vigil coma

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vigil coma

Etymology: L, vigil + Gk, koma, deep sleep
a semiconscious state of delirium in which the patient may appear awake, with eyes open and staring, and may make verbal sounds.


(ko'ma) [Gr. koma, a deep sleep]
A state of unconsciousness from which one cannot be aroused. Coma is the most severe of the alterations of consciousness. It differs from sleep in that comatose patients will not awaken with stimulation. It differs from lethargy, drowsiness, or stupor (states in which patients are slow to respond) in that comatose patients are completely unresponsive. Finally, it differs from delirium, confusion, or hallucinosis (states in which patients' sense of reality is distorted and expressions are bizarre) in that comatose patients cannot express themselves at all. See: Glasgow Coma Scale


Two thirds of the time, coma results from diffuse brain injury or intoxication, such as may be caused by drug overdose, poisoning, hypoglycemia, uremia, liver failure, infection, or closed-head trauma. In about one third of cases, coma results from intracranial lesions, such as massive strokes, brain tumors, or abscesses. For these focal injuries to depress consciousness, the lesion must result in compression or injury to the brain's reticular activating system (the network of cells responsible for arousal). Rarely, coma is feigned by patients with psychiatric illnesses.


The airway, breathing, and circulation are supported. The cervical spine is protected if there is any question of traumatic injury to the head and neck. A rapid physical examination is performed to determine whether the patient has focal neurological deficits. Simultaneously, intravenous dextrose, naloxone, and thiamine are given (to try to reverse narcotic overdose or diabetic coma). If the examination reveals focal findings, an intracranial lesion may be present and should be quickly diagnosed (with brain scans) and treated (e.g., with neurosurgery if appropriate). If the patient is neurologically nonfocal, treatment focuses on metabolic support, the administration of antidotes for any proven intoxications, and treatment for infections. Seizures, if present, should be promptly controlled with anticonvulsants. Blood-sugar levels should be tightly controlled (between 80 and 110 mg/dl). Fevers should be suppressed with antipyretics. Acid-base disturbances should be corrected.


If there is a question whether the coma is due to an overdose of insulin or to hypoglycemia, it is crucial to give glucose intravenously. Administration of naloxone is also standard care.

Patient care

A patent airway is maintained. If neck trauma is suspected (e.g., if the patient was found on the floor), the patient should not be moved, except after protecting the cervical spine. Neurological status is monitored with the Glasgow Coma Scale. Frequency of assessment depends on protocol and the patient's stability. Findings are documented, and evidence of clinical deterioration is reported.

Fluid and electrolyte balance is monitored and maintained; gastrointestinal and urinary functions are assessed; care for the indwelling urinary catheter, intravenous line, and nasogastric or PEG feeding tube is provided, as well as adequate enteral or parenteral nutrition; and bowel elimination is maintained with stool softeners, suppositories, or enemas. Ventilatory status is assessed by auscultating for abnormal lung sounds, and adequate ventilation and oxygenation are determined by arterial blood gases or oxygen saturation values. The nurse or respiratory therapist assists with intubation and provides mechanical ventilation as required. The patient is repositioned to improve aeration of lung bases, and drainage of secretions is encouraged. The oropharynx (and endotracheal tube) is suctioned gently but briefly as necessary, considering concerns for increased intracranial pressure. The corneas are protected from ulceration by applying artificial tears to moisturize the eyes and by patching the eyes closed if the patient is unable to close them. Skin status is assessed and a plan instituted to prevent or manage pressure areas; passive range-of-motion exercises are provided; the patient is repositioned frequently; distal extremities are supported and elevated to prevent dependent edema; and appropriate supportive devices are used to prevent external hip rotation, flexion and extension contractures, and footdrop. Therapy to prevent deep venous thrombosis should be given (for example, heparin, warfarin, or compression stockings). Early enteral feeding of the patient prevents malnutrition.

Verbal and tactile stimulation are provided; the patient is assessed per orders (or hospital protocol) to person, time, place, and activities; nothing is said in the patient's presence that the patient should not hear, because the unresponsive patient may occasionally be somewhat aware of his or her surroundings. Emotional and educational support is offered to family members. See: shock

alcoholic coma

A coma due to ingestion of alcohol.

apoplectic coma

A coma produced by intracranial hemorrhage and its associated increase in intracranial pressure. One side of the body and one or more extremities may be paralyzed, usually on the opposite side of the injury in the brain. One pupil may be larger than the other, usually on the same side as the brain injury.
See: cerebral hemorrhage; diabetic coma; hypoglycemic coma

barbiturate coma

A coma caused by ingestion or injection of barbiturates. It is used clinically in the treatment of elevated intracranial pressure.

Patient care

The patient usually requires intubation and mechanical ventilation. Ventilatory status and oxygenation are monitored, adequate ventilation is maintained, and pulmonary toilet is provided. Aseptic technique is used for all procedures to prevent nosocomial infections.

diabetic coma

Coma resulting from extremely low or extremely high blood sugar levels. Although both hyperglycemia and hypoglycemia can cause coma in diabetic patients, hypoglycemia is much more common. As a result, emergency treatment of hypoglycemia (with an ampule of intravenous dextrose) is always given first to comatose patients before initiating blood sugar testing. If high blood sugar levels are the cause of altered consciousness, insulin and massive hydration are usually needed.

