request if needed.
C - Circulation
Pulse Rate: Check.
Skin Color and Temperature: Assess.
Capillary Refill Time: Measure.
Blood Pressure: Sometimes check.
Peripheral Skin Temperature: Measure.
Body Temperature: Measure.
Effects of Inadequate Circulation: Increased respiratory rate and decreased mental state.
IV Access: Establish with two large cannulae.
Intra-Osseous Needle: Consider if IV access is not quickly established.
Blood Tests: Take blood for BSL, FBC, crossmatch.
Fluid Bolus: Give 20mL/kg of normal saline if circulation is inadequate.
Tamponade: For any continuing external hemorrhage.
Repeat Fluid Bolus: If circulation remains unstable, using normal saline or colloid solution.
Packed Cells: Consider if a third bolus is necessary, and arrange early surgical intervention.
D - Disability
Level of Consciousness: Initial assessment using AVPU (Awake, Voice, Pain, Unresponsive).
Formal GCS Assessment: If AVPU shows impairment.
Pupil Response: Check reaction to light.
Movement in Limbs: Assess and check reflexes where possible.
BSL: Measure on arrival and periodically.
E - Exposure/Environment
Remove Clothing: To check for any obvious life-threatening injury.
Avoid Hypothermia: Limit exposure of the body and warm all ongoing fluids.
F - Fluids
Fluid Charts: Monitor fluid input and output.
Patient’s Urine: Check if available.
Skin Turgor: Assess for hydration status.
G - Glucose
Rapid Finger Prick: To check for hypoglycemia.
Further Information and Family and Friends
Gather Additional Information: From drug charts, medical notes, investigation results, friends, and relatives.
Social Assessment: Determine the patient’s next of kin or close relatives, living situation, and access to the building.
Goals
Patient Goals: Establish both short-term and long-term goals for the patient.
Monitoring Plan: Develop a plan for continuous monitoring.
Describe the patient monitoring and process of the Between the Flags model, and the Paediatric CERS and Escalation Matrix
Between the flags model
The standard observation charts have 3 colour-coded zones:
Blue zone = criteria for which increasing the frequency of observations and/or increased vigilance is required.
Yellow zone = clinical review required.
Red zone = rapid response call is required.
In paediatrics, observations are taken 6 times per day at 4 hourly intervals.
A newborn’s vitals must be taken before leaving the birthing environment.
Frequency of assessment is to be increased above the minimum requirements when:
The patient’s vital sign observations fall within a coloured zone on a standard observation chart
Assessment identifies other signs and symptoms of deterioration
A CERS call has been made.
Paediatric CERS
CERS = Clinical Emergency Response Systems
CERS refers to a health service/facility’s response to a deteriorating patient within its care.
The main components include:
Clinical review - respond within 30 minutes to a breach in clinical review criteria.
Rapid response - immediately in response to breach in the rapid response criteria.
Escalation Matrix
The Escalation Matrix determines local criteria that are a best fit for the organisation’s context and services.
It allows for a unified approach to levels of escalation across the facilities and LHD.
Demonstrate appropriate charting patient observations in children (use of BTF in SPOC charts)
Learning Points: Health society and environment
List the public Health notifiable infectious illness in children and describe the rationale and process for reporting
List of Public Health Notifiable Infectious Illnesses in Children
All notifiable diseases can be found in the Public Health Act 2010 No 127. Below are some of the most relevant preventable diseases which are mandatory for reporting in schools and daycare centers:
Diphtheria
Mumps
Poliomyelitis
Haemophilus influenzae Type b (Hib)
Meningococcal disease
Rubella ("German measles")
Measles
Pertussis ("whooping cough")
Tetanus
Gastroenteritis (among people of any age in an institution, foodborne illness in two or more related cases)
Rationale for Reporting
Prevent Spread of Infectious Diseases: Enables public health units to take immediate action to control and prevent the spread of infectious diseases.
Protect Community Health: Reporting helps in safeguarding the community by ensuring that outbreaks are contained.
Identify Disease Patterns: Assists in identifying patterns of disease spread and potential patient zero, which is crucial for effective outbreak management.
Improve Healthcare Policy: Provides data that helps in the formulation and improvement of healthcare policies and standards.
Uphold Healthcare Standards: Ensures compliance with public health standards and protocols.
Process for Reporting
Complete the NSW Health Communicable Diseases Notification Form:
Fill out the form with all relevant information about the case.
Submission:
Send the completed form to the local Public Health Unit (for example, Hunter New England LHD - Wallsend).
Immediate Phone Notification:
Some diseases require immediate phone notification, which is indicated by a phone icon on the form. This ensures prompt action is taken for highly contagious or severe diseases.
Detailed Steps in Disease Reporting
Identification of a Notifiable Disease:
Once a notifiable disease is identified, healthcare providers must report it to the public health authorities.
Form Completion:
Complete the NSW Health Communicable Diseases Notification form accurately with details such as patient information, disease specifics, and any relevant clinical information.
Sending the Form:
The completed form must be sent to the appropriate local Public Health Unit. This can be done through various means, including electronic submission, fax, or mail.
Phone Notification:
For certain diseases, an immediate phone call to the public health unit is required. This is to ensure that the authorities can take swift action to manage and control the spread of the disease.
Follow-Up:
The public health unit may follow up with the reporting entity for additional information or to provide further instructions on managing the case and preventing further spread.
Describe the societal and environmental influences on growth and nutrition
Societal Influences
Cost:
The cost of food and the ability to purchase it are primary determinants of food choice.
Low-income groups are reported to consume more unbalanced diets and have a lower intake of fresh fruits and vegetables due to financial constraints.
Social Class:
Higher social classes are associated with higher intakes of fruits, lean meats, oily fish, and wholemeal foods compared to lower social classes.
Economic disparities influence the quality and variety of food available to different social classes.
Social Context:
Peer Influences: Individuals, especially children and adolescents, are influenced by their peers' eating habits and preferences.
Parental Influences: Parents play a critical role in shaping their children's dietary habits through the foods they provide and their own eating behaviors.
Family Eating Practices: Regular family meals and shared eating practices can promote healthier eating habits.
Social Norms: Societal norms and cultural expectations can impact food choices and dietary practices.
Cultural Factors:
Cultural background influences food preferences, methods of preparation, and religious practices related to food.
Different cultures have unique dietary practices that can affect nutritional status and health outcomes.
Environmental Determinants
Access and Availability:
The availability of food and access to transportation can significantly influence dietary choices.
"Food deserts" are areas with little to no access to shopping facilities that provide fresh, healthy food, leading to reliance on processed and unhealthy food options.
Education, Knowledge, and Skills:
A lack of cooking skills can inhibit families from preparing fresh, healthy meals.
Education level is linked to better eating habits, as higher education often correlates with greater nutritional knowledge and healthier food choices.
Parents' ability to pass on cooking skills and nutrition education to their children is crucial for promoting long-term healthy eating habits.
Time Constraints:
Increasing numbers of dual-income families and longer working hours make it challenging to find time for preparing healthy meals.
Time constraints often lead to reliance on convenience foods, which are typically less nutritionally dense and can contribute to poor dietary choices.
Parental Monitoring and Motivation:
Parents' ability to monitor their children's growth and diet is essential for ensuring proper nutrition and preventing malnutrition or obesity.
Parental motivation and behavioral capability to encourage and provide healthy diets for their children play a significant role in shaping their children's eating habits and overall health.
Describe the population health strategies employed for weight management in Children
Policies Influencing Food Environments
Marketing Restrictions:
Unhealthy Foods and Beverages: Strong links exist between TV advertising and children's food knowledge, preferences, purchase requests, and consumption patterns. Policies aim to limit the marketing of unhealthy foods to children.
Food Taxes and Subsidies:
Economic Measures: Implementing taxes on unhealthy foods and providing subsidies for healthier options like fruits and vegetables. Evidence shows that price has a significant effect on consumption choices.
Initiatives Promoting Healthy Foods:
Fruit and Vegetable Initiatives: Programs aimed at increasing the consumption of fruits and vegetables among children.
Other Food Policies: Includes restrictions on trans-fatty acids and policies ensuring healthy food service options in government institutions.
Policies Influencing Physical Activity Environments and Social Marketing
Physical Activity Recommendations:
WHO Guidelines: Children aged 5-17 should accumulate at least 60 minutes of moderate to vigorous intensity physical activity daily.
Social Marketing Campaigns:
Media Campaigns: Use of both paid and non-paid forms of media to increase knowledge and change attitudes towards diet and physical activity. Campaigns typically target both nutrition and physical activity behaviors.
National and Regional Initiatives
Australian Dietary Guidelines:
Dietary Advice: Provides up-to-date advice on the types and amounts of foods that should be consumed for health and wellbeing. Recommendations are based on scientific evidence.
Health Star Rating System:
Nutritional Labelling: A front-of-pack labelling system that rates the overall nutritional profile of packaged food from ½ a star to 5 stars, helping consumers make healthier choices.
Healthy Food Partnership:
Collaborative Efforts: A mechanism for the government, public health sector, and food industry to tackle obesity, encourage healthy eating, and empower food manufacturers to make positive changes.
Australia’s Physical Activity & Sedentary Behaviour Guidelines:
Guidance on Exercise: Provides guidelines on the duration and intensity of physical activity and sedentary behavior for different age groups to benefit overall health and wellbeing.
Clinical Practice Guidelines Portal:
Access to Guidelines: Provides access to clinical practice guidelines that have been adapted to the Australian context, ensuring relevance and applicability to local practice.
Healthy Weight Guide:
Information Resource: A comprehensive source of information developed by the Australian Government on how to achieve and maintain a healthy weight, based on recent Australian and international research.
Girls Make Your Move Campaign:
Inspiration for Physical Activity: Aims to inspire, energize, and empower young women to be more active through physical activities and sports.
These comprehensive strategies aim to create supportive environments for children, promoting healthy eating habits and physical activity to manage weight and prevent obesity.
Aboriginal & Torres Strait Islander Health:
What are some factors that contribute to higher prevalence of growth restriction and lower nutrition status of Aboriginal and Torres Strait Islander children?
Socio-Economic Factors
Income:
Indigenous Australians are significantly more likely to experience food insecurity due to financial constraints. They are seven times more likely to go without food in the previous 12 months compared to non-Indigenous Australians.
Poverty often leads to maximizing calories per dollar spent, which typically results in lower nutritional quality as nutritious plant-based diets can be expensive.
Socio-Economic Disadvantage:
Lower socioeconomic status impacts the ability to afford and access nutritious food.
Socio-economic disadvantage also affects other areas of life, including housing, education, and employment, which in turn impact nutritional status and growth.
Health and Lifestyle Factors
Smoking During Pregnancy:
There is a strong relationship between smoking during pregnancy and low birthweight, which is a factor for growth restriction.
Smoking and other harmful behaviors during pregnancy, such as excessive alcohol consumption, contribute to poor prenatal health and low birthweight.
Maternal Health:
Factors such as maternal age, illness during pregnancy, low socioeconomic status, multiple pregnancies, and poor antenatal care can contribute to low birthweight and growth restriction.
Geographical and Environmental Factors
Food Security and Access:
Food security is a significant issue, particularly in rural and remote areas where access to fresh and nutritious food is limited.
Issues of supply and availability of food in remote communities lead to reliance on less nutritious, processed foods.
Geographical Isolation:
Remote and rural locations often have limited access to healthcare and support services, which can impact prenatal and postnatal care and subsequently children's growth and nutrition.
Housing and Infrastructure:
Overcrowding in housing and lack of appropriately designed and maintained homes can hinder safe storage, preparation, and consumption of food.
Poor housing conditions and infrastructure contribute to an unhealthy living environment that affects overall health and nutrition.
Cultural and Social Factors
Cultural Food Values:
Traditional dietary practices and cultural food preferences may not always align with modern nutritional guidelines, leading to potential gaps in nutritional intake.
Cultural practices around food preparation and consumption are significant in understanding the nutritional status of Indigenous children.
Education and Literacy:
Low levels of education, particularly in nutrition and food literacy, contribute to poor dietary choices.
Lack of knowledge and skills in preparing nutritious meals impacts food choices and overall nutrition.
Social Factors:
Social norms and family practices around food and eating can influence children's nutritional status.
Peer influences and family eating practices play a role in shaping dietary habits.
Health Disparities
High Rates of Low Birthweight (LBW):
Aboriginal and Torres Strait Islander babies are 2.5 times more likely to be born with low birthweight compared to non-Indigenous babies. This is often due to preterm birth or intrauterine growth restriction.
Contributing factors include poor maternal nutrition, inadequate prenatal care, and higher rates of maternal smoking and alcohol use.
Chronic Diseases:
Poor nutrition contributes to higher rates of chronic diseases such as obesity, cardiovascular disease, type 2 diabetes, and tooth decay.
These conditions are exacerbated by the high prevalence of over-nutrition and under-nutrition among Indigenous populations.
Health Inequities:
Five out of the seven leading factors contributing to the health gap between Indigenous and non-Indigenous Australians (obesity, high blood cholesterol, alcohol, high blood pressure, and low fruit and vegetable intake) are related to poor diet.
What are some of the strategies currently used by the Australian government to address factors affecting growth and nutritional status of Aboriginal and Torres Strait Islander children?
National and Community-Based Programs
General Australian Government Department of Health Programs:
Various programs contribute to the prevention and management of diet-related disorders among Aboriginal and Torres Strait Islanders at a national level.
Since the expiration of the National Aboriginal and Torres Strait Islander Nutrition Strategy and Action Plan (NATSINSAP) 2002-2010, there has been no national coordination of nutrition efforts.
Community-Based Nutrition Programs:
Effective programs adopt a multi-strategy approach, addressing both food supply (availability, accessibility, and affordability) and demand for healthy foods.
Community involvement is crucial in all stages of program initiation, development, implementation, and evaluation to ensure cultural appropriateness and tailored interventions.
Food Supply Improvement Programs:
Focus on food retail outlets, local food production (e.g., school or community gardens), food provided by community organizations, and food aid.
Community store nutrition policies play a significant role in influencing food supply and dietary intake in remote areas.
Nutrition Education:
While alone it may not improve food security or dietary intake, it is effective when combined with strategies such as cooking programs, peer education, budgeting advice, and group-based lifestyle modification programs.
Support for Nutrition Workforce:
A well-supported, resourced, and educated Aboriginal and Torres Strait Islander nutrition workforce is essential for successful nutrition interventions.
Specific Government Initiatives and Funding
Better Start to Life Approach:
$94 million over three years from July 2015, aimed at expanding efforts in child and maternal health.
Includes $54 million for increasing sites providing New Directions: Mothers and Babies Services, offering antenatal care, parenting advice, and health checks for children.
$40 million to expand the Australian Nurse–Family Partnership Programme (ANFPP), improving pregnancy outcomes and supporting child health and development.
National Aboriginal and Torres Strait Islander Nutrition Strategy and Action Plan (NATSINSAP):
Key achievements in food supply in remote and rural communities, disseminating good practice, and developing a nutrition workforce.
Examples include Remote Indigenous stores and takeaways resources, nationally accredited nutrition training materials for Indigenous health workers, and the revival of the National Nutrition Networks conference.
Aboriginal and Torres Strait Islander Guide to Healthy Eating:
Educational resources to support healthy dietary choices.
Health Star Rating System:
Launched in December 2014 to help consumers make more nutritious choices when purchasing packaged foods.
