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Multiple sclerosis etiology
- unknown cause
- unlikely related to a single cause
- genetics and environmental related to infectious, immunologic, and genetic factors
- precipitating factors can turn on MS in someone with a genetic disposition
- precipitating factors: infection, smoking, physical injury, emotional stress, excessive fatigue, pregnancy, and a poorer state of health
Multiple sclerosis classification scheme
Relapsing-remitting
- clearly defined relapses with full recovery or minimal residual
- 80+% are diagnosed with this type of relapse
Primary-progressive
- accumulation of disease
- no distinct relapse or recovery
- 10% of MS
Secondary-progressive
- start with relapse-remitting
- there is also progression
- 50% of patients diagnosed with relapse-remitting develop this within 10 years
Clinically isolated syndrome (CIS)
- episode that is indicative of MS
- clinical episode with symptoms similar to MS
Multiple sclerosis diagnosis
- no definitive diagnostic test
- based on: history, clinical manifestations, and results of imaging studies
- diagnosis of exclusion
Imaging and tests that can assist in diagnosis
- MRI
- CSF analysis
- evoked potentials: electrical events generated in by peripheral stimulation of a sensory organ to measure response time (somatosensory, visual, or brainstem auditory) (patients with MS have delayed visual response 50-90% of the time)
3 Criteria for Diagnosis
- lesions in 2 different locations
- damage/attack interval (usually a month apart)
- rule out
Multiple sclerosis clinical manifestations
Motor
- weakness or paralysis
- double vision
- scanning speech
- muscle spasticity (interferes with speech and gait)
Sensory
- Lhermitte's sign: electrical shock radiating down spine and neck
- numbness
- tingling
- blurred vision
- dizziness (vertigo)
- loss of balance
- patchy blindness
- reticular nerve root pain
Cerebellar
- nystagmus
- involuntary eye movement
- ataxia
- dysarthria
- dysphagia
- difficulty swallowing
Fatigue
- increased energy needs
- heat
- decreased fluids
Bowel and Bladder
- constipation
- spastic bladder: possible dribbling or incontinence
- flaccid bladder
Sexual dysfunction
- erectile dysfunction
- decreased libido
- decreased vaginal lubrication
- pain during intercourse
Emotional changes
Cognition
- 50% may experience short-term conversational or planning issues
Multiple sclerosis pseudo relapse
- also known as pseudo-exacerbation or pseudo-flare
- common triggers: stress, fatigue, illness, and heat
- not causing new damage
- very distressing to patients
- treat underlying cause
Impact of Pregnancy on a Patient with Multiple Sclerosis
- pregnancy can exacerbate symptoms and progression
goals of disease modifying therapy
- decrease relapse rate
- slower accumulation of brain lesions on MRI
- will not heal scarring
- may not improve current functioning
- may have some effect on progression
Adjunctive pharmacologic treatment for multiple sclerosis
- acute exacerbations: glucocorticoids (methylprednisolone, prednisone, etc.) (reduces edema at the site of demyelination) and plasma exchange (for a bad reaction to glucocorticoids)
- anticholinergics: treating bladder symptoms, increasing the amount of urine that can be held
- CNS stimulants for fatigue
- muscle relaxants for spasticity
- nerve conduction enhancer - improves walking speed (cautioned in CKD and seizure disorder)
- tricyclic antidepressants for chronic pain
- antispasmodics for spasticity (baclofen)
- anti seizure for chronic pain
Functional limitation in patients with multiple sclerosis
- impaired physical mobility
- impaired urinary elimination
- interrupted family processes
- risk for falls
Multiple sclerosis patient teaching
- good balance of exercise and rest
- nutrition
- treatment regimen (medication management and adherence)
- self-catheterization if necessary
- adequate intake of fiber to aid in regular bowel habits
- emotional adjustments
- lifestyle changes
ALS etiology-classifications
- sporadic: without family history, random, 90-95% of cases
- familial: one occurrence in family, dominant inheritance
- onset: 40-70 years of age
- men vs. women - 2:1 men to women
- 5000 people in US diagnosed annually
ALS clinical manifestions UMN vs. LMN
Typical manifestations: muscle weakness, dysarthria, dysphagia
Other manifestations: pain, sleep disorders, spasticity, drooling, emotional lability, depression, esophageal reflux, constipation
Upper Motor Neuron manifestations
- loss of dexterity or ability to coordinate movements
- weakness
- spasticity
- hyperreflexia
Lower Motor Neuron manifestations
- weakness
- paralysis
- hyporeflexia
- fasciculations
- flaccidity
- muscle cramps
ALS diagnosis
- difficult to diagnose
- thorough neurological examination is key
- diagnosis of exclusion: electrodiagnostic tests, blood and urine studies, spinal tap, x-rays, MRI, pyelogram of cervical spine, and muscle and/or nerve biposy
- El Escorial criteria
ALS drug therapy
Riluzole
- decreases body's level of glutamate
- slows progression of disease
Edaravone
- slows functional deterioration
- prevents oxidative stress
- came out 2 years ago
ALS nursing interventions
Facilitating communication: over articulation, limit distractions, sit face to face, yes/no systems, eye blinking, smartphone, letter board, speech generating devices
Aspiration precautions: honey or nectar thick food, coughing and deep breathing exercises, secretion management with coughalator and chest physiotherapy, incentive spirometry, suctioning
Falls precautions: bed alarm, bed in lowest position, lifts, wheelchair safety, promote safe mobility
Skin management: turn q2hr, promote adequate nutritional intake, avoid boney prominences, reposition in wheelchair, incontinence management
Nutrition: appropriate consistency, small bites, eat slowly, positioning after eating, small frequent meals, high fiber, hydration, G tube, parenteral nutrition as the disease progresses
ALS prognosis
- no cure
- death typically occurs from a respiratory tract infection
- 2-6 years after diagnosis
- focus on symptom management
SLE etiology
- unknown
SLE risk factors
- potentially due to genetics, hormones, or environmental factors
- possible environmental factors: sun or UV exposure, stress, viruses, chemicals, toxins, medications
SLE pathophysiology
- the immune system produces auto reactive B cells and T cells, which make a type of protein called autoantibodies
- these autoantibodies in turn attack the bodies' cells, leading to inflammation
- these autoantibodies target various components of the cell nucleus and result in a Type III hypersensitivity response
SLE clinical manifestations
General
- fever
- weight loss
- joint pain
- excessive fatigue
Dermatologic
- malar/butterfly rash
- alopecia
- mouth ulcers
- photosensitivity
Musculoskeletal
- arthritis
- swelling
- pain
- stiffness
- deformity
- subluxation
- swan neck of finger
- ulnar deviation
Pulmonary
- pleurisy: inflammation of tissue that lines the lungs
Cardiac
- pericarditis
- myocarditis
- endocarditis
- fibrosis of sinoatrial and atrioventricular nodes (can lead to heart block)
- antiphospholipid syndrome: formation of abnormal blood clots
- Raynaud's phenomenon: narrowing of blood vessels
Renal
- mild proteinuria
- glomerulonephritis
Nervous System
- seizures
- headaches
- peripheral neuropathy
- cognitive problems: disordered thinking, disorientation, memory deficits
- depression
- anxiety
Hematologic
- anemia: low RBC
- leukopenia: low WBC
- thrombocytopenia: low platelets
- coagulation disorders: excess bleeding or clotting
SLE diagnosis
Labs
- ANA test
- Anti-DSDNA test
- Anti-smith antibody
- antiphospholipid antibodies
X-ray
- can be used to assess affected joints
ECG
- can be used to access cardiac abnormalities
SLE pharmacologic treatment
- NSAIDS: reduce inflammation
- antimalarial agents: decrease autoantibody production
- corticosteroids: decrease inflammation (should be limited to the lowest dose)
- steriod-sparing medications: suppress immune system; control inflammation
- anticoagulants: increases blood clotting time
- monoclonal antibodies: target B-cells
- respiratory corticotropin injection: contains naturally occurring hormone ACTH, stimulates body to produce cortisol, helps reduce inflammation
