History

Chief complaints relating to depressed consciousness vary widely. Family members may report the patient as being more difficult to arouse from sleep or less interactive. Often, family members or friends have alerted emergency medical services after the patient is “found down” or unarousable even with vigorous stimulation.

Often, information from alternate sources guides the diagnostic workup. Common sources of information include family members, neighbors, prehospital personnel, law enforcement, and nursing home staff.³ They may know of preceding symptoms such as headache, nausea, vomiting, or fever. Key historical information includes the rate of symptom onset, a history of trauma, exposure to drugs or toxins, or new medications or change in dosage. Rate of symptom onset is important, as an abrupt onset of decreased alertness may suggest structural phenomena or vascular insult, whereas a gradual onset would be more indicative of the slow, indolent course frequently seen with toxic, metabolic, or infectious causes. Family members usually have some knowledge regarding the patient’s past medical history, which may include diabetes, liver or renal disease, vascular disease such as hypertension, coronary disease, stroke or transient ischemic attacks, malignancy, seizures, immunocompromised states such as human immunodeficiency virus (HIV) infection, sickle cell disease, organ transplantation, or psychiatric illness. Family members may also be able to relay additional diagnostic clues such as rate of onset or waxing-waning characteristics of the patient’s symptoms.

In addition, previous medical records should be reviewed whenever possible to augment or confirm the information provided. Items with the patient such as a card in the wallet containing lists of medical conditions and/or medications or a medical alert bracelet or necklace can provide valuable information. If the patient’s historical baseline mental status cannot be established, the current presentation is assumed to be an acute change.⁴

Causes of depression of consciousness vary with patient age (Box 16-2). The elderly are particularly vulnerable to infectious causes, medication changes, and alterations in their living environments. Young adults and adolescents are more likely to be affected after recreational drug use or trauma. Accidental toxic ingestions are often seen in younger children. In infants, infectious causes of depressed consciousness are most common; however, trauma secondary to physical abuse and metabolic derangements from inborn errors of metabolism can be seen.⁵

Physical Examination

The severity of presenting symptoms dictates the speed needed for stabilization and diagnosis. After necessary stabilization measures have been instituted (e.g., intubation of the frankly comatose patient), a systematic physical examination is conducted. Level of consciousness is determined by the patient’s ability to speak in full, coherent sentences and to respond appropriately to the examiner. A rapid, directed neurologic screening examination can determine whether the patient has a significant focal motor deficit. The presence of a distinctive odor on the breath, although uncommon, can cue the examiner to the presence of alcohol, ketones (diabetic or alcoholic ketoacidosis), or bitter almonds (cyanide toxicity). Undressing the patient completely permits evaluation for signs of trauma or skin lesions suggesting overwhelming infection or needle track marks.

Significant hypotension with depressed consciousness suggests shock with resultant cerebral hypoperfusion, and both causes and therapy should be addressed immediately. Hypertension can be seen as a result of subarachnoid hemorrhage or cerebral or brainstem infarction or may be secondary to any condition resulting in increased ICP. Late-stage, severe elevation in ICP can cause bradycardia and hypertension, also known as the Cushing reflex. This is an ominous sign and is seen most commonly in lesions affecting the posterior fossa and in children. Bradycardia is also seen in medication overdoses such as with beta-blockers, calcium channel blockers, cardiac glycosides, and clonidine. Myocardial conduction blocks may also cause severe bradycardia, hypotension, and subsequent stupor or coma. Tachycardia has a broad differential in the altered patient and can be the result of hypovolemia, fever, severe anemia, thyrotoxicosis, and drugs such as anticholinergics and stimulants. Both hypothermia and hyperthermia can result in altered mental status whether from infectious, structural, toxic or metabolic, or environmental causes. Hyperventilation, Kussmaul’s or Cheyne-Stokes breathing, agonal breathing, apnea, or other alterations in respiratory patterns can suggest primary CNS abnormalities or toxic or metabolic derangements. Changes in respiratory patterns can be challenging for the clinician in an unresponsive patient, as they can represent the sequelae of a primary CNS insult or compensation for an underlying toxic or metabolic process.

Immediately after an assessment of the patient’s vital signs, a head-to-toe physical examination is performed.⁶ A methodical and complete head and neck examination is conducted, with particular emphasis on examination of the pupillary reflexes and eye movements (see later discussion) and any indications of head trauma, including hemotympanum, periorbital ecchymosis, Battle’s sign, scalp hematoma, or CSF otorrhea or rhinorrhea. The hydration of the mucous membranes may give clues to specific toxidromes. Laceration or bruising of the tongue may indicate a recent seizure.