Campaigns include specific media targeting Indigenous communities.
Healthy Bodies Need Healthy Drinks Resource Package:
Launched in 2014, culturally appropriate materials encouraging school-aged children and their families to choose water over high-sugar drinks to prevent obesity, chronic disease, and dental caries.
Implementation Plan for the National Aboriginal and Torres Strait Islander Health Plan 2013–2023:
Recognizes the importance of addressing social and cultural determinants of health contributing to poor dietary choices and health outcomes through coordinated whole-of-government action.
State and Territory Initiatives
Move Well Eat Well Program in Tasmania:
Operates in primary schools and early childhood settings to improve policies and practices supporting nutrition and physical activity.
Resources
Aboriginal and Torres Strait Islander Health performance framework 2017 report
https://www.pmc.gov.au/sites/default/files/publications/indigenous/hpf-2017/tier2/219.html#important
Learning Points: Professional Development
Demonstrate discharge summary documentation and communication to parents of sick child via examples of dehydration or abdominal pain
Demonstrate communication and escalation using the ISBAR model
Learning Points: Science & Scholarship
Describe the pathophysiological basis of vomiting
Vomiting, or emesis, is a complex protective reflex designed to expel harmful substances from the stomach and upper intestine.
This reflex involves multiple components and pathways, integrating signals from the central nervous system, gastrointestinal tract, and other areas. Here’s a detailed explanation of the pathophysiology of vomiting:
Central Nervous System Components
Vomiting Center:
Location: Medulla oblongata
Function: The primary control center that initiates the vomiting reflex
Receptors: Muscarinic receptors
Input: Receives signals from various sources, including the chemoreceptor trigger zone, labyrinth of the inner ear, higher brain centers, and the gastrointestinal tract.
Chemoreceptor Trigger Zone (CTZ):
Location: Area postrema, outside the blood-brain barrier, in the floor of the fourth ventricle.
Receptors: Dopamine and serotonin receptors
Function: Detects blood-borne toxins and chemicals (e.g., chemotherapy agents) and activates the vomiting center through muscarinic receptors
Labyrinth of the Inner Ear:
Function: Involved in motion sickness.
Pathway: Movements activate the vestibulocochlear nerve, which sends signals to the vestibular nuclei in the pons. This activates histamine and muscarinic receptors, relays to the CTZ, and finally to the vomiting center.
Higher Brain Centers:
Function: Emotional and sensory inputs (e.g., pain, repulsive sights or smells) can trigger vomiting.
Pathway: These inputs directly stimulate the vomiting center.
Gastrointestinal Tract
Mechanoreceptors and Chemoreceptors:
Location: Throughout the gastrointestinal tract.
Function: Detect irritation, distension, and chemical stimuli.
Pathway: Signals from the vagal afferent nerves synapse in the nucleus tractus solitarius (NTS) in the medulla. Some neurons extend to the area postrema and other brain regions, contributing to the sensation of nausea.
Vomiting Reflex Mechanism
Initiation:
The vomiting center sends efferent signals via cranial nerves V, VII, IX, X, and XII.
Physiological Responses:
Tachycardia: Increased heart rate.
Increased Saliva Production: Protects the teeth and mucosa from stomach acid.
Closure of Epiglottis: Prevents aspiration of vomitus.
Diaphragm Contraction: Creates negative thoracic pressure aiding in the expulsion of gastric contents
Relaxation of Lower Esophageal Sphincter: Allows contents to move from the stomach into the esophagus.
Contraction of Abdominal Muscles: Increases intra-abdominal pressure.
Anti-peristalsis: Reversal of normal peristaltic movement to push contents upwards.
Ejection Phase:
Gastric and Lower Esophageal Sphincter Relaxation: Facilitates the movement of stomach contents.
Retching: Preceding phase where the glottis closes, and respiratory muscles counteract abdominal contraction, preventing expulsion.
Final Expulsion: Chyme is forced upwards and expelled through the mouth.
Neurotransmitters Involved
Muscarinic M1 Receptors: Involved in the activation of the vomiting reflex
Dopamine D2 Receptors: Triggered by toxins and drugs in the CTZ
Histamine H1 Receptors: Play a role in motion sickness
5-Hydroxytryptamine (5-HT)3 Receptors: Activated by serotonin in the gastrointestinal tract
Neurokinin 1 (NK1) Receptors: Substance P acts on these receptors in the vomiting center
List the common causes of vomiting in infants and children including surgical and other causes
Infancy
Gastroenteritis
Symptoms: Diarrhea (fluid stools), vomiting.
Cause: Viral or bacterial infection.
Acute Infections
Examples:
Tonsillitis
Otitis media
Pneumonia
Meningitis
Urinary Tract Infection (UTI)
Lesions of the GI Tract
Examples:
Duodenal obstruction from volvulus complicating malrotation
Strangulated inguinal hernia
Intussusception
Gastroesophageal Reflux Disease (GORD)
Symptoms: Recurrent fussiness during or after feedings, poor weight gain, recurrent respiratory symptoms (e.g., cough, stridor, wheezing).
Pyloric Stenosis
Symptoms: Recurrent projectile vomiting immediately after feeding in neonates aged 2–12 weeks, infrequent stools.
Infants may be emaciated (extremely thin or dehydrated) and dehydrated. Sometimes a palpable "olive" in the right upper quadrant.
Significance: Sudden onset of forceful, projectile vomiting, infants remain hungry/keen to feed, may contain blood, thickened pylorus felt.
Malabsorption
Examples: Coeliac disease (not common).
Intestinal Obstruction
Examples:
Meconium ileum
Meconium ileus is a condition in newborns where the meconium, which is the first stool passed by an infant, is abnormally thick and sticky, causing a blockage in the ileum, the final part of the small intestine
Volvulus
Intestinal malrotation
Intestinal malrotation refers to an abnormal rotation of the intestine during fetal development. This condition can lead to improper positioning of the intestines within the abdomen
Intestinal atresia
Intestinal atresia is a congenital condition where a portion of the intestine is absent, leading to a complete obstruction.
Increased Intracranial Pressure (ICP)
Examples: Space-occupying lesion (e.g., trauma, tumor).
Cyclical Vomiting Syndrome
Characteristics: Severe, discrete attacks of vomiting or nausea at varying intervals, with normal health between episodes and no demonstrable structural abnormalities.
Children
Infections
Examples:
Respiratory tract infections
Gastrointestinal tract infections
Acute Appendicitis and Peritonitis
Symptoms: Guarding, sometimes diarrhea.
Poisoning
Examples: Ingestion of toxic substances.
Migraine
Symptoms: Severe paroxysmal frontal headache with pallor, positive family history common.
Intracranial Neoplasm
Symptoms: Signs of increased ICP, vomiting in the morning before breakfast.
Psychological/Psychogenic Causes
Examples: Stress or anxiety-related vomiting.
Cyclical Vomiting Syndrome
Characteristics: Exclusion diagnosis, periodic severe vomiting.
Surgical and Other Causes
Intussusception
Symptoms: Colicky abdominal pain, inconsolable crying, lethargy, drawing of legs up to chest, later bloody ("currant jelly") stool. Typically ages 3–36 months but can be outside this range.
Malrotation with Volvulus
Symptoms: In neonates, bilious emesis, abdominal distention, and pain, bloody stool.
Sepsis
Symptoms: Fever, lethargy, tachycardia, tachypnea, widened pulse pressure, hypotension.
Food Intolerance
Symptoms: Abdominal pain, diarrhea, possibly eczematous rash or urticaria.
Other Medical Causes
Examples:
Urinary tract infection (UTI)
Meningitis
Raised intracranial pressure (ICP)
Metabolic disorders
Surgical Causes
Examples:
Appendicitis
Surgical obstruction (e.g., adhesions)
Meckel’s diverticulum
Vomiting Clinical Scenarios
Acute Vomiting
Description: Discrete episode of moderate to high intensity, most common, usually associated with an acute illness.
Investigations:
Full Blood Count (FBC)
Urea & Electrolytes (U&E)
Creatinine
Stool for culture and virology
Abdominal X-ray (AXR)
Surgical opinion if obstruction or acute abdomen possible
Exclude systemic disease
Causes: GI infection, non-GI infection (e.g., UTI), GI obstruction (congenital or acquired), adverse food reaction, poisoning, raised intracranial pressure, endocrine/metabolic disease (e.g., diabetic ketoacidosis).
Chronic Vomiting
Description: Low-grade daily pattern, frequently with mild illness.
Investigations:
FBC
Erythrocyte Sedimentation Rate (ESR)/C-Reactive Protein (CRP)
U&E
Liver Function Tests (LFT)
Helicobacter pylori serology
Urinalysis
Abdominal ultrasound
Small bowel enema
Sinus X-rays
Test feed or abdominal ultrasound for pyloric stenosis
Brain imaging (CNS tumor)
Consider urine pregnancy testing in teenage girls
Upper GI endoscopy
Causes: Peptic ulcer disease, gastroesophageal reflux, chronic infection, gastritis, gastroparesis, food allergy, psychogenic, bulimia, pregnancy.
Cyclic Vomiting
Description: Severe, discrete episodes associated with pallor, lethargy, +/- abdominal pain. The child is well between episodes. Often a family history of migraine or vomiting.
Investigations:
As for chronic vomiting, plus:
Serum amylase
Serum lipase
Blood glucose
Serum ammonia
Causes: Usually non-GI cause, idiopathic, CNS disease, abdominal migraine, endocrine (e.g., Addison’s disease), metabolic (e.g., acute intermittent porphyria), intermittent GI obstruction, fabricated illness.
More information
Distinguishing Features and Important Points for Vomiting in Infants and Children
Nature of Vomiting
Bilious Vomiting
Indicates: Gastrointestinal (GIT) obstruction until proven otherwise.
Action: Requires urgent surgical referral.
Blood in Vomit
Swallowed Blood:
Causes: Epistaxis (nosebleed), maternal blood due to delivery, or nipple trauma.
Action: Investigate source of blood.
Upper GI Hemorrhage:
Causes: Potential source if blood is present.
Action: Requires endoscopic evaluation.
Projectile Vomiting
Indicates: Pyloric stenosis.
Action: Requires investigation and often surgical management.
Early Morning Vomiting
Indicates: Raised intracranial pressure (ICP).
Action: Requires urgent evaluation for possible space-occupying lesion
Associated Signs and Symptoms
Evidence of Diarrhea
Indicates: Gastroenteritis
Fever or Systemic Illness
Indicates: Infection or sepsis
Action: Requires full sepsis workup and treatment
Abdominal Distension and Tenderness
Indicates: GIT obstruction
Additional Clues: “Tinkling” or absent bowel sounds
Headache
Indicates: Possible migraine, raised ICP, or infection
Action: Requires neurological evaluation
Rectal Bleeding
Indicates: Gastroenteritis, colitis, intussusception, Meckel’s diverticulum.
Bulging Fontanelle in Infants
Indicates: Raised ICP.
Action: Requires immediate investigation.
Specific Conditions
Meconium Ileus
Definition: Failure to pass the first stool in neonates (usually within the first 24-48 hours).
Cause: Cystic fibrosis (90% of cases)
Clinical Features: Signs of small bowel obstruction (bilious vomiting, abdominal distention, no passing of meconium)
Investigations: Abdominal X-ray (dilated small bowel loops, microcolon, Neuhauser signs - soap bubble appearance).
Management: Enema with a contrast agent, surgery in complicated cases.
Intestinal Malrotation
Definition: Abnormal or incomplete rotation of the gastrointestinal tract during fetal development.
Pathophysiology: Arrest in normal gut rotation leading to abnormal orientation of the bowel and mesentery.
Clinical Features: Mostly asymptomatic unless complicated by volvulus.
Associated Congenital Anomalies: Congenital diaphragmatic hernia, congenital heart defects, omphalocele (a birth defect in which the infant's intestine or other abdominal organs protrude through a hole in the belly button area and are covered with a membrane), Meckel’s diverticulum, esophageal atresia, biliary atresia.
Investigations: Upper GI series, barium enema, abdominal ultrasound, abdominal X-ray.
Management: Elective surgery (Ladd procedure).
Volvulus
Definition: Twisting of a loop of bowel on its mesentery.
Pathophysiology: Torsion of a malrotated gut leading to mechanical bowel obstruction.
Clinical Features:
Midgut Volvulus: Bilious vomiting, abdominal distention, signs of bowel ischemia (hematochezia, hematemesis, hypotension, tachycardia).
Gastric Volvulus: Severe abdominal pain, retching, inability to pass an NG tube.
Duodenal Obstruction: Bilious vomiting without abdominal distention.
Investigations: Upper GI series (duodenal obstruction, corkscrew duodenum), barium enema (Bird’s peak sign at the site of the twist), abdominal ultrasound (whirlpool sign), abdominal X-ray.
Management:
Initial: NPO, NGT insertion, IV fluids, broad-spectrum antibiotics.
Emergency Surgery (Ladd Procedure): Reduce/untwist the volvulus and remove Ladd bands.
Duodenal Atresia
Definition: Complete occlusion or absence of the duodenal lumen.
Epidemiology: Associated with chromosomal abnormalities, especially Down syndrome.
Pathophysiology: Failed or partial reuniting of the duodenum during the embryonic period.
Clinical Features:
Intrauterine: Polyhydramnios (excessive accumulation of amniotic fluid — the protective liquid contained within the amniotic sac of a pregnant woman)
Postpartum: Vomiting (bilious if stenosis is distal to the major duodenal papilla), distended upper abdomen, scaphoid lower abdomen, delayed meconium passage.
Investigations:
Prenatal: Ultrasound (double bubble sign).
Postnatal: Abdominal X-ray (gasless distal bowel).
Management:
Initial Management: IV fluids, NGT for gastric decompression.
Surgical Management: Bypass of the atresia or stenosis.
List the common causes of abdominal pain in infants and children; Including surgical causes
Infants and Children
Gastrointestinal Causes
Gastroenteritis
Appendicitis
Mesenteric Lymphadenitis
Constipation
Abdominal Trauma
Intestinal Obstruction
Peritonitis
Food Poisoning
Peptic Ulcer
Meckel's Diverticulum
Inflammatory Bowel Disease (IBD)
Lactose Intolerance
Hepatitis
Cholecystitis
Cholelithiasis
Choledocholithiasis
Splenic Infarction
Splenic Rupture
Pancreatitis
Genitourinary Causes
Urinary Tract Infection (UTI)
Urinary Calculi
Dysmenorrhea
Mittelschmerz
Pelvic Inflammatory Disease (PID)
Threatened Abortion
Ectopic Pregnancy
Ovarian/Testicular Torsion
Endometriosis
Metabolic Disorders
Diabetic Ketoacidosis (DKA)
Hypoglycemia
Porphyria
Acute Adrenal Insufficiency
Hematologic Disorders
Sickle Cell Anemia
Henoch-Schonlein Purpura
Hemolytic Uremic Syndrome
Miscellaneous Causes
Drugs and Toxins
Erythromycin
Salicylates
Lead Poisoning
Venoms
Pulmonary Causes
Pneumonia
Diaphragmatic Hernia
Pleurisy
Time-Critical Causes of Abdominal Pain by Age
Neonates
Hirschsprung Enterocolitis
Hirschsprung enterocolitis is an inflammatory condition of the bowel that occurs in patients with Hirschsprung disease. It involves inflammation of the colon and can lead to severe complications such as sepsis and bowel perforation.
