If poisoning or drug overdosage is suspected, aspiration and analysis of the gastric contents are sometimes helpful, but greater reliance should be placed on chromatographic analysis of the blood and urine (“toxic screen”). Accurate means are available for measuring the blood concentrations of most antiepileptic drugs, opiates, diazepines, barbiturates, alcohol, and a wide range of other toxic substances. These screening procedures vary widely between hospitals and certain toxins must be specifically sought. A specimen of urine is obtained by catheter for determination of specific gravity and for glucose, acetone, and protein content. Proteinuria may also be found for 2 or 3 days after a subarachnoid hemorrhage or with high fever. Urine of high specific gravity, glycosuria, and acetonuria occurs almost invariably in diabetic coma; but transient glycosuria and hyperglycemia may be precipitated solely by a massive cerebral lesion. Blood counts should be obtained and in malarial districts, a blood smear should be examined for parasites. Neutrophilic leukocytosis occurs in bacterial infections and mild elevations of the white blood cell counts also with brain hemorrhage and infarction, although rarely exceeding 12,000/mm3. Venous blood should be examined for the concentrations of glucose, urea, carbon dioxide, bicarbonate, ammonia, sodium, potassium, chloride, calcium, and AST (aspartate serum transaminase); analysis of blood gases and carboxyhemoglobin should be obtained in appropriate cases of anoxia or exposure to carbon monoxide by smoke inhalation or faulty heating systems. Determination of ammonia level may be added in instances where hepatic failure is a possible cause of stupor or coma.
It should be kept in mind that disorders of water and sodium balance, reflected in hyperor hyponatremia, may be the result of cerebral disease (excess antidiuretic hormone [ADH] secretion, diabetes insipidus, atrial natriuretic factor release), as well as being the proximate cause of coma.
An EEG is informative if no adequate explanation for coma is forthcoming from the initial examinations.
At times, this is the only way to reveal nonconvulsive status epilepticus as the cause of stupor.
Classification of Coma and Differential Diagnosis
The demonstration of focal brain disease by hemiparesis, and meningeal irritation with abnormalities of the CSF serve to divide the diseases that cause coma into three classes, as follows:
I.  Diseases that cause no focal or lateralizing neurologic signs, usually with normal brainstem functions. CT scan and cellular content of the CSF are normal.
A.	Exogenous intoxications: alcohols, barbiturates and other sedative drugs, opiates (Chaps. 41
B.	Endogenous metabolic disturbances: anoxia, diabetic acidosis, uremia, hepatic failure, nonketotic hyperosmolar hyperglycemia, hypoand hypernatremia, hypoglycemia, addisonian crisis, profound nutritional deficiency, carbon monoxide poisoning, thyroid states, hypercalcemia (Chaps. 39 and 40)
C.	Severe systemic infections: pneumonia, peritonitis, typhoid fever, malaria, septicemia, Waterhouse-Friderichsen syndrome
D.	Circulatory collapse (shock) from any cause
E.	Postseizure states and convulsive and nonconvulsive status epilepticus (Chap. 15)
F.	Hypertensive encephalopathy and eclampsia (Chap. 33)
G.	Hyperthermia and hypothermia (Chap. 39)
H.	Concussion (Chap. 34)
I.	Acute hydrocephalus (Chap. 29)