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Hyperglycemia
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Two syndromes have been de ned, mainly in diabetics: (1) hyperglycemia with ketoacidosis and (2) hyperosmolar nonketotic hyperglycemia In diabetic acidosis, the familiar picture is one of dehydration, fatigue, weakness, headache, abdominal pain, dryness of the mouth, stupor or coma, and Kussmaul type of breathing Usually the condition has developed over a period of days in a patient known or proven to be diabetic Often, the patient had failed to take a regular insulin dose The blood glucose level is found to be more than 400 mg/dL, the pH of the blood less than 720, and the bicarbonate less than 10 meq/L Ketone bodies and B-hydroxybutyric acid are elevated in the blood and urine, and there is a marked glycosuria The prompt administration of insulin and repletion of intravascular volume correct the clinical and chemical abnormalities over a period of hours Of considerable interest is a small group of patients with diabetic ketoacidosis, such as those reported by Young and Bradley, in whom deepening coma and cerebral edema develop as the elevated blood level of glucose is corrected Mild cerebral edema is commonly observed in children during treatment with uids and insulin (Krane et al) This condition has been attributed by Prockop to an accumulation of fructose and sorbitol in the brain The latter substance, a polyol that is formed during hyperglycemia, crosses membranes slowly, but once it does so is said to cause a shift of water into the brain and an intracellular edema However, according to Fishman, the increased polyols in the brain in hyperglycemia are not present in suf cient concentration to be important osmotically; they may induce other metabolic effects related to the encephalopathy These are matters of conjecture, since the increase of polyols has never been found The brain edema in this condition is probably due to reversal of the osmolality gradient from blood to brain, which occurs with rapid correction of hyperglycemia The pathophysiology of the cerebral disorder in diabetic ketoacidosis is not fully understood No consistent cellular pathology of the brain has been identi ed in the cases we have examined Factors such as ketosis, tissue acidosis, hypotension, hyperosmolality, and hypoxia have not been identi ed Attempts at therapy by the administration of urea, mannitol, salt-poor albumin, and dexamethasone are usually unsuccessful, though recoveries are reported In hyperosmolar nonketotic hyperglycemia, the blood glucose
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THE ACQUIRED METABOLIC DISORDERS OF THE NERVOUS SYSTEM
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is extremely high, over 600 mg/dL, but ketoacidosis does not develop or is mild Osmolality is usually around 350 mosmol/L There is also hemoconcentration and prerenal azotemia Appreciation of the neurologic syndrome is generally credited to Wegierko, who published descriptions of it in 1956 and 1957 Most of the patients are elderly diabetics, but some were not previously known to have been diabetic An infection, enteritis, pancreatitis, or a drug known to upset diabetic control (thiazides, prednisone, phenytoin) leads to polyuria, fatigue, confusion, stupor, and coma Often the syndrome arises in conjunction with the combined use of corticosteroids and phenytoin (which inhibits insulin release), for example, in elderly patients with brain tumors The use of osmotic diuretics enhances the risk If the patient is seen before coma supervenes, seizures and focal signs such as a hemiparesis, a hemisensory defect, or a homonymous visual eld defect may have erroneously suggested the possibility of a stroke The mortality rate has been as high as 40 percent Fluids should be replaced cautiously, using isotonic saline and potassium Correction of the markedly elevated blood glucose requires relatively small amounts of insulin, since these patients often do not have a high degree of insulin resistance
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Hepatic Stupor and Coma (Hepatic or Portal-Systemic Encephalopathy)
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Chronic hepatic insuf ciency with portocaval shunting of blood is punctuated by episodes of stupor, coma, and other neurologic symptoms a state referred to as hepatic stupor, coma, or encephalopathy It was delineated by Adams and Foley in 1949 This state complicates all varieties of liver disease and is unrelated to jaundice or ascites Less widely known is the fact that a surgical portalsystemic shunt (Eck stula) is attended by the same clinical picture, in which case the liver itself may be little or not at all affected (see further on) Also, there are a number of hereditary hyperammonemic syndromes, usually rst apparent in infancy or childhood (see Chap 37), that lead to episodic coma with or without seizures In all these states, it is common for an excess of protein derived from the diet or from gastrointestinal hemorrhage to induce or worsen the encephalopathy Additional predisposing factors are hypoxia, hypokalemia, metabolic alkalosis, excessive diuresis, use of sedative hypnotic drugs, and constipation Reye syndrome, a special type of acute nonicteric hepatic encephalopathy of children, is also associated with very high levels of ammonia in the blood (see further on) Clinical Features The clinical picture of acute, subacute, or chronic hepatic encephalopathy consists essentially of a derangement of consciousness, presenting rst as mental confusion with decreased psychomotor activity, occasionally with hyperactivity, followed by progressive drowsiness, stupor, and coma The confusional state, before coma supervenes, is combined with a characteristic intermittency of sustained muscle contraction; this phenomenon, which was originally described in patients with hepatic stupor by Adams and Foley and called asterixis (from the Greek sterixis, a xed position ), is now recognized as a sign of various metabolic encephalopathies but is most prominent in this disorder (page 86) It is conventionally demonstrated by having the patient hold his arms outstretched with the wrists extended, but the same tremor can be elicited by any sustained posture, including that of the protruded tongue A variable, uctuating rigidity of the trunk and limbs, grimacing, suck and grasp re exes, exaggeration
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or asymmetry of tendon re exes, Babinski signs, and focal or generalized seizures round out the clinical picture in a few patients The EEG is a sensitive and reliable indicator of impending coma, becoming abnormal during the earliest phases of the disordered mental state Watson and Adams noted an EEG abnormality consisting of paroxysms of bilaterally synchronous slow or triphasic waves in the delta range, which at rst predominate frontally and are interspersed with alpha activity and later, as the coma deepens, displace all normal activity (Fig 2-3H, page 27) A few patients show only random high-voltage asynchronous slow waves This syndrome of hepatic encephalopathy is remarkably diverse in its course and evolution It usually appears over a period of days to weeks and may terminate fatally; or, with appropriate treatment, the symptoms may regress completely or partially and then uctuate in severity for several weeks or months Persistent hepatic coma of the latter type proves fatal in about half of patients (Levy et al) In many patients, the syndrome is relatively mild and does not evolve beyond the stage of mental dullness and confusion, with asterixis and EEG changes In yet others, a subtle disorder of mood, personality, and intellect may be protracted over a period of many months or even years; this chronic but nevertheless reversible mental disturbance need not be associated with overt clinical signs of liver failure (mainly jaundice and ascites) or other neurologic signs Characteristically in these patients, an extensive portal-systemic collateral circulation can be demonstrated (hence the term portal-systemic encephalopathy) and an association established between the mental disturbance and an intolerance to dietary protein as well as raised blood ammonia levels (Summerskill et al) The diversion of blood from the portal system into the vena cava after ligation of the portal veins was rst performed in dogs by Eck in 1877 Probably the rst and certainly most striking example in man was the case of pure Eck stula reported by McDermott and Adams, in which a portacaval shunt was created during the removal of a pancreatic tumor The liver was normal Episodic coma occurred thereafter whenever dietary protein increased Consciousness was restored on a protein-free diet, and coma could be induced again by ammonium chloride Postmortem examination 2 years later con rmed the normal liver and showed cerebral changes of hepatic encephalopathy, as described below Finally, there is a group of patients (most of whom have experienced repeated attacks of hepatic coma) in whom an irreversible mild dementia and a disorder of posture and movement (grimacing, tremor, dysarthria, ataxia of gait, choreoathetosis) gradually appear This condition of chronic acquired hepatocerebral degeneration must be distinguished from other dementing and extrapyramidal syndromes (see further on) A few cases of isolated spastic-ataxic paraplegia (so-called hepatic myelopathy) of unclear nature have also been described (page 1078) The concentrations of blood NH3, particularly if measured repeatedly in arterial blood samples, usually are well in excess of 200 mg/dL, and the severity of the neurologic and EEG disorders roughly parallels to the ammonia levels With treatment, a fall in the NH3 levels precedes clinical improvement In the past, a provocative test of an oral dose of 60 g of NH3Cl was used in uncertain cases to produce mild symptoms of hepatic encephalopathy Neuropathologic Changes The striking nding by Adams and Foley in patients who die in a state of hepatic coma is a diffuse increase in the number and size of the protoplasmic astrocytes in the deep layers of the cerebral cortex, lenticular nuclei, thalamus, substantia nigra, cerebellar cortex, and red, dentate, and pontine
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