Etiology (Causes)
Hirschsprung Disease:
The primary underlying cause is Hirschsprung disease, where a segment of the colon lacks nerve cells (ganglion cells), leading to chronic obstruction and stasis of intestinal contents.
Bacterial Overgrowth:
Stasis of intestinal contents can promote bacterial overgrowth and translocation, contributing to the development of enterocolitis.
Mucosal Barrier Dysfunction:
The absence of ganglion cells can impair mucosal barrier function, making the bowel more susceptible to inflammation and infection.
Incarcerated Hernia
Intussusception
Necrotizing Enterocolitis
Volvulus
Infants and Children
Abdominal Trauma
Appendicitis
Constipation
Gastroenteritis
Incarcerated Hernia
Intussusception
Meckel's Diverticulum
Mesenteric Adenitis
Ovarian Torsion
Pyloric Stenosis
Testicular Torsion
Volvulus
Adolescents
Appendicitis
Abdominal Trauma
Cholecystitis/Cholelithiasis
Constipation
Ectopic Pregnancy
Gastroenteritis
Inflammatory Bowel Disease (IBD)
Ovarian Cyst – Torsion/Rupture
Pancreatitis
Pelvic Inflammatory Disease (PID)
Renal Calculi
Testicular Torsion
Important Non-Abdominal Causes of Abdominal Pain
Diabetic Ketoacidosis (DKA)
Headache (Migraine)
Henoch-Schonlein Purpura
Hip Pathology
Pneumonia
Psychological Factors
Sepsis
Sexually Transmitted Infection
Sickle Cell Disease (Vaso-occlusive Crisis)
Toxin Exposure or Overdose
UTI/Pyelonephritis
Detailed Information on Specific Conditions
Hirschsprung Enterocolitis
Characterized by: An aganglionic colon segment (usually rectosigmoid) that fails to relax.
Epidemiology: Affects 1 in 5000 newborns, more common in males (4:1).
Cause: RET gene mutations associated with MEN2 and familial Hirschsprung disease.
Pathophysiology: Genetic mutation → defective migration of parasympathetic neuroblasts → absence of Meissner and Auerbach plexuses → aganglionic colon segment → inability to control intestinal wall muscles → uncoordinated peristalsis + slow motility → stenosis and functional obstruction → megacolon.
Clinical Features:
Early: Delayed passage of meconium, distal intestinal obstruction, tight anal sphincter, explosive stool on DRE.
Late: Chronic constipation, poor feeding, failure to thrive.
Investigations: Abdominal X-ray, barium enema.
Complications: Toxic megacolon, fecal incontinence, urinary dysfunction, erectile dysfunction, bowel perforation.
Management: Initial medical management (fluids, NGT, IV antibiotics), surgical correction.
Intussusception
Characterized by: Invagination of a proximal bowel segment into a distal lumen, most often occurs at the ileocecal valve.
Epidemiology: Most common between 2 months and 2 years, more common in males.
Cause: Idiopathic (90%) or pathological lead points (e.g., Meckel's diverticulum, polyps).
Pathophysiology: Imbalance in bowel wall → invagination (Invagination, in a medical context, refers to the process where a part of the intestine folds into an adjacent section) → venous impairment → ischemia → sloughed bowel wall → necrosis and perforation.
Clinical Features: Cyclic colicky abdominal pain, palpable sausage-shaped mass, red currant jelly stools, vomiting, high pitched bowel sounds, lethargy, pallor.
Investigations: Enema, ultrasound, abdominal X-ray.
Management: IV fluid resuscitation, NPO, analgesia, NGT, IV antibiotics, enema, surgical reduction if necessary.
Necrotizing Enterocolitis
Characterized by: Hemorrhagic necrotizing inflammation of the intestinal wall.
Epidemiology: Most common cause of acute abdomen in premature infants, typically between 2-4 weeks of life.
Cause: Unknown; factors include intestinal wall perfusion and motility disorders, microbial overgrowth, formula feeding, rapid increase in enteral nutrition.
Clinical Features: Lethargy, distended abdomen, gastric retention, vomiting, diarrhea, rectal bleeding, abdominal tenderness.
Investigations: FBC, ESR/CRP, coagulation studies, ABG, blood cultures, abdominal X-ray, portal vein gas.
Management: Supportive care, stop enteral feeding, decompression via NGT, IV antibiotics, radiographic monitoring, surgical intervention if needed.
Meckel's Diverticulum
Characterized by: A true diverticulum located approximately 2 feet proximal to the ileocecal valve.
Epidemiology: Most common congenital GIT abnormality, present in 2% of the population.
Pathophysiology: Persistence of the omphalomesenteric duct.
Clinical Features: Lower GI bleeding, bowel obstruction symptoms, diverticulitis symptoms.
Investigations: Meckel scintigraphy scan, CT angiography.
Management: Surgical resection if symptomatic.
Mesenteric Lymphadenitis
Characterized by: Enlargement and inflammation of mesenteric lymph nodes.
Epidemiology: Common in children under 15.
Cause: Yersinia species, beta-hemolytic streptococcus, E. coli, Strep viridans.
Clinical Features: Abdominal pain, fever, diarrhea, malaise, anorexia, nausea, vomiting.
Investigations: CT abdomen and pelvis.
Management: Supportive care, empirical antibiotics.
Pyloric Stenosis
Characterized by: Hypertrophy and hyperplasia of the pyloric sphincter.
Epidemiology: Most common cause of gastric outlet obstruction in infants, more common in males and firstborn children.
Causes: Environmental factors, genetic factors, macrolide antibiotics.
Clinical Features: Projectile non-bilious vomiting, palpable olive-shaped pylorus, peristaltic wave, "hungry vomiter."
Investigations: Abdominal ultrasound, UEC.
Management: Pyloromyotomy.
Pyloromyotomy involves making an incision in the outer layer of the hypertrophied pyloric muscle to relieve the obstruction.
Describe the main causes and mechanisms for abnormal growth patterns
Abnormal Growth Patterns
Abnormal growth patterns can be divided into:
Failure to thrive
Short stature
Tall stature
Failure to Thrive
Causes
Mechanism | Specific Causes |
---|---|
Inadequate Calorie Intake/Retention | - Inadequate nutrition (breastmilk, formula, and/or food) |
- Breastfeeding difficulties | |
- Error in infant formula preparation | |
- Restricted diet (e.g., restricting food groups, vegan, sensory aversions) | |
- Structural (e.g., cleft palate) | |
- Persistent vomiting | |
- Appetite loss due to chronic disease | |
- Early (<4 months) or delayed (>6 months) introduction of solids | |
Inadequate Absorption | - Cow milk protein allergy |
- Coeliac disease (if having gluten-containing diet) | |
- Pancreatic insufficiency (e.g., cystic fibrosis) | |
- Chronic diarrhea | |
- Chronic liver disease | |
Excessive Caloric Utilization | - Urinary tract infection |
- Chronic illness/inflammation | |
- Chronic respiratory disease (e.g., cystic fibrosis) | |
- Congenital heart disease | |
- Diabetes mellitus | |
- Hyperthyroidism | |
Psychosocial Factors | - Parental mental illness, disability, or chronic illness |
- Poor carer understanding (e.g., language barrier, limited literacy) | |
- Non-secure attachment patterns | |
- Behavioral disorders | |
- Difficulties at meal times | |
- Coercive feeding (including feeding child while asleep) | |
- Food insecurity | |
- Social isolation | |
- Failure to attend appointments | |
- Parental substance abuse | |
- Family violence | |
- Trauma or neglect | |
- Current or past child protection involvement | |
Other Medical Conditions | - Genetic syndromes |
- Inborn errors of metabolism |
Investigations
Bedside: Urinalysis, urine MCS, stool MCS, fat globules, fatty acid crystals, fecal calprotectin.
Bloods: FBC, UEC, LFT, ESR, iron studies, TSH, glucose, coeliac serology and total IgA (if on solid or feeds containing gluten), vitamin B12.
Short Stature
Causes
Mechanism | Specific Causes |
---|---|
Normal Variants of Growth | - Familial short stature |
- Constitutional delay of growth and puberty | |
- SGA (small gestational age) infant with catch-up growth | |
Systemic | - Undernutrition |
- Glucocorticoid therapy | |
- GI disease (especially IBD) | |
- Rheumatological disease (e.g., systemic-onset juvenile idiopathic arthritis) | |
- Renal disease (e.g., CKD, renal tubular acidosis) | |
- Cancer | |
- Pulmonary disease (e.g., cystic fibrosis, severe asthma) | |
- Immunodeficiency | |
Endocrine Diseases | - Hypothyroidism |
- GH deficiency | |
- Precocious puberty | |
- Cushing syndrome | |
- Pseudohypoparathyroidism type 1 | |
Genetic Diseases | - Turner syndrome |
- SHOX mutations | |
Skeletal Dysplasias | - Osteogenesis imperfecta |
- Achondroplasia | |
- Hypochondroplasia |
Investigations
Bedside: Urinalysis
Bloods: FBC, UEC, CMP, CRP/ESR, TSH, cortisol studies, coeliac serology, ANA screening, GH, IGF-1, FSH, LH
Imaging: Bone age (X-ray of the wrist)
Other: GH stimulation test, karyotype analysis
Tall Stature
Causes
In Infancy
Mechanism | Specific Causes |
---|---|
Causes in Infancy | - Infant of a diabetic mother |
- Cerebral gigantism | |
- Beckwith-Wiedemann syndrome |
In Childhood or Adolescence
Mechanism | Specific Causes |
---|---|
Endocrine Disorders | - Familial/constitutional tall stature |
- Precocious puberty | |
- Growth hormone excess | |
- Hyperthyroidism | |
- Sex hormone deficiency or insensitivity | |
- Familial glucocorticoid deficiency/resistance | |
Non-Endocrine Disorders | - Exogenous obesity |
- MC4R mutation | |
- Klinefelter syndrome (47XXY) | |
- 47, XYY | |
- Marfan syndrome |
Investigations
Bloods: TSH, GH, IGF-1, LH, FSH, testosterone levels, serum cortisol, serum prolactin
Imaging: Bone age (X-ray of the wrist)
Other: Karyotype analysis
Detailed Information on Specific Conditions
Cow Milk Protein Allergy
Epidemiology: One of the most common food allergies in children, affects 1-2% of preschool children.
Pathophysiology: IgE antibodies against milk proteins.
Risk Factors: Family history, atopic disease, allergic disease.
Clinical Features:
Mild to Moderate Reactions: Hives, swelling of the lips/face/eyes, tingling of the mouth, abdominal pain, vomiting.
Severe Reactions (Anaphylaxis): Difficulty/noisy breathing, swelling of the tongue, persistent cough, dizziness, collapse.
Investigations: Allergy skin prick test, RAST test.
Management: Diet free of cow’s milk and cow’s milk products.
Prognosis: 90% of children with delayed reactions and 50% with immediate reactions will outgrow their allergy by 3-5 years of age.
Short Stature
Physiological Causes:
Familial short stature
Constitutional delay of growth and puberty
Small for gestational age infant with catch-up growth
Idiopathic short stature
Pathological Causes:
Defects of nutrition, digestion, or absorption
Social and emotional deprivation
Chronic disease (e.g., rheumatologic, CKD, cancer)
Genetic syndromes (e.g., Turner syndrome in girls)
Endocrine (e.g., deficiency of thyroid or growth hormone)
Iatrogenic (e.g., long-term steroid therapy)
Disorders of bone growth (e.g., skeletal dysplasia)
Investigations: Urinalysis, blood tests (FBC, UEC, CMP, etc.), imaging (bone age X-ray), GH stimulation test, karyotype analysis.
Tall Stature
Causes of Overgrowth in Infancy:
Infant of a diabetic mother
Cerebral gigantism
Beckwith-Wiedemann syndrome
Causes of Overgrowth in Childhood or Adolescence:
Familial/constitutional tall stature
Endocrine disorders (e.g., precocious puberty, growth hormone excess, hyperthyroidism)
Non-endocrine disorders (e.g., exogenous obesity, Klinefelter syndrome, Marfan syndrome)
Investigations: TSH, GH, IGF-1, LH, FSH, testosterone levels, serum cortisol, serum prolactin, bone age X-ray, karyotype analysis.
Describe the pathophysiology for the common causes of chronic abdominal pain and or diarrhoea in children (Coeliac disease, IBD)
Coeliac Disease
Coeliac disease is an autoimmune disorder characterized by an abnormal immune response to gluten, a protein found in wheat, rye, and barley.
Genetic Predisposition:
Majority of patients carry one of two major histocompatibility complex class-II molecules: HLA-DQ2 (95%) and HLA-DQ8 (5%).
Immune Response:
Loss of immune tolerance to gluten-derived peptides (gliadin) leads to the activation of an antigen-specific T-cell response.
Gluten peptides are resistant to human proteases and persist intact in the small intestinal lumen.
These peptides access the lamina propria through:
Faulty tight junctions.
Endothelial cell transcytosis.
Dendritic cell sampling of the intestinal lumen.
Passage during the resorption of apoptotic villous enterocytes.
Innate and Adaptive Immune Activation:
In the intestinal submucosa, gluten peptides trigger both innate and adaptive immune activation:
Innate Response:
Gluten peptides stimulate IL-15 production by dendritic cells, macrophages, and intestinal epithelial cells, leading to epithelial damage via intra-epithelial lymphocytes.
Adaptive Response:
In the submucosa, gluten peptides are deamidated by tissue transglutaminase (tTG), allowing high-affinity binding to HLA-DQ2 or DQ8.
This triggers activation of helper T (Th) cells, leading to:
Cell death and tissue remodeling with villous atrophy and crypt hyperplasia.
Th2-mediated plasma cell maturation and production of anti-gliadin and anti-tTG antibodies.
Associated Conditions:
Positive family history, Type 1 diabetes, Down syndrome, and IgA deficiency.
Presentation:
Initial Features:
Pallor, diarrhea, pale bulky floating stools, anorexia, failure to thrive (FTT), irritability.
Later Features:
Apathy, gross motor developmental delay, ascites, peripheral edema, anemia, delayed puberty, arthralgia, hypotonia, muscle wasting, specific nutritional disorders.
Investigations:
Bedside: Urinalysis, stool MCS.
Bloods: IgA tissue transglutaminase antibody (tTG IgA), total IgA, deamidated gliadin peptide, FBC (iron, folate, B12 deficiency anemia), endomysial antibody (EMA), HLA testing.
Other: Upper endoscopy and biopsy (villous atrophy, crypt hyperplasia, intraepithelial lymphocyte infiltration), skin biopsy (if dermatitis herpetiformis).
Management:
Consultation with a dietician.
Education about the disease.
Lifelong adherence to a strict gluten-free diet.
Identification and treatment of nutritional deficiencies (iron, vitamin D, B12, folate).
Continuous long-term follow-up by a multidisciplinary team (serology, FBC, TSH, vitamin D).
Inflammatory Bowel Disease (IBD)
IBD encompasses Crohn's disease and ulcerative colitis, both of which involve chronic relapsing inflammation of the gastrointestinal tract.
Crohn's Disease
Pathology:
Chronic relapsing inflammation with "skip lesions" affecting any part of the GIT.
Involves transmural inflammation (including the serosa), fissured ulceration, "cobblestone" appearance, and granuloma formation.
