ca-cna-critical-care-pediatrics cheat sheet

Glasgow Coma Scale for children under 5 uses age-specific verbal and motor anchors; the pediatric score (infant to <5 years) differs from the adult GCS, so scores must be labeled with the scale version used.

GCS total = eye (1-4) + verbal (1-5) + motor (1-6), range 3-15; intubated patients score verbal as 1T and the total should be reported with the T modifier rather than assumed.

Pupillary exam: record size in mm, symmetry, and reactivity to light; a fixed dilated pupil suggests ipsilateral uncal herniation, while pinpoint pupils suggest pontine injury or opioid effect.

Brainstem reflexes to document in coma: pupillary light, corneal, oculocephalic (only with cervical spine cleared), oculovestibular (cold caloric), gag, and cough.

Decorticate posturing (flexion of arms, extension of legs) localizes above the red nucleus; decerebrate posturing (extension of all limbs) localizes at or below the red nucleus and carries worse prognosis.

Pediatric early warning scores and nursing neurologic checks (GCS, pupils, vital signs, motor exam) are typically performed hourly in acute deterioration risk; trends matter more than single values.

Age-specific normal values: infants have a sunken or flat fontanelle, open sutures, and lower blood pressure; hypotension in a child is a late sign, so mean arterial pressure should be maintained near age-appropriate targets.

Sedation confounds the neurologic exam; use validated sedation scales (e.g., Comfort-B, Richmond Agitation-Sedation Scale) and document the sedative infusion rate alongside GCS to interpret changes.

Severe pediatric TBI is defined as post-resuscitation GCS 3-8; management targets normoxia (SpO2 >94%), normocapnia (PaCO2 35-38 mmHg), normotension, normothermia, and normonatremia.

Avoid hypotension: pediatric age-based systolic targets approximate 70 + (2 x age) mmHg; a single episode of hypotension in severe TBI increases morbidity and mortality.

Hyperventilation to PaCO2 30-35 mmHg is reserved for acute herniation signs only, because hypocapnia causes cerebral vasoconstriction and ischemia.

Hypertonic saline (3%) and mannitol are osmotic therapies for intracranial hypertension; mannitol is avoided in hypovolemia and hypertonic saline requires monitoring of serum sodium and osmolality.

Cervical spine injury is uncommon but must be assumed in TBI with high-energy mechanism; maintain inline stabilization until imaging and clinical clearance.

Spinal cord injury: spinal shock causes flaccidity and areflexia below the lesion with bradycardia and hypotension (neurogenic shock); after days to weeks, spasticity and hyperreflexia develop.

Neurogenic shock is treated with volume and vasopressors (norepinephrine or phenylephrine); avoid isolated fluid loading because it can worsen cord edema and pulmonary edema.

Autonomic dysreflexia occurs with lesions at T6 or above: hypertension, bradycardia, headache, flushing, and sweating triggered by bladder or bowel distension; treat by removing the stimulus and using antihypertensives.

Status epilepticus is continuous seizure activity lasting 5 minutes or more, or recurrent seizures without return to baseline between events; treatment begins at 5 minutes.

Time-based treatment: benzodiazepine at 5 minutes (lorazepam 0.1 mg/kg IV, midazolam 0.2 mg/kg IM/intranasal, or diazepam 0.3 mg/kg IV), repeat once; second-line at 20 minutes (levetiracetam 60 mg/kg, fosphenytoin 20 mg PE/kg, or valproate 40 mg/kg); refractory at 40 minutes requires continuous infusion.

Refractory status epilepticus is defined as seizures persisting despite two appropriately dosed antiseizure medications; super-refractory is status persisting 24 hours or more after anesthesia initiation.

Nonconvulsive status epilepticus should be suspected in a child with unexplained persistent altered mental status; continuous EEG is required for diagnosis.

Febrile status epilepticus in a child 6 months to 5 years with fever and no CNS infection has a low risk of epilepsy; evaluation focuses on source of fever and excluding meningitis when indicated.

Neonatal seizures are often subtle (automatisms, apnea, cycling) and frequently electrographic only; phenobarbital is first-line, with levetiracetam or fosphenytoin as alternatives.

Monitor for benzodiazepine respiratory depression and hypotension; have airway equipment and flumazenil awareness, and check glucose and electrolytes (calcium, magnesium, sodium) at seizure onset.

Status epilepticus complications include hyperthermia, rhabdomyolysis, acidosis, aspiration, and excitotoxic neuronal injury; continuous EEG monitoring guides titration of anesthetic infusions.

Monro-Kellie doctrine: the skull is a fixed volume containing brain, blood, and CSF; an increase in one compartment must be offset by a decrease in another or intracranial pressure rises.

Normal intracranial pressure in children is lower than in adults; thresholds for treatment are commonly above 20 mmHg sustained for more than 5 minutes in older children, with lower thresholds in infants.

Cerebral perfusion pressure = mean arterial pressure minus intracranial pressure; CPP targets are age-dependent and generally aim for at least 40-50 mmHg in young children.

Signs of raised intracranial pressure: headache, vomiting, sunsetting eyes, bulging fontanelle, cranial suture separation, papilledema, and a Cushing response (hypertension, bradycardia, irregular respirations).

External ventricular drain allows both CSF drainage and pressure measurement; nursing care includes leveling the transducer to the tragus or foramen magnum, avoiding overdrainage, and strict sterile technique.

Hydrocephalus types: communicating (impaired absorption) versus noncommunicating (obstruction); shunt malfunction presents with headache, vomiting, lethargy, and possibly upward gaze palsy.

CSF analysis: bacterial meningitis typically shows elevated opening pressure, neutrophilic pleocytosis, low glucose (CSF to serum ratio below 0.4), and high protein; viral patterns are lymphocytic with normal glucose.

Osmotic therapy and CSF diversion are temporizing; definitive management of hydrocephalus is shunt or endoscopic third ventriculostomy, and shunt infection must be considered with fever and meningismus.

Pediatric stroke presents with acute focal deficit; the pediatric NIH Stroke Scale can be used, and time-critical imaging (MRI with diffusion-weighted imaging) is preferred over CT for early detection.

Arterial ischemic stroke in children is associated with arteriopathy, cardiac disease, sickle cell disease, and prothrombotic states; thrombolysis and thrombectomy are considered only in selected centers with protocols.

Hemorrhagic stroke in children may result from arteriovenous malformation, aneurysm, or coagulopathy; management includes blood pressure control, reversal of anticoagulation, and neurosurgical consultation.

Cerebral venous sinus thrombosis presents with headache, papilledema, seizures, and focal deficits; anticoagulation with low-molecular-weight heparin is standard even in the presence of hemorrhagic infarction.

Sickle cell disease stroke: exchange transfusion to reduce hemoglobin S and target hemoglobin around 30% is the acute therapy; hydroxyurea is used for prevention.

Posterior reversible encephalopathy syndrome (PRES) presents with headache, seizures, visual changes, and hypertension; treatment is blood pressure control and removal of the offending agent.

Cerebral salt wasting and syndrome of inappropriate antidiuretic hormone both cause hyponatremia after brain injury; distinguish by volume status: cerebral salt wasting is hypovolemic, SIADH is euvolemic.

Brain death evaluation in children requires documentation of etiology, absence of brainstem reflexes, apnea testing, and consideration of ancillary studies; protocols differ for neonates and young infants.

Bacterial meningitis in children: empiric therapy is vancomycin plus a third-generation cephalosporin (ceftriaxone or cefotaxime); add ampicillin for neonates and Listeria risk, and add dexamethasone before or with the first antibiotic dose for Haemophilus influenzae type b suspicion.

Do not delay antibiotics for lumbar puncture when the child is unstable or has signs of raised intracranial pressure; obtain blood cultures and start empiric therapy first.

Contraindications to immediate lumbar puncture: focal neurologic deficit, seizures, papilledema, altered consciousness, hemodynamic instability, or coagulopathy.

Neonatal meningitis pathogens: group B Streptococcus, Escherichia coli, and Listeria monocytogenes; presentation may be subtle with poor feeding, temperature instability, and apnea.

Viral meningitis is usually self-limited; enteroviruses and herpes simplex virus are common. HSV encephalitis presents with fever, seizures, and temporal lobe findings and requires intravenous acyclovir.

Brain abscess presents with headache, fever, focal deficits, and ring-enhancing lesions; treatment includes prolonged antibiotics and possible stereotactic drainage.

Tuberculous meningitis presents with subacute headache, cranial nerve palsies, and basilar meningeal enhancement; treatment is multidrug antituberculous therapy plus corticosteroids.

Prevention: Haemophilus influenzae type b, pneumococcal, and meningococcal conjugate vaccines reduce meningitis incidence; chemoprophylaxis is indicated for close contacts of meningococcal disease.

Guillain-Barre syndrome presents with ascending symmetric weakness, areflexia, and albuminocytologic dissociation (elevated CSF protein with normal cell count); treatment is intravenous immunoglobulin or plasma exchange.

Respiratory failure in Guillain-Barre syndrome is predicted by vital capacity below 15-20 mL/kg, inability to count to 20 in one breath, or bulbar dysfunction; monitor with serial negative inspiratory force and vital capacity.

