Coma is a state of reduced alertness and responsiveness from which the patient cannot be aroused.18,19 The Glasgow Coma Scale (Table 168-6; see also chapter 257, Head Trauma) is a widely used clinical scoring system for alterations in consciousness. Advantages are the simplicity of the scoring system and assessment of separate verbal, motor, and eye-opening functions. Disadvantages include lack of acknowledgment of hemiparesis or other focal motor signs and lack of testing of higher cognitive functions. Interrater variability has been noted in assessments using the Glasgow Coma Scale.20 Another coma scale, the FOUR (Full Outline of UnResponsiveness) score, has been used in intensive care units and has the advantages of assessing simple brainstem functions and respiratory patterns, as well as eye and motor responses.21 Causes of coma likely to be encountered in the ED are noted in Table 168-7.
TABLE 168-6Glasgow Coma Scale ||Download (.pdf) TABLE 168-6 Glasgow Coma Scale
|Component ||Score ||Adult ||Child <5 y ||Child >5 y |
|Motor || |
Withdraws to pain
Normal spontaneous movements
Localizes to supraocular pain (>9 mo)
Withdraws from nail bed pressure
Flexion to supraocular pain
Extension to supraocular pain
|Follows commands |
|Verbal || |
Less than usual ability; irritable cry
Cries to pain
Moans to pain
No response to pain
|Eye opening || |
TABLE 168-7Differential Diagnosis of Coma ||Download (.pdf) TABLE 168-7 Differential Diagnosis of Coma
Coma from causes affecting the brain diffusely
Hyperosmolar state (e.g., hyperglycemia)
Electrolyte abnormalities (e.g., hypernatremia or hyponatremia, hypercalcemia)
Organ system failure
Endocrine (e.g., Addison's disease, hypothyroidism, etc.)
Carbon dioxide narcosis
Drug reactions (e.g., neuroleptic malignant syndrome)
Environmental causes—hypothermia, hyperthermia
Deficiency state—Wernicke's encephalopathy
Coma from primary CNS disease or trauma
Direct CNS trauma
Diffuse axonal injury
The pathophysiology of coma is complex. Coma can result from deficiency of substrates needed for neuronal function (as with hypoglycemia or hypoxia). With systemic causes, the brain is globally affected, and signs that localize dysfunction to a specific area of the brainstem or cortex are usually lacking. With primary CNS causes, coma may result from a brainstem disorder such as hemorrhage or from bilateral cortical dysfunction. Signs localizing to specific areas of CNS dysfunction such as hemiparesis or cranial nerve abnormalities may be present. Unilateral hemispheric disease, such as stroke, should not alone result in coma. The function of the brainstem and/or both hemispheres must be impaired for unresponsiveness to occur.
The herniation syndromes are models for alterations of consciousness, but their mechanisms are unknown. In uncal herniation syndrome, the medial temporal lobe shifts to compress the upper brainstem, which results in progressive drowsiness followed by unresponsiveness.19,22 The ipsilateral pupil is sluggish, eventually becoming dilated and nonreactive as the third cranial nerve is compressed by the medial temporal lobe. Hemiparesis may develop ipsilateral to the mass from compression of the descending motor tracts in the opposite cerebral peduncle. Central herniation syndrome is characterized by progressive loss of consciousness, loss of brainstem reflexes, decorticate posturing, and irregular respiration.19 Because midline shift without herniation, as demonstrated by neuroimaging, seems to correlate with a decreased level of consciousness, vascular compression due to local cerebral edema or local increased intracranial pressure (ICP) may be an underlying mechanism for these syndromes.
A diffuse increase in ICP can cause diffuse CNS dysfunction. Cerebral blood flow is constant at mean arterial pressures (MAPs) of 50 to 100 mm Hg due to the process of cerebral autoregulation. At MAPs outside this range, cerebral blood flow may be reduced, and diffuse ischemia may develop. Cerebral perfusion pressure is equal to the MAP minus the ICP (cerebral perfusion pressure = MAP – ICP). In extreme uncontrolled elevation of the ICP, cerebral perfusion pressure is diminished as the ICP approaches the MAP, which causes brain ischemia.