Commonly involves the ileum (80% of cases) and rectum (25% of cases).
Aetiology:
Genetic: Mutations in CARD15 (NOD2).
Environmental: Cigarette smoking, oral contraceptives, high refined sugar diet, nutritional deficiencies, infectious agents, NSAIDs.
Main Clinical Features:
Persistent or grumbling pain with severe acute attacks.
Diarrhea less prominent (without blood), rectal bleeding less common.
Abdominal mass relatively common, abdominal pain/tenderness.
Extra-intestinal manifestations include arthritis, uveitis, erythema nodosum, pyoderma gangrenosum, primary sclerosing cholangitis, vitamin B12 deficiency.
Complications:
Strictures, fistulae, anal and perianal lesions, massive hemorrhage, incomplete obstruction, toxic megacolon.
Ulcerative Colitis
Pathology:
Recurrent acute inflammation with intervening quiescent phases, continuous involvement of the affected colon.
Confined to the mucosa and submucosa, with widespread superficial ulceration, pseudopolyps.
Aetiology:
Genetic: 10% have a 1st-degree relative affected, higher incidence in Ashkenazi Jews.
Environmental: Higher incidence in developed countries, smoking protective, previous enteric infections increase risk.
Immunologic: Impaired epithelial barrier, reduced dendritic cell numbers, exaggerated Th2 cell response.
Main Clinical Features:
Severe diarrhea with blood, tenesmus, rectal bleeding very common.
Abdominal pain and tenderness.
Extra-intestinal manifestations include arthropathy, eye, skin, and biliary tract disorders, anemia.
Complications:
Strictures rare, fistulae rare, massive hemorrhage, toxic megacolon, high risk of malignant change with severe or longstanding disease.
Pathophysiology Overview
Condition | Pathophysiology |
---|---|
Coeliac Disease | Autoimmune response to gluten, leading to villous atrophy, crypt hyperplasia, and malabsorption due to an immune response triggered by gliadin peptides. |
Crohn's Disease | Immune dysregulation and chronic relapsing inflammation with transmural involvement, skip lesions, granuloma formation, leading to fibrosis, strictures, and fistulae. |
Ulcerative Colitis | Chronic inflammation confined to the mucosa and submucosa with continuous colonic involvement, leading to widespread ulceration, pseudopolyps, and increased risk of colorectal cancer. |
Detailed Descriptions:
Coeliac Disease:
Epidemiology: Females > males, bimodal peak incidence (8-12 months, 30-40s), more common in individuals of northern European descent.
Cause: Genetic predisposition (HLA-DQ2, HLA-DQ8), associated with autoimmune diseases.
Pathophysiology: Consumption of gluten triggers chronic intestinal inflammation due to an autoimmune response, leading to epithelial damage, villous atrophy, crypt hyperplasia, and malabsorption.
Clinical Features:
Gastrointestinal: Chronic or recurring diarrhea (steatorrhea), flatulence, abdominal bloating and pain, nausea, vomiting, lack of appetite.
Extraintestinal: Vitamin deficiency, iron deficiency anemia, fatigue, weight loss, osteoporosis, hypocalcemia, failure to thrive, growth failure, delayed puberty, dermatitis herpetiformis, neuropsychiatric symptoms, reduced fertility or infertility, autoimmune thyroid disease, type 1 diabetes mellitus, Turner syndrome, Down syndrome, rheumatoid arthritis, sarcoidosis, selective IgA deficiency.
Investigations: IgA tissue transglutaminase antibody (tTG IgA), total IgA, deamidated gliadin peptide, FBC, endomysial antibody (EMA), HLA testing, upper endoscopy and biopsy, skin biopsy (if dermatitis herpetiformis).
Management:
Consultation with dietician
Education about disease
Lifelong adherence to strict gluten-free diet - abdominal discomfort lessens within days and diarrhoea within weeks.
Identification and treatment of nutritional deficiencies - iron, vitamin D, B12, folate.
Access to an advocacy group
Continuous long term follow up by a multidisciplinary team
Serology at 6 month intervals until levels normalise, then annually.
Measure FBC, TSH, vitamin D.
Monitor growth of child
IBD (Crohn's Disease and Ulcerative Colitis):
Epidemiology: More common in whites, particularly individuals of Ashkenazi Jewish descent, with 10-20% of IBD cases diagnosed during childhood. Peak age of onset at 15-29 years.
Risk Factors: Genetic predisposition (HLA-B27), smoking, oral contraceptive use, NSAIDs, high refined sugar diet, previous intestinal infection.
Pathophysiology:
Crohn's Disease: Dysregulation of Th17 signaling, immune dysregulation, NOD2 mutations leading to unregulated inflammation, transmural involvement, "skip lesions," granuloma formation.
Ulcerative Colitis: Abnormal host immune response to commensal bacteria, Th2-mediated response, continuous inflammation from the rectum proximally, confined to mucosa and submucosa.
Pattern of involvement
Ulcerative colitis
Inflammation is limited to the mucosa and submucosa.
Ascending inflammation beginning in the rectum and moves retrograde the colon.
In children, the disease is often pancolonic at diagnosis.
Crohn’s disease
Inflammation is transmural (i.e. affects the full thickness of the GI wall)
Most commonly infects the terminal ileum and colon.
Any part of the GIT can be involved, but the rectum is generally spared.
Inflammation is irregular and does not occur continuously throughout the GIT.
In children, upper GI involvement is more common than in adults.
Clinical Features:
Crohn's Disease: Chronic watery diarrhea, perianal fistulas and abscesses, malabsorption, abdominal pain, palpable abdominal mass.
Ulcerative Colitis: Bloody diarrhea with mucus, fecal urgency, abdominal pain and cramps, tenesmus.
Investigations:
Laboratory studies and stool tests
FBC: anaemia
LFT
UEC: electrolyte abnormalities from diarrhoea and dehydration.
↑ ESR + CRP
Stool:
MCS: Microscopy, culture, sensitivities
OCP: Ova, cysts, parasites
Confirm diagnosis: colonoscopy & biopsy
Colonoscopy findings:
Ulcerative colitis: Circumferential inflammation or ulceration that is continuous throughout a section of rectum/ colon. Friable mucosa with bleeding on contact with endoscope.
Crohn’s disease: “Skip lesions” with cobblestone appearance - linear patches of damaged tissue with normal patches of mucosa in between. Usually does not involve the rectum.
Biopsy findings:
Ulcerative colitis: Neutrophil infiltration limited to the mucosa and submucosa. Crypt abscesses (due to aggression of lymphocytes) => crypt atrophy.
Crohn’s disease: Transmural inflammation. Inflammatory cells and non-caseous sarcoid granulomas.
Radiological studies
Plain x ray
Barium enema radiography
Management
Non-pharmacological therapy
Multidisciplinary team involvement - paediatrician, gastroenterologist, GP.
Education
Dietetic assessment
Consider social work, psychological or other allied health services.
Group support
Vaccination - ensure vaccinations are up to date and commence live vaccinations prior to starting immunosuppressive therapy. After therapy begins, NO LIVE vaccinations.
Pharmacological therapy
Ulcerative colitis
Acute flare
Mild to moderate:
Oral 5-aminosalicylate (induction)
If unresponsive, add oral prednisone
Moderate to severe:
IV hydrocortisone or methylprednisolone
If unresponsive, add IV infliximab or ciclosporin
Chronic (i.e. maintenance therapy)
Rectal and/or Oral 5-aminosalicylate
If unresponsive, add oral azathioprine, mercaptopurine or methotrexate
If unresponsive, add IV infliximab
Gastroenteritis in children
Briefly describe common causes, investigations and treatment; antibiotics, fluid management, electrolyte management, antiemetics / antidiarrhoeal agents
Gastroenteritis in Children:
Common Causes
Viral Gastroenteritis:
Transmission: Faecal-oral route, often through contaminated water. Common during winter. Breastfeeding provides some protection. More severe in malnourished children.
Causes:
Rotavirus (most common before vaccination)
Norovirus
Enteric adenovirus
Astrovirus
Cytomegalovirus (CMV in immunocompromised patients)
Bacterial Gastroenteritis:
Sources of Infection: Contaminated water, poor food hygiene (meat, fresh produce, chicken, eggs, previously cooked rice). Most common in children under 2 years old.
Causes:
Salmonella spp.
Campylobacter jejuni
Shigella spp.
Yersinia enterocolitica
Escherichia coli
Clostridium difficile
Bacillus cereus
Vibrio cholerae
Presentation
Viral Gastroenteritis:
Watery diarrhea (rarely bloody)
Vomiting
Cramping abdominal pain
Fever
Dehydration
Electrolyte disturbances
Upper respiratory tract signs common with rotavirus
Vomiting predominates with norovirus
Bacterial Gastroenteritis:
Secretory and inflammatory diarrhea
Symptoms similar to viral gastroenteritis plus:
Malaise
Dysentery (bloody and mucous diarrhea)
Abdominal pain mimicking appendicitis or IBD
Tenesmus
Complications
Viral:
Prominent UGI symptoms (N/V)
Acute, resolves within 24-48h
Possible secondary cases due to person-to-person transmission
Bacterial:
Bacteraemia
Secondary infections (pneumonia, osteomyelitis, meningitis)
Reiter’s syndrome (Shigella, Campylobacter)
Haemolytic-uraemic syndrome (E. coli O157, Shigella)
Guillain-Barré syndrome (Campylobacter)
Reactive arthropathy (Yersinia)
Haemorrhagic colitis
Toxin-mediated:
N/V and abdominal pain prominent
Diarrhoea occurs later
Short incubation period (several hours)
Closely clustered cases
Infections arise from a single point source
Investigations
Assess degree of dehydration: Use weight change, signs, vital signs, pallor (blood loss), abdominal tenderness, signs of associated illness (e.g., petechial rash in HSP).
Calculate fluid deficit
Faecal samples for bacterial culture if significant abdominal pain or blood in faeces.
C. difficile infection: Based on clinical features (diarrhoea, ileus, toxic megacolon) and microbiological evidence or colonoscopy findings.
Stool microbiological investigations: If diarrhea persists beyond 7 days, suspicion of septicaemia, blood/mucus in stool, or immunocompromised child.
Blood tests: For severe dehydration, renal disease, altered conscious state, 'doughy' skin (hypernatraemia), home therapy with hypertonic/hypotonic fluids, profuse losses, ileostomy.
Treatment
Antibiotics:
Most acute diarrhoea is viral and does not require antibiotic therapy
Empirical antibiotics are usually not indicated for community-acquired infectious diarrhoea
In children with bloody diarrhoea without fever or sepsis, empirical antibiotic therapy is not recommended due to the risk of precipitating haemolytic uraemic syndrome (HUS) if the infection is caused by enterohaemorrhagic Escherichia coli
Empirical therapy is indicated or should be considered in some groups.
Empirical antibiotics are indicated for patients with manifestations of severe disease
Consider empirical antibiotics in immunocompromised patients, even if they do not have clinical features suggesting severe disease, as they are at greater risk of rapid deterioration and poor outcomes
There is evidence that empirical antibiotic therapy shortens the duration of illness by 1-3 days in returned travellers with acute diarrhoea
If empirical antibiotic therapy for acute infectious diarrhoea is indicated, obtain samples for faecal testing before starting therapy → use:
Ciprofloxacin 500mg (child: 12.5mg/kg up to 500mg) orally, 12-hourly for 3 days
Norfloxacin 400mg (child: 10mg/kg up to 400mg) orally, 12-hourly for 3 days
If the infection is likely to have been acquired in an area where quinolone resistance is common (e.g. South and East Asia), or an oral suspension is required (e.g. for young children), consider: azithromycin 500mg (child: 10mg/kg up to 500mg) orally, daily for 3 days
If oral therapy is not tolerated or absorption is likely to be impaired, consider: ceftriaxone 2g (child ≥1mth: 50mg/kg up to 2g) IV, daily for 3 days
C. difficile infection:
First episode:
Metronidazole 400mg (child: 10mg/kg up to 400mg) orally or enterally, 8-hourly for 10 days
OR vancomycin 125mg (child: 10mg/kg up to 125mg) orally or enterally, 6-hourly for 10 days
There is evidence that vancomycin has similar efficacy to metronidazole in this setting; however, for antimicrobial stewardship reasons, it is not the preferred drug
First recurrence or refractory disease
Vancomycin 125mg (child: 10mg/kg up to 125mg) orally or enterally, 6-hourly for 10 days
OR fidaxomicin 200mg orally, 12-hourly for 10 days
Second and subsequent recurrences or ongoing refractory disease
Vancomycin 10mg/kg up to 125mg orally or enterally, 6-hourly for 14 days
OR nitazoxanide 100mg (for children 1-3y/o) or 200mg (for children ≥4y/o) orally, 12-hourly for 10 days
Severe infection
Vancomycin 125mg (child: 10mg/kg up to 125mg) orally or enterally, 6-hourly for 10 days
IV vancomycin is not effective against C. difficile infection due to inadequate penetration of the drug into the lumen of the colon
In complicated cases (e.g. hypotension or shock, ileus, megacolon), in addition to oral or enteral vancomycin à use: metronidazole 500mg (child: 12.5mg/kg up to 500 mg) IV, 8-hourly for 10 days
Consider adding intracolonic vancomycin, particularly in the presence of ileus → use: vancomycin 500mg in 100mL sodium chloride 0.9% rectally (via rectal tube), administered as a retention enema, 6-hourly
Early surgical referral is indicated for patients with severe disease, because outcomes are poor after organ dysfunction is established
Patients with severe disease may require a colectomy to survive, particularly if toxic megacolon develops
Faecal microbiota transplantation (FMT) can also be considered
Fluid Management:
Children with minimal or no dehydration should be encouraged to continue eating and drinking as tolerated
Oral rehydration solutions are strongly recommended for patients at risk of dehydration (e.g. infants and toddlers, children having frequent episodes of vomiting or diarrhoea)
Children with mild to moderate dehydration can be adequately rehydrated with an oral rehydration solution
Contain a balanced quantity of sodium and glucose and other electrolytes e.g. potassium and chloride
Sodium concentrations of 45-60mmol/L, glucose concentrations of 80-120mmol/L and total osmolarity of about 240mOsm/L
Nasogastric rehydration (NGTR)
Most children stop vomiting after NGT fluids are started
If vomiting continues, consider ondansetron and slow NG fluids temporarily
Rapid nasogastric rehydration: 25mL/kg/h for 4h
Treatment is divided into the rehydration phase and the maintenance phase
Rehydration phase: replace the fluid deficit à give 50-100mL/kg of fluids (depending on the degree of dehydration) over 4h, then reassess hydration status
Maintenance phase: provide the usual maintenance fluid requirement and replace ongoing losses from diarrhoea or vomiting (10mL/kg body weight for each loose or watery stool, and 2mL/kg for each episode of vomiting)
Maintenance fluid requirements (24h)
100mL/kg: for the first 10kg of weight (4mL/h)
+50mL/kg: for the second 10kg of weight (2mL/h)
+20mL/kg: for the remaining weight above 20kg (1mL/h)
Severe dehydration
Severely dehydrated children should be admitted to hospital for rehydration and close monitoring → IV rehydration is usually necessary
A fluid bolus of sodium chloride 0.9% (20mL/kg) is given, and may be repeated until the child’s mental state and perfusion improves
The child’s hydration status should be reassessed after each fluid bolus to determine ongoing fluid therapy, and serum electrolyte (especially sodium, potassium and bicarbonate) and glucose concentrations should be measured
Lack of response to intravenous rehydration may indicate an underlying condition such as infection, septic shock, or a cardiac or metabolic disorder
Electrolyte Management:
Use Plasma-Lyte 148 and 5% Glucose OR 0.9% sodium chloride (normal saline) and 5% Glucose for rehydration after any required boluses
If serum K <3mmol/L, add KCl 20mmol/L, or give oral supplements
Measure Na, K and glucose at the outset and at least 24-hourly from then on (more frequent testing is indicated for patients with comorbidities or if more unwell)
24-hr electrolyte requirements
Antiemetics/Antidiarrhoeal Agents:
Antiemetics
Ondansetron reduces vomiting, improves intake of oral rehydration solutions, and reduces the need for intravenous fluids and hospitalisation
Well tolerated, non-sedating and does not cause extrapyramidal adverse effects (like dopamine receptor antagonists e.g. metoclopramide)
Ondansetron can worsen diarrhoea (possibly due to retention of fluids and toxins normally eliminated by vomiting)
If ondansetron is considered appropriate, use: ondansetron 0.15mg/kg up to 8mg orally or IV; repeat dose after 8-12h if necessary
Antidiarrhoeals: not recommended for acute diarrhoea in infants and children
Urinary Tract Infection in children
Briefly describe common causes, investigations and treatment; Diagnosis, Investigations, Treatment, Follow up
Common Causes
Bacterial Infections:
Escherichia coli (E. coli): Causes 85-90% of pediatric UTIs.
