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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-five serious cases of diabetic ketoacidosis, representing 23 patients, with ages ranging from 4 to 15 years are reported. School agers and adolescents were the groups most affected without existing significant predilection for sex. In 40% there was no success in finding the precipitating cause of the crisis; 32% was attributed to infectious processes, specially of the respiratory ducts and the rest, due to negligence in the application of insulin. The clinical signs showed: vomiting, dehydration, Kussamaul's respiration, sopor, stupor and in 5 cases a state of coma. Determinations of glucose, were integrated in 88% within the range of 451 to 750 mg % and the rest in lower figures. The pH in most was reported below 7.10 and CO2 lower than 10 mEq/l. Electrolytes in blood were generally evaluated within normal limits. Potassium in 20% was reported high, but we consider this was due to dehydration and because of its influence we recommend an electrocardiographic evaluation. Our classification which attempts to correlate the clinic and the laboratory is reported and our therapeutic scheme is discussed as well as the possible causes in two patients who died.
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PMID:[Diabetic ketoacidosis in children and adolescents. Clinical and therapeutical considerations in 25 severe cases]. 2 Sep 2

In a field study comprising 678 patients with arterial hypertension efficacy and tolerance of the stable combination VKB 105 consisting of 10 mg Pindolol (Visken) and 5 mg Clopamid (Brinaldix) were investigated. Treatment with 1--2 tablets of VKB per day resulted in a successful therapy in 94% of all patients corresponding on the average to a reduction in blood pressure to 145/85 mm Hg within 14 days. In mean arterial pressures ranging between 120 and 170 mm Hg a positive linear relationship between the individual initial value and the hypotensive effect of the combination could be observed. A controlled omission trial disclosed qualitatively the respective contribution to the effect of the two components Pindolol and Clopamid. With a systematic case control of the serum potassium under the combined therapy with VKB 105 and during a monotherapy with Clopamid and antihypokalaemic effect of Pindolol could be demonstrated diminishing the tendency for potassium loss. The result revealed a far-reaching potassium neutrality of diuresis-depending stimulation of renin by the beta-receptor blocker. In 61 patients altogether subjective side-effects could be recorded, such as vertigo (5%), palpitations (2.8%), fatigue (2%), insomina (1.9%), nausea (1.7%) and vomiting (0.8%). Laboratory controls gave no indication for clinically relevant changes.
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PMID:[A field study with the combination of Pindolol and Clopamid in antihpertensive therapy (author's transl)]. 3 34

Classic renal tubular acidosis is characterized by a primary defect in establishment of a large hydrogen ion gradient across the distal renal tubule. Thus the development of hyperchlorenic metabolic acidosis follows. In addition, hypokalemia results from renal potassium wasting secondary hyperaldosteronism from sodium wasting and contraction of the extracellular fluid. The presenting signs and symptoms are growth retardation, fatigue, periodic paralysis, polyuria, polydipsia, vomiting and constipation as well as nephrocalcinosis and nephrolithiasis. It is suggested that effective treatment with alkali therapy requires markedly higher doses than formerly recommended, and may related to a higher rate of endogenous acid production from (1) intermediary metabolism of sulfur amino acids and organic acids, (2) impaired tubular reabsorption of bicarbonate and (3) hydrogen ion release from hydroxyapatite formation. It is also suggested that acidosis may interfere with vitamin D metabolism and thus play an important role in the pathoetiology of the growth failure in children with this disorder.
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PMID:Acid-base, calcium, potassium and aldosterone metabolism in renal tubular acidosis. 3 60

The use of sucrose in oral rehydration therapy solutions in place of glucose was tested in 18 patients, 17 males and 1 female, admitted for treatment of severe dehydration due to diarrhea and vomiting. 13 of these patients were positive for cholera (1 with untyped vibrio), whereas 4 others cultured no recognizable pathogen. Patients received an average 1100 ml of intravenous fluids to keep the intravenous drip open during the oral therapy period, and the intravenous therapy was stopped or slowed during oral (or nasogastric) therapy. Average patient age was 32 years. Oral solutions contained either 48 or 38 gm of sucrose per liter plus (in all solutions) sodium chloride (4.2 gm/liter), sodium bicarbonate (2 gm/liter), and potassium citrate (2.7 gm/liter). Of the 18 patients, 15 could be maintained using this solution, but 3 developed massive increases in net fluid losses with increases in plasma specific gravity, which necessitated terminating the therapy. In these failure cases, plasma specific gravity increased over 1.031. Stool samples of 12 patients tested were found to contain reducing sugar: prehydrolysis 436 mg/100 ml, posthydrolysis 957 mg/100 ml. The breakdown of sucrose by intestinal enzymes or by bacteria accounts for the presence of reducing sugar in the stool. These data contrast with the rarity of treatment failures of oral glucose therapy; therefore, glucose is the preferable component in oral rehydration electrolyte solution therapy.
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PMID:Sucrose in oral therapy for cholera and related diarrhoeas. 4 61