- immunosuppressive medications: suppress the immune system
SLE non-pharmacologic treatment
Nutrition
- no special diet
- consider: alcohol use, fat & salt intake, and calcium intake
- avoid alfalfa and garlic
Exercise
- low impact: walking, swimming, yoga, pilates, cycling
SLE complications
- infections
- end-stage renal disease
- stroke
- heart attack
- pregnancy complications
- skin scarring
SLE nursing management
- pain management
- patient education
- maintain optimal role function
- positive self-image
Primary prevention of abdominal trauma
- seatbelts: most effective way to reduce injury with MVC and reduces serious injury in crash by 50%
- helmets: most effective way to reduce injury in MCC; estimated to prevent 37% of fatal motorcycle injuries
trauma primary survey
A - airway (with cervical spine protection)
B - breathing (and ventilation)
C - circulation (with hemorrhage control - stop the bleed)
D - disability (neurological status)
E - exposure and environmental control (completely undress patient but avoid hypothermia)
- vital signs, IV's, drugs, transfusions, foley, gastric tube, documentation
trauma secondary survey
- History: AMPLE (allergies, medications, PMH, last meal, and events surrounding injury)
- physical examination: neurologic, head and skull, maxillofacial, neck, chest, abdomen, perineum/rectum, musculoskeletal, and tubes/fingers
common injuries in blunt trauma
- liver laceration
- splenic laceration
- renal laceration
- bowel hematoma
- pelvic hematoma
- retroperitoneal hematoma
pre-op nursing management of abdominal trauma
- prep for surgical intervention (pending diagnostic data)
- fluid resuscitation
- protection of ABC's
- management of pain
- frequent abdominal assessments (observe for abdominal distention and palpate for pain and firmness)
- prevention of lethal triad
post-op nursing management of abdominal trauma
Respiratory
- protect and monitor airway and breathing
- ensure latency of airway
- monitor vital signs
- position patient to ensure optimal lung expansion
- monitor color and character of secretions (suction as needed)
Cardiovascular
- maintain hemodynamic stability
- monitor VS
- frequent assessment of peripheral vascular system
- monitor mental status
- provide fluid resuscitation
- crystalloid: lactated ringers or normal saline(20-30 mL/kg)
- colloids
- monitor I/O
- vasopressors: study at Penn showed that vasopressin along with crystalloid and colloid resuscitation had no mortality benefit but did show statistically significant benefit of less overall fluid resuscitation
Hematologic
- prevent trauma triad of death
- stop the bleed
- keep the patient warm: keep patient covered as much as possible, apply warm blankets, keep room temp. high
- administer fluids, both crystalloid and colloid
- ensure they are warm
- monitor and maximize oxygenation
Gastrointestinal
- abdominal assessment: observe for increasing abdominal distention, auscultate for bowel sounds, and palpate to assess for pain or tenderness as well as firmness of abdominal wall
- trend bladder pressure: measures the intra-abdominal pressure and considered reliable only when patient is heavily sedated or chemically paralyzed
- nutrition: early involvement of nutrition team, advocate for 1.5-2.5g/kg/day of protein to start, monitor nutritional status with weekly labs (albumin, pre-albumin, C-reactive protein), monitor and replace electrolytes, weigh patient daily
- if contraindications to TEN exist, advocate for patient to start TPN within 48 hours of initial damage control procedure
Surgical Site
- incision assessment
- midline incision with full abdominal closure
- partial closure (such as a fascial closure where the skin remains open)
- open abdomen with ABThera, VAC, or other closure device
- indications for the open abdomen: damage control surgery, abdominal compartment syndrome, massive fluid replacement, requirement for second-look surgery (to assess bowel viability or to evaluate and treat continued intra-abdominal contamination)
Neurologic exam
- glasgow coma scale
- pupils: CN II and III = midbrain
- not unilateral or bilateral dilated pupils (can be signed of increased ICP or herniation)
- extremity movement (equal?)