Particularly in unresponsive patients with a history of seizures, the possibility of ongoing nonconvulsive seizures must be considered. Subtle status epilepticus or ictal coma may represent transformed generalized convulsive status epilepticus. Electrical seizures may continue in the absence of clinical seizures.23
The clinical features of coma vary with both the depth of coma and the cause. For example, a patient in a coma with a hemispheric hemorrhage and midline shift may have decreased muscle tone on the side of the hemiparesis. The eyes may conjugately deviate toward the side of the hemorrhage. With expansion of the hemorrhage and surrounding edema, increase in ICP, or brainstem compression, unresponsiveness may progress to a complete loss of motor tone and loss of the ocular findings as well.
A variety of abnormal breathing patterns may be seen in the comatose patient.19 They offer little information in the acute setting. Pupillary findings, the results of other cranial nerve evaluation, hemiparesis, and response to stimulation are all part of the clinical picture that need assessment. These findings can assign the cause of the coma into a probable general category—diffuse CNS dysfunction (toxic-metabolic coma) or focal CNS dysfunction (structural coma). A further division of structural coma into hemispheric (supratentorial) or posterior fossa (infratentorial) coma is often possible at the bedside.
Many different toxic and metabolic conditions cause coma. The diffuse CNS dysfunction is reflected by the lack of focal physical examination findings that point to a specific region of brain dysfunction. For example, in toxic-metabolic coma, if the patient demonstrates either spontaneous movements or reflex posturing, the movements are symmetric without evidence of hemiparesis. Muscle stretch reflexes, if present, are symmetric. Pupillary response is generally preserved in toxic-metabolic coma. Typically the pupils are small but reactive. If extraocular movements are present, they are symmetric. If extraocular movements are absent, however, this sign is of no value in differentiating toxic-metabolic from structural coma. A noTable exception is severe sedative poisoning as from barbiturates; the pupils may be large, extraocular movements absent, muscles flaccid, and the patient apneic, which simulates the appearance of brain death.
Coma from Supratentorial Lesions
Coma caused by lesions of the hemispheres, or supratentorial masses, may present with progressive hemiparesis or asymmetric muscle tone and reflexes. The hemiparesis may be suspected with asymmetric responses to stimuli or asymmetric extensor or flexor postures. Uncal herniation syndrome, as described earlier in Pathophysiology, is an example of a supratentorial syndrome. Frequently, however, large acute supratentorial lesions are seen without the features consistent with temporal lobe herniation. Coma without lateralizing signs may result from decreased cerebral perfusion secondary to increased ICP. Reflex changes in blood pressure and heart rate may be observed with increased ICP or brainstem compression. Hypertension and bradycardia in a comatose patient may represent the Cushing reflex from increased ICP.
Coma from Infratentorial Lesions
Posterior fossa or infratentorial lesions comprise another structural coma syndrome. An expanding lesion, such as cerebellar hemorrhage or infarction, may cause abrupt coma, abnormal extensor posturing, loss of pupillary reflexes, and loss of extraocular movements. The anatomy of the posterior fossa leaves little room for accommodating an expanding mass. Early brainstem compression with loss of brainstem reflexes may develop rapidly. Another infratentorial cause of coma is pontine hemorrhage, which may present with the unique signs of pinpoint-sized pupils.
Pseudocoma or psychogenic coma is occasionally encountered and may present a perplexing clinical problem. Adequate history taking and observation of responses to stimulation reveal findings that differ from those in the syndromes described in the previous sections. Pupillary responses, extraocular movements, muscle tone, and reflexes are shown to be intact on careful examination. Tests of particular value include responses to manual eye opening (there should be little or no resistance in the truly unresponsive patient) and extraocular movements. Specifically, if avoidance of gaze is consistently seen with the patient always looking away from the examiner, or if nystagmus is demonstrated with caloric vestibular testing, this is strong evidence for nonphysiologic or feigned unresponsiveness.
In the approach to the comatose patient, perform stabilization, diagnosis, and treatment actions simultaneously. Examination, laboratory procedures, and neuroimaging allow differentiation between structural and metabolic causes of coma in almost all patients in the ED. History and physical examination findings allow that initial assignment in many patients, but liberal use of CT scanning is encouraged because exceptions to the tentative clinical diagnosis are frequent.
Address airway, breathing, and circulation immediately. Consider reversible causes of coma, such as hypoglycemia or opiate overdose. Access all available historical sources (EMS personnel, caregivers, family, witnesses, medical records, etc.) to aid in diagnosis.
The tempo of onset of the coma is of great diagnostic value. Abrupt coma suggests abrupt CNS failure with possible causes such as catastrophic stroke or seizures. A slowly progressive onset of coma may suggest a progressive CNS lesion such as tumor or subdural hematoma. Metabolic causes, such as hyperglycemia, may also develop over several days.
