Coma

Coma

Nicholas S. Abend

INTRODUCTION

Consciousness is a state of arousal (wakefulness) with awareness of self and surroundings. Arousal is mediated by the brainstem and subcortical structures, including the ascending reticular activating system, hypothalamus, thalamus, and bilateral cerebral cortex. Awareness is mediated primarily by the cerebral cortex, but requires subcortical connections. Coma is a state of altered consciousness with loss of both wakefulness and awareness and characterized by an unarousable unresponsiveness. Coma is a temporary state that is followed by return of consciousness, progression to the minimally conscious state or vegetative state, or progression to brain death. Coma is a clinical diagnosis, made by history and physical examination. History and examination, in addition to diagnostic testing, may elucidate an etiology, direct treatment, and establish prognosis. Between normal consciousness and coma is a spectrum of states of diminished consciousness, subdivided by convention into lethargy, obtundation, and stupor (Table 21-1). Coma must be distinguished from delirium, akinetic mutism, locked-in syndrome, minimally conscious state, persistent vegetative state, and brain death (Table 21-2).

DIFFERENTIAL DIAGNOSIS LIST

Traumatic brain injury
Parenchymal injury (contusions and diffuse axonal injury)
Intracranial hemorrhage
Epidural hematoma
Subdural hematoma
Subarachnoid hemorrhage
Intracerebral hematoma
Cerebral edema
Acute hydrocephalus
Anoxic ischemic encephalopathy
Vascular
- Intracranial hemorrhage
- Arterial ischemic infract
Venous sinus thromboses
Vasculitis

TABLE 21-1 States of Altered Consciousness

Lethargy	Reduced wakefulness, deficits in attention
Obtundation	Blunted alertness, diminished interaction with environment
Stupor	Unresponsiveness with little/no spontaneous movement resembling deep sleep; temporary arousal with vigorous stimulation
Coma	Unarousable unresponsiveness

TABLE 21-2 Coma and Other Disease States of Altered Consciousness

Coma	Arousal and awareness are absent. Sleep/wake cycles are absent. Movements are reflexive and are not purposeful or reproducible. The EEG generally demonstrates diffuse slowing. It is a temporary state that evolves into other states.
Vegetative state	Arousal is present but awareness is absent. Sleep/wake cycles are present. Brainstem and hypothalamic function is sufficiently intact to allow prolonged survival with care. Movements are reflex and are not purposeful or reproducible. The EEG generally demonstrates diffuse slowing. It is considered permanent if it lasts more than 12 mo after traumatic brain injury or 3 mo after nontraumatic brain injury.
Minimally conscious state	Arousal is present and there is partial awareness consisting of minimal but definite behavioral evidence of self or environmental awareness such as following simple commands, making verbalizations, making simple nonreflexive gestures, or reacting appropriately to emotional content of stimuli. A sleep/wake cycle is present. The EEG may contain mild slowing or may be normal. Distinguishing a minimally conscious state from a vegetative state often requires a multidisciplinary team using a responsiveness program.
Akinetic mutism	Both arousal and awareness are present but there is extreme slowing or absence of bodily movement loss and slowed cognition. Sleep/wake cycles are present. The EEG demonstrates diffuse slowing. Caused by damage to bilateral inferior frontal lobes, extensive bihemispheric disease, lesions of the paramedian mesencephalic reticular formation, or posterior diencephalon.
Locked-in syndrome	A state of preserved arousal and awareness, intact sleep/wake cycles, and normal EEG activity with complete paralysis of voluntary muscles. If due to severe neuromuscular disease (e.g., botulism, Guillain-Barre syndrome, neuromuscular blocking medications), then no movement occurs. If due to damage to the corticospinal and corticobulbar pathways below the level of the midbrain, then vertical eye movements may be preserved.
Brain death	Permanent absence of all brain activity, including brainstem function.
Delirium (acute confusional state)	Characterized by impaired attention, fluctuating level of consciousness, disorganization, perceptual disturbances, and increased or decreased psychomotor activity. Recall problems and disorientation are found on examination. It is often associated with acute metabolic, toxic, or endocrine disturbances but may also occur with focal lesions (especially frontal) and seizures.

Infections/postinfectious/inflammatory
- Meningitis and encephalitis: bacterial, viral, rickettsial, and fungal
- Acute demyelinating diseases
  - Acute disseminated encephalomyelitis (ADEM)
  - Multiple sclerosis
  - Acute leukodystrophy
Inflammatory/autoimmune
- Sarcoidosis
- Sjogren syndrome
- Lupus cerebritis
Abscess
Granuloma
Acute metabolic derangement
- Hypoglycemia
- Hyperglycemia (diabetic ketoacidosis and non-ketotic hyperosmolar)
- Hyponatremia or hypernatremia
- Hypercalcemia
- Addison disease
- Hypothyroidism or panhypopituitarism
- Uremic coma
- Hepatic coma
- Hypercapnia
- Hyperbilirubinemia
- Cofactors: thiamine, niacin, and pyridoxine
- Inborn errors of metabolism
- Urea cycle disorders
- Amino acidopathies
- Organic acidopathies
- Mitochondrial disorders
Neoplastic
- Lymphoma
- Gliomatosis cerebri
- Multiple metastases
- CNS neoplasm causing compression or hydrocephalus or within brain stem
Toxins
- Medications: narcotics, sedatives, antiepileptics, antidepressants, analgesics, and aspirin
- Environmental toxins: organophosphates, heavy metals, cyanide, and mushroom poisoning
- Illicit substances: alcohol, heroine, amphetamines, and cocaine
Paroxysmal neurologic disorders
- Seizures/status epilepticus
- Acute confusional migraine
Intussusception
Psychogenic unresponsiveness

EVALUATION OF COMA

History, physical examination, and diagnostic testing are essential in determining coma etiology so that specific therapies may be instituted. Initial efforts must identify reversible causes of coma and normalize vital functions in order to prevent secondary brain injury. An initial approach is listed in Table 21-3. Recent guidelines have also been published online (see “Suggested Readings”).