Examination of the neck should focus on evidence of meningismus, which can be seen in meningitis, subarachnoid hemorrhage, and some cases of herniation. The cervical spine should be immobilized if there are signs of neck trauma, such as cervical spine tenderness or evidence of blunt external trauma, or if the history indicates a potential mechanism for neck injury. Stridor indicates respiratory distress typically from infection, allergic reaction, or foreign body aspiration. Presence of a goiter may indicate underlying thyroid pathology.

Cardiopulmonary examination should focus on respiratory effort, ventilatory patterns, presence of arrhythmia or murmurs, cardiac output, and the presence of injury. Potentially helpful abdominal findings include hepatosplenomegaly, pulsatile masses, ecchymosis, or sequelae of liver failure such as ascites, caput medusa, or spider angiomata. Gross blood, purulent drainage, or retained foreign bodies should be sought on genitourinary and rectal examination. In the absence or presence of signs of trauma, lesions on the skin such as rashes, signs of drug use (needle tracks or medication patches), or embolic phenomena can be differential clues.

A systematic neurologic examination, with particular attention paid to the eyes, is the most useful tool in differentiating a structural from a systemic or metabolic cause of depressed consciousness or coma. A head-to-toe approach is a proven strategy. This should include evaluation of the patient’s Glasgow Coma Scale (GCS) score (Box 16-3), level of alertness, cranial nerves, strength, reflexes, and cerebellar functions with emphasis on gait, pronator drift, finger-to-nose, heel-to-shin, rapid alternating movements, and Romberg testing. The GCS measures the best motor and verbal responses and the degree of stimulus required to elicit eye opening and is measured serially, as level of consciousness frequently is dynamic after the initial insult and subsequent response to therapy. The GCS does not differentiate among causes of altered mental status or coma or assess cognition but is useful in monitoring changes in mental status when serial examinations are performed and serves as an objective reference for communicating with consultants.⁷ A change of two or more points in serial GCS testing represents a significant change.

Discovery of a focal neurologic deficit is suggestive of a structural cause. Particular attention should be paid to a focused eye examination, during which a helpful amount of information can be obtained. Unilateral dilatation of a pupil (“blown pupil”) and loss of reactivity in a comatose patient are ominous signs of uncal herniation and necessitate immediate neurosurgical consultation and intervention. Papilledema, which may indicate increased ICP or retinal hemorrhages associated with trauma, can be identified on funduscopic examination. The eye examination should also include testing of eye movements, which are coordinated by the medial longitudinal fasciculus located in the brainstem and ocular centers located in the cerebral cortex. Cranial nerves III, IV, and VI are responsible for control of the extraocular muscles. Cranial nerve III paralysis results in a persistently abducted eye, whereas a persistently adducted eye is caused by paralysis of cranial nerve VI. In the setting of trauma, a unilateral third cranial nerve palsy suggests an ipsilateral compressive lesion such as seen with epidural hematoma. Cranial nerve VI palsies are often nonlocalizing, as the nerve has a long intracranial course and compressive forces from intracranial mass effects (e.g., tumor, traumatic hematoma, increased ICP) may compromise cranial nerve function anywhere in its course. Horizontal disconjugate gaze is an important finding and is commonly seen in patients who are sedated, drowsy, or intoxicated. Disconjugate gaze found in the vertical plane is usually more serious and suggests cerebellar or pontine dysfunction. Normal ocular motility suggests that a significant portion of the brainstem remains intact.

Oculocephalic (doll’s eyes) and oculovestibular reflex testing are useful in looking at the functional integrity of the brainstem. These tests, if results are negative, make structural lesions in the brainstem very unlikely as the source of the patient’s altered mental status.

If there are no contraindications, such as suspected cervical spine injury, oculocephalic testing is accomplished by observing the patient’s eye movements while the head is turned from side to side. Patients who exhibit a maintained forward gaze despite head turning (doll’s eye reflex) are unlikely to have a brainstem-mediated cause of coma. If the eyes remain in a fixed position within the orbits, turning in unison with the head, brainstem dysfunction is suggested. Oculovestibular or “cold water caloric” testing is a more sensitive test for brainstem involvement and cannot voluntarily be resisted (Fig. 16-2). After elevation of the patient’s head to 30 degrees (this can be done in patients whose cervical spine is not cleared by placing the bed in the reverse Trendelenburg position), 10 to 30 mL of ice water is used to irrigate the external auditory canal. Tympanic membrane perforation and cerumen impaction should be ruled out before this test is performed. In patients who have an intact brainstem, the response is a slow conjugate deviation of gaze toward the side of the cold water stimulus for 30 to 120 seconds. The reflex is short-lived and followed by corrective fast beats of nystagmus toward the midline. This corrective nystagmus is described by the mnemonic COWS, which stands for “cold-opposite, warm-same.” If there is no response to the irrigation, brainstem dysfunction is possible.