Proteus mirabilis: Found in 30% of boys with uncomplicated cystitis.
Staphylococcus saprophyticus: Found in adolescents of both sexes with acute UTI.
Staphylococcus aureus: Common cause of renal abscess.
Pseudomonas species, Serratia marcescens, Citrobacter species, Staphylococcus epidermidis: Cause low-virulence infections in patients with urinary tract malformation or dysfunction.
Other Bacteria: Klebsiella aerogenes, Enterococcus species.
Risk Factors:
Younger Children:
Malformations and obstruction of the urinary tract.
Prematurity.
Indwelling urinary catheters.
Lack of circumcision (in males).
High-grade vesicoureteral reflux (VUR).
Older Children:
Diabetes.
Trauma.
Sexual intercourse (in females).
Epidemiology
Bimodal Peak Age Incidence: Infancy, 2-4 years.
Gender Ratio:
First 2 months: males > females.
2 months to 2 years: females > males.
4 years: females > males.
Clinical Presentation
Young Children (Infants and Pre-verbal):
Fever
Vomiting
Poor feeding
Lethargy
Irritability
Older Children:
Dysuria
Urinary frequency
Lower abdominal and loin pain
Diagnosis
Clinical Symptoms: Dysuria, frequency, loin pain.
Positive Urine Culture:
Urine bag: Not recommended due to high contamination rates.
Clean catch: >10^5 organisms/mL with pyuria/bacteriuria.
Catheterisation: 10% contamination rate.
Suprapubic aspiration: Gold standard with 1% contamination rate.
Urine Collection Methods:
Urine Bag: Adhesive plastic bag applied to perineum; used if all else fails.
Clean Catch (CCU or MSU): Stream of urine caught in a specimen jar; used if child can void on request.
Catheterisation (CSU): Mid-stream sample collected using an in/out catheter; used if unable to obtain CCU/MSU.
Suprapubic Aspiration (SPA): Needle inserted into the bladder under US guidance; used if child is unable to void.
Contamination Rates and Suitability:
Urine Bag: 50% contamination, not recommended (false positive rate 88-99%).
Clean Catch: 25% potential contamination.
Catheterisation: 10% potential contamination.
Suprapubic Aspiration: 1% contamination, gold standard.
Investigations
Initial Testing:
Infants and children presenting with unexplained fever of 38°C or higher should have a urine sample tested within 24h
Dipstick test in the urine: ‘leucocytes’ and ‘nitrites’ strongly suggests UTI
Urine should be sent for microscopy, culture, and sensitivity
In infants and children who are suspected to have acute pyelonephritis/upper UTI
In infants and children with a high to intermediate risk of serious illness
In infants <3mths
In infants and children with a positive result for leukocyte esterase or nitrite
In infants and children with recurrent UTI
In infants and children with an infection that does not respond to treatment within 24-48h, if no sample has already been sent
When clinical symptoms and dipstick tests do not correlate
Laboratory tests for localising UTI: CRP alone should not be used to differentiate acute pyelonephritis/upper urinary tract infection from cystitis/lower urinary tract infection
Imaging tests for localising UTI: routine use of imaging is not recommended
In the rare instances when it is clinically important to confirm or exclude acute pyelonephritis/upper urinary tract infection, power Doppler ultrasound is recommended
When this is not available or the diagnosis still cannot be confirmed, a dimercaptosuccinic acid (DMSA) scintigraphy scan is recommended
Treatment
Conservative:
For asymptomatic bacteriuria, improve hygiene, hydration, and bowel habits.
Medical:
Oral Antibiotics:
First Line: Trimethoprim or Trimethoprim-sulfamethoxazole.
Second Line: Cephalexin.
For non-severe UTI in infants >3 months.
IV Antibiotics:
Indicated for severe UTI, sepsis, or infants <3 months.
Antibiotics: Gentamicin with amoxicillin (or ampicillin), switch to oral when improving.
Specific Treatment for UTI:
Non-severe UTI in Infants >3 months:
Trimethoprim or Trimethoprim-sulfamethoxazole.
Cephalexin.
Severe UTI (e.g., sepsis, shock) or Infants <3 months:
Gentamicin with amoxicillin (or ampicillin).
Switch to oral when improving.
Special Considerations:
Circumcision: May lower the risk of UTIs; not routinely recommended but considered if recurrent UTIs.
Assess for Hypospadias: If indicated.
Follow-Up
Repeat Urine Culture: On completion of antibiotics.
Imaging: If <6 months, atypical UTI, or recurrent UTIs.
Specialist Follow-Up: For pyelonephritis, recurrent pyrexial UTIs, or known renal anomalies.
NICE Guidelines on Imaging Tests:
<6 Months:
Uncomplicated: USS as outpatient.
Atypical: Acute USS.
Recurrent: Acute USS, DMSA at 3 to 6 months after infection.
6 Months to 3 Years:
Uncomplicated: No imaging for the first episode.
Atypical: Acute USS.
Recurrent: Routine USS, DMSA at 3 to 6 months after infection.
3 Years:
Uncomplicated: No imaging for the first episode.
Atypical: Acute USS, nothing else if normal.
Recurrent: Routine USS.
CRP Testing:
Not recommended to differentiate acute pyelonephritis/upper UTI from cystitis/lower UTI.
Detailed Treatment Guidelines
Antibiotic Choices for Children
Trimethoprim 4mg/kg BD
Cefradine 25mg/kg BD
Cefalexin 25mg/kg BD
Co-amoxiclav 125/31 (1-6y/o), 5mL TDS
Co-amoxiclav 250/62 (7-12y/o), 5mL TDS
IV cefuroxime 25mg/kg 8-hourly
IV gentamicin 2.5mg/kg/dose 8-hourly
Antibiotic Treatment Duration
Cystitis: Oral antibiotics for 3-7 days.
Pyelonephritis: Oral antibiotics for 7-10 days or IV antibiotics for 2-4 days followed by oral antibiotics for a total duration of 10 days.
Follow-Up Imaging
<6 Months:
USS During Acute Infection: Yes for atypical and recurrent UTI.
USS Within 6 Weeks: Yes for uncomplicated.
DMSA 4-6 Months After Acute Infection: Yes for atypical and recurrent UTI.
Micturating Cystourethrography (MCUG): Yes for atypical and recurrent UTI.
6 Months to 3 Years:
USS During Acute Infection: Yes for atypical and recurrent UTI.
USS Within 6 Weeks: No.
DMSA 4-6 Months After Acute Infection: Yes for atypical and recurrent UTI.
MCUG: Yes for recurrent UTI.
3 Years:
USS During Acute Infection: Yes for atypical UTI.
USS Within 6 Weeks: No.
DMSA 4-6 Months After Acute Infection: No.
MCUG: Yes for recurrent UTI.
Prophylaxis
Oral Antibiotic Prophylaxis: May be needed and continued until investigations are complete.
Trimethoprim: 2mg/kg at night.
Nitrofurantoin: 1mg/kg.
Indications: Vesicoureteric reflux (VUR), recurrent UTIs (more than 2-3 episodes).
Additional Considerations from Uploaded Images
Diagnosis and Investigations:
Diagnosis is based on clinical symptoms and positive urine culture.
Clinical Symptoms: Dysuria, frequency, loin pain.
Positive Urine Culture: Varies depending on the method of collection:
Urine Bag: Adhesive plastic bag applied to perineum; if all else fails.
Clean Catch (CCU or MSU): Stream of urine caught in a specimen jar; child capable of voiding on request.
Catheterisation (CSU): Mid-stream sample collected using an in/out catheter; unable to obtain CCU/MSU sample.
Suprapubic Aspiration (SPA): Needle inserted into the bladder under US guidance; child unable to void on request.
Contamination Rates:
Urine Bag: 50% contamination, not recommended.
Clean Catch: 25% potential contamination from foreskin or reflux of urine into the vagina.
Catheterisation: 10% potential contamination.
Suprapubic Aspiration: 1% contamination, gold standard.
Positive Urine Culture:
Urine Bag: Not suitable due to high contamination rates.
Clean Catch: >10^5 organisms/mL clinically relevant organisms + pyuria/bacteriuria.
Catheterisation: >10^5 organisms/mL clinically relevant organisms + pyuria/bacteriuria.
Suprapubic Aspiration: Any growth of clinically relevant organisms + pyuria/bacteriuria.
DMSA = Technetium-99m-labeled dimercaptosuccinic acid scan of kidneys (for renal scarring from pyelonephritis)
Learning Points: Clinical Practice
Professional skills in growth and GI problems
Demonstrate the accurate measurement and charting of growth
Weighing Children Less Than 2 Years
Equipment:
Use a levelled pan scale, either high-quality electronic digital or beam balance.
Scale should weigh up to 20kg, in 5g (0.005kg) increments.
The tray needs to be large enough to support children up to 2 years of age.
Scales should be located on a stable, non-carpeted surface.
Clean the scales after every use.
Service the scale (including calibration) according to manufacturers’ guidelines.
Preparation:
Place a sheet/paper towel on the scale.
Child is undressed with the nappy removed.
Procedure:
Turn on scale and ‘tare’ to zero.
Place the baby in the center of the scale and ensure that weight is evenly distributed.
Weigh with parent/carer on a platform scale if unable to weigh alone. This can be done either using a scale which can be ‘zeroed’ after the parent/carer stands on them (a ‘taring’ scale) or by subtraction as follows:
Example:
Weigh the parent/carer and record weight = 60kg
Weigh the parent carer with child = 66.5kg
Difference is the weight of the child. e.g. 66.5-60 = 6.5kg
Recording:
Wait until the scales settle at a reading.
Record weight to the nearest 5g (0.005kg).
Make a note if the child is in plaster, harness, or any other item unable to be removed.
Plot the World Health Organization (WHO) weight-for-age growth chart.
Children less than 2 who can stand without assistance may be weighed on either infant or platform scales.
Include measurements and weight status description on relevant clinical documents such as discharge summaries and in the Child Personal Health Record where appropriate.
Weighing Children 2 Years and Over
Equipment:
Scales for weighing children can be either high-quality beam balance with movable weights, or high-quality electronic.
The scale should weigh in 100g (0.1kg) increments and can be ‘locked’ in.
The scale can be easily ‘zeroed’.
Scales should have a stable weighing platform, which is large enough to support the child.
Preparation:
Place the scale on a firm surface (not carpet).
Explain to the child that you are measuring their weight.
Make sure that any outer heavy clothing such as a coat, jacket, or jumper is removed. Light clothing can be worn.
Remove shoes and socks and ensure pockets are empty.
Procedure:
Turn the scales on and wait until they zero.
Ask the child to stand on the middle of the scales, look straight ahead, and stand still.
You may need to move them into the right position.
Check the child is not holding onto a wall or table; and arms are at their side.
Wait until the scales settle at a reading.
Bend down if necessary to read the scale at eye level.
Record weight to the nearest 100g (0.1kg).
Plot weight on the appropriate weight-for-age growth chart.
Include measurements and weight status description on relevant clinical documents such as discharge summaries, and in the Child Personal Health Record where appropriate.
Length Measurement for Children Less Than 2 Years
Equipment:
Length is measured in the recumbent position using an infantometer (infant length board or mat) designed for the purpose.
The measuring board or mat should have a firm, flat, horizontal surface with a fixed measure in 1mm (0.1cm) increments.
The device has a fixed head-board at right angles to the measuring board or mat, and a smoothly-moving foot-board perpendicular to the measuring board or mat.
Preparation:
Ask the child to remove their shoes and socks.
Procedure:
Ask the parent/carer to place the child on the length-board.
The child should be facing vertically upwards with the crown of the head firmly on the headboard.
Ensure the child’s body and pelvis are straight along the measuring device.
Parent holds the child’s head against the immovable headboard.
A second person straightens both of the child’s legs, holds the feet with toes pointing directly up, and moves the foot-board into position against the child’s feet.
Recording:
Record length to the nearest 1mm (0.1cm).
Plot length on the WHO length-for-age chart.
Record whether length or height/stature has been measured because length is greater than height/stature. If measuring length of a child over 2 years, subtract 0.7 centimeters from the length to convert it to height because length measurements are usually larger than height measurements by this amount.
Include measurements and weight status description on relevant clinical documents such as discharge summaries, and in the Child Personal Health Record where appropriate.
Height/Stature Measurement for Children 2 Years and Older
Equipment:
Height is measured in the standing position using a stadiometer (height measurer).
A stadiometer consists of a vertical board with an attached metric ruler with an easily moveable horizontal headboard that can be brought into contact with the most superior part of the head.
The equipment has a wide and stable platform, or firm uncarpeted floor as the base.
Equipment should be accurately and firmly mounted on a wall.
Ensure that fixed position devices have been installed correctly, and re-check after moving or re-location.
Should have an easy-to-read, stable metric ruler or digital readout in 1mm (0.1cm) increments.
Preparation:
Show the child the stadiometer and explain you are going to see how tall they are.
It can be helpful to measure the parent first if the child is hesitant.
Take the child over to the stadiometer and make sure they face away from the equipment.
Remove the child’s shoes and socks.
Procedure:
Position the child facing away from the stadiometer or wall with bare feet close together, legs straight, arms at side, and shoulders relaxed.
Ask the child to look straight ahead and take a big breath in and out to relax.
Double-check their position, making sure their knees are straight, heels on the floor, and head, shoulder blades, bottom, and heels are in contact with the stadiometer (height measurer) or the wall. Check that their arms are by their sides, and shoulders relaxed. Check that a horizontal line can be drawn from the lower border of the eye to the tragus, located over the ear canal.
Bring the measuring device down to rest on the child’s head.
Recording:
Record height to the nearest 1mm (0.1cm).
Plot height on the appropriate height-for-age growth chart.
Record whether height/stature has been measured because length is greater than height/stature.
Include measurements and weight status description on relevant clinical documents such as discharge summaries, and in the Child Personal Health Record where appropriate.
