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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperglycemic hyperosmolar coma is a life-threatening emergency with a mortality much higher than that of other forms of hyperosmolarity such as hypernatremia or diabetic ketoacidosis. Despite the differences in the three conditions, present evidence suggests that correction of hyperosmolarity should proceed slowly to avoid the seizures that may occur in all three conditions. This report describes a 9-month-old diabetic child who initially had hyperglycemic hyperosmolar coma and who is one of the youngest survivors of this syndrome in the American literature. This case report points out the limited understanding of the pathophysiology of this syndrome and the consequent problems of therapy.
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PMID:Hyperglycemic hyperosmolar coma in a 9-month-old child. 42 Jan 89

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

Magnesium is gaining recognition as a clinically important electrolyte. Hypomagnesemia has been associated with a variety of disorders including seizures, malignant ventricular dysrhythmias, and sudden death. The emergency department patients who are most likely to be magnesium deficient include alcoholics, patients who take diuretics, and those in diabetic ketoacidosis. Hypokalemia and hypocalcemia may represent unrecognized hypomagnesemia. Clinical trials and case reports also document increasing interest in magnesium as an effective therapeutic agent for potentially life-threatening problems such as torsade de pointes, digitalis toxicity, bronchospasm, and alcohol withdrawal. We present an overview of hypomagnesemia, review the current literature, and focus on the role of magnesium in the acute care setting and the implications for the emergency physician.
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PMID:Magnesium: clinical considerations. 149 Nov 57

Cerebral cell volume regulatory mechanisms are activated by sustained disturbances in plasma osmolality. Acute hypernatremia causes a predictable shrinkage of brain cells due to the sudden imposition of a plasma-to-cell osmolal gradient. However, during chronic hypernatremia cerebral cell volume is maintained close to the normal range as a result of the accumulation of electrolytes and organic osmolytes including myo-inositol, taurine, glutamine, glycerophosphorylcholine, and betaine. The increased cytosolic level of these molecules is generally accomplished via increased activity of sodium (Na+)-dependent cotransport systems. The slow dissipation of these additional osmotically active solutes from the cell during treatment of hypernatremia necessitates gradual correction of this electrolyte abnormality. Acute hyponatremia leads to cerebral cell swelling and severe neurological dysfunction. However, prolonged hyponatremia is associated with significant reductions in brain cell electrolyte and organic osmolyte content so that cerebral cell volume is restored to normal. While acute hyponatremia can be treated with the administration of moderate doses of hypertonic saline in order to control seizure activity, chronic hyponatremia should be corrected slowly in order to prevent subsequent neurological deterioration. If the rate of correction exceeds 0.5 mmol/l per hour, or if the total increment in serum [Na+] exceeds 25 mmol/l in the first 48 h of therapy, then there is an increased risk of the development of cerebral demyelinating lesions. Chronic hyperglycemia activates the brain cell volume regulatory adaptations in the same manner as hypernatremia. Therefore, during the treatment of diabetic ketoacidosis, it is imperative to restore normoglycemia gradually in order to prevent the occurrence of cerebral edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cell volume regulation: a review of cerebral adaptive mechanisms and implications for clinical treatment of osmolal disturbances: II. 153 29

Severe hypophosphatemia (i.e., serum phosphorus concentration below 1 mg/dl) occurs infrequently in veterinary patients. It is most often associated with diabetic ketoacidosis in small animals. Phosphate is necessary for the production of 2,3 diphosphoglycerate (2,3-DPG) and adenosine triphosphate (ATP); both are important for normal cellular metabolism. Consequences of severe hypophosphatemia may include hemolytic anemia, seizures, altered mentation, cardiomyopathy, and skeletal muscle weakness. Parenteral phosphate therapy is necessary in most cases of severe hypophosphatemia.
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PMID:Hypophosphatemia. Causes and clinical consequences. 267 24

The effects of pregnancy on acute metabolic complications of diabetes may have important consequences for both mother and fetus. The consequences of pregnancy for chronic complications of diabetes, including retinopathy, nephropathy, neuropathy, and hypertension, are not clear. Recent data are reviewed so that health care providers will be able to provide reasonable advice to insulin-dependent diabetic women contemplating pregnancy both for problems that may potentially arise during gestation and those that may affect long-term health and survival. Diabetic ketoacidosis is an uncommon problem that arises during gestation. Acute alterations in pH and electrolyte concentrations as well as hyperglycemia, however, may have important consequences for mother and fetus, including perinatal asphyxia and reduced fetal oxygen delivery. Hypoglycemia, on the other hand, may result in maternal coma or seizures and, when frequent, has been associated with infant respiratory distress syndrome. Background retinopathy often worsens during gestation, with regression common postpartum. Data suggest that progression of background disease is related to both glycemic control and the acute institution of intensive insulin therapy with those patients with poor control requiring more aggressive therapeutic intervention most adversely affected. The course of proliferative retinopathy is more variable, with both progression and regression reported. Preconception photocoagulation may prevent progression. Preconceptional ophthalmologic evaluation with frequent assessments during pregnancy is advised. Increases in 24-hour protein excretion are common during gestation in patients with preexisting renal disease and resolve in many patients postpartum. Serum creatinine and creatinine clearance increase during the first trimester and generally do not change during the remainder of pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impact of pregnancy on complications of insulin-dependent diabetes mellitus. 313 6