Patient care

The primary treatment measures for diabetic ketoacidosis are replacing fluids and electrolytes and then administering insulin, which usually will resolve metabolic acidosis. The nurse or laboratory technician draws blood for glucose, acetone, complete blood count, electrolytes, and arterial blood gases and obtains urine for urinalysis. The patient is assessed for neurological signs and symptoms; aspiration precautions are instituted as warranted. Intravenous (IV) access is initiated, and 1 L or 15 ml/kg of normal saline solution (NS) is administered over the first hour. Some physicians prescribe an IV bolus of 0.1 to 0.15 units/kg of regular insulin once fluid resuscitation begins, but usually insulin is held until 1 to 2 L of fluid have been administered. The first liter of fluid is followed by NS (or 0.45% saline solution [SS] if the patient's sodium level is elevated) at 7.5 ml/kg/hr for 2 to 4 hr, then at 3.75 ml/kg/hr for 24 to 36 hr until fluid losses are corrected. The patient's lungs are auscultated every hour, then every 2 to 4 hr for crackles related to fluid overload. Regular insulin is added to all fluids after the first or second liter (depending on protocol), to infuse at a rate of 0.1 units/kg/hr, with the intent of reducing glucose levels by 75 to 100 mg/dl/hr. The patient's blood glucose is monitored hourly, and electrolyte and serum acetone studies are repeated in 4 hr. The patient's heart rhythm also is monitored for potassium-related arrhythmias, such as ventricular ectopy. Once the patient's blood glucose is below 300 mg/dL, the prescribed IV fluid is changed to D5/0.45% NS to prevent hypoglycemia. Throughout initial resuscitation and ongoing fluid and insulin therapy, health care providers search for and treat the underlying cause (infection being the most common). The patient is monitored closely until ketones are no longer present in the blood and the bicarbonate level in the serum is > 21.

When the patient is considered stable, has bowel sounds, is awake, and is able to tolerate food, insulin is administered subcutaneously as prescribed. The patient is then allowed to eat a diabetic meal. Another 2 hr pass before the patient's insulin infusion is discontinued, until the subcutaneous regular insulin is absorbed. IV insulin has a 5- to 7-min half-life, so premature discontinuance could lead to a return of ketoacidosis. Blood glucose levels are assessed every 2 to 4 hr as warranted. The dietitian assesses and evaluates the patient's nutritional needs, and helps him or her to understand the importance of meal planning for optimal glucose control. The patient is ready for discharge when normal hydration and functional digestion are present and acidosis is absent. He or she is taught how to manage blood sugars and to continue to take prescribed insulin or hypoglycemic agents even when food cannot be consumed, because illness makes blood sugars vary. The signs of hyperglycemia, how to perform glucose monitoring, and when and how to test for urine ketones are reviewed. The patient learns how to substitute liquids for solid foods during illness in order to maintain adequate carbohydrate and fluid intake, the need for more frequent glucose monitoring when ill, and when to contact the primary care provider (blood glucose above 300 mg/dl, inability to eat, or vomiting). The patient also is referred to a home care nurse for further monitoring as necessary, and to a community-based diabetic education course for enhanced understanding and control of diabetes.

hepatic coma

Coma resulting from portal-systemic encephalopathy.

hyperosmolar nonketotic coma

Abbreviation: HNC
A coma in which the patient has a relative insulin deficiency and resulting hyperglycemia, but enough insulin to prevent fatty acid breakdown. The condition occurs in individuals with type 2 diabetes and is caused by hyperosmolarity of extracellular fluids and subsequent intracellular dehydration. It often is precipitated by severe physical stress or by extreme or prolonged dehydration.

hypoglycemic coma

Unconsciousness caused by very low blood sugars, usually less than 40 mg/dl. The most common cause is a reaction to insulin or an oral hypoglycemic agent. The patient typically will recognize, after reviving, that coma was preceded by heavy exercise, limited caloric intake, or a recent increase in the dose of diabetic medications. Occasionally alcoholic patients, patients with salicylate overdoses, or severely malnourished patients will present with coma and low blood sugar. Very rarely, the hypoglycemic patient will be found to have an insulin-secreting tumor of the pancreas.

irreversible coma

A coma from which the patient cannot recover.

Kussmaul's coma

See: Kussmaul, Adolph

myxedema coma

Unresponsiveness or lethargy that results from severe or neglected hypothyroidism. It is marked by neurological dysfunction, by respiratory depression, and by lowered body temperature, blood pressure, blood sugar, and serum sodium. The condition is an endocrinological crisis that requires treatment with thyroid and adrenocortical hormones, fluids, and glucose; gradual rewarming; ventilatory support; and intensive monitoring.

uremic coma

Loss of consciousness caused by the toxic effects of the nitrogen-containing wastes and inorganic acids that accumulate in the bloodstream of patients in renal failure. Coma in renal failure usually occurs after other uremic symptoms, such as loss of appetite, confusion, lethargy, or seizures.

vigil coma

Akinetic mutism.