Determining Weight Status in Children
For Children Aged Up to 2 Years Old:
Appropriate interpretation of serial measurements on the weight-for-age and length-for-age growth charts will allow determination of the child’s weight status. For example:
If the percentile recorded on the weight-for-age chart is roughly the same as the
Demonstrate the key steps for evidence-based assessment of hydration status in children
Degree of Dehydration and Corresponding Clinical Features:
Clinical Feature | Mild Dehydration (<5%) | Moderate Dehydration (5-9%) | Shock (≥10%) |
---|---|---|---|
Conscious State | Alert and responsive | Lethargic, irritable | Reduced conscious state |
Heart Rate | Normal | Normal/mild tachycardia | Tachycardia |
Breathing | Normal | Increased respiratory rate | Increased respiratory rate, deep acidotic breathing |
Blood Pressure | Normal | Normal | Hypotension |
Skin Color | Normal | Normal | Pale or mottled |
Extremities | Warm | Warm | Cold |
Peripheral Pulses | Normal | Normal | Weak |
Eyes and Fontanelle | Not sunken | Sunken | Deeply sunken |
Mucous Membranes | Moist | Dry | Dry |
Skin Turgor | Instant recoil | Mildly decreased | Decreased |
Central Capillary Refill Time | Normal | Prolonged | Markedly prolonged |
Additional Clinical Features:
Clinical Feature | Minimal (<3%) | Mild to Moderate (3-9%) | Severe (>9%) |
---|---|---|---|
Mental State | Alert, well | Normal to irritable | Apathetic, lethargic |
Thirst | Normal, may refuse liquids | Thirsty | Drinks poorly |
Pulse | Normal and strong | Tachycardia | Tachycardia, weak |
Respiration | Normal | Tachypnoea | Tachypnoea and deep |
Capillary Refill | Normal (<2s) | Prolonged | Prolonged |
Skin Turgor | Normal | Recoil <2s | Recoil >2s |
Extremities | Warm peripheries | Cool peripheries | Cold, mottled, acrocyanosis |
Eyes and Fontanelle | Normal | Mildly sunken | Deeply sunken |
Oral Mucous Membranes | Moist | Dry | Parched |
Urine Output | Normal to reduced | Reduced | Minimal to anuric |
Measured Weight Loss or Percentage Dehydration:
5% dehydration = loss of 5mL of fluid per 100g body weight, or 50mL/kg or 10 x percent dehydrated/kg.
Deficit Calculation:
Calculated following an estimation of the degree of dehydration expressed as % of body weight.
Example: A 10kg child who is 5% dehydrated has a water deficit of 500mL.
The deficit is replaced over a time period that varies according to the child's condition. The rate of rehydration should be adjusted with ongoing assessment of the child.
Assessment Steps:
History:
Intake: Foods and fluids intake compared to normal.
Output: Urine and stool output compared to normal.
Excessive Loss: Vomiting, polyuria, diarrhea.
Recent Consumption: Intake of hypertonic or hypotonic fluids (e.g., diluted formula, lots of water, fortified feeds).
Risk Factors for Severe Dehydration and Electrolyte Disturbances:
Infants <6 months old.
GI issues (e.g., Hirschsprung, short gut syndrome, ileostomy, colostomy).
Cystic Fibrosis (CF).
Renal impairment.
Diuretic use.
Metabolic disorders.
Dehydration is especially dangerous in children with:
Congenital heart disease (especially if they have cardiac shunts).
Slow weight gain.
Immunocompromised.
Previous organ transplant.
Use of nephrotoxic medications.
Examination:
Vitals: Check vital signs.
Weight: Compare current weight with previous readings from the last two weeks.
Mucous Membranes: Assess for moisture.
Capillary Refill: Check time taken for capillary refill.
Skin Appearance and Turgor: Evaluate skin turgor and general appearance.
Investigations:
UEC: Check urea, electrolytes, and creatinine levels.
Blood Glucose Level: Assess blood glucose levels.
Additional Considerations:
Calculation of hydration status using clinical signs is typically inaccurate. However, a combination of examination findings is often utilized to assess hydration status.
"No single symptom or clinical sign reliably predicts the degree of dehydration" – NSW Health.
Weighing a child bare and comparing with previous readings from within the last two weeks is the most reliable measure, although this is not often available.
The most useful clinical signs are abnormal capillary refill time, abnormal skin turgor, and abnormal respiratory pattern. These can be used to guide a rough percentage loss:
Mild Dehydration (<4%): No clinical signs. May have increased thirst.
Moderate Dehydration (4-6%): Delayed CRT (>2 seconds), increased respiratory rate, and mild decreased tissue turgor.
Severe Dehydration (≥7%): Very delayed CRT (>3 seconds), mottled skin, other signs of shock (tachycardia, irritable or reduced conscious level, hypotension), deep, acidotic breathing, and decreased tissue turgor.
Other 'Signs of Dehydration':
Sunken eyes, lethargy, and dry mucous membranes may be considered in the assessment of dehydration. Although their significance has not been validated in studies, they are less reliable than the signs listed above.
Describe an evidence-based approach to the standards for paediatric IV fluid management (Clinical Practice Guidelines)
IV Fluid Content for Children (Excluding Neonates)
For Resuscitation/Bolus:
Fluid: 0.9% Sodium Chloride
Alternative (only under specialist direction): Other crystalloids (e.g., balanced salt solutions) or colloids may be used.
For Replacement Fluids (Dehydration or Ongoing Losses):
Fluid: 0.9% Sodium Chloride + 5% Glucose +/- Potassium Chloride 20mmol/L
Alternative (only under specialist direction): Plasma-Lyte148 + 5% Glucose
For Maintenance Fluids:
Fluid: 0.9% Sodium Chloride + 5% Glucose +/- Potassium Chloride 20mmol/L
Alternative (only under specialist direction):
0.45% Sodium Chloride + 5% Glucose +/- Potassium Chloride 20mmol/L
Plasma-Lyte148 + 5% Glucose
Note: If electrolytes are outside the normal range, discussion with a specialist is necessary.
IV Fluid Content for Neonates (<1 Month)
For Resuscitation/Bolus:
Fluid: 0.9% Sodium Chloride
For Replacement (Dehydration or Ongoing Losses) or Maintenance:
Special Care Nurseries:
Day 1: 10% Glucose
Day 2 Onwards:
0.225% Sodium Chloride + 10% Glucose +/- Potassium Chloride 10mmol/500mL (Special Care Nurseries)
0.45% Sodium Chloride + 10% Glucose (No Potassium Chloride) (Emergency Departments)
0.45% Sodium Chloride + 10% Glucose +/- Potassium Chloride 10mmol/500mL (Paediatric Wards)
Note: If electrolytes are outside the normal range, discussion with a specialist is necessary.
Detailed Guidelines for Paediatric IV Fluid Management
Resuscitation:
Indication: Shock
Fluid: 0.9% Sodium Chloride (NB: must write this in full)
Amount:
For infants and children (>28 days old): 20mL/kg bolus
For neonates (<28 days old): 10mL/kg bolus
Speed: Over 15-60 minutes
Maintenance:
Indication: Fasting or unable to tolerate oral fluids.
Fluid:
For infants and children (>28 days old): 0.9% Sodium Chloride + 5% Dextrose (+/- 20mmol/L Potassium Chloride).
For neonates (<28 days old):
Day 1: 10% Dextrose
Day 2 Onwards: 0.225% Sodium Chloride + 10% Dextrose (+/- 10mmol/500mL Potassium Chloride).
Amount:
For 1st 10kg: 100mL/kg/day (4mL/kg/hr)
For 2nd 10kg: 50mL/kg/day (2mL/kg/hr)
For every kg above 20kg: 20mL/kg/day (1mL/kg/hr)
Example Calculation:
33kg child:
Total fluid per day = 1000mL + 500mL + 20 * 13mL = 1760mL/day
Hourly rate = 40mL + 20mL + 13mL = 73mL/hour
Rehydration:
Indication: Dehydration
Fluid:
For infants and children (>28 days old): 0.9% Sodium Chloride + 5% Dextrose (+/- 20mmol/L Potassium Chloride).
For neonates (<28 days old):
Day 1: 10% Dextrose
Day 2 Onwards: 0.225% Sodium Chloride + 10% Dextrose (+/- 10mmol/500mL Potassium Chloride).
Amount:
Volume deficit = weight (kg) x deficit (%) x 10
Only replace a max of 5% per 24 hours due to the risk of cerebral or pulmonary edema.
Example: If 10% dehydrated, give 5% replacement per 24 hours over 48 hours.
Example Calculation:
22kg child with estimated 5% dehydration:
Maintenance = 1000mL + 500mL + 40mL = 1540mL/day
Replacement (5%) = 22kg x 5% x 10 = 1100mL/day
Total fluids = 1540 + 1100 = 2640mL/day
Hourly rate = 110mL/hour
Ongoing Losses:
Indication: Additional fluids may be required (i.e., beyond rehydration) if very high stoma/gut or renal losses.
Fluid: 0.9% Sodium Chloride
Amount:
Measure losses over 4-6 hours. Divide by the number of hours to find the hourly losses. Give this amount over the same timeframe in addition to other IV fluids.
Example: Child has stoma losses of 200mL over 4 hours. Give 50mL/hr of additional fluids for the next 4 hours.
Demonstrate communication of appropriate oral rehydration management
Criteria for Oral Rehydration Management:
Suitable for Intervention:
The patient has been assessed and triaged as category 4 or 5, and allocated to the waiting room.
The patient has vomiting, with or without diarrhea.
The child shows signs of dehydration consistent with mild dehydration.
Exclusion Criteria:
Abdominal distension
Bile-stained vomiting
Blood in vomitus or stool
Severe abdominal pain
Moderate to severe headache
Age less than 6 months
Respiratory distress
Moderate tachycardia or hypotension
Oral Rehydration Guidelines:
Appropriate Fluids for Rehydration:
Inappropriate Fluids: Lemonade, homemade oral rehydration solutions (ORS), and sports drinks.
Recommended ORS: Gastrolyte™, HYDRAlyte™, Pedialyte™.
Feeding and Hydration:
Stop any feed fortifications (e.g., extra scoops of formula, Polyjoule).
Encourage parents to use methods to help children drink (e.g., cup, icy pole, syringe), aiming for small amounts of fluid often.
Continue breastfeeding.
Early feeding (as soon as rehydrated) reduces stool output and aids gastrointestinal tract recovery.
Recommend returning to the usual diet once rehydrated.
If diarrhea worsens with formula feeding, consider temporary (2 weeks) use of lactose-free formula.
Trial of Oral Fluids in the Emergency Department:
Most children with mild/no dehydration can be discharged without a trial of fluids after appropriate advice and follow-up.
Aim for 10-20mL/kg fluid over 1 hour of ORS; give frequent small amounts.
Significant ongoing GI losses (frequent vomiting or profuse diarrhea) reduce the chance of successful rehydration at home.
Additional Causes of Vomiting to Consider:
Gastroenteritis: Common cause, but other causes should be ruled out.
Obstruction: Intussusception, volvulus.
Infection: Pneumonia, appendicitis, meningitis, urinary tract infection.
Raised Intracranial Pressure: Brain tumor.
Metabolic Disease: Diabetes.
Demonstrate charting oral rehydration and IV fluids for children
IV Fluids
Total fluid requirement = Maintenance + Replacement of deficit + Replacement of ongoing losses
Calculating fluid deficit
Deficit (mL) = Weight (kg) change (premorbid weight minus current weight) x 1000
g. a 10 kg child who now weighs 9.5 kg has a 500 mL water deficit and is 5% dehydrated
You need to replace the deficit over 24-48 hours
For children with ≤5% dehydration, replace deficit in the first 24 hours
For children with >5% dehydration, replace deficit more slowly. Give 5% in the first 24 hours and the remainder over the following 24 hours
Ongoing losses
Measure any ongoing loss and replace at the same rate it is lost
g. if there is a 200mL loss over 4 hours replace this by delivering 50mL/hr of fluids over the next 4 hours
GI losses are usually replaced with NaCl 0.9% + KCl 20mmol/L
Maintenance fluid rates
The preferred fluid type for IV maintenance is sodium chloride 0.9% with glucose 5%
Demonstrate appropriate history and examination in assessment of pain in children, including acute abdominal pain
History Taking:
General Information:
Age: of the child
SOCRATES: (Site, Onset, Character, Radiation, Associated symptoms, Timing, Exacerbating/relieving factors, Severity) for pain assessment
Recent Trauma: Assess for any recent trauma or injury
Past Medical History: Including immunizations, allergies, previous illnesses, surgeries
Prenatal and Birth History: Complications, Apgar score, NICU admission, term or preterm
Developmental History: Milestones, delays
Growth and Nutrition Status: Weight, height, dietary habits
Sleep Patterns: Normal sleep habits and changes
Gynecological History: (if applicable)
Family History and Social History: Conditions, family dynamics
GI-Specific History:
Stool Color and Character: Diarrhea, constipation, blood in stool
Vomiting: Frequency, color, presence of blood
Hematemesis: Presence of blood in vomit
Jaundice: Yellowing of skin/eyes
Abdominal Pain: Location, intensity, duration, radiation
Colic: Patterns of crying and discomfort
Appetite: Changes in eating habits
GU-Specific History:
Urinary Symptoms: Frequency, dysuria, hematuria, discharge
Abdominal Pain: Related to urination
Quality of Urinary Stream: Changes or difficulties
Polyuria: Increased frequency of urination
Previous Infections: History of UTIs or other infections
Facial Edema: Swelling around the face
Physical Examination:
General Inspection:
Alertness and Activity Level: How alert and active is the child?
Skin Color: Pallor, jaundice, cyanosis
Rash: Presence of any obvious rash
Healthy Weight: Does the child appear to be of a healthy weight?
Signs of Pain: Does the child look in pain?
Overall Appearance: Does the child look well or sick?
Genetic Condition Indicators: Stature, syndromic facial features
Position During Exam:
Parent’s Lap vs. Exam Table: Depending on the child's comfort
Order of Examination:
Least Distressing to Most Distressing: Use distraction as a valuable tool
Pediatric Assessment Triangle (PAT):
Appearance:
Tone, interactiveness, consolability, look/gaze, speech/cry
Work of Breathing:
Abnormal airway sounds, positioning, retractions, flaring
Circulation to Skin:
Pallor, mottling, cyanosis
Hands:
Finger Clubbing: Cystic fibrosis, liver disease, inflammatory bowel disease
Leukonychia: (whitened nail bed) – hypoalbuminaemia
Palmar Erythema: Liver disease, polycythaemia, Kawasaki disease, thyrotoxicosis
Peripheral Edema: Nephrotic syndrome, liver disease
Pulse Assessment: Radial pulse, femoral pulse in babies, assess rate and rhythm
Face:
Oedema: Nephrotic syndrome, liver disease
Pallor: Anemia
Conjunctival Pallor: Anemia
Scleral Icterus: Jaundice (hepatic pathology, hemolysis)
Aniridia: Wilm’s tumor, WAGR syndrome
Kayser-Fleischer Rings: Wilson’s disease
Neuroblastoma: Loss of the eye’s red reflex
Xanthelasma and Corneal Arcus: Hyperlipidaemia
Angular Stomatitis: Inflammation of mouth corners (iron or vitamin B12 deficiency)
Glossitis: Smooth tongue swelling with erythema (iron/B12/folate deficiency)
Aphthous Ulcers: Benign, Crohn’s disease, Bechet’s disease
Dental Caries: Neglect, gastroesophageal reflux disease
Macroglossia: Down’s syndrome, hypothyroidism, mucopolysaccharidoses, Beckwith-Wiedemann syndrome
Pigmentation/Polyps: Peutz-Jeghers syndrome
Lymph Nodes: Palpate cervical and supraclavicular lymph nodes – may indicate infection or malignancy
Abdomen:
Inspection:
Distension, caput medusae, spider naevi, hernia, drains/tubes/access
Palpation:
Tenderness (focal vs. generalized), rebound tenderness, guarding, rigidity, abdominal masses, distension, palpable feces
Percussion and Auscultation:
Assess for bowel sounds and other abnormalities
Special Techniques for Abdominal Exam:
Play Techniques: To elicit subtle guarding
"Can you jump up and down?"
"Blow out your tummy as big as you can, then suck it in as far as you can"
Specific Organ Examination:
Liver Palpation: Right upper quadrant for hepatomegaly or masses
Splenic Palpation: Left upper quadrant for splenomegaly
Kidneys: Bilateral palpation for masses
Ascites: Fluid wave test or shifting dullness
Auscultation: Bowel sounds, bruits
Genital Examination:
Penile and Scrotal Development: Hypospadias, chordee, descended testicles, scrotal swelling
Female Genital Examination: Confirm external genitalia normalcy
Rectal Examination:
Indicated Situations: Confirm anus looks normal and patent, assess for tags, prolapse, staining of underwear
Lower Limbs:
Inspection: Ankle edema (nephrotic syndrome/liver disease)
History of Presenting Complaint:
Site:
RLQ pain suggests appendicitis
Epigastric pain suggests peptic ulcer disease
Diffuse pain may indicate perforation or peritonitis
Onset:
Gastroenteritis lasting >10 days suggests parasitic or non-infectious cause
Recurrent, self-resolving episodes of pain characteristic of biliary colic
Sudden-onset flank pain may indicate nephrolithiasis or pyelonephritis
Character:
Peptic ulcer disease pain is dull, appendicitis is sharp/stabbing
Radiation:
Abdominal pain radiating to the back suggests cholecystitis or pancreatitis
Associated Symptoms:
Fever, nausea, vomiting, diarrhea (gastroenteritis)
Jaundice (viral hepatitis)
Blood in stool (ulcerative colitis)
Blood or bile in vomitus (small bowel obstruction)
Genitourinary symptoms: dysuria, frequency, hematuria (UTI)
Timing:
History of trauma: blunt or penetrating, accidental or non-accidental
Exacerbating or Relieving Factors:
Movement, food, medication
Severity:
Assess using pain scales appropriate for the child's age
Past Medical History:
Previous Conditions:
Operations, medication use, immunizations, allergies, and current comorbidities
Conditions like sickle cell disease, cystic fibrosis, spina bifida, developmental delay, cerebral palsy, splenic infarction, recent or current URTI
Potential Complications Causing Abdominal Pain:
Hirschsprung Disease:
Enterocolitis
Cystic Fibrosis:
Abdominal distension, bloody diarrhea, electrolyte disturbances
Liver Disease/Ascites:
Primary bacterial peritonitis
Nephrotic Syndrome:
Pancreatitis
VP Shunt:
Pancreatitis
Chemotherapy:
Pancreatitis
Immunocompromised:
Toxic megacolon
Sickle Cell Disease:
Vaso-occlusive crisis
Family and Social History:
Family History:
Risk factors for inflammatory bowel disease, nephrolithiasis
Social History:
Travel history to developing countries, dietary habits, family dynamics, social and psychiatric history, sexual history in reproductive-age females
Examination Techniques:
Comprehensive Physical Examination:
Including vital signs, abdominal examination, checking for non-abdominal causes
Observation:
Child's movements, gait, position, level of comfort
Pelvic Examination:
Reserved for sexually active adolescents
Abdominal Examination:
Thorough inspection, palpation, percussion, and auscultation.
Describe the evidence-based approach to managing abdominal pain in children (Clinical Practice Guidelines)
General Management of Abdominal Pain
Fluid Resuscitation: May be required in cases of dehydration or shock.
Analgesia: Provide pain relief based on the severity of the pain (see detailed table below).
NPO (Nil Per Os): Keep the child fasting, especially if surgical intervention is being considered.
Consider NG Tube: If bowel obstruction is suspected.
Early Referral: If surgical or gynecological management may be required.
Analgesic Options Based on Pain Severity
Pain Severity | Analgesic | Route |
---|---|---|
Mild to Moderate Pain | Sucrose | Oral |
Paracetamol | Oral, PR (per rectum), IV | |
Ibuprofen | Oral | |
Moderate to Severe Pain (in addition to the above) | Oxycodone | Oral |
Morphine | IV, subcutaneous | |
Fentanyl | Intranasal | |
Tramadol | Oral, IV |
Assessment and Monitoring
Repeated Examination: To look for persistence or evolution of signs and to evaluate the response to treatment.
Pain Assessment Tools:
Wong-Baker FACES Pain Rating Scale: For children 3 years and older.
FLACC Scale: Face, Legs, Activity, Cry, Consolability for behavioral observation.
Neonatal Infant Pain Scale (NIPS): For infants.
Common and Time-Critical Causes of Abdominal Pain by Age
Age Group | Causes |
---|---|
Neonates | Hirschsprung enterocolitis, Incarcerated hernia, Intussusception, Necrotizing enterocolitis, Volvulus |
Infants/Children | Abdominal trauma, Appendicitis, Constipation, Gastroenteritis, Incarcerated hernia, Intussusception, Meckel diverticulum, Mesenteric adenitis, Ovarian torsion, Pyloric stenosis, Testicular torsion, Volvulus |
Adolescents | Appendicitis, Abdominal trauma, Cholecystitis, Cholelithiasis, Constipation, Ectopic pregnancy, Gastroenteritis, Inflammatory bowel disease, Ovarian cyst - torsion/rupture, Pancreatitis, Pelvic Inflammatory Disease, Renal calculi, Testicular torsion |
Important Non-Abdominal Causes to Consider
Diabetic ketoacidosis (DKA)
Headache (Migraine)
Henoch-Schonlein Purpura
Hip pathology
Pneumonia
Psychological factors
Sepsis
Sexually transmitted infections
Sickle Cell Disease (vaso-occlusive crisis)
Toxin exposure or overdose
Urinary Tract Infection (UTI)/Pyelonephritis
Investigations
Most children need no investigations.
Investigations may include:
Urine analysis: (+/- culture, +/- pregnancy test if indicated)
Electrolytes +/- Liver Function Tests (LFTs)
Lipase: For pancreatitis
Venous blood gas
Blood sugar: For DKA
Imaging:
Abdominal X-Ray (AXR): If obstruction is suspected.
Chest X-Ray (CXR): If pneumonia is suspected.
Ultrasound: After discussion with senior staff, appropriate for suspected ovarian torsion or intussusception.
Treatment
Fluid Resuscitation: May be required.
Analgesia:
Mild Pain (Pain Score 1-3, NIPS Score 1-2): Oral paracetamol and/or ibuprofen.
Moderate Pain (Pain Score 4-6, NIPS Score 3-4): Oral paracetamol or ibuprofen and oral oxycodone.
Severe Pain (Pain Score 7-10, NIPS Score 5-7): Oral paracetamol or ibuprofen and intranasal fentanyl or oral oxycodone or IV morphine.
Opioid and Non-Opioid Analgesia
Non-Opioid Analgesia:
AnGel/EMLA
Paracetamol
NSAIDs (e.g., ibuprofen, ketorolac)
Tramadol
Local anesthesia blocks
Opioid Analgesia:
Oral: Morphine/MS Contin, Oxycodone IR/oxycontin SR
IV: Morphine, Fentanyl, Hydromorphone
Additional Management Considerations
Keep children fasting: Consider enteral or intravenous fluids if assessment or diagnosis is delayed (consult local fasting guidelines).
Early referral: For possible diagnoses requiring surgical or gynecological management.
Consider a nasogastric tube: If bowel obstruction is suspected.
Describe the key features for recognising a presentation of Diabetic Ketoacidosis in children
Overview
Diabetic ketoacidosis (DKA) in children is a critical medical emergency requiring immediate hospital admission.
It primarily occurs in children with type 1 diabetes but can also be seen in type 2 diabetes under stress conditions.
Pathophysiology
Decrease in Effective Circulating Insulin: This is associated with elevations in counter-regulatory hormones (glucagon, catecholamines, cortisol, growth hormone).
Hyperglycemia: Increased glucose production by the liver and kidney and impaired peripheral glucose utilization.
Hyperosmolality: Due to high blood sugar levels.
Lipolysis: Increased fat breakdown leading to the production of ketone bodies (beta-hydroxybutyrate, acetoacetate).
Acidosis: Metabolic acidosis from ketone bodies.
Osmotic Diuresis: Leads to dehydration and electrolyte imbalances.
Ketoacid Accumulation: Causes nausea, vomiting, and exacerbation of dehydration.
Major Complications:
Clinical Features
History: Weight loss, abdominal pain, vomiting, polyuria, and polydipsia.
Examination:
Dehydration
Kussmaul breathing (deep and laboured), chest pain
Altered level of consciousness (due to cerebral oedema - occurs in severe DKA)
Abdominal pain and vomiting
Hx of polyuria and polydipsia
Hx of nocturnal enuresis (bed wetting)
Hx of weight loss
Precipitants
Inadequate Insulin: In known diabetics (e.g., missed doses, pump failure).
First Presentation of Type 1 Diabetes Mellitus.
Illness: Such as infections (e.g., pneumonia, UTI), surgery, or trauma.
Diagnostic Criteria
Serum Glucose > 11 mmol/L
Venous pH < 7.3 or Bicarbonate < 15 mmol/L
Presence of Ketonaemia/Ketonuria
Severity Assessment
Mild: Venous pH < 7.3, Bicarbonate < 15 mmol/L
Moderate: Venous pH < 7.2, Bicarbonate < 10 mmol/L
Severe: Venous pH < 7.1, Bicarbonate < 5 mmol/L
Investigations
Urine Analysis: To check for ketonuria and glucose.
Blood Tests: Serum glucose, electrolytes (UEC), liver function tests (CMP), venous blood gas (VBG), blood ketones, full blood count (FBC), HbA1c, and septic workup if infection is suspected.
Imaging: May include chest X-ray if pneumonia is suspected, abdominal X-ray if bowel obstruction is suspected, and ultrasound if indicated for other conditions.
Management
Goals:
Correct Dehydration
Reverse Ketosis, Correct Acidosis, and Glucose Levels
Monitor for Complications: Cerebral edema, hypoglycemia, hypo/hyperkalemia.
Identify and Treat Precipitating Causes
Supportive Measures and Monitoring:
Nurse Head Up: To prevent aspiration.
Airway Monitoring: Especially in children with reduced consciousness.
NPO (Nil Per Os): Until the child is alert and acidosis resolves.
IV Access: For fluid and insulin administration.
Neurological Observations: To monitor for cerebral edema.
Cardiac Monitoring: For electrolyte disturbances (e.g., hyperkalemia, hypokalemia).
Antibiotics: If febrile, after obtaining cultures.
Urinary Catheterization: For strict fluid balance in unconscious children.
Fluid Resuscitation:
Initial Bolus: 10 mL/kg 0.9% sodium chloride for children with tachycardia and delayed capillary refill.
Potassium Management: Add potassium to fluids if serum potassium < 5.5 mmol/L and child is passing urine.
Glucose Addition: Once blood glucose levels drop to 15 mmol/L, switch to 0.9% sodium chloride with 5% glucose and potassium chloride.
Insulin Therapy:
Infusion: Start with 0.1 units/kg/hour (0.05 units/kg/hour in specific cases).
Transition to Subcutaneous Insulin: Once the child is alert and stable.
Monitoring for Complications:
Cerebral Edema: Symptoms include headache, vomiting, altered consciousness, and rising blood pressure. Managed with mannitol infusion or hypertonic saline.
Hypoglycemia: Managed with glucose infusion.
Electrolyte Imbalances: Managed based on regular monitoring and adjustments.
Timeline of Monitoring and Management:
Demonstrate patient assessment leading to the recognition of serious illness using A-G assessment
A - Airway
Is the airway patent?
Signs of Airway Obstruction: Look for chest and abdomen rising and falling alternately and vigorously.
Skin Color: Is it blue or mottled?
Noises of Obstruction: Listen for snoring, expiratory wheezing, or gurgling.
Additional points for detailed airway assessment:
Facial Fractures: Look for signs.
Contaminants: Check for blood, vomit, or teeth in the mouth/airway.
Epistaxis: Note any nosebleeds.
Examine the Anterior Neck:
Tracheal deviation
Wounds
Subcutaneous emphysema
Laryngeal tenderness/crepitus
Venous distension
Esophageal injury (unlikely if the child can swallow easily)
Carotid hematoma/bruits/swelling
Management of Airway Obstruction:
Positioning: Age-appropriate positioning of the head into a neutral position (use a thoracic elevation device if <8 years old or a towel under the shoulder blades).
Suction: Gentle suction to remove blood/vomit/secretions.
Oxygen: Apply high-flow oxygen.
Jaw Thrust: Avoid head-tilt or chin lift.
Airway Devices: Use an oropharyngeal airway if tolerated, or a nasopharyngeal airway (if head injury is excluded/unlikely).
Intubation: To be performed by an experienced operator.
Cervical Spine Protection: Manual in-line stabilization, followed by the application of a properly fitted hard collar, sandbags, and strap.
B - Breathing
Observation: Look, listen, and feel.
Oxygen Saturation: Measure.
High-Flow Oxygen: Apply to all spontaneously breathing patients (10-15L O2 via a non-rebreather mask).
Work of Breathing: Check for recession, respiratory rate, and accessory muscle use.
Effectiveness of Breathing: Assess oxygen saturation, symmetry and degree of chest expansion, and breath sounds.
Effects of Inadequate Respiration: Check heart rate and mental state.
Signs of Injury: Look for seat belt marks, bruising, and wounds.
Thoracic Cage Assessment: Feel for emphysema/crepitus and clavicle/chest wall tenderness.
CXR: Request if needed.
C - Circulation
Pulse Rate: Check.
Skin Color and Temperature: Assess.
Capillary Refill Time: Measure.
Blood Pressure: Sometimes check.
Peripheral Skin Temperature: Measure.
Body Temperature: Measure.
Effects of Inadequate Circulation: Increased respiratory rate and decreased mental state.
IV Access: Establish with two large cannulae.
Intra-Osseous Needle: Consider if IV access is not quickly established.
Blood Tests: Take blood for BSL, FBC, crossmatch.
Fluid Bolus: Give 20mL/kg of normal saline if circulation is inadequate.
Tamponade: For any continuing external hemorrhage.
Repeat Fluid Bolus: If circulation remains unstable, using normal saline or colloid solution.
Packed Cells: Consider if a third bolus is necessary, and arrange early surgical intervention.
D - Disability
Level of Consciousness: Initial assessment using AVPU (Awake, Voice, Pain, Unresponsive).
Formal GCS Assessment: If AVPU shows impairment.
Pupil Response: Check reaction to light.
Movement in Limbs: Assess and check reflexes where possible.
