• Lethargy indicates a patient who is incoherent but arousable and has a tendency to sleep.
• Stupor is used when the patient is responsive only to pain.
• Vegetative state suggests a chronic state in which sleep–wake cycles persist but there is no evidence of cognition.
• Locked-in must be distinguished from coma; that is, cognitive functions are intact, though the patient may appear unconscious.

• Trauma: epidural, subdural, intracerebral hematoma, diffuse cerebral swelling
• Poisoning
• Hypoxia/ischemia
• Infection—meningitis, encephalitis, toxic shock
• Subdural empyema
• Hemorrhagic shock
• Metabolic disorders
  • Hypoglycemia (salicylate or ethanol intoxication, hyperinsulinemia)
  • Diabetic ketoacidosis (DKA): rare catastrophic neurologic deterioration seen on initiation of insulin and/or fluid therapy
  • Reye syndrome
  • Electrolyte abnormalities (Na, K, Ca, Mg)
  • Hepatic/uremic encephalopathy
  • Inborn errors of metabolism
  • Hormonal abnormalities (thyroid, adrenal, pituitary)
  • Hypothermia/hyperthermia
• Tumor
• Seizure
• Vascular: hemorrhage [from arteriovenous malformation (AVM), aneurysm, coagulopathy, infarction, cerebral venous thrombosis, hypertensive encephalopathy]
• Hydrocephalus: ventriculoperitoneal (VP) shunt obstruction
• Mass/bleed obstructing ventricular outflow

• Respiratory failure
• Deep venous thrombosis
• Pneumonia
• Aspiration

• Psychogenic coma: patient may resist passive eye opening, regard self in mirror, and avoid passive arm fall over face
• Locked-in state: complete paralysis with normal cerebral function may occur in severe neuromuscular disorders (acute polyneuropathy) or in ventral pontine lesions (hemorrhage, demyelination)

• Head trauma
• Ingestion
• Drugs/toxins in home
• Fever
• Nausea
• Headache
• Preceding viral illness
• Seizures
• Diabetes
• Preexisting neurologic disease
• Previous episodes of coma

• Vital signs
• Abnormal respiratory pattern
• Bradycardia
• Hypertension
• HEENT—look for signs of head trauma: raccoon eyes (Battle signs, ecchymosis at mastoid equals basilar skull fracture)
• Retinal hemorrhages
• Bulging fontanelle
• Neck: nuchal rigidity, Kernig and Brudzinski signs associated with meningitis
• Neurologic: verbal or motor response to voice, touch, pain; eye opening/fixation; spontaneous movements/posturing; pupil symmetry/reactivity, abnormal oculocephalic response (doll eyes); worsening signs in any of the above may indicate increased intracranial pressure (ICP)
• Reflexes specific to rostral brainstem function include pupillary light reflex, corneal reflex, jaw jerk
• Reflexes specific to caudal brainstem function include oculocephalic reflex (horizontal eye deviation with passive head rotation), gag, spontaneous respirations

• Glucose
• Electrolytes
• BUN/creatinine
• Calcium
• Arterial blood gas
• CBC
• Toxicology screen
• Ammonia
• Liver transaminases
• Radiology—non-contrast head CT scan first to look for hemorrhage, may be followed by contrasted images for infection/mass lesions
• Cervical spine series (CT or lateral and AP x-ray studies)—indicated if evidence of trauma by history or on examination
• Cervical spine must be stabilized until injury is ruled out
• Lumbar puncture, to rule out infection, bleed; defer until after CT if focal exam or signs of increased ICP
• Question of “traumatic tap” can be settled by spinning out red cells promptly and examining fluid for xanthochromia
• EEG—helpful to rule out non-convulsive status epilepticus

• First priority is stabilization of respiratory and hemodynamic status.
• Endotracheal intubation is usually required to ensure airway protection and adequate oxygenation.
• Large-bore IV lines should be placed and isotonic fluids administered as needed to replace intravascular volume and maintain adequate blood pressure.
• If finger-stick glucose determination is low, give 2 to 4 mL of 25% dextrose (D25) per kilogram intravenously (D10 if young infant).
• If ingestion is suspected, administer naloxone (0.01 mg/kg IV).
• When there is evidence of increased ICP:
  • Hyperventilate to decrease blood CO₂ to 25 to 30 Torr and give mannitol (0.5–1 g/kg IV).
  • Dexamethasone, 1 to 2 mg/kg IV, can also be administered.
  • All fluids given should be isotonic and the volume limited to that needed to maintain adequate perfusion.
  • Head should be elevated 30 degrees above horizontal to maximize cerebral venous drainage.
  • Hospitalization is usually in the intensive care unit for close monitoring for changes in respiratory status or signs of increased ICP.
  • Drug indications depend on underlying etiology.
  • IV antibiotics should be given if infection is suspected.

• Quadriparesis due to neuromuscular weakness may resemble coma; responsiveness is determined by patient questioning, using whatever movements may be preserved (often, eye movements).
• In psychogenic coma, defensive movements may be elicited (resistance to passive eye opening, arm falls away from face); presentation of a mirror may induce involuntary visual fixation.

Q: What is the role of EEG in the diagnosis of coma?
A: EEG is useful in diagnosis of psychogenic coma (should be normal) and in coma from brainstem lesions, in non-convulsive status epilepticus (shows electrographic seizures), and in possible herpes encephalitis (temporal or frontal sharp activity).

Q: Should anticonvulsants be given to comatose victims of trauma?
A: While there is no clear evidence that anticonvulsants improve outcome or reduce incidence of post-traumatic seizures, they are often given when post-traumatic intracranial hypertension and/or edema is suspected because seizures are known to raise ICP.

Ashwal S, Bale JF, Coulter DL, et al. The persistent vegetative state in children: report of the Child Neurology Society Ethics committee. Ann Neurol 1992;32:570.

Chiappa KH, Hill RA. Evaluation and prognostication in coma. Electroencephalogr Clin Neurophysiol 1998;106(2):149–155.

Feske SK. Coma and confusional states: emergency diagnosis and management. Neurol Clin 1998;16(2):237–256.

Johnston B, Seshia SS. Prediction of outcome in non-traumatic coma in childhood. Acta Neurol Scand 1984;69:417.