Coma, Pediatric

Basics

Description

Coma is defined as a state in which the patient appears to be asleep, shows no awareness of his or her surroundings, and cannot be aroused. Coma frequently is only a transient state, whereby patients recover, die, or progress to a permanent state of impairment. Often a medical emergency, immediate intervention may be required to preserve life and brain function.

Coma is at the far end of a spectrum of acute impaired consciousness, which also includes the following:
- Lethargy or stupor: patient arousable but does not stay awake; impaired responses to commands
- Delirium: a confused, agitated patient with fragmented attention, concentration, and memory
Coma may progress to
- Persistent vegetative state: chronic state of unconsciousness with no awareness or cognition, no voluntary responses, and no language abilities; preserved autonomic functions and sleep/wake cycles
- Brain death: coma, apnea, and lack of cortical and brainstem responses

Epidemiology

Incidence varies by age, season (infection), and ethnicity (inborn errors of metabolism [IEM]).

Pathophysiology

Dysfunction of the reticular activating system in the brainstem or bilateral cerebral dysfunction causes impaired arousal and consciousness.

Etiology

Coma etiology can be traumatic or nontraumatic. Infection is a common cause of nontraumatic coma. Traumatic coma is more likely in older children.

Diagnosis

Differential Diagnosis

Trauma
- Epidural/subdural or intracerebral bleeding, cerebral swelling, and/or diffuse axonal injury
Intoxication
- Household drug ingestion including barbiturates, opiates, psychotropics, and salicylates; street drugs; alcohol; smoke or carbon monoxide inhalation; ethylene glycol; lead; and others
Hypoxia/diffuse ischemia
- Drowning, suffocation/strangulation, cardiac disease, or complications
Infection
- Bacterial or viral meningitis, encephalitis, postinfectious encephalomyelitis, toxic or systemic shock, subdural empyema. Pathogens leading to coma include HSV, Mycoplasma pneumoniae, influenza, and Neisseria meningitidis.
Postinfectious/autoimmune mediated
- Anti-NMDA receptor encephalitis, acute disseminated encephalitis (ADEM), acute necrotizing encephalitis (ANE), febrile infection-related epilepsy syndrome (FIRES), CNS lupus
Metabolic disorders
- Hypoglycemia (salicylate or ethanol intoxication, insulin overdose/hyperinsulinemia), diabetic ketoacidosis (DKA) (neurologic deterioration on initiation of insulin therapy), hyperglycemic nonketotic coma, Reye syndrome, electrolyte abnormalities (Na, K, Ca, Mg), hepatic/uremic encephalopathy, IEM, endocrine abnormalities (hypothyroidism, Addisonian crisis), hypothermia/hyperthermia
Tumor
- Can cause increased intracranial pressure and herniation
Seizure
- Nonconvulsive status
Vascular
- Infarction, hemorrhage from arteriovenous malformation (AVM), aneurysm, coagulopathy, cerebral venous thrombosis, hypertensive encephalopathy, basilar-type migraine
Hydrocephalus
- Ventriculoperitoneal (VP) shunt obstruction, mass/bleed obstructing ventricular outflow

Disorders mimicking coma include the following:

Psychogenic coma
- Patient may resist passive eye opening, regard self in a mirror, and avoid passive arm fall over face and other noxious stimuli.
Catatonia
- A form of psychogenic coma; patients may hold a posture, sit, or stand.
Locked-in state/complete paralysis
- Patient is paralyzed with intact cerebral function; may occur in severe neuromuscular disorders or in ventral pontine lesions

History

Question: Evidence or history of head trauma, drowning, or other trauma?
Significance: Are there concerns for nonaccidental trauma?
Question: What medications are in the home? Has the patient been depressed or displayed suicidal behaviors? Is there a history of illicit drug use?
Significance: Ingestion/drugs/toxins
Question: Recent fevers, viral or bacterial illnesses, mental status changes, sick contacts, immunosuppression, infectious risk factors?
Significance: Infection
Question: Past medical history risk factors?
Significance: Epilepsy, diabetes, heart disease, neurologic disease including previous episodes of coma, history of failure to thrive (IEM)
Question: Recent nausea, vomiting, mental status change?
Significance: Increased intracranial pressure

Physical Exam

Vital sign changes: Hyperthermia suggests infection, intoxication, and neuroleptic malignant syndrome. Tachycardia suggests fever, pain, hypovolemia, arrhythmia, and heart failure.
Skin changes: Look for rashes suggesting infection, bruising, and other evidence of trauma; neurocutaneous stigmata may be associated with seizures; feel anterior fontanelle in infants for evidence of increased intracranial pressure (ICP).
Neurologic exam: Focus on general level of awareness, eye movements, and motor responses to accurately define coma versus lethargy or delirium. Findings can be used in various coma scales.
Eye movements: Persistent eye deviation is associated with contralateral seizure activity or ipsilateral brain lesions. Impaired upward gaze may indicate high ICP. Nystagmus can be seen in intoxications.
Pupillary reaction: Small reactive or large reactive pupils suggest intoxication. Anisocoria suggests unilateral brainstem compression. Fixed, dilated pupils indicate global herniation/brain death. Perform oculocephalic (doll's eye) and oculovestibular (calorics) to confirm.
Motor exam: Assess tone, reflexes, and motor responses to stimuli. Flaccid tone and areflexia are serious signs if not related to medications or lower motor neuron disease. Pressure on the supraorbital notch beneath medial eyebrow will avoid reflex pain responses. Localizing pain entails purposeful movements to remove the stimulus. Withdrawal from pain is less purposeful. Decorticate (adduction with elbow and wrist flexion) and decerebrate (extension, internal rotation of arms) may be provoked by stimulation. They can be asymmetric and intermittent and should not be mistaken for seizures.
Glasgow Coma Scale/Pediatric Glasgow Coma Scale-associated with prognosis in certain situations (see Appendix, Tables 5 and 6)
- Eye opening (score range 1-4)
- Verbal response (score range 1-5)
- Motor response (score range 1-6)

Alert

Hypertension, bradycardia, and irregular respirations (Cushing reflex) herald impending brain herniation.

Diagnostic Tests & Interpretation

Initial blood studies obtained with placement of an IV line include the following:

Glucose, electrolytes, blood urea nitrogen/creatinine, calcium, magnesium, phosphorous
CBC and blood culture
Arterial blood gas
Toxicology screen (consider EKG)
Ammonia, liver transaminases, CK

Other helpful studies based on the clinical picture may include the following:

Metabolic labs (urine organic acids, serum amino acids, lactate), urinalysis, urine culture, thyroid function tests, cortisol, coagulation studies, carboxyhemoglobin (CO poisoning), ANA, anti-NMDA receptor antibodies
LP (opening pressure, glucose, cell count, protein, Gram stain, culture) to rule out infection or bleed; defer until after CT if focal exam or signs of increased ICP. If question of traumatic tap, spin out red cells promptly and examine fluid for xanthochromia. Simultaneous fingerstick blood glucose is ideal.
EEG can be helpful to rule out nonconvulsive status epilepticus, especially in patients with a history of seizures or clinically suspected seizures. Continuous EEG may be needed to make this diagnosis.
Electrophysiologic studies including somatosensory evoked (SEP), brainstem auditory evoked, and visual evoked potentials may be helpful for diagnosis and prognosis.

Imaging

Head CT: Quick noncontrast scan can detect hemorrhage, hydrocephalus, herniation, and masses; may be followed by contrast images or MRI; should be done prior to LP to rule out a mass (risk for herniation from LP)
Cervical spine series (CT or lateral and anterior-posterior radiograph studies): indicated if with evidence of trauma by history or on physical exam. Spine must be stabilized until injury is ruled out.
Brain MRI: can help with diagnosis and prognosis if prior workup is unrevealing. Consider MRA to evaluate arteries and MRV to rule out venous thrombosis. MRS can help clarify hypoxic and metabolic etiologies.

Treatment

Surgery/Other Procedures

Neurosurgical intervention may be required in cases of head trauma, hemorrhage, mass lesion, or hydrocephalus. Neurology consultation is usually indicated.