Myasthenia gravis crisis presents with worsening bulbar and respiratory weakness; treat with acetylcholinesterase inhibitors, corticosteroids, intravenous immunoglobulin, or plasma exchange, and avoid aminoglycosides and magnesium.

Spinal muscular atrophy and Duchenne muscular dystrophy require attention to respiratory support, secretion clearance, and cardiomyopathy; Duchenne is associated with dilated cardiomyopathy and arrhythmia.

Cerebral palsy is a nonprogressive motor disorder; critical care issues include aspiration, spasticity, seizures, and malnutrition, and acute deterioration should prompt evaluation for other causes.

Rett syndrome and other neurodevelopmental disorders carry risks of autonomic instability, prolonged QT interval, and sudden respiratory arrest; monitor cardiac rhythm and breathing patterns.

Neuromuscular respiratory failure causes a restrictive pattern with decreased vital capacity and preserved lung compliance; hypoxemia is a late sign, so hypercapnia and weak cough are earlier clues.

Botulism presents with descending symmetric flaccid paralysis, ptosis, and bulbar weakness; treatment is botulinum antitoxin and supportive ventilation.

Analgesia-first sedation: treat pain before adding sedatives; validated pediatric tools include the FLACC scale for younger children and the numeric rating scale for older children.

Opioids (fentanyl, morphine) cause dose-dependent respiratory depression, bradycardia, and hypotension; naloxone reverses opioid effects but may precipitate withdrawal and seizures.

Benzodiazepines (midazolam, lorazepam) cause respiratory depression and hypotension, especially with rapid infusion; flumazenil is avoided in chronic benzodiazepine users due to seizure risk.

Dexmedetomidine provides sedation without respiratory depression but causes bradycardia and hypotension; it is not appropriate for deep sedation requiring airway protection.

Continuous propofol is avoided for prolonged sedation in children because of propofol infusion syndrome (metabolic acidosis, rhabdomyolysis, hyperkalemia, cardiac failure).

Ketamine provides analgesia and amnesia with preserved airway reflexes; it can increase intracranial pressure and cause emergence reactions, so it is used cautiously in TBI.

Antiepileptic drug monitoring: phenytoin and fosphenytoin require cardiac monitoring and slow infusion; valproate requires liver enzymes and ammonia monitoring; levetiracetam may cause behavioral changes.

Withdrawal from prolonged sedation presents with agitation, tachycardia, tachypnea, and seizures; use a weaning protocol and consider clonidine or methadone transitions.

CT is fast and detects hemorrhage and fractures but has lower sensitivity for early ischemia; MRI with diffusion-weighted imaging is more sensitive for acute infarction and edema.

Radiation dose reduction: use pediatric-specific protocols and avoid repeat CT when MRI is feasible; document cumulative dose exposure.

Continuous EEG is indicated for unexplained altered mental status, refractory status epilepticus, and titration of anesthetic infusions; detect nonconvulsive seizures and burst suppression.

Amplitude-integrated EEG is used for neonatal monitoring and can detect background suppression and seizures but requires confirmation with full EEG.

Transcranial Doppler measures cerebral blood flow velocity and can detect vasospasm after subarachnoid hemorrhage; it is operator dependent.

Near-infrared spectroscopy monitors regional cerebral oxygen saturation; trends, not absolute values, guide interpretation.

Pupillometry provides quantitative pupillary size and reactivity; it detects early herniation better than manual exam and should be interpreted with intracranial pressure and clinical findings.

Multimodal monitoring combines intracranial pressure, cerebral perfusion pressure, EEG, and oxygen saturation data; no single parameter should drive therapy without clinical correlation.

Family-centered care includes parents in rounds, explains findings in plain language, and supports presence during resuscitation when safe and feasible.

Surrogate decision-making: parents provide consent for minors; for older children, assent should be sought, and mature minor laws vary by state.

Brain death determination requires institutional protocol, two examinations by qualified clinicians, apnea testing, and ancillary studies when indicated; family meetings should explain the process in advance.

Withdrawal of life-sustaining therapy requires consensus, palliative care involvement, and symptom management; do not conflate withdrawal with euthanasia.

Rehabilitation begins in the intensive care unit with early mobilization, positioning, splinting, and speech and swallow evaluation to prevent contractures and aspiration.

Discharge planning for a child with a new neurologic deficit includes a tracheostomy or ventilator plan, gastrostomy feeding plan, school reentry, and caregiver training.

Transition to adult care for chronic neurologic conditions should begin in adolescence with a written plan covering medications, emergency protocols, and guardianship or supported decision-making.

Ethical principles in pediatric neurocritical care: best interest standard, proportionality of treatment, informed consent, and attention to the family's cultural and religious values.