- in a comatose patient, checking protective reflexes such as blink (corneal reflex), gag, and cough are used to determine presence or absence of brain death
- observe for signs of trauma: lacerations, CSF rhinorrhea, peri-orbital hematoma, battles sign (bruising behind ear), raccoon eyes
- note PMH
TBI classification and types of injury
Penetrating Injury
- a head injury in which the dura mater (outer layer of the meninges) is breached
- less common than closed head trauma but worse prognosis
- penetrating: foreign object penetrate and remains lodged
- tangential: foreign objects glances off skulls driving bone fragments into the brain
- perforating: through and through
- most common is GSW
Concussion
- low velocity injury resulting in functional deficit without pathological injury
- most common symptoms is headache
- neuroimaging is typically normal
- recovery from symptoms within 7 days to 6 weeks
- balance and coordination may be affected
- concussion clinics and outpatient therapy are useful for symptom management (which can affect QOL)
Acceleration and Deceleration Injuries
- coup: site of impact with blunt object
- contrecoup: opposite the area of impact
Diffuse Axonal Injury
- long connecting fibers in the brain (axons) are sheared as the brain accelerates and decelerates
- causes injury to many places in the brain
- patients are often in a coma without obvious lesion on CT scan; punctate hemorrhages can be seen on MRI
- supportive care
- poor outcomes
Subdural Hematoma
- bleeding between dura and arachnoid membranes
- elderly are prone d/t fragile vessels and brain atrophy
- can occur with relatively low impact or be spontaneous
- typically venous (tearing of bridging veins)
- close near observation/serial near exams: gradually increasing headache and confusion can indicate expansion
- potential surgery for evacuation
- seizure prophylaxis (presenting symptom can be seizure)
- possible drain
Epidural Hematoma
- bleeding between skull and dura layer
- typically arterial
- close near observation/serial near exams: lucid initially to unconsciousness (can happen quickly)
- potential surgery
- seizure prophylaxis
Subarachnoid
- bleeding between the Pia mater and the arachnoid membrane
- trauma is most common cause of SAH
- seizure prophylaxis
- occurs in 35% of TBI, typically in combination with other hemorrhage
- rarely causes vasospasm
- medical management only
Intracerebral Hemorrhage
- intraparenchymal hemorrhage: blood in brain tissue
- intraventricular hemorrhage: blood in ventricles
- seizure prophylaxis
- surgery: possibly
Potential complications of head injury
- cerebral edema and herniation
- seizures
- hydrocephalus
- alternations of neuroendocrine function of hypothalamus and pituitary system (diabetes isipidus and syndrome of inappropriate anti-diuretic hormone)
Cushing's triad
- increased BP (sympathetic response to cerebral ischemia, worsening problem)
- decreased HR (HTN is detected and stimulates vagus nerve)
- decrease RR or irregular respiratory pattern (compression or respiratory center)
means acute herniation (near emergency)
TBI nursing management
Neuro
- serial neurologic exams (Q15min-Q4hours)
- monitoring/managing ICP; ICP
- manage pain/agitation
- EVD management
- repeat imaging - urgency
- seizures (clinical vs sub-clinical)
- HOB elevated (unless contraindicated)
- management of paroxysmal sympathetic hyperactivity
CV
- BP goals: avoid HTN in bleed; avoid hypotension to optimize CPP
- monitor HR: high risk of arrhythmias d/t sympathetic surge
- treat shock (fluid/vasopressors)
Respiratory
- monitor status; GCS
SCI: traumatic vs. non-traumatic
Traumatic
- flexion/extension/compression
- fractures
- hematomas
Non-Traumatic
- tumors
- infection
- stenosis
- ischemic injury
- AVMs
- neuromuscular disease can present with weakness
SCI major cause of death
- aspiration and shock
ASIA scoring
