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COMA AND SOMNOLENCE

COMA AND SOMNOLENCE: Excerpt from Differential Diagnosis in Primary Care

Somnolence is a deep sleep from which the patient can be aroused. Coma is an unconscious state from which the patient cannot be aroused. Because somnolence may be simply an early stage of coma, its etiologies are almost all identical to the etiologies of coma. The few exceptions are mentioned at the close of this discussion.

COMA AND SOMNOLENCE

COMA AND SOMNOLENCE

COMA AND SOMNOLENCE

While in medical school, I discovered a little text, Aids to Medical Diagnosis by G. E. F. Sutton2. I have never forgotten the unique little mnemonic provided in the text for remembering the causes of coma, A-E-I-O-U, the vowels.

1. A—Accidents suggest cerebral concussion and epidural and subdural hematomas. The A also stands for arterial occlusions, arteriosclerosis, aneurysms, and autoimmune disorders.
2. E—Endocrine disorders such as myxedema coma, hyperparathyroidism, diabetic coma, and insulin shock are included in this category. The E also stands for the coma following an epileptic seizure.
3. I—Inflammatory and Intoxication disorders such as encephalitis, cerebral abscess, meningitis, alcoholism, and opiates or barbiturates are included in this category.
4. O—Organ failure should suggest hepatic coma, respiratory failure, and uremia.
5. U—Uremia was used by Sutton, but because it is included above in organ failure, I prefer to use the U to designate the “undefined” disorders such as narcolepsy and conversion hysteria.

Therefore, with the vowels A, E, I, O, U, one has a useful system for recalling the causes of coma and somnolence. VINDICATE can be used in a similar manner, but I prefer to let the reader develop the etiologies using this mnemonic as an exercise. There are two other approaches to the differential diagnosis of coma that may be more instructive. These are the anatomic and physiologic approaches.

If one visualizes the anatomy of the head from the skull on into the ventricles and cross-indexes the various layers with the mnemonic MINT, one will have an excellent means of recalling the causes of coma and somnolence demonstrated in Table 17. The important conditions resulting from disease of each anatomic structure are reviewed here.

Thinking of the skull reminds one of depressed skull fractures and epidural and subdural hematomas. In visualizing the meninges meningitis and subarachnoid hemorrhages are recalled. Moving deeper into the brain itself will suggest encephalitis, encephalopathies (e.g., alcoholic), and brain tumors. Considering the arteries at the base of the brain, one should recall arterial occlusions, hemorrhages, and emboli. The blood supply prompts the recall of anoxia and other metabolic disorders that may be responsible for coma. The veins suggest venous sinus thrombosis as the cause of coma. Finally, the pituitary should help recall not only the coma of hypopituitarism but all the other endocrinopathies. This, then, is the anatomic approach to the differential diagnosis of coma and somnolence.

For the physiologic approach simply ask the question, What does the brain cell need to “keep awake” or to continue functioning? It needs a good supply of oxygen, glucose, and vitamins; the proper amount of insulin; an appropriate electrolyte and acid–base medium; and a proper amount of fluid in that medium. In addition, the brain cell cannot afford to have any toxic substance in that medium that might block the use or action of these metabolic substances. Now one is in a position to take each category and discuss the diseases that may result in a disturbance of brain cell function.

1. Decreased supply of oxygen. Focal anoxia from an arterial thrombosis, embolism, or hemorrhage falls in this category. Generalized anoxia from severe anemia and pulmonary or heart disease can also be recalled here.
2. Decreased or increased supply of glucose. Any hypoglycemic state (e.g., malabsorption syndrome, severe cirrhosis, glycogen storage disease, and hypopituitarism) may cause coma. On the other hand, coma may be caused by hyperglycemia (nonketotic hyperosmolar diabetic coma).
3. Too much or too little insulin. In this category one should recall excessive exogenous insulin, insulinomas, and functional hypoglycemia, as well as diabetic acidosis (too little insulin).
4. Avitaminosis. Wernicke encephalopathy from thiamine deficiency, the hypocalcemia and possible tetany of rickets, and the dementia with somnolence of pellagra might be recalled here.
5. Disturbances of electrolyte and acid–base equilibrium. Here one should recall the coma of hyponatremia, hypokalemia, hyperkalemia (e.g., Addison disease, uremia, and diuretics), hypocalcemia (hypoparathyroidism, rickets, uremia, and malabsorption syndrome), hypercalcemia (e.g., hyperparathyroidism and metastatic tumors of the bone), and hypomagnesemia. The coma of diabetic acidosis, lactic acidosis, carbon dioxide (CO2) narcosis, and alkalosis (hyperventilation syndrome) will also be recalled here.
6. Increased fluid in the cell medium. This should suggest cerebral edema from brain tumors, hemorrhages, hydrocephalus, encephalitis and meningitis, and cerebral concussions.
7. Toxic substances that block the utilization or action of metabolic substances. In this category are extrinsic substances like lead, alcohol, lysergic acid diethylamide (LSD), opiates, and a list of other drugs. It should also include intrinsic toxins from hepatic coma, uremia, and CO2 narcosis.

Somnolence, as suggested in the introduction, is an indication of a few conditions that are not as likely to present with frank coma: These are endogenous depression narcolepsy, cerebral arteriosclerosis, and encephalitis lethargica. The physiologic approach should also suggest myxedema coma, but it is difficult to fit it into any of the aforementioned categories.

Approach to the Diagnosis

Obviously, the neurologic examination and a good history from a member of the family or friend are invaluable in the diagnosis of coma. However, one should not delay ordering laboratory work until the examination and history are accomplished. A CBC, BUN, fasting blood sugar (FBS), serum osmolality, electrolytes, blood gases, urinalysis, and drug screen are ordered immediately. If there is little or no history available and insulin shock is suspected, glucose or glucagon is administered before the laboratory reports are back, although this is done with more caution today for fear of aggravating a case of nonketotic, hyperosmolar diabetic coma.

It has been my experience that the neurologic examination is best performed simultaneously with the taking of a history from a relative or friend. In this way, various telltale neurologic signs can be found with alacrity. A unilateral dilated pupil (suggesting a subdural hematoma or aneurysm), acetone breath (suggesting diabetic acidosis), contusion of the skull (suggesting cerebral concussion or hematoma), and nuchal rigidity (suggesting a subarachnoid hemorrhage in meningitis) are just a few of the signs that can help identify the cause of the coma rapidly.

Coma without focal neurologic findings should suggest a metabolic or toxic cause. In that case, an intensive laboratory workup as listed below would be indicated. A spinal tap maybe indicated if there is fever as well. On the other hand, coma with focal neurologic signs suggests tumor, abscess, hematoma or cerebral embolism, thrombosis, or hemorrhage. The clinician should proceed with a skull x-ray film and CT scan immediately. When these are not available, immediate referral to a large medical center is necessary. Electroencephalography (EEG) and a spinal tap may identify the cause. A spinal tap should be considered with extreme caution even if there is no papilledema. Of course, a spinal tap is never done in the presence of papilledema unless a neurologist is consulted and CT findings are negative. One indication for a spinal tap under these circumstances might be meningitis. Another might be “benign intracranial hypertension.”

Other Useful Tests

1. CBC (septicemia, meningitis)
2. Sedimentation rate (inflammation)
3. Chemistry panel (diabetic acidosis, hypoglycemia, uremia, electrolyte imbalance)
4. Drug screen (drug intoxication)
5. Arterial blood gas (hypoxia, hypercarbia)
6. Blood lead level (lead encephalopathy)
7. Urine porphobilinogens (porphyria)
8. Blood cultures (septicemia)
9. Thyroid profile (myxedema coma)
10. Blood ammonia level (hepatic coma)
11. ECG (CHF, cardiac arrhythmia)
12. CT scan of the brain (encephalitis, hematoma, abscess)
13. EEG (level of coma assessment, epilepsy)
14. Spinal tap (meningitis, encephalitis, subarachnoid hemorrhage)

Book Source Details

• Book Title: Differential Diagnosis in Primary Care
• Author(s): R. Douglas Collins
• Year of Publication: 2007
• Copyright Details: Differential Diagnosis in Primary Care, Copyright © 2007 Lippincott Williams & Wilkins.

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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

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More About This Book: Title: Differential Diagnosis in Primary Care Authors: R. Douglas Collins Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 0-7817-6812-8

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