Recently, literature on the phenomenon of basilar artery stenosis or occlusion manifesting as depressed consciousness or coma has increasingly been published. A review of the Lausanne Stroke Registry showed that 100% of patients with poor outcome from high-grade basilar stenosis or occlusion had either stupor or coma or the triad of pupillary abnormalities, dysarthria, and bulbar findings on presentation.¹

Laboratory Studies

Bedside glucose testing definitively confirms or excludes hypoglycemia and can frequently limit further extensive metabolic testing in diabetic or intoxicated patients. Serum electrolytes and renal function measurement identify the presence of a metabolic acidosis, anion gap, uremia, or derangements in sodium or potassium. Changes in serum calcium can be a marker for metastatic disease, and severe hypercalcemia can cause altered mental status. Arterial blood gas analysis rapidly assesses acid-base status and the presence of hypercarbia or hypoxia and allows calculation of arterial-alveolar gradient in conditions in which shunting is suspected. Carbon monoxide (CO)–oximetry can be added to confirm methemoglobinemia or carbon monoxide exposure.

A urine dip test is a quick way to screen for the presence of ketones, the spilling of glucose as seen in hyperosmolar states, or infection, which can frequently precipitate changes in mentation, especially in the elderly. Urinalysis itself provides valuable information regarding hydration status (specific gravity) and the possible presence of calcium oxalate crystals in the setting of ethylene glycol ingestion. Urine drug testing may confirm a suspected ingestion or be helpful if another cause is not readily apparent.

A complete blood count can be useful. Although an elevated white blood cell count can be a marker for infection, it is nonspecific and rarely helpful in discerning a toxic or metabolic cause. An abnormally low white blood cell count, however, suggests an immunocompromised state and should urgently direct clinical investigation toward an infectious cause. Profound anemia may be seen from witnessed or occult blood loss. Thrombocytopenia can be a marker for sepsis, intracranial hemorrhage, or disseminated intravascular coagulation.

Elevated results from serum coagulation studies can be a marker for bleeding dyscrasias, liver disease, or supratherapeutic levels of anticoagulation drugs. Both platelets and coagulation studies should be checked before invasive procedures are performed at noncompressible sites such as lumbar punctures and central venous access, if the patient’s condition allows.

Serum ammonia levels are controversial and have not been shown to be a reliable marker for the cause of depressed consciousness. Although usually associated with severe liver disease, ammonia levels can be elevated in other conditions such as valproic acid toxicity and inborn errors of metabolism and can be normal in patients with hepatic encephalopathy.⁸ Thyroid function studies can help confirm myxedema coma or thyrotoxicosis. When CNS pathology such as infection or hemorrhage is suggested but not seen on neuroimaging studies, cerebrospinal fluid analysis is undertaken.

Imaging Studies

Noncontrast computed tomography (CT) of the brain is the initial imaging modality of choice in the setting of depressed consciousness and coma. In the majority of ED settings, it is available and quickly obtained, and this makes CT more suitable than other imaging tests for the patient with borderline hemodynamic instability. Brain CT is sufficiently sensitive to detect most intracranial hemorrhages that are large enough to cause coma. In addition, the presence of hydrocephalus can quickly be assessed. Despite its utility, linear artifacts created by the thick skull base can limit the view of the posterior fossa on CT. In this case, magnetic resonance imaging (MRI) of the brain is generally much better for identifying structural lesions in this region. However, this modality is less practical in most ED settings because of its cost, limited availability, and duration of acquiring each study, which consequently limits the ability to monitor or access the unstable patient.⁴

Contrast-enhanced CT may be used if a tumor, metastatic disease, or intracerebral infection is suspected. CT or magnetic resonance angiography or venography may be available in larger tertiary care centers for use in the diagnosis and/or treatment of intracerebral aneurysms, arteriovenous malformations, cerebral venous sinus thrombosis, or basilar or vertebral artery stenosis or occlusion.

Plain radiography may identify severe pneumonia or acute respiratory distress syndrome. In ingestions, it may rarely reveal specific types of heavy metals such as mercury, iron, or lead in the pediatric population or packages of ingested illicit substances in body packers or stuffers.

Additional Testing

Electrocardiograms (ECGs) can reveal cardiac ischemia, conduction blocks, or arrhythmia or can help corroborate certain ingestions (tricyclic antidepressants), electrolyte abnormalities (e.g., potassium, calcium), or hypothermia. If nonconvulsive status epilepticus is suggested, or if a patient with status epilepticus has required neuromuscular blockade, continuous electroencephalographic monitoring, if available, can provide key information about the patient’s status and guide therapy.