A - complete; no motor or sensory function is preserved in the sacral segments S4-S5
B - incomplete; sensory but not motor function is preserved below the neurological level and includes sacral segments S4-5
C - incomplete; motor function is preserved below the neurological level and more than half of key muscles below the neurological level have a muscle grade less than 3
D - incomplete; motor function is preserved below the neurological level, and at least half of key muscles below the neurological level have a muscle grade of 3 or more
E - norma; motor and sensory function are normal
types of SCI injuries
Complete
- no residual function more than three levels below the injury affecting both sides equally
Incomplete
- any residual sensory or motor function below the injured level
spine syndromes
Central Cord Syndrome
- most common type of incomplete injury
- injury to the center portion of the cervical cord - cervical motor fibers are located towards the center of the cord
- results in weakness in arms (loss of fine motor) more than legs
- surgical treatment remains controversial
- commonly found in hyperextension injury: older persons with cervical spondylosis/stenosis and younger persons with traumatic injury
- recovery is possible but variable
Brown-Sequard syndrome
- rare
- ipsilateral loss of motor and contralateral loss of sensation
- damage to half of the spinal cord; can be seen in patients with spinal cord tumor, trauma, infection and inflammatory disease, as well as disc herniation
Anterior Cord Syndrome
- complete motor paralysis and loss of temp. and pain perception distal to the lesion with preserved light touch, vibration, and proprioception
- caused by compression of the anterior spinal artery
- associated with burst fractures
Cauda Equina Syndrome
- nerve roots of the caudal equine are compressed (herniated disc, tumor, abscess)
- symptoms: weakness, difficulty urinating, loss of rectal tone, saddle anesthesia
- medical emergency
Management of cardiogenic shock
- restore blood flow
- oxygen supply and demand
- thrombolytics
- angioplasty with senting
- coronary revascularization
- reduce workload of the heart with intra-aortic balloon pump (IABP) or ventricular assistive device (VAD)
- airway and oxygenation management
- drug therapy: positive inotropes (dopamine and dobutamine) ventodilation (nitroglycerin), and vasodilation (sodium nitroprusside), diuretics, and beta blockers
- supportive therapy
common problems experiences by people who shift work
- characterized by insomnia, sleepiness, and fatigue
- sleep debt grows
- complications: mood, impact work performance, testosterone, higher accident risk, and substance use
insomnia etiology
- behaviors
- lifestyle
- diet
- medical conditions
- medications
- stressful life events
prevention of organ rejection
- both the donor and recipient are tested to identify HLA antigen variations, which minimizes rejection
- activation of lymphocytes are cellular rejection
- activation of antibodies are humoral rejection
treatment of organ rejection
- calcineurin inhibitors
- corticosteroids
- antimetabolites
- antibody products
diabetes insipidus clinical manifestations
- polydipsia
- polyuria
- excretion of large quantities of urine (2-20L/day, very low specific gravity, very low urine osmolality, serum osmolality is elevated)
- nocturia
- generalized weakness
- dehydration
acute thyrotoxicosis management
- medical emergency
- propylthiouracil
- beta blockers
- IV fluids
- cardiac monitoring
- adequate oxygenation
Cushing's syndrome etiology
- iatrogenic administration of exogenous corticosteroids
- ACTH-secreting pituitary adenoma: large cause of endogenous cases
- adrenal tumors: less common
Hyperparathyroidism diagnosis
- serum PTH levels
- serum Ca
- serum P+
- bone density measurements
- urine
Hyperparathyroidism management
Surgical
- partial vs. complete (outpatient)
- auto transplantation of normal parathyroid tissue
