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1. A chronic alcoholic with severe metabolic acidosis presents a difficult diagnostic problem. The most common cause is alcoholic ketoacidosis, a syndrome with a typical history but often misleading laboratory findings. This paper will focus on this important and probably underdiagnosed syndrome. 2. The disorder occurs in alcoholics who have had a heavy drinking-bout culminating in severe vomiting, with resulting dehydration, starvation, and then a beta-hydroxybutyrate dominated ketoacidosis. 3. Awareness of this syndrome, thorough history-taking, physical examination and routine laboratory analyses will usually lead to a correct diagnosis. 4. The treatment is simply replacement of fluid, glucose, electrolytes and thiamine. Insulin or alkali should be avoided. 5. The most important differential diagnoses are diabetic ketoacidosis, lactic acidosis and salicylate, methanol or ethylene glycol poisoning, conditions which require quite different treatment. 6. The diagnostic management of unclear cases should always include toxicological tests, urine microscopy for calcium oxalate crystals and calculation of the serum anion and osmolal gaps. 7. It is suggested here, however, that the value of the osmolal gap should be considered against a higher reference limit than has previously been recommended. An osmolal gap above 25 mosm/kg, in a patient with an increased anion gap acidosis, is a strong indicator of methanol or ethylene glycol intoxication.
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PMID:Severe metabolic acidosis in the alcoholic: differential diagnosis and management. 879 30

A 9-year-old male Doberman Pinscher was referred to the Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, for polyuria/polydipsia, anorexia, and vomiting. Laboratory examination of blood and urine revealed hyperglycemia, glucosuria, and acidosis. Diabetes mellitus was diagnosed but was very resistant to subsequent insulin treatment. At the owners' request, the dog was euthanatized and a postmortem examination was performed. In addition to hepatic, pancreatic, and renal changes compatible with diabetes mellitus, an acidophilic adenoma of the adenohypophysis was found. Immunohistochemical staining for growth hormone, adrenocorticotropic hormone, and prolactin showed a strong immunolabeling for growth hormone within the cytoplasm of the tumor cells. Although growth hormone level was not measured in the plasma, our findings suggest that the diabetes mellitus in this dog was caused by excess growth hormone secreted by the pituitary neoplasm.
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PMID:Diabetes mellitus in a dog with a growth hormone-producing acidophilic adenoma of the adenohypophysis. 881 49

We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.
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PMID:Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC. 884 91

The purpose of the present study was to examine the presentation and outcomes associated with diabetic ketoacidosis (DKA) in pregnancies complicated by diabetes. Eleven episodes (2%) of DKA were diagnosed during the 10-year study period. All patients were under close observation by the Diabetes-in-Pregnancy Service. Plasma glucose levels of less than 200 mg/dL were present in 4 of the 11 patients (36%), 10 (90%) of whom presented with nausea, vomiting, and decreased caloric intake. Two subsequently had fetal distress necessitating cesarean section. One fetal death occurred in a patient treated with subcutaneous insulin. Despite contemporary methods of diabetes care, near-normal plasma glucose levels are not enough to preclude diabetic ketoacidosis. Nausea, vomiting, and decreased caloric intake in an otherwise normal pregnant, diabetic woman requires evaluation to exclude ketosis.
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PMID:The changing presentations of diabetic ketoacidosis during pregnancy. 896 Jun 16

We undertook the present study to examine the acid-base and electrolyte disturbances in relation to hydration status in patients with diabetic ketoacidosis (DKA). A total of 40 insulin-dependent diabetes mellitus patients (22 male, 18 female), aged 18-61 years with DKA admitted to our hospital during the last 2 years, were studied. The duration of diabetes averaged 9 +/- 2 years. In all cases a detailed investigation of the acid-base status and electrolyte parameters was performed. Twenty-one patients had a pure metabolic acidosis with an increased serum anion gap, seven had DKA combined with hyperchloremic metabolic acidosis, nine had DKA coexisting with metabolic alkalosis, while three had DKA with a concurrent respiratory alkalosis. Hydration status as evidenced by the ratio of urea/creatinine seems to play an important role in the development of mixed acid-base disorders (detected by changes in the ratios delta anion gap/delta bicarbonate (delta AG/delta HCO3) and sodium/chloride (Na/Cl)). In fact, hyperchloremic acidosis developed in the patients with the better hydration status. However, contradictorily, the severely dehydrated patients who experienced recurrent episodes of vomiting developed DKA with a concurrent metabolic alkalosis. Finally, patients with pneumonia or gram-negative septicemia exhibited DKA combined with a primary respiratory alkalosis. We conclude that patients with DKA commonly develop mixed acid-base disorders, which are partly dependent on patients' hydration status.
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PMID:Acid-base and electrolyte disturbances in patients with diabetic ketoacidosis. 896 87

In adults with diabetes mellitus, hepatomegaly and abnormalities of liver enzymes occur as a consequence of hepatocellular glycogen accumulation, as has been well described in children. During periods of hyperglycemia glucose freely enters the hepatocytes driving glycogen synthesis, which is augmented further by administration of insulin to supraphysiologic levels. The accumulation of excessive amounts of glycogen in the hepatocytes is a function of intermittent episodes of hyperglycemia and hypoglycemia and the use of excessive insulin. Hepatic glycogenosis occurs in patients with poorly controlled insulin-dependent type I or type II diabetes. The clinical manifestations of this phenomenon may include abdominal pain and obstructive symptoms such as early satiety, nausea, and vomiting. Ascites has rarely been reported. The typical biochemical findings are mildly to moderately elevated aminotransferases, with or without mild elevations of alkaline phosphatase. Liver synthetic function is usually normal. All these abnormalities, including the hepatomegaly, are readily reversible with sustained euglycemic control. The other major cause of hepatomegaly in patients with diabetes is steatosis. This is a function of the body habitus and state of insulin resistance rather than glycemic control. However, the distinction between steatosis and glycogenosis is important: whereas steatosis may progress to fibrosis and cirrhosis, glycogenosis does not, but reflects the need for better diabetic control. Glycogenosis and steatosis cannot be distinguished reliably on ultrasound examination. The histology, however, is definitive. In glycogenosis, as in primary glycogen storage diseases, there is excess glycogen in the cytoplasm, and often also in the nucleus, of hepatocytes. The hepatocytes throughout the lobule appear pale and swollen with clearly defined cell boundaries. Ultrastructural examination reveals cytoplasmic glycogen in clumps displacing organelles to the periphery of the cell, and there is little if any steatosis. We have shown that hepatomegaly due to glycogenosis in adults with diabetes is similar in all respects to the condition seen in children. As in children, liver enzyme abnormalities are unreliable in predicting the presence or the extent of glycogenosis. Hepatic glycogenosis can occur at any age, and therefore should be included in the differential diagnosis of hepatomegaly in all insulin-requiring diabetics.
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PMID:Hepatomegaly and abnormal liver tests due to glycogenosis in adults with diabetes. 898 49

A 41-year-old black woman with a history of well-controlled, insulin-dependent diabetes mellitus was in her usual state of relatively good health when she had acute onset of right upper quadrant and epigastric abdominal pain, nausea, and vomiting. Physical examination and laboratory evaluation revealed gastrointestinal hemorrhage, decreased mental status, and acidemia, and emergency exploratory laparotomy elucidated ischemic bowel, of which 90 cm was resected. Postoperatively, the patient had cardiac arrest and could not be resuscitated. Autopsy was remarkable for mesenteric venous thrombosis and pylethrombosis, with ischemic necrosis of bowel and passive hyperemia. The arterial side of the cardiovascular system was relatively unaffected. Although arterial vascular complications of diabetes mellitus are well known, venous complications are less well described.
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PMID:An unusual complication of diabetes mellitus: the zebra that became a horse. 900 34

Based on case reports pathogenesis and treatment of the following diabetic emergencies were discussed: 1. The hyperosmolar non-ketotic coma without or with only modest ketosis occurring mainly in type II diabetics and the severe ketoacidosis with or without disturbed consciousness occurring mainly in type I diabetics are the two forms of severe metabolic decompensation of diabetes mellitus. 2. Severe hypoglycaemia may be caused by treatment with sulfonylureas and insulin. 3. The most dangerous life threatening adverse effect of biguanides is lactic acidosis. The incidence of ketoacidosis is about 1-5% in type I diabetics with a mortality of 3-9%. Mortality rates of hyperosmolar non-ketotic comas are much higher, approaching 20-40%, and are explained by severe concomitant complications and older age. The most important triggering factors of diabetic coma are infections, insulin dispensing errors and non-compliance. Carefully instructing patients about the risks of loosing appetite and vomiting as early signs of ketoacidosis is essential. Adequate replacement of fluid, electrolyte and water are the most important therapeutical aspects of ketoacidosis and hyperosmolar non-ketotic coma. Early diagnosis and appropriate treatment of infection by antibiotics are important. Complication of therapy (hypokalemia, hypovolemia and rapid full of oncotic pressure) should be avoided by clinical and laboratory monitoring. Treatment of acidosis with bicarbonate has been found more dangerous than useful. Severe hypoglycaemia is the most important and most dangerous side effect of sulfonylurea and insulin. The incidence of severe hypoglycaemia under glibenclamide ist 3-5 fold higher than under treatment with tolbutamide or glibornurid. Glibenclamide should not be recommended anymore. Longterm experience of the therapeutic security of new sulfonylurea derivates like glimepirid is lacking. Blood-glucose-measurements in the afternoon are important for recognizing disposition to sulfonylurea hypoglycaemia, because at this time the blood-glucose-values tend to be lower than in the morning fasting state. Under insulin treatment the following risk factors for severe hypoglycaemia need to be considered: metabolic control in the near normal range, intensified treatment with rapidly decreasing HbA1c-levels, impaired renal function, unawareness o hypoglycaemia. When the renal function is impaired, biguanide treatment is not indicated because of the risk of lactic acidosis. Most of the diabetic emergency situations are avoidable by proper education of the patients.
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PMID:[Diabetic emergencies]. 914 92

Sudden death caused by the acute onset of diabetic coma is reported. A 15-year-old female had been suffering from insulin-dependent diabetes mellitus for the prior 8 years and had a fever and vomiting for the past few days. On the 4th day, after the onset of fever and vomiting, she died suddenly, and was autopsied to clarify the cause of death. Macroscopic examination revealed that the pancreas was atrophic (40 g) whereas the liver was markedly enlarged (2,740 g). Histological findings were: 1) The islets of Langerhans were decreased in size and number. They were not positive for aldehyde-fuchsin staining, 2) There were severe fatty changes in the liver cells. The retained blood in the left ventricle was analyzed: glucose, 1,016 mg/dl; acetone, 345 mg/l; acetoacetate, 5.91 mmol/l: D-3-hydroxybutyrate, 4.17 mmol/l; hemoglobin A1c, 10.2%; fructosamine, 416 mumol/l; total serum cholesterol, 220 mg/dl; triglycerides, 205 mg/dl; free fatty acid, 8.0 mEq/l; urea nitrogen, 40 mg/dl. Although the biochemical estimation of the glucose and ketone levels in post-mortem body fluids was recognized as being unreliable, many of these values were far elevated in comparison with those of normal individuals. Thus, we concluded that the cause of death was diabetic ketoacidosis. We also discuss the diagnostic problems of postmortem blood chemistry.
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PMID:Sudden death due to diabetic coma in insulin-department diabetes mellitus: an autopsy report. 918 21

We report a 30 years old woman with sporadic poliglandular autoimmune syndrome type II, first seen with an insulin-dependent diabetes mellitus and a Graves-Basedow disease that became spontaneously hypothyroid with positive antimicrosomal antibodies. Six years later she presented with persistent vomiting and a remarkable reduction in insulin requirements. She had low basal and stimulated-cortisol levels and the diagnosis of severe adrenal failure was reached. A CT scan showed normal adrenal glands, she did not have cutaneous hyperpigmentation nor evidences of mineralocorticoid deficit. A selective autoimmune damage of the fascicular zone was assumed but a selective damage of ACTH producing pituitary cells cannot be discarded. The importance of investigating adrenal function in cases of unexplained reduction of insulin requirements is emphasized.
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PMID:[Asymptomatic Addison disease: cause of striking reduction of insulin requirements in a patient with diabetes, Hashimoto thyroiditis and Basedow disease]. 929 4


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