Address general examination and measurement of vital signs (including oxygen saturation and temperature) following stabilization and resuscitation. General examination may reveal signs of trauma or suggest other diagnostic possibilities for the unresponsiveness. For example, a toxidrome may be present that suggests diagnosis and treatment, such as the opiate syndrome with hypoventilation and small pupils.
Neurologic testing deviates from the standard examination. Fine tests of weakness, such as testing for pronator drift of the outstretched upper extremities, are not possible in the unresponsive patient. However, asymmetric findings on examination of cranial nerves through pupillary examination, assessment of corneal reflexes, and testing of oculovestibular reflexes may suggest focal CNS lesions. Abnormal extensor or flexor postures are nonspecific for localization or cause of coma but suggest profound CNS dysfunction. Asymmetric muscle tone or reflexes raise the suspicion of a focal lesion. The goal of the physician is to rapidly determine if the CNS dysfunction is from diffuse impairment of the brain or if signs point to a focal (and perhaps surgically treatable) region of CNS dysfunction.
CT is the neuroimaging procedure of choice. Acute hemorrhage is readily identified, as is midline shift and mass lesions. Consider lumbar puncture if CT scan findings are unremarkable and subarachnoid hemorrhage or CNS infection is suspected. Suspect basilar artery thrombosis in a comatose patient with "normal" results on head CT, in which the only finding may be a hyperdense basilar artery.24 MRI or cerebral angiography is needed to make the diagnosis of basilar artery thrombosis.
SPECIAL CONSIDERATIONS IN COMA
If trauma is suspected, maintain stabilization of the cervical spine during assessment. If protection of the airway is in doubt or the coma state is likely prolonged, then protect the airway by intubating the patient. Rapid-sequence intubation techniques are discussed at length in chapter 29, Intubation and Mechanical Ventilation. ingestions, infections, and child abuse in the appropriate clinical setting.
Patients who have had generalized seizures and remain unresponsive may be in a continuing state of electrical seizures without corresponding motor movements. This is called nonconvulsive status epilepticus or subtle status epilepticus and can be described as electromechanical dissociation of the brain and body. If the motor activity of the seizure stops and the patient does not awaken within 30 minutes, then consider nonconvulsive status epilepticus. Obtain neurologic consultation and electroencephalography.23
Treatment of coma involves identification of the cause of the brain failure and initiation of specific therapy directed at the underlying cause. Attend to airway, ventilation, and circulation. Evaluate and treat for readily reversible causes of coma, such as hypoglycemia and opioid toxicity.
Rapid point-of-care glucose determination can identify the need for dextrose. Although thiamine should be administered before glucose infusion in patients with a suspected history of alcohol abuse or malnutrition, thiamine is not necessary for all patients. Routine use of flumazenil in coma of unknown cause is not recommended.25 Naloxone, the opiate antagonist, is useful in coma because typical signs of opiate overdose may be absent.
Increased Intracranial Pressure
If history, physical examination, or neuroimaging findings suggest increased ICP, specific steps can reduce or ameliorate any further rise in ICP. Any noxious stimulus, including "bucking" the ventilator, can increase ICP, so use paralytic and sedative agents. A general recommendation is to keep the head elevated about 30 degrees and at midline to aid in venous drainage. Mannitol (0.5 to 1.0 gram/kg IV) can decrease intravascular volume and brain water and may transiently reduce ICP. In cases of brain edema associated with tumor, dexamethasone, 10 milligrams IV, reduces edema over several hours. Hyperventilation with reduction of partial pressure of arterial carbon dioxide can reduce cerebral blood volume and transiently lower ICP. Current recommendations are to avoid excessive hyperventilation (partial pressure of arterial carbon dioxide ≤35 mm Hg) during the first 24 hours after brain injury. Brief hyperventilation may be necessary for refractory intracranial hypertension. Data to recommend specific therapy are lacking, and preferences among individuals and institutions vary greatly, so communicate early with consultants and admitting physicians.
DISPOSITION AND FOLLOW-UP
Patients with readily reversible causes of coma, such as insulin-induced hypoglycemia, may be discharged if home care and follow-up care are adequate and a clear cause for the episode is suspected. Admit patients with persistent altered consciousness. Most institutions depend on emergency physicians to stabilize the patient's condition and correctly assign a tentative diagnosis so that the patient may be admitted to the proper specialty service. If the appropriate service is not available, then consider transfer to another hospital after patient stabilization.