Calcium supplementation for life if surgical interventions fail
Conservative approach if asymptomatic or mild symptoms
- labs
- annual x-rays or DEXA scans
- drug therapy
Multiple sclerosis pathophysiology
Three Characterizing Pathologic Processes
- chronic inflammation
- demyelination
- gliosis in the CNS: scarring, nonspecific reaction-like changes
Primary Neuropathologic Condition
- autoimmune process orchestrated by activated T cells
- T cells migrate to the CNS, causing a blood-brain disruption
Onset
- insidious
- vague symptoms
- intermittent
Golden hour vs. platinum 10
Golden hour
- the first hour after injury will largely determine a critically injured person's chances for survival
Platinum 10
- later coined to restrict the time of pre-hospital care of critically injured trauma patients to no more than 10 minutes of on-scene stabilization time prior to initiation of transport
- resulted in a scoop and run approach to encourage rapid transport to the local trauma center
Etiology: blunt vs. penetrating
Blunt
- MVC
- MCC
- pedestrian vs car
- assault with blunt force
- fall
Penetrating
- stab wound
- gunshot wound
abdominal trauma complications
Abdominal compartment syndrome
- condition caused by abnormally increased pressure within the abdomen that is associated with organ dysfunction
- risk factors: trauma, surgery, infection
- intra-abdominal hypertension can impair the function of nearly every organ system
- clinical manifestations: abdominal distention worsening to tense, rigid abdomen; abdominal pain out or proportion to injury; tachypnea and/or dyspnea
- treatment: relief the pressure; emergency that needs to go to the OR immediately for exploratory laparotomy
Renal injury
- causes: pre-renal and intra-renal (secondary to prolonged hypotension; toxins such as antibiotics and IV contrast dye)
- monitor urine output
- inform provider if patient produces less than 0.5mL/kg/hr
- obtain labs as ordered
- monitor creatinine, BUN, and electrolytes
Infection
- prevent and treat
- monitor for sepsis (shivering, extreme pain or general discomfort, pale or discolored skin, sleepy/confused, "I feel like I might die" statements, shortness of breath
- antibiotics (prophylaxis and treatment)
Trauma triad of death
- hypothermia
- coagulopathy
- acidosis
Motor strength scaling
- musculoskeletal strength graded out of 5
TBI signs
- use GCS
- decorticate (flexor) posturing: damage to cerebral hemispheres
- decerebrate (extensor) posturing: deeper brain structures, including midbrain, pons, brain stem
TBI symptoms: mild vs. severe
Mild
- LOC for secs to min or none but state of being dazed/disoriented
- headache
- N/V
- fatigue
- speech problems
- dizziness
Moderate to Severe
- LOC for several mins to hours
- headache
- repeated N/V
- seizures
- dilation of one or both pupils
- clear fluids from nose or ears
- weakness
- agitation
- slurred speech
- come (GCS
SCI etiology
- fractures
- dislocation
- masses such as tumors
- hematomas
- abscesses
- ischemic injuries (spinal stroke)
- penetrating injuries to the spine accounts for about half of spinal injuries in urban centers
SCI mechanisms of injury
- must always be presumed until it is excluded (a missed injury can have devastating consequences)
- compression
- flexion
- extension
- rotation
- lateral bending/stress
- distraction
- penetration
SCI acute complications
Spinal Shock
- transient depression or loss of reflex activity below the level of an acute spinal cord injury
Neurogenic shock
- form of distributive shock
- a sudden loss of autonomic tone due to spinal cord injury causes hypotension and bradycardia - unopposed parasympathetic innervation
- usually occurs in patients with injury T6 and above but can happen in any injury above L2
- management: airway support if needed, fluids and vasopressor support as needed, to maintain MAP
- atropine for bradycardia vs pacing (temporary or permanent?)
