Coma





The causes of coma are varied and include a number of immediately life-threatening conditions for which emergent intervention is necessary. Close attention to general stabilization measures is necessary for all patients with coma. Simultaneously, laboratory studies should be sent and a brief history obtained from bystanders, family, and emergency medical first responders. At times the etiology of coma is obvious or known, such as traumatic brain injury or witnessed drug overdose. When the cause of coma is unknown, initial therapy is often empiric. Causes of coma may be divided into primary brain disorders and systemic disorders that secondarily cause brain dysfunction. Primary brain disorders may be structural, such as pontine infarction, large intracerebral hemorrhage, or hydrocephalus; or nonstructural, such as seizures or encephalitis. Examples of systemic disorders that cause coma include shock (e.g., from sepsis or hemorrhage), exposure to toxins or drugs (e.g., pesticides, opiates), and severe metabolic derangements (e.g., hypoglycemia).



  • A.

    Coma is frequently accompanied by respiratory and/or hemodynamic instability. Initial resuscitation includes securing an airway (usually with an endotracheal tube), mechanical ventilation, and hemodynamic support. Laboratory evaluation includes serum glucose, electrolytes, liver and thyroid function tests, ammonia, osmolality, blood count, arterial blood gas, and toxicology testing.


  • B.

    A focused clinical examination includes both a neurologic assessment (“coma exam”) and a systemic survey. The coma examination focuses on level of arousal, cranial nerve function—especially the pupils and position of the eyes—and the motor examination with particular attention to motor asymmetry and abnormal reflexive movements (posturing). The goal of the initial neurologic examination is to help determine whether the coma is due to (1) brainstem dysfunction or a large focal hemispheric lesion (in which case a structural lesion is more likely) or (2) to bihemispheric dysfunction (in which case a systemic cause is more likely). Structural lesions may require emergent neurosurgery, whereas systemic causes typically require medical therapy. To facilitate rapid assessment and communication of severity, clinical scales such as the Glasgow Coma Scale are frequently used. A systemic survey should include full exposure of the patient and a search for etiological clues (e.g., the presence of traumatic injuries, skin temperature, needle marks suggesting intravenous drug abuse).


  • C.

    When a structural cause is suspected, emergent noncontrast head computed tomography (CT) should be performed. This will identify many intracranial catastrophes leading to coma, such as large intracerebral hemorrhage or other mass lesions leading to herniation and acute hydrocephalus. Diffuse cerebral edema is typically identifiable on head CT, though in a young person the changes may not be as obvious as in older patients. Posterior reversible encephalopathy syndrome sufficient to cause coma is usually apparent on head CT, though better defined on brain magnetic resonance imaging (MRI).


  • D.

    Two important though infrequent causes of coma often missed on initial noncontrast head CT are basilar thrombosis and deep cerebral vein thrombosis. In the case of basilar thrombosis, it often takes 12–24 hours for ischemic changes consistent with infarction to be visible in the posterior circulation. Deep cerebral vein thrombosis may cause bi-thalamic venous edema and infarction, but this also may take hours to appear on CT, or the signs may be subtle and symmetric causing them to be unappreciated. CT angiography will rapidly and accurately identify basilar thrombosis, and CT venography deep cerebral vein thrombosis.


  • E.

    When coma is of unknown etiology, initial therapy is usually empiric. Empiric measures might include the following: (1) hyperventilation if elevated intracranial pressure is suspected; (2) administration of naloxone (0.4–2 mg SC/IM/IV every 2–3 minutes as needed) to address possible opiate intoxication; (3) gastric lavage with activated charcoal if recent medication overdose is suspected; (4) antibiotic administration if meningitis, encephalitis, or sepsis is suspected; and (5) administration of thiamine (500 mg IV tid × 3 days, then 250 mg IV/IM daily × 5 days) followed by glucose (75 mL of 20% glucose or 150 mL of 10% glucose IV) to treat possible thiamine deficiency and hypoglycemia, respectively. In the setting of significant thiamine depletion, glucose may precipitate acute thiamine deficiency, so thiamine should be given first. Severe thiamine deficiency causes Wernicke encephalopathy, which classically presents with confusion, ataxia, and ophthalmoplegia, but in its extreme form may manifest as coma.


  • F.

    The etiology of coma is sometimes known or obvious. Whether neuroimaging is indicated depends on the specific etiology. For example, in the case of traumatic brain injury, neuroimaging is mandatory to determine if the patient requires immediate surgery, whereas in the case of cardiac arrest, neuroimaging might be deferred. When indicated, noncontrast head CT is usually the initial study, given speed of acquisition compared to MRI.


  • G.

    Further testing might include lumbar puncture for cerebrospinal fluid analysis, electroencephalography to assess for status epilepticus, or further neuroimaging (e.g., brain MRI).


Algorithm 11.1


Flowchart for the treatment of a comatose patient. CT, Computed tomography; CTA, computed tomography angiography; CTV, computed tomography venography; EEG, electroencephalogram; MRI, magnetic resonance imaging; TBI, traumatic brain injury.

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May 3, 2021 | Posted by in NEUROLOGY | Comments Off on Coma

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