Ketoacidosis is one of the common complications of Type I insulin-dependent diabetes mellitus. Several neurologic (cerebral) deficiencies have been associated with diabetic ketoacidosis, including cerebral edema with increased intracranial pressure resulting in coma; partial and generalized seizures; and cerebrovascular occlusive disease resulting in motor and/or sensory dysfunction. Intracerebral hematomas have not been reported. A child is described who had insulin-dependent diabetes mellitus with hyperglycemic ketoacidosis who developed multiple spontaneous intracerebral hematomas. Possible mechanisms are discussed.
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PMID:Spontaneous intracerebral hematomas in juvenile diabetic ketoacidosis. 315 Feb 80

A case of diabetic ketoacidosis in a 64-year-old black woman with maturity-onset diabetes receiving phenytoin for a seizure disorder is reported. The woman was admitted to the hospital with a one-day history of polyuria and polydipsia. For the 10 months before admission, her diabetes was controlled with isophane insulin suspension 27 units daily. She also took phenytoin 100 mg orally three times a day. This was prescribed approximately six weeks earlier for right-sided focal seizures that were detected by electroencephalogram during a previous hospitalization for nonketotic hyperosmolar coma. No other medications were taken. The patient was treated with i.v. fluids and intermittent doses of i.v. insulin. Her condition rapidly improved and insulin zinc suspension 35 units daily was prescribed on discharge. Phenytoin was discontinued because the seizure disorder was considered secondary to the previous episode of hyperosmolar coma. A literature review of phenytoin-induced hyperglycemia is presented, including previous case reports, possible mechanisms of action, monitoring guidelines, and potential therapeutic uses. If hyperglycemia occurs in a patient taking phenytoin, especially after starting phenytoin therapy or increasing the dose, drug-induced hyperglycemia should be considered in the differential diagnosis.
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PMID:Phenytoin-induced hyperglycemia. 729 47

Although hypophosphatemia is relatively uncommon, it may be seen in anywhere from 20% to 80% of patients who present to the ED with alcoholic emergencies, diabetic ketoacidosis (DKA), and sepsis. Severe hypophosphatemia, as defined by a serum level below 1.0 mg/dL, may cause acute respiratory failure, myocardial depression, or seizures. Because hypophosphatemia is not as often treated by ED physicians, becoming familiar with a single intravenous phosphate solution and specific guidelines for phosphate repletion are essential. One mL of the most commonly available phosphate solution (K2PO4) contains 4.4 meq of potassium and 3 mmol (93 mgs) of phosphate. Administering K2PO4 at a rate of 1 mL per hour is almost always a very safe and appropriate treatment for hypophosphatemia. This article provides guidelines for phosphate therapy in hypophosphatemic ED patients including those in DKA, those presenting with alcohol-related complaints including alcoholic ketoacidosis and patients with acute exacerbation of asthma and chronic obstructive pulmonary disease.
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PMID:Hypophosphatemia in the emergency department therapeutics. 1091 39

We herein report a rare case of MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) and diabetes mellitus with ketoacidosis. An 18-year-old female patient was diagnosed to have diabetes mellitus and insulin therapy was thereafter initiated. At 26 years of age, she was hospitalized for diabetic ketoacidosis, soon followed by a loss of consciousness, left-sided dysmetria, and ataxic speech. MELAS was diagnosed because of the presence of ragged red fibers in a muscle biopsy. At 33 years of age, she was admitted to our hospital because of ketoacidosis and partial status epilepticus. A blood gas examination revealed as follows; arterial pH, 6.88; bicarbonate, 2.1 mmol/l; base excess - 29.8 mmol/l. The serum level of glucose had also increased to 30 mmol/l. The serum levels of lactate and B-hydroxybutyrate were elevated to 11.4 mmol/l and 1,990 micromol/l, respectively. Ketoacidosis improved by fluid replacement and continuous intravenous insulin infusion. A brain MRI demonstrated hyperintensity areas on FLAIR images in the bilateral temporal lobes and the cerebellum. A proton MRS demonstrated the abnormal lactate accumulation in the bilateral temporal and occipital lobes. Since epileptic seizures are rare in patients with diabetic ketoacidosis, such seizures may indicate the existence of MELAS syndrome.
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PMID:Ketoacidosis accompanied by epileptic seizures in a patient with diabetes mellitus and mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). 1111 21


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