hyperosmolar nonketotic coma

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Related to hyperosmolar nonketotic coma: diabetic ketoacidosis


a state of unconsciousness from which the patient cannot be aroused, even by powerful stimuli. Traumatic brain injuries are the most frequent cause; other causes include severe uncontrolled diabetes mellitus, liver disease, kidney disease, and neurologic conditions. Evaluation of a patient in a coma is comprehensive. The underlying cause should be identified so that appropriate treatment can be initiated. magnetic resonance imaging, electroencephalography, and brainstem auditory evoked potentials give information about electrical activity of the brain in a patient who is comatose, although the results are not predictive of recovery. Some patients are able to emerge from a coma. In others, the coma may progress to a persistent vegetative state in which the functions of the brainstem and circulation remain relatively intact or may be supported with assistive technologies. Patients in irreversible coma may meet the criteria of brain death.
Schematic representation of major brain stem reflexes used in coma examination. From Marx et al., 2002.
Patient Care. Assessment of the patient in a coma includes an evaluation of vital signs, determination of level of consciousness, neuromuscular responses, and reaction of the pupils to light. In most hospitals a standard form is used to measure and record the patient's responses to stimuli in objective terms. The glasgow coma scale is a standardized tool that aids in assessing a comatose patient and eliminates the use of ambiguous and easily misinterpreted terms such as unconscious and semicomatose. Additional assessment data are gathered relating to the underlying cause and the patient's immobility; these include evaluation of the gag and corneal reflexes. In the absence of gag reflex, regurgitation and aspiration are potential problems.

Abnormal rigidity and posturing in response to noxious stimuli are motor responses to coma. Decorticate rigidity is abnormal flexor posturing, with the arms, wrists, and fingers drawn up. The legs may be extended with plantar flexion. This type of rigidity usually indicates a lesion in the cerebral hemispheres or a disruption of the corticospinal tracts. Decerebrate rigidity is abnormal extensor posturing: in response to painful stimuli the extremities extend rigidly and the palms turn outward. This type of rigidity is indicative of damage to the brainstem and as a rule is a sign of greater cerebral impairment than is decorticate rigidity.

Comatose patients are predisposed to all the hazards of immobility, including impairment of skin integrity and development of pressure ulcers and contractures. A multidisciplinary, coordinated plan of care is essential. Families should be encouraged to be actively involved in care of the patient. The health care team should also recognize the family's need for support; the emotional and financial impacts of coma are usually significant.
alcoholic coma coma accompanying severe alcoholic intoxication.
alpha coma coma in which there are electroencephalographic findings of dominant alpha-wave activity.
diabetic coma the coma of severe diabetic acidosis; see also diabetes mellitus.
hepatic coma coma accompanying cerebral damage resulting from degeneration of liver cells, especially that associated with cirrhosis of the liver.
hyperglycemic hyperosmolar nonketotic coma (hyperosmolar nonketotic coma) see hyperglycemic hyperosmolar nonketotic coma.
irreversible coma brain death.
Kussmaul's coma the coma and air hunger of diabetic acidosis.
myxedema coma an often fatal complication of long-term hypothyroidism in which the patient is comatose with hypothermia, depression of respiration, bradycardia, and hypotension; usually seen in elderly patients during cold weather.
coma vigil locked-in syndrome.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

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.
See also: coma
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