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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to confirm or refute the previously held view that electrocardiographic (ECG) abnormalities are frequent in diabetic ketoacidosis, we have undertaken continuous ECG monitoring for 24 h, with subsequent computer analysis, in 14 diabetic patients admitted with severe ketoacidosis. There was a steady fall in heart rate during the 24-h except in 3 severely dehydrated patients. Depression of the ST-segment was minimal and ST-segment height correlated significantly with heart rate, whereas no consistent relationship was found between T-wave amplitude and either heart rate or plasma potassium. Two patients developed short periods of supraventricular ectopic beats. Although ECG monitoring has been claimed to be a useful aid in the management of diabetic ketoacidosis, this study clearly demonstrates that significant ECG changes are rare and ECG monitoring thereafter adds little to careful clinical observation and regular biochemical assessment.
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PMID:The value of continuous ECG monitoring during treatment of diabetic ketoacidosis. A computer study. 10 99

Stupor in patients with nonketotic hyperglycemia has been ascribed to hyperosmolarity, but the cause of depressed consciousness in patients with ketoacidosis has been puzzling. In this study, blood pH, serum glucose and sodium concentrations, and serum osmolality were measured in eighty-five consecutive episodes of diabetic ketoacidosis and forty-seven of nonketotic hyperglycemia. In the acidotic patients, as in those with nonketotic hyperglycemia, stupor closely paralleled hyperosmolarity and not the severity of acidemia. Indeed, the mean elevations of serum osmolarity were almost the same in the ketotic and in the nonketotic patients who were deeply obtunded. It seems likely that depression of consciousness in patients with severely uncontrolled diabetes mellitus, if not due to a nonmetabolic disorder, such as acute stroke, is attributable to hyperosmolarity, whether or not ketoacidosis is present.
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PMID:Hyperosmolar nature of diabetic coma. 23 99

Coma and other neurologic abnormalities are present in patients with either diabetic ketoacidosis (DKA) or nonketotic coma (NKC), and the cause of such phenomena are not known. Patients with NKC also manifest seizures and focal neurologic changes. Treatment of diabetic coma with insulin may induce cerebral edema by as yet undefined mechanism(s). In patients with DKA, cerebral oxygen utilization is impaired, and there is hyperviscosity of the blood. A substantial part of the brain's energy source is derived from ketones, which in themselves can depress sensorium. Extracellular hyperosomolality is present, which may also contribute to the genesis of coma. In addition, most ketoacidotic patients have associated medical conditions, which may further impair consciousness. Biochemical changes in the brains of animals with DKA include impairment of both phosphofructokinase activity and pyruvate oxidation, and accumulation of citrate. The net effect upon sensorium in ketoacidotic patients probably represents the interaction of most of the above factors and differs markedly among individuals. Patients with NKC manifest not only depression of sensorium, but also focal motor seizures, hemiparesis, and other neurologic changes, such as aphasia, hypereflexia, sensory defects, autonomic changes, and brainstem dysfunction. Most of the aforementioned changes revert to normal after correction of hyperosomolality. Gamma amino butyric acid, which has been shown to elevate the seizure threshold, is normal in brains of ketoacidotic animals, but may be low in nonketotic coma. Also, hyperosomolality per se may produce seizures. Cerebral edema may complicate the treatment of either DKA or NKC. The available experimental evidence suggests that many of the commonly held theories for the production of such brain swelling probably do not occur. There is no breakdown of the sodium pump, sorbitol or fructose do not accumulate in brain, and brain glucose is only about 25 percent of that in plasma; Cerebral edema is probably produced largely by a direct action of insulin on brain at a time when plasma glucose is approaching normal values. Cerebral edema can thus theoretically be avoided by stopping insulin when plasma glucose has been lowered to values approaching normal.
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PMID:Neurologic manifestations of diabetic comas: correlation with biochemical alterations in the brain. 80 37

A 24-year-old newly diagnosed male patient with diabetes presented with diabetic ketoacidosis (DKA) (pH 7.16, HCO3 6.0) and extreme hypertriglyceridemia (239.35 mmol/L). The diagnosis of DKA was delayed because of the apparent depression of the true serum glucose (to 11 mmol/L). He was treated with intravenous (IV) insulin and rehydration, which normalized his pH, HCO3, and triglyceride levels. To the authors' knowledge, this is both the highest triglyceride level recorded and the first report of a high triglyceride level as the apparent cause of a factitiously low glucose level.
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PMID:Pseudonormoglycemia in diabetic ketoacidosis with elevated triglycerides. 189 2

Deep venous thromboses in the lower extremities were observed in three boys aged 8, 10, and 12 years. In one case, it must have originated from circulatory depression during diabetic ketoacidosis. In two children, osteomyelitis was detected in the proximity; they developed septic pulmonary embolism. Osteomyelitis and septic arthritis as possible cause or consequence should be actively looked for in septic thromboembolism.
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PMID:[Pelvic and femoral vein thrombosis in childhood]. 314 16

The widespread presence of fingernail polish remover in the home makes the product a common source of ingestion, as evidenced by recent poison center data. Its principal component, acetone, is present in relatively high concentration. The syndrome of acetone intoxication presents as generalized central nervous system/respiratory depression, hyperglycemia, and ketosis. Despite its ubiquitous presence and high potential for severe intoxication, no reports are found describing the toxicity and supportive care following its ingestion by children. The authors present a 30-month-old patient with severe acetone intoxication secondary to fingernail polish remover ingestion. Also noted is the need to include acetone ingestion in the differential diagnosis of apparent diabetic ketoacidosis.
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PMID:Acute acetone intoxication in a pediatric patient. 336 29

Cerebral edema as a complication of the therapy of diabetic coma has been described for over 50 years, although modern awareness dates to about 1967. Almost all cases have occurred in patients with diabetic ketoacidosis (DKA). Although a few cases of cerebral edema have been reported in patients with nonketotic hyperosmolar coma (NKHC), these are in general not well documented by either autopsy data of cat scans. Over a period of 9 years, I have encountered 5 patients who developed cerebral edema as a complication of the therapy of NKHC. The initial plasma glucose in these patients was 1,496 +/- (SD) 296 mg/dl and plasma osmolality was 382 +/- 29 mosm/kg. All had depression of sensorium to at least a stupor (stage I coma or greater). All were treated with intravenous insulin and either 77 or 154 mM NaCl, and plasma glucose fell at a mean rate of 38 mg/dl/h. In all patients, plasma glucose fell below 250 mg/dl (mean of 18 +/- 66 mg/dl) and all patients experienced increased depression of sensorium, elevated csf pressure, and brain swelling as diagnosed by cat scanning. Therapy with various combinations of glucose, mannitol and steroids were without effect. In 1 patient, insertion of a subdural intracranial screw lowered intracranial pressure from 24 to 3 cm of H2O. Three of the 5 patients died and 2 remain in a persistent vegetative state, 1 of whom is also quadriplegic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral edema complicating nonketotic hyperosmolar coma. 354 38

The response of four Type I diabetic patients to long term (1,4,4, and 8 months) intravenous insulin infusion is reported. As compared to their usual subcutaneous depot insulin treatment, glycosylated hemoglobin (HbAl) decreased from 12.2 +/- 0.7 to 8.8 +/- 0.9 (p less than 0.05). However, only 49 to 76.5% of self blood glucose monitoring results were between 60-179 mg/dl range. Although 6.3 to 15.2% of capillary blood glucose levels were less than 60 mg/dl, severe hypoglycemia occurred only on one occasion. Plasma cholesterol, triglyceride and high density lipoprotein all decreased significantly (p less than 0.005). The major motivating factors for participation in this study were: (1) the hope of preventing diabetic complications; (2) the wish for more knowledge about diabetes; (3) a sense of special purpose and (4) a general interest in science and research. Catheter obstruction as a result of insulin aggregation terminated the study in two subjects. A third subject requested the study be stopped primarily because of imposed travel restrictions. In one subject, the study was stopped because of a disrupted personal life and developing depression. Diabetic ketoacidosis or sepsis from the centrally placed intravenous catheter did not occur. Although long term intravenous insulin infusion is feasible in a clinical research setting, insulin aggregation continues to be a major limiting factor. The widespread clinical use of implantable pumps will have to await the development of a suitable insulin formulation.
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PMID:Long term open loop intravenous insulin infusion in type I diabetes: feasibility, problems and promise. 639 75

Severe intercurrent nonthyroidal illnesses (diabetic ketoacidosis, myocardial infarction, fulminant hepatitis and bacterial pneumonia) in four thyrotoxic patients were associated with depression of total serum thyroxine (T(4)) and triiodothyronine (T(3)) values into the normal or even subnormal range. A diagnosis of hyperthyroidism was established by a combination of elevated radioactive iodine uptake, absent thyroid-stimulating hormone response to thyrotropin-releasing hormone or an elevated free T(4) by dialysis values. In the two of four cases that had a fatal outcome, there was a progressive decline in total T(4) and total T(3) values. In contrast, the two surviving patients had a progressive increase of total T(3) and total T(4) values into the hyperthyroid range as their underlying illness resolved. As has been seen with severe nonthyroidal illnesses, pronounced depression of total T(3) and total T(4) levels in hyperthyroid patients may also portend a poor prognosis.
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PMID:Influence of nonthyroidal illnesses on serum thyroid hormone indices in hyperthyroidism. 688 Jan 82

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85


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