Coma, Seizures, and Other Disorders of Consciousness
Patients who present to the emergency department (ED) with a history of transient loss of consciousness or impaired consciousness require a thorough and systematic evaluation by the physician. It is important to obtain as much history as possible from family, friends, and other observers. A history of trauma; previous illness; medication, alcohol, or drug use; or psychiatric illness is important to elicit to guide appropriate additional studies and therapy.
COMMON CAUSES OF IMPAIRED CONSCIOUSNESS
Head trauma
Intracerebral hemorrhage
Thromboembolic cerebrovascular disease
Seizure disorder*
Hypoglycemia*
Alcohol or drug intoxication
Diabetic ketoacidosis*
Hyperosmolar hyperglycemic nonketotic coma*
Syncope (see Chapter 40)
Orthostatic hypotension
Lactic acidosis*
OTHER CAUSES OF IMPAIRED CONSCIOUSNESS NOT TO BE MISSED
Subarachnoid hemorrhage
Meningitis
Encephalitis
Wernicke encephalopathy
Hypertensive encephalopathy
Intracranial neoplasm
Uremic encephalopathy
Hepatic encephalopathy
Hyponatremia
Myxedema*
Hypocalcemia
Hypercalcemia
Dehydration
Carbon monoxide inhalation
Chronic obstructive pulmonary disease with acute decompensation
Hyperthermia
Hypothermia
Hyperthyroidism (thyroid storm)*
HISTORY
The use of medications, alcohol, or illicit drugs or a history of trauma, which may have been remote or trivial, is an important differential feature to ascertain early in the evaluation of all patients with an alteration in mental status.
The presence of palpitations, chest or abdominal pain, headache, fever, or neck stiffness should specifically be investigated.
A history of diabetes mellitus, hypothyroidism, hypoparathyroidism or hyperparathyroidism, liver disease, hypertension, renal failure, or chronic obstructive pulmonary disease is important to determine.
Changes in mental status or loss of consciousness associated with standing or on arising from sitting or recumbency suggest postural hypotension.
PHYSICAL EXAMINATION
A complete set of vital signs including an oral or rectal temperature should be obtained in all patients; postural vital signs should also be obtained when a history of syncope is present. Pulse oximetry must be measured.
Signs of trauma, the stigmata of liver disease, needle tracks, and infectious or embolic phenomena should be sought in the examination of the skin.
Examination of the head may reveal “raccoon’s eyes,” suggesting an orbital or basilar skull fracture; Battle sign, suggesting a mastoid fracture; or nasal or aural bleeding, suggesting a basilar skull fracture.
Examination of the eyes is a crucial aspect of the neurologic examination of the comatose patient. The position of the eyes with respect to the head and to one another should be ascertained. Conjugate displacement of the eyes occurs toward the side of a destructive cortical mass lesion, away from the side of an irritable (epileptiform) cortical focus, and away from the side of a pontine lesion. Dysconjugate eye positions virtually always suggest a brainstem abnormality. Pupils that are midposition (3-5 mm diameter) and nonreactive to light are found in patients with midbrain damage. Conversely, if the pupils react to light, the midbrain is intact. A unilaterally dilated, unreactive pupil implies third nerve compression secondary to temporal lobe herniation. Small, reactive pupils with a dysconjugate gaze directed toward the nose suggest a pontine lesion.
Funduscopy should also be performed and may reveal papilledema, suggestive of increased intracranial pressure, or a subhyaloid hemorrhage, occasionally noted in patients with ruptured intracranial aneurysms.
Both subarachnoid hemorrhage and meningitis may produce neck stiffness.
Fetor hepaticus, the fruity smell of ketoacidosis, alcohol, or acetaldehyde on the breath may be noted.
Posturing is helpful in discerning the cause of coma. Decorticate posturing consists of flexion and adduction of the arms and extension of the legs and suggests a deep hemispheric process. Decerebrate posturing consists of extension, adduction, and internal rotation of the arms and extension of the legs; this posturing localizes the lesion to the upper brainstem.
Spontaneous seizure activity is also important to note; diffuse, generalized tonic-clonic movements suggest a grand mal seizure, whereas lip smacking and other automatisms indicate a temporal lobe focus. Focal seizures or generalized seizures that begin with a discrete focus suggest a local structural lesion.