Autonomic dysreflexia
- uncontrolled sympathetic response secondary to a stressor in patients with a SCI T6 and above (unlikely to occur with injuries below T10)
- life threatening HTN and bradycardia when there is a noxious stimulus below the level of injury
- initial complaint is headache - any patient with headache and SCI above T6 should have their BP checked immediately
- common triggers are bladder dissension, fecal impaction/constipation, pressure injury
SCI nursing management
Neuro
- serial neurologic exams, especially motor strength and sensation
- maintain proper spinal precautions/alignment
- pain management (neuropathic pain)
- patient/family education and support
- encourage patient to be active participant in their care/recovery (give them back some control)
Respiratory
- close monitoring
- pulmonary toileting (cough assist, chest PT, quad cough)
- management of secretions
CV
- BP monitoring
- HR/telemetry
- optimize perfusion - patients may require MAP goals of >80 or higher in initial injury period to optimize spine perfusion
- manage shock
GI/GU
- bowel regimen (may need standing suppository/rectal stimulation)
- strict bladder training
Skin
- frequent turns and skin assessments - offload pressure
- mobilize
Heme
- DVT prophylaxis
Discharge planning
- early PT/OT/Speech
- SCI rehabilitation/PM&R
Medical management of spinal injury
- stabilization of spin
- distributive shock management: fluid resuscitation, atropine for bradycardia, vasopressors PRN
- no current support for steroids
- intensive support care
causes of spinal tumors
- viruses
- defective genes
- exposure to certain chemicals and hazardous materials
- immune system disorders
- genetic diseases, such as tuberous sclerosis
- exposure to radiation
SCI clinical manifestations
- trouble waking (abnormal gait)
- numbness/tingling
- bowel/bladder dysfunction
- general midback pain
SCI diagnostic approach
- can take weeks
- often other causes ruled out first
- usually first diagnosed on MRI
Management of spinal tumors
- surgical resection and stabilization of spine if possible
- radiation therapy
- chemo
- steroids to reduce swelling
- serial neuro assessments and spine exams
- pain management
- incentive spirometry
- prevent atelectasis
- peri-op abx
- wound and drain care/monitoring
- bowel regimen
- monitor for urinary retention
- mobilize
leading causes of death in spinal cord injury after initial injury
- pneumonia
- PE
- sepsis
Classifications of shock
- cardiogenic
- hypovolemic (absolute and relative)
- distributive (neurogenic, anaphylactic, and septic)
- obstructive
Clinical manifestations of cardiogenic shock
- problem with the pump
- early: tachycardia, hypotension, narrowed pulse pressure
- respiratory: tachypnea, crackles, cyanosis, rhonchi
- cardiovascular: tachycardia, decrease in BP, decrease in cap refill, chest pain may or may not be present
- integumentary: pallor, cool, clammy
- renal: increase Na&H2O retention, decreased renal blood flow and urinary output
- neuro: anxiety, confusion, agitation
- GI: decreased BS, nausea, vomiting
Clinical manifestations of hypovolemic shock
- dependent on age, extent of injury or insult, and overall state of health
- respiratory: tachypnea and bradypnea (late)
- cardiovascular: decreased preload, SV, and cap refill
- integumentary: pallor, cool, clammy
- renal: decreased u/o
- neuro: anxiety, confusion, agitation
- GI: absent bowel sounds
Clinical manifestations of neurogenic shock
- main symptoms: hypotension, bradycardia, inability to regulate body temperature that leads to poikilothermia
-respiratory: related to injury level
- cardio: decreased BP, bradycardia, increase/decrease in temperature
- integumentary: pallor, cool, clammy
- renal: bladder dysfunction
- neuro: flaccid paralysis below level of lesion, loss of reflex activity
- GI: bowel dysfunction
Clinical manifestations of anaphylactic shock
- main symptoms: dizziness, chest pain, incontinence, swelling of lips and tongue, wheezing, stridor, flushing, pruritus, uticaria, angioedema, and sense of impending doom
