Coma

Article Author:
J. Stephen Huff
Article Editor:
Prasanna Tadi
Updated:
3/8/2019 4:02:19 PM
PubMed Link:
Coma

Introduction

Coma is defined as a state of deep unconsciousness, with the eyes closed, that lasts for a prolonged or indefinite period. Altered mental status is a catch-all term that includes a spectrum of behaviors from confusion to coma. There are gradations of consciousness that are described as stupor, obtundation, and lethargy. Though these are explicitly defined, they are often misused and miscommunicated. It is suggested that providers should determine the patient’s response to stimulation and describe that response rather than use imprecise jargon. The first goal of the clinician is to stabilize the patient and diagnose the rapidly reversible causes of coma such as hypoglycemia. Then, one can focus on how to pursue evaluation that will sort the case into structural or nonstructural causes of coma.[1][2][3]

Etiology

Coma may result from diffuse neuronal dysfunction due to structural and nonstructural brain diseases. Several structural brain diseases such as subdural or epidural traumatic hematomas, spontaneous intracerebral hemorrhage, venous thrombosis, tumors, raised intracranial pressure, anoxic brain injury, brain stem strokes (locked-in syndrome) can cause coma. Metabolic or infectious etiologies including elevated ammonia levels due to liver disease, uremic encephalopathy due to renal failure, excessive alcohol intake, and illicit drug use are nonstructural causes of coma. Of all the nonstructural causes of coma, Hypoglycemia and systemic infections likely account for the majority of patients presenting with coma.[4][5] With the increasing use of EEG monitoring in intensive care units, patients are now being identified with abnormal electroencephalograic findings suggesting seizure activity but are clinical without generalized seizures. This new entity is known as Nonconvulsive status epilepticus (NCSE) which is a prolonged seizure that presents as an altered mental status. The mortality associated with this subtle status epilepticus exceeds 30%.[6]

Epidemiology

Though coma is a typical clinical presentation to the emergency department, the frequency of presentation is difficult to discern. Coma is a clear clinical condition, and diagnostic coding often reflects the etiology of the altered mental status. The use of many terms to describe patients with depressed mental states also leads to multiple coding options, making any retrospective reviews challenging.[7][8][9]Brain hemorrhage (43.5%) and drug overdose (37.5%) are the most common among structural and nonstructural causes of coma respectively.[10] 

Pathophysiology

The most commonly accepted pathophysiology of coma is due to a decrease in the supply of glucose to the brain and oxygen diffuse neuronal dysfunction from either structural or nonstructural causes. A myriad of medical physiologies may lead to substrate disruption and central nervous system (CNS) dysfunction, with coma as the extreme clinical condition. For example, any clinical process that causes circulatory collapse or profound hypoxemia may manifest as coma.  Fifteen seconds of circulatory collapse will result in loss of consciousness. If the cause of the circulatory collapse is brief and promptly restored, such as from a simple faint, consciousness is regained. If hypotension or hypoxemia continues, the altered mental state continues, and secondary CNS damage will occur.[11][12][13]

Hypoglycemia is encountered frequently in clinical practice, most often in the association of treatment for diabetes mellitus or as a complication of alcoholism. The pathophysiology of other causes of metabolic coma is not clear but may involve false neurotransmitters as is suggested in hepatic encephalopathy. Electrolyte abnormalities such as hyponatremia or hypercalcemia may disrupt normal neuronal metabolism.

Structural lesions of the CNS, such as intracerebral hemorrhage, may lead to the direct destruction of the brain tissue as well as secondary damage from either shifting of intracranial structures or increased intracranial pressure. Herniation Syndromes describe clinically recognizable physical examination features that suggest the anatomic location of the CNS lesion. The most discussed of the herniation syndromes is the uncal herniation, where the medial portion of the temporal lobes shifts with resulting loss of consciousness from brainstem compression. The pathophysiologic findings are compression of the brainstem and Cranial nerve three as it exits the brainstem and crosses the tentorium cerebelli. This results impairment of the parasympathetic fibers (pupilloconstrictors) that travel with the third nerve, and in most cases pupillary dilatation on the same side (roughly 90%) of the mass lesion.  

Increased intracranial pressure is a more frequent cause of coma than the herniation syndromes. The brain is enclosed in a closed cranial vault, hence the conditions that increase intracranial pressure will disrupt cerebral perfusion. The equation that approximates this relationship is unforgiving CPP (cerebral perfusion pressure) = MAP (mean arterial pressure estimated as 1/3 systolic BP [blood pressure] + 2/3 diastolic BP) - ICP (intracranial pressure).  If ICP approaches MAP, cerebral perfusion diminishes. Thus, it is essential to maintain CPP by avoiding hypotension and reducing increased intracranial pressure. Global depression of neuronal functioning is the most common mechanism of coma in toxins and poisonings.

History and Physical

When evaluating, it is axiomatic that the fundamentals of emergency care – airway, breathing, circulation – be addressed. Physical examination should include the response to pain, a brief assessment of motor function, eye-opening, and verbalization and can be summarized in the Glasgow Coma Scale or other rating scales. Cranial nerve examination will include an evaluation of extraocular movements, pupillary, corneal, cough, and gag reflex. The presence of ipsilateral dilation of the pupil suggests the uncal herniation syndrome with compression of the third cranial nerve from a mass or edema. Lack of focal findings suggests a metabolic, infectious, or toxicologic cause of coma. Physical examination should be directed to detect any signs of trauma.

Evaluation

The differential diagnosis of coma is extensive. Unless a recognizable infectious or metabolic cause is established, additional testing including imaging is necessary. CT and MRI brain scanning may detect hemorrhage, mass effect, or other structural abnormalities. EEG should be considered in a patient following generalized convulsive status epilepticus with continued altered mental status.[14][15]

Treatment / Management

Determination of the serum glucose by the point of care testing or empiric administration of glucose is recommended. Naloxone is considered in patients with narcotic toxidrome as slow respiratory rate, small pupils, and altered mental status. Thiamine should be administered to individuals at risk for poor nutrition such as alcoholics, bariatric surgery patients, or patients with chronic malabsorptive states. Maintenance of cerebral perfusion pressure by preserving the mean arterial pressure to avoid hypotension is the key to the management strategy. One should consider the possibility of increased intracranial pressure and continue supportive care with airway protection and blood pressure.[16][17][18]

Pearls and Other Issues

Patients with reversible causes of coma, such as hypoglycemia, may be discharged after appropriate intervention and considering their safe home environment. Patients with persistent coma need hospital admission with ongoing monitoring, supportive care, and targeted care to the underlying cause of coma. The etiology of the coma determines the admission service.

Enhancing Healthcare Team Outcomes

There are many causes of the coma but irrespective of the cause, the treatment is similar. These individuals require care of many organ systems, and thus a multidisciplinary team approach is essential. Patients with coma need attention in the ICU, and many may be on a ventilator. Since the 1970s, the prognosis of patients with coma has markedly improved. However, very few long-term data are available on people who survive coma. While short-term prognosis varies from good to poor, depending on the cause, it appears that full recovery often takes months or years. Two negative prognostic factors include the depth of coma and the duration. Also, those without any brain stem reflexes tend to have the worst outcomes. Some patients remain in a persistent vegetative state, and the recovery of these individuals remains debatable. Current recommendations are that once a patient had developed a coma, a team of healthcare professionals should determine the prognosis and if a decision of hopelessness is made, this should be communicated to the family, who may or may not accept the decision. Life support should not be withdrawn until one is entirely sure that recovery is not possible. Prematurely deciding to end life can lead to medicolegal disputes and tarnish the reputation of the healthcare providers.[19][20][21]


References

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