In patients with coma, the respiratory pattern is useful in localizing lesions. Cheyne-Stokes respirations, characterized by periods of hyperventilation tapering to periods of apnea, suggest bilateral deep hemispheric disease or basal ganglia dysfunction and may be seen as well in congestive heart failure, uremia, or hypertensive encephalopathy. Central neurogenic hyperventilation refers to continued, regular, rapid respirations that have no specific localizing significance but are said to increase in regularity with increasing depth of coma. A prolonged inspiratory phase followed by expiratory apnea defines apneustic breathing, which implies lower pontine damage. Ataxic breathing suggests a lesion in the medullary respiratory center and is best described as a chaotic, random respiratory pattern.
Motor responses must also be observed during the neurologic examination of the comatose patient, both spontaneous and induced by painful stimuli. Focal seizures may be of localizing value, whereas generalized seizures are not. Myoclonic jerks and asterixis should be noted and imply metabolic encephalopathy. Localized absence of movement may be caused by a structural lesion or may be a manifestation of the postictal state (Todd paralysis). Higher level motor movements, such as yawning or withdrawal from painful stimuli, imply that the corticospinal tracts are intact.
DIAGNOSTIC TESTS
Measurement of sodium, BUN, creatinine, glucose, calcium, magnesium, and blood ammonia, a toxic screen; computed tomography (CT) or magnetic resonance imaging (MRI) studies of the head; an electrocardiogram (ECG); and lumbar puncture may all provide useful information.
The selection and sequential performance of each of these tests must be judicious and guided by both history and physical examination. If meningitis or encephalitis is suspected, a lumbar puncture is indicated.
TREATMENT
The physician’s immediate therapeutic responses to comatose patients should include standard airway maintenance and ventilation, intravenous catheter placement, and, after drawing blood for the appropriate studies, the intravenous administration of one ampule of 50% D/W, 100 mg of thiamine, and 0.8 to 2.0 mg of naloxone. Comatose and semicomatose patients who cannot protect their airways will need endotracheal intubation and ventilator support. Care should be taken not to overhydrate the patient with suspected brain edema. In patients with malignant hypertension, intravenous labetalol or continuous infusion nitroprusside should be
administered as described in Chapter 24. In patients with suspected bacterial meningitis, antibiotics should be administered as early as possible.
Most patients with unexplained abnormalities of mental status require admission. In addition, patients with syncope that is not clearly benign (i.e., vasovagal syncope in a young person, intoxication, rapidly resolving insulin-induced hypoglycemia) must be admitted to the hospital or an observation unit for monitoring and further evaluation. Importantly, patients with hypoglycemia secondary to treatment with one of the oral sulfonylurea agents (tolazamide, acetohexamide, and especially chlorpropamide) may require admission because of the long half-life of these agents and the consequent need for continuous intravenous glucose therapy.
CLINICAL REMINDERS
Consider postural vital signs, a pregnancy test, an ECG, a complete blood count, and stool for occult blood analysis in patients who present with a history of syncope; observation and monitoring may be appropriate (see Chapter 40).
Administer thiamine to patients in coma before the administration of glucose to prevent the precipitation of acute Wernicke encephalopathy.
Administer antibiotics to all patients with suspected bacterial meningitis as soon after lumbar puncture as possible. If the lumbar puncture will be delayed or if it is unobtainable for any reason, antibiotics should then be given before obtaining cerebrospinal fluid.
Do not overhydrate patients with suspected brain edema.
Hyperventilate to a Pco2 of 25 to 30 mm Hg, and administer mannitol (1.0-1.5 g/kg over 20-30 minutes) to patients with increased intracranial pressure. Dexamethasone (10 mg followed by 4-6 mg every 6 hours) should be administered early.
SPECIFIC DISORDERS
Seizure Disorder
Diagnosis
Seizures may be classified as generalized or partial (focal). Generalized seizures include tonic-clonic (grand mal), absence (petit mal), and febrile seizures. Partial seizures may be either simple (focal seizures) or complex (focal with alteration in mental status).
Patients may present to the ED during a seizure or postictally. Because most grand mal seizures last no more than 5 or 10 minutes, patients are usually postictal on arrival.
Confusion, evidence of fecal or urinary incontinence, postictal paralysis, and perioral injury are commonly noted and suggest a recent tonic-clonic seizure.
Most patients presenting to the ED with a seizure have a prior history of seizures. Medication noncompliance and alcohol or benzodiazepine withdrawal are common causes of recurrent seizures.
Head trauma is the leading cause of seizures in all age groups.
In the absence of head trauma, in infants and children up to age 5, fever is the likeliest cause of a first seizure. From ages 5 to 30, idiopathic convulsive disorders predominate, whereas from ages 30 to 60, intracranial malignancy and AIDS-related intracranial processes become increasingly more common. Beyond age 60, cerebrovascular disease represents the greatest single cause of seizures, including both acute embolic and thrombotic events.
A first-time seizure in pregnant women in the third trimester or postpartum period may represent eclampsia.
The physical examination must be directed toward uncovering any underlying disease processes, including neoplasia or infarct of the central nervous system, evidence of head trauma, metabolic derangements (e.g., hypocalcemia, hypoglycemia, or hypomagnesemia), or drug abuse.
The neck should be examined for evidence of rigidity and the anterior neck should be specifically examined for signs of previous surgery, suggesting possible hypocalcemia related to thyroid or parathyroid disease.
In particular, the neurologic examination should be directed at defining lateralizing or focal signs. A Todd or postictal paralysis, although suggesting a focus, may be noted in patients with generalized epilepsy for 24 to 48 hours after the seizure. In this case, the usefulness of neurologically defined focal findings is minimal; beyond 48 hours, however, any focality noted on examination likely has a structural counterpart.
Diagnostic Tests
Testing in all patients having a first seizure should include a measurement of serum electrolytes, calcium, BUN, and glucose. All women of childbearing age should have a pregnancy test. A noncontrast CT of the brain should be completed in the ED or arranged for as an outpatient in the near future. Toxicology screening and ECG should be considered on a case by case basis. If CNS infection is suspected, a lumbar puncture should be performed after elevated intracranial pressure (related to focal mass effect) has been excluded. A CT scan of the head should be obtained immediately and before lumbar puncture in all patients with suspected focal processes, continued abnormal mental status, and elevated intracranial pressure.
Patients with recurrent seizures should have anticonvulsant medication levels measured.
Generalized Seizures
An initial and immediate loss of consciousness and extensive autonomic phenomena are common clinical features. Motor activity may be either absent (akinetic) or convulsive (tonic-clonic or grand mal). Frequently, this seizure pattern is preceded by a preictal phase consisting of bilateral, generalized myoclonic jerks, usually occurring in flexion and lasting several seconds. Autonomic changes begin in the preictal phase, are maximal toward the end of the tonic phase, and decrease during the clonic phase; these consist of tachycardia, hypertension, bladder distention, piloerection, glandular hypersecretion, mydriasis, and apnea. Tonic contractions, in flexion then extension, herald the ictal phase. Tonic rigidity lasts from 10 to 20 seconds and evolves through a vibratory tonus while progressing into clonus. Tonic tremors slow in frequency but increase in amplitude until distinct clonic activity, manifested by alternating muscular relaxation and violent flexor contractions, appears. Clonus usually lasts for approximately 30 seconds, during which time the relaxation cycles progressively increase in duration until the seizure terminates with a final flexor jerk. Intraoral injury is common during the clonic phase, while urinary and fecal incontinence typically occur in the immediate postictal period.
Febrile Convulsions
Febrile convulsions typically manifest as generalized tonic-clonic seizures. These constitute the most common childhood neurologic problem and affect 2% to 5% of all children younger than 5 years of age. In general, a febrile seizure may be defined as a convulsive episode in a child between the ages of 6 months and 5 years in whom other causes have been excluded. Most febrile seizures are generalized from the outset and subside within 10 to 20 minutes. Episodes usually develop 2 to 6 hours after
the onset of fever and are most commonly noted in children with upper respiratory tract infection, otitis media, pharyngitis, roseola infantum, or Shigella gastroenteritis. Fifty percent of patients report a family history of febrile seizures. Two percent of children with febrile seizures will develop idiopathic epilepsy while up to 33% will have a recurrence associated with fever.
The physician must bear in mind that the diagnosis of febrile seizure is one of exclusion; other causes, such as trauma and meningoencephalitis, must be ruled out before concluding that the convulsion was due only to fever. A first seizure in a febrile child in whom a central nervous system infection cannot be excluded remains an indication for lumbar puncture and a period of observation. Typically, these are children less than 1 year of age. Meningitis can often be excluded in older children based upon clinical appearance after the seizure and postictal period.
After the airway, breathing, and circulation have been evaluated and secured and the diagnosis of febrile seizure has been made, promptly reducing fever with antipyretics and sponging with tepid water as needed is essential for the prevention of short-term recurrences. Occasionally, treatment with intravenous lorazepam (0.05 to 0.1 mg/kg intravenous) or diazepam (0.1-0.25 mg/kg intravenous given at 1 mg/min up to 10 mg) may be required to terminate the seizure.