BSL: Measure on arrival and periodically.
E - Exposure/Environment
Remove Clothing: To check for any obvious life-threatening injury.
Avoid Hypothermia: Limit exposure of the body and warm all ongoing fluids.
F - Fluids
Fluid Charts: Monitor fluid input and output.
Patient’s Urine: Check if available.
Skin Turgor: Assess for hydration status.
G - Glucose
Rapid Finger Prick: To check for hypoglycemia.
Further Information and Family and Friends
Gather Additional Information: From drug charts, medical notes, investigation results, friends, and relatives.
Social Assessment: Determine the patient’s next of kin or close relatives, living situation, and access to the building.
Goals
Patient Goals: Establish both short-term and long-term goals for the patient.
Monitoring Plan: Develop a plan for continuous monitoring.
Describe the patient monitoring and process of the Between the Flags model, and the Paediatric CERS and Escalation Matrix
Between the flags model
The standard observation charts have 3 colour-coded zones:
Blue zone = criteria for which increasing the frequency of observations and/or increased vigilance is required.
Yellow zone = clinical review required.
Red zone = rapid response call is required.
In paediatrics, observations are taken 6 times per day at 4 hourly intervals.
A newborn’s vitals must be taken before leaving the birthing environment.
Frequency of assessment is to be increased above the minimum requirements when:
The patient’s vital sign observations fall within a coloured zone on a standard observation chart
Assessment identifies other signs and symptoms of deterioration
A CERS call has been made.
Paediatric CERS
CERS = Clinical Emergency Response Systems
CERS refers to a health service/facility’s response to a deteriorating patient within its care.
The main components include:
Clinical review - respond within 30 minutes to a breach in clinical review criteria.
Rapid response - immediately in response to breach in the rapid response criteria.
Escalation Matrix
The Escalation Matrix determines local criteria that are a best fit for the organisation’s context and services.
It allows for a unified approach to levels of escalation across the facilities and LHD.
Demonstrate appropriate charting patient observations in children (use of BTF in SPOC charts)
Learning Points: Health society and environment
List the public Health notifiable infectious illness in children and describe the rationale and process for reporting
List of Public Health Notifiable Infectious Illnesses in Children
All notifiable diseases can be found in the Public Health Act 2010 No 127. Below are some of the most relevant preventable diseases which are mandatory for reporting in schools and daycare centers:
Diphtheria
Mumps
Poliomyelitis
Haemophilus influenzae Type b (Hib)
Meningococcal disease
Rubella ("German measles")
Measles
Pertussis ("whooping cough")
Tetanus
Gastroenteritis (among people of any age in an institution, foodborne illness in two or more related cases)
Rationale for Reporting
Prevent Spread of Infectious Diseases: Enables public health units to take immediate action to control and prevent the spread of infectious diseases.
Protect Community Health: Reporting helps in safeguarding the community by ensuring that outbreaks are contained.
Identify Disease Patterns: Assists in identifying patterns of disease spread and potential patient zero, which is crucial for effective outbreak management.
Improve Healthcare Policy: Provides data that helps in the formulation and improvement of healthcare policies and standards.
Uphold Healthcare Standards: Ensures compliance with public health standards and protocols.
Process for Reporting
Complete the NSW Health Communicable Diseases Notification Form:
Fill out the form with all relevant information about the case.
Submission:
Send the completed form to the local Public Health Unit (for example, Hunter New England LHD - Wallsend).
Immediate Phone Notification:
Some diseases require immediate phone notification, which is indicated by a phone icon on the form. This ensures prompt action is taken for highly contagious or severe diseases.
Detailed Steps in Disease Reporting
Identification of a Notifiable Disease:
Once a notifiable disease is identified, healthcare providers must report it to the public health authorities.
Form Completion:
Complete the NSW Health Communicable Diseases Notification form accurately with details such as patient information, disease specifics, and any relevant clinical information.
Sending the Form:
The completed form must be sent to the appropriate local Public Health Unit. This can be done through various means, including electronic submission, fax, or mail.
Phone Notification:
For certain diseases, an immediate phone call to the public health unit is required. This is to ensure that the authorities can take swift action to manage and control the spread of the disease.
Follow-Up:
The public health unit may follow up with the reporting entity for additional information or to provide further instructions on managing the case and preventing further spread.
Describe the societal and environmental influences on growth and nutrition
Societal Influences
Cost:
The cost of food and the ability to purchase it are primary determinants of food choice.
Low-income groups are reported to consume more unbalanced diets and have a lower intake of fresh fruits and vegetables due to financial constraints.
Social Class:
Higher social classes are associated with higher intakes of fruits, lean meats, oily fish, and wholemeal foods compared to lower social classes.
Economic disparities influence the quality and variety of food available to different social classes.
Social Context:
Peer Influences: Individuals, especially children and adolescents, are influenced by their peers' eating habits and preferences.
Parental Influences: Parents play a critical role in shaping their children's dietary habits through the foods they provide and their own eating behaviors.
Family Eating Practices: Regular family meals and shared eating practices can promote healthier eating habits.
Social Norms: Societal norms and cultural expectations can impact food choices and dietary practices.
Cultural Factors:
Cultural background influences food preferences, methods of preparation, and religious practices related to food.
Different cultures have unique dietary practices that can affect nutritional status and health outcomes.
Environmental Determinants
Access and Availability:
The availability of food and access to transportation can significantly influence dietary choices.
"Food deserts" are areas with little to no access to shopping facilities that provide fresh, healthy food, leading to reliance on processed and unhealthy food options.
Education, Knowledge, and Skills:
A lack of cooking skills can inhibit families from preparing fresh, healthy meals.
Education level is linked to better eating habits, as higher education often correlates with greater nutritional knowledge and healthier food choices.
Parents' ability to pass on cooking skills and nutrition education to their children is crucial for promoting long-term healthy eating habits.
Time Constraints:
Increasing numbers of dual-income families and longer working hours make it challenging to find time for preparing healthy meals.
Time constraints often lead to reliance on convenience foods, which are typically less nutritionally dense and can contribute to poor dietary choices.
Parental Monitoring and Motivation:
Parents' ability to monitor their children's growth and diet is essential for ensuring proper nutrition and preventing malnutrition or obesity.
Parental motivation and behavioral capability to encourage and provide healthy diets for their children play a significant role in shaping their children's eating habits and overall health.
Describe the population health strategies employed for weight management in Children
Policies Influencing Food Environments
Marketing Restrictions:
Unhealthy Foods and Beverages: Strong links exist between TV advertising and children's food knowledge, preferences, purchase requests, and consumption patterns. Policies aim to limit the marketing of unhealthy foods to children.
Food Taxes and Subsidies:
Economic Measures: Implementing taxes on unhealthy foods and providing subsidies for healthier options like fruits and vegetables. Evidence shows that price has a significant effect on consumption choices.
Initiatives Promoting Healthy Foods:
Fruit and Vegetable Initiatives: Programs aimed at increasing the consumption of fruits and vegetables among children.
Other Food Policies: Includes restrictions on trans-fatty acids and policies ensuring healthy food service options in government institutions.
Policies Influencing Physical Activity Environments and Social Marketing
Physical Activity Recommendations:
WHO Guidelines: Children aged 5-17 should accumulate at least 60 minutes of moderate to vigorous intensity physical activity daily.
Social Marketing Campaigns:
Media Campaigns: Use of both paid and non-paid forms of media to increase knowledge and change attitudes towards diet and physical activity. Campaigns typically target both nutrition and physical activity behaviors.
National and Regional Initiatives
Australian Dietary Guidelines:
Dietary Advice: Provides up-to-date advice on the types and amounts of foods that should be consumed for health and wellbeing. Recommendations are based on scientific evidence.
Health Star Rating System:
Nutritional Labelling: A front-of-pack labelling system that rates the overall nutritional profile of packaged food from ½ a star to 5 stars, helping consumers make healthier choices.
Healthy Food Partnership:
Collaborative Efforts: A mechanism for the government, public health sector, and food industry to tackle obesity, encourage healthy eating, and empower food manufacturers to make positive changes.
Australia’s Physical Activity & Sedentary Behaviour Guidelines:
Guidance on Exercise: Provides guidelines on the duration and intensity of physical activity and sedentary behavior for different age groups to benefit overall health and wellbeing.
Clinical Practice Guidelines Portal:
Access to Guidelines: Provides access to clinical practice guidelines that have been adapted to the Australian context, ensuring relevance and applicability to local practice.
Healthy Weight Guide:
Information Resource: A comprehensive source of information developed by the Australian Government on how to achieve and maintain a healthy weight, based on recent Australian and international research.
Girls Make Your Move Campaign:
Inspiration for Physical Activity: Aims to inspire, energize, and empower young women to be more active through physical activities and sports.
These comprehensive strategies aim to create supportive environments for children, promoting healthy eating habits and physical activity to manage weight and prevent obesity.
Aboriginal & Torres Strait Islander Health:
What are some factors that contribute to higher prevalence of growth restriction and lower nutrition status of Aboriginal and Torres Strait Islander children?
Socio-Economic Factors
Income:
Indigenous Australians are significantly more likely to experience food insecurity due to financial constraints. They are seven times more likely to go without food in the previous 12 months compared to non-Indigenous Australians.
Poverty often leads to maximizing calories per dollar spent, which typically results in lower nutritional quality as nutritious plant-based diets can be expensive.
Socio-Economic Disadvantage:
Lower socioeconomic status impacts the ability to afford and access nutritious food.
Socio-economic disadvantage also affects other areas of life, including housing, education, and employment, which in turn impact nutritional status and growth.
Health and Lifestyle Factors
Smoking During Pregnancy:
There is a strong relationship between smoking during pregnancy and low birthweight, which is a factor for growth restriction.
Smoking and other harmful behaviors during pregnancy, such as excessive alcohol consumption, contribute to poor prenatal health and low birthweight.
Maternal Health:
Factors such as maternal age, illness during pregnancy, low socioeconomic status, multiple pregnancies, and poor antenatal care can contribute to low birthweight and growth restriction.
Geographical and Environmental Factors
Food Security and Access:
Food security is a significant issue, particularly in rural and remote areas where access to fresh and nutritious food is limited.
Issues of supply and availability of food in remote communities lead to reliance on less nutritious, processed foods.
Geographical Isolation:
Remote and rural locations often have limited access to healthcare and support services, which can impact prenatal and postnatal care and subsequently children's growth and nutrition.
Housing and Infrastructure:
Overcrowding in housing and lack of appropriately designed and maintained homes can hinder safe storage, preparation, and consumption of food.
Poor housing conditions and infrastructure contribute to an unhealthy living environment that affects overall health and nutrition.
Cultural and Social Factors
Cultural Food Values:
Traditional dietary practices and cultural food preferences may not always align with modern nutritional guidelines, leading to potential gaps in nutritional intake.
Cultural practices around food preparation and consumption are significant in understanding the nutritional status of Indigenous children.
Education and Literacy:
Low levels of education, particularly in nutrition and food literacy, contribute to poor dietary choices.
Lack of knowledge and skills in preparing nutritious meals impacts food choices and overall nutrition.
Social Factors:
Social norms and family practices around food and eating can influence children's nutritional status.
Peer influences and family eating practices play a role in shaping dietary habits.
Health Disparities
High Rates of Low Birthweight (LBW):
Aboriginal and Torres Strait Islander babies are 2.5 times more likely to be born with low birthweight compared to non-Indigenous babies. This is often due to preterm birth or intrauterine growth restriction.
Contributing factors include poor maternal nutrition, inadequate prenatal care, and higher rates of maternal smoking and alcohol use.
Chronic Diseases:
Poor nutrition contributes to higher rates of chronic diseases such as obesity, cardiovascular disease, type 2 diabetes, and tooth decay.
These conditions are exacerbated by the high prevalence of over-nutrition and under-nutrition among Indigenous populations.
Health Inequities:
Five out of the seven leading factors contributing to the health gap between Indigenous and non-Indigenous Australians (obesity, high blood cholesterol, alcohol, high blood pressure, and low fruit and vegetable intake) are related to poor diet.
What are some of the strategies currently used by the Australian government to address factors affecting growth and nutritional status of Aboriginal and Torres Strait Islander children?
National and Community-Based Programs
General Australian Government Department of Health Programs:
Various programs contribute to the prevention and management of diet-related disorders among Aboriginal and Torres Strait Islanders at a national level.
Since the expiration of the National Aboriginal and Torres Strait Islander Nutrition Strategy and Action Plan (NATSINSAP) 2002-2010, there has been no national coordination of nutrition efforts.
Community-Based Nutrition Programs:
Effective programs adopt a multi-strategy approach, addressing both food supply (availability, accessibility, and affordability) and demand for healthy foods.
Community involvement is crucial in all stages of program initiation, development, implementation, and evaluation to ensure cultural appropriateness and tailored interventions.
Food Supply Improvement Programs:
Focus on food retail outlets, local food production (e.g., school or community gardens), food provided by community organizations, and food aid.
Community store nutrition policies play a significant role in influencing food supply and dietary intake in remote areas.
Nutrition Education:
While alone it may not improve food security or dietary intake, it is effective when combined with strategies such as cooking programs, peer education, budgeting advice, and group-based lifestyle modification programs.
Support for Nutrition Workforce:
A well-supported, resourced, and educated Aboriginal and Torres Strait Islander nutrition workforce is essential for successful nutrition interventions.
Specific Government Initiatives and Funding
Better Start to Life Approach:
$94 million over three years from July 2015, aimed at expanding efforts in child and maternal health.
Includes $54 million for increasing sites providing New Directions: Mothers and Babies Services, offering antenatal care, parenting advice, and health checks for children.
$40 million to expand the Australian Nurse–Family Partnership Programme (ANFPP), improving pregnancy outcomes and supporting child health and development.
National Aboriginal and Torres Strait Islander Nutrition Strategy and Action Plan (NATSINSAP):
Key achievements in food supply in remote and rural communities, disseminating good practice, and developing a nutrition workforce.
Examples include Remote Indigenous stores and takeaways resources, nationally accredited nutrition training materials for Indigenous health workers, and the revival of the National Nutrition Networks conference.
Aboriginal and Torres Strait Islander Guide to Healthy Eating:
Educational resources to support healthy dietary choices.
Health Star Rating System:
Launched in December 2014 to help consumers make more nutritious choices when purchasing packaged foods.
Campaigns include specific media targeting Indigenous communities.
Healthy Bodies Need Healthy Drinks Resource Package:
Launched in 2014, culturally appropriate materials encouraging school-aged children and their families to choose water over high-sugar drinks to prevent obesity, chronic disease, and dental caries.
Implementation Plan for the National Aboriginal and Torres Strait Islander Health Plan 2013–2023:
Recognizes the importance of addressing social and cultural determinants of health contributing to poor dietary choices and health outcomes through coordinated whole-of-government action.
State and Territory Initiatives
Move Well Eat Well Program in Tasmania:
Operates in primary schools and early childhood settings to improve policies and practices supporting nutrition and physical activity.
Resources
Aboriginal and Torres Strait Islander Health performance framework 2017 report
https://www.pmc.gov.au/sites/default/files/publications/indigenous/hpf-2017/tier2/219.html#important
Learning Points: Professional Development
Demonstrate discharge summary documentation and communication to parents of sick child via examples of dehydration or abdominal pain
Demonstrate communication and escalation using the ISBAR model