- respiratory: SOB, edema of larynx and epiglottis, wheezing, stridor, rhinitis
- cardio: CP, third spacing of fluid
- integumentary: flushing, pruritus, urticaria, angioedema
- renal: incontinence
- neuro: anxiety, feeling of impending doom, decreased LOC
- GI: cramping, ABD pain, diarrhea, vomiting, nausea
Clinical manifestations of septic shock
- pathophysiologic effects: vasodilation, maldistribution of blood flow, and myocardial depression
- respiratory: hyperventilation, crackles, respiratory alkalosis leading to acidosis, hypoxemia, ARDS (acute respiratory distress syndrome), and pulmonary hypertension
- cardio: increase/decrease in temp, myocardial dysfunction, ventricular dilation, decrease in EF
- integumentary: warm and flushed and then cool and mottled (late)
- renal: decreased urine output
- neuro: altered MS, confusion, agitation
- GI: GI bleed, paralytic ileus
Clinical manifestations of obstructive shock
- main symptoms: decreased CO, increased afterload, and variable left ventricular filling pressure
- respiratory: tachypnea, SOB, bradypnea (late)
- cardio: decreased BP and preload
- integumentary: pallor, cool, clammy
- renal: decreased urine output
- neuro: anxiety, confusion, agitation
- GI: decreased or absent bowel sounds
Management of hypovolemic shock
- treat the underlying cause
- large bore peripheral IVs or central venous catheter (CVC)
- fill the tank with crystalloids (LR, normal saline) and colloids (PRBCs, FFP, albumin, plasma volume expanders like hetastarch and dextran)
- invasive hemodynamic monitoring
- airway and oxygenation management
- no specific drug therapy
Management of neurogenic shock
- based on the cause
- spine stability
- vasopressors (phenylephrine)
- atropine
- fluids must be used cautiously as there is a risk of fluid overload (change in resistance, not volume)
- body temperature
- airway and oxygenation management
Management of anaphylactic shock
- prevention
- removal of offending cause
- airway and oxygenation management (endotracheal intubation or cricothyroidotomy)
- fluid resuscitation
- drug therapy: epinephrine, Benadryl, bronchodilators, corticosteroids
Management of septic shock
- blood cultures identifying the organism
- labs
- abx
- aggressive fluid resuscitation
- vasopressors (norepinephrine)
- inotrope (dobutamine)
- prophylactic anticoagulants
- stress ulcer prophylaxis
- airway and oxygenation management
- invasive hemodynamic monitoring
Management of obstructive shock
- treat the underlying cause: pericardiocentesis, needle decompression, chest tube insertion, embolectomy
- fluid resuscitation (temporary)
- airway and oxygenation management
- no specific drug therapy
SIRS criteria
- temp over 100.9
- heart rate over 90 bpm
- respiratory rate of 22 bpm or PCO2 less than 32 mmHg
- WBC over 12 or WBC less than 4
Sepsis
- 2 SIRS + infection
Severe sepsis
- sepsis + 1 sepsis induced organ dysfunction
Septic shock
- severe sepsis + hypotension without response to fluid resuscitation
Stages of shock
1. Initial
- cellular level
- usually not clinical apparent
- metabolism changes (lactic acid build-up)
2. Compensatory
- attempt to equilibrilate
- activation of neural, hormonal, and biochemical mechanisms
3. Progressive
- begins as compensatory mechanisms begin to fail
- changes in mental status
- CV system profoundly affected
- pulmonary system
- aggressive interventions (key to preventing MODS)
4. Irreversible/Refractory
- decreased perfusion, which leads to anaerobic metabolism
- decreased CO
- increasing capillary permeability
- increasing dilation
- profound hypotension and hypoxemia
- unlikely recovery
- sequelae: cerebral ischemia, worsening cardiac depression, and failure of one organ system
How SVR, CO, and CVP relate to the presentation of cardiogenic shock
- increase in CVP, PAWP, and SVR
- decrease in CO
- related to systolic dysfunction (ineffective forward movement of blood) or diastolic dysfunction (ineffective filling)