Inpatient Considerations

Initial Stabilization

First priority is airway, breathing, and circulation management.
If head trauma is suspected, stabilize the cervical spine with a collar while securing the airway.
Endotracheal intubation: often required for airway protection and adequate oxygenation
Place large-bore IV lines for isotonic fluids to maintain intravascular volume and blood pressure as needed.
Evidence of increased ICP
- Hyperventilate to decrease blood carbon dioxide to 30-35 torr.
- Consider 3% hypertonic saline (HS) as bolus or continuous infusion, which may be more efficacious than other osmotic agents.
- Consider mannitol (0.5-1 g/kg IV); can also give dexamethasone 1-2 mg/kg IV
- Treat fever with antipyretics and environmental cooling methods.
- Elevate head to 30 degrees above horizontal; avoid head-turned posture to maximize cerebral venous drainage.
- Hospitalization in the intensive care unit for close monitoring of changes in respiratory status or signs of increased ICP
- Neurosurgical consultation; consider role for decompression craniectomy.
If fingerstick glucose is low, give 2-4 mL/kg of 25% dextrose (D25) IV (D10 for infant).
If opiate ingestion is suspected, administer naloxone (0.1 mg/kg IV for infants <5 years of age or <20 kg; 2 mg for older, larger children).
Correct electrolyte and acid-base abnormalities.
Empiric treatment with IV antibiotics and acyclovir should be started if bacterial or viral meningitis is suspected.
Consider benzodiazepine (lorazepam 0.05-0.1 mg/kg IV) for suspected seizure activity, although this may compromise neurologic examination.

Ongoing Care

Prognosis

Prognosis depends on underlying etiology and patient's clinical course. It is not advised to prognosticate too early.
Serial exams combined with diagnostic tests (electrophysiology, imaging) will provide more complete information.
The following portend poor prognosis: absent motor responses to painful stimuli on day 3, no spontaneous eye opening after 1 week, bilaterally absent SEP, and isoelectric baseline or burst suppression on EEG at 1 week.
Conversely, a reactive EEG is associated with improved outcomes. Some of these findings are more firmly established in adults but, in the right clinical context, may be applicable to pediatric patients.

Complications

Acute coma
- Brain injury
- Respiratory failure/aspiration
- Seizures
- Infection
Chronic sequelae
- Epilepsy
- New cognitive and/or motor baseline

Additional Reading

Abend NS, Licht DJ. Predicting outcome in children with hypoxic-ischemic encephalopathy. Pediatr Crit Care Med. 2008;9(1):32-39. [View Abstract]
Gwer S, Gatakaa H, Mwai L, et al. The role for osmotic agents in children with acute encephalopathies: a systematic review. BMC Pediatr. 2010;10:23. [View Abstract]
Martin C, Falcone RA Jr. Pediatric traumatic brain injury: an update of research to understand and improve outcomes. Curr Opin Pediatr. 2008;20(3):294-299. [View Abstract]
Seshia SS, Bingham WT, Sadanand V. Nontraumatic coma in children and adolescents: diagnosis and management. Neurol Clin. 2011;29(4):1007-1043. [View Abstract]

Codes

ICD09

780.01 Coma
781.99 Other symptoms involving nervous and musculoskeletal systems
780.03 Persistent vegetative state
779.2 Cerebral depression, coma, and other abnormal cerebral signs in fetus or newborn
780.01 Coma

ICD10

R40.20 Unspecified coma
R40.1 Stupor
R40.3 Persistent vegetative state
P91.5 Neonatal coma

SNOMED

371632003 Coma (disorder)
247917007 Catatonia (finding)
24473007 Persistent vegetative state (disorder)
90224001 coma in the newborn (disorder)

FAQ

Q: What is the value of the Pediatric Glasgow Coma Scale (PGCS)?
A: The PGCS is helpful in predicting prognosis but not for diagnosing the cause of coma. The etiology of coma can impact the usefulness of the scale. For example, PGCS has a better correlation with outcomes following traumatic brain injury than for cold water drowning.
Q: When a bacterial infection is suspected as a potential etiology of coma, should antibiotic therapy be delayed until CSF has been obtained for testing?
A: Starting antibiotic therapy prior to obtaining CSF may lead to a false-negative CSF culture. However, if there is any concern for increased ICP or mass effect, a CT should be obtained prior to an LP, and antibiotics should be started in the meantime.

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