History

History taking should include a detailed description of events leading to the onset of coma, with particular attention to timing, exposures, and accompanying symptoms. Rapidly developing somnolence suggests a metabolic, toxic, or infectious etiology. Sudden onset of coma without trauma suggests spontaneous intracranial hemorrhage or seizure. Slowly progressive loss of consciousness suggests hydrocephalus, expanding mass lesion, or indolent infection. Preceding headache with positional changes or with Valsalva maneuver suggests increased intracranial pressure (ICP) from hydrocephalus or mass lesion. Headache with neck pain or stiffness suggests meningeal irritation from inflammation, infection, or hemorrhage. Fever suggests infection, but its absence does not rule it out, particularly in infants under 3 to 6 months of age or in immunocompromised children. Recent fevers or illness suggests an autoimmune process like ADEM. Abnormal movements or a fluctuating mental status may suggest nonconvulsive seizures or post-ictal state. Questions about possible toxic ingestions should include a survey of medications and poisons in the home and environment, even if not readily accessible to the child. Travel history may explain exposure to infections prevalent in certain areas, such as Lyme in the northeastern United States; insect bite history is also helpful but may be misleading. Recent exposure to kittens in a comatose child with axillary or inguinal lymphadenopathy may be a clue to infection with Bartonella henselae (cat scratch encephalopathy). A history of recurrent abdominal pain may suggest intussusception.

TABLE 21-3 Initial Evaluation of Coma

Airway, breathing, and circulation assessment and stabilization.
- Ensure adequate ventilation and oxygenation.
- Blood pressure management depends on considerations regarding underlying coma etiology. If hypertensive encephalopathy or intracranial hemorrhage, then lower blood pressure. If perfusion-dependent state such as some strokes or elevated intracranial pressure (ICP), then reducing blood pressure may reduce cerebral perfusion.
- Identify and treat hypoglycemia (thiamine may be given first in adult patients).
Draw blood: Consider electrolytes, ammonia, arterial blood gas, liver and renal function tests, complete blood count, lactate, pyruvate, and toxicology screen.
Neurological assessment.
- GCS score.
- Assess for evidence of raised ICP and herniation.
- Assess for abnormalities suggesting focal neurologic disease.
- Assess for history or signs of seizures.
If there is concern for infection and LP must be delayed, then provide broad-spectrum infection coverage (including bacterial, viral, and possibly fungal).
Give specific antidotes if toxic exposures are known.
- For opiate overdose administer naloxone.
- For benzodiazepine overdose consider administering flumazenil.
- For anticholinergic overdose consider administering physostigmine.
Identify and treat critical elevations in ICP.
- Neutral head position, elevated head by 20-30 degrees, sedation.
- Hyperosmolar therapy with mannitol 0.5-1 g/kg or hypertonic saline.
- Hyperventilation as temporary measure.
- Consider intracranial monitoring.
- Consider neurosurgical intervention.
Head CT (noncontrast).
Treat seizures with IV anticonvulsants. Consider prophylactic anticonvulsants.
Investigate source of fever and use antipyretics and/or cooling devices to reduce cerebral metabolic demands.
Detailed history and examination.
Consider: lumbar puncture, EEG or extended long-term EEG monitoring, magnetic resonance imaging, metabolic testing (amino acids, organic acids, acylcarnitine profile), autoimmune testing (ANA panel, anti-thyroid antibodies), thyroid testing (TSH, T3, T4).

Eliciting a history of trauma, whether accidental or nonaccidental, is crucial and understanding the mechanism of injury can direct further investigation. Delay of hours between trauma and loss of consciousness can be seen with epidural hematoma. Discordance between the history of trivial trauma and the findings of extensive injury or delay in seeking treatment should raise suspicion of child abuse.

The child’s past medical history may provide valuable information. Prior episodes of unexplained coma suggest intermittent metabolic disease, recurrent toxic ingestions, or Munchausen by proxy syndrome. Developmental delay and preexisting neurological abnormalities may suggest inborn errors of metabolism, but are also independent risk factors for epilepsy, thus raising suspicion of a prolonged post-ictal state. Recent weight changes or other constitutional abnormalities suggest endocrine dysfunction or an oncologic process. In a child with known cardiac disease, circulatory collapse and hypoxic ischemic encephalopathy should be considered.

Examination

The Glasgow coma scale (GCS) is a reproducible way to rate any patient with altered consciousness using three areas of response to stimuli, eye opening, verbal response, and motor response, and has been adapted for use in children (Table 21-4). Often, intubation and mechanical ventilation are indicated in a child with deteriorating mental status whose GCS is ≤8.

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