This study is a description of a patient who exhibited diabetic ketosis associated with an alkalosis rather than acidosis and a review of eight previously reported cases. Precipitating factors for this syndrome are severe vomiting with loss of hydrogen, potassium, and chloride ions, and dehydration. The ingestion of alkali may also result in this mixed acid-base disturbance. Treatment consists primarily of replacement of potassium and chloride. All reported patients had received large doses of insulin for initial therapy; however, limited insulin (20 U) therapy in this patient almost completely reversed the metabolic abnormality with 12 hours.
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PMID:Mixed acid-base abnormalities in diabetes. 10 96

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
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PMID:Electrolyte and acid-base disturbances in the management of leukemia. 26 90

Under the circumstances of limited health resources and immediate need for preventing the dehydration associated with diarrhea in infants, breastfeeding should be encouraged throughout the diarrheal episode. When this is not possible because of cessation or failure of lactation, an oral electrolyte solution should be administered. It should be sterile and provide a quantity of electrolytes not greatly in excess of 30 mEq/liter of sodium and potassium. There should be little possibility of an error in the dilution of the mixture if it is to be supplied in powdered form. Milk should be reintroduced after 24 hours and the electrolyte mix rapidly discontinued so as to minimize nutritional deficits. If no such electrolyte mixture is available, it is reasonable to alternate feedings of commercial soft drinks or bland teas with milk feedings. There should be specific instructions that the infant should be brought to the hydration center if more than 3 sequential feedings are lost by vomiting, if fever is present, or it the stools exceed the volume of 3 feedings. In general, dehydration of less than 5% of body weight can be managed by this program in the house, dehydration greater than 5% but less than 10% requires supervision by health authorities, and dehydration greater than 10% requires intravenous therapy in a hydration center. In those countries with cholera and during epidemics of shigellosis or enterotoxigenic Escherichia coli, solutions containing 90 mEq/liter of sodium should be given under ambulatory supervision. This solution should be discontinued when fecal losses moderate (less than 60 ml/kg/day) and the lower electrolyte solution (30 mEq/liter) substituted.
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PMID:A critique of oral therapy of dehydration due to diarrheal syndromes. 33 34

Hypokalemia is seen most often with the use of diuretics and in patients with emesis. Other common clinical settings in which it may be significant include corticosteroid therapy, antibiotic usage, diarrhea, diabetic ketoacidosis, or psychiatric illness. Occasionally the cause may be obscure. In such situations the determination of urine potassium and arterial pH may prove helpful. Subclassification of hypokalemia into such categories as "acidosis", "alkalosis", "extra-renal", or "renal" loss is then possible. The cases discussed demonstrate the utilization of these methods to define the etiology and to understand the pathophysiology in hypokalemia.
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PMID:Mechanisms in hypokalemia: clinical correlation. 35 75

In infants and children acute dehydration is mainly caused by gastroenteritis with vomiting and diarrhoea, and by feeding failures. Since in the German speaking literature very different therapeutic regimens for rehydration are discussed the principles of oral and parenteral treatment are described. The rational therapy is based on the knowledge of physiology and pathophysiology of water and electrolyte metabolism. Therefore a few basic aspects are described, i.e. compartments of body fluids, turnover rates, the balance, types of dehydration, concentration of electrolytes in body fluids and their relevance to dehydration. Special problems exist in the treatment of hypertonic dehydration. In order to avoid cerebral edema the rehydration should not be attempted quickly with very hypotonic salt solutions, but should be performed with a 1/2--1/3 isotonic Ringer-lactate solution and early begin of potassium substitution over a period of 48 h.
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PMID:[The treatment of acute dehydration (author's transl)]. 35 53

The usual metabolic derangement in uncontrolled diabetes mellitus is metabolic acidosis, with an increase in the anion gap because of increased ketoacids and lactate. However, diabetic ketoalkalosis may occasionally be encountered, the prominent clinical feature of which is vomiting, with depletion of potassium, chloride, and hydrogen ions. Self-medication with absorbabe alkali may also contribute to the alkalosis. It would be dangerous to treat hyperlgycemic patients with alkali if their condition is ketoalkalosis instead of ketoacidosis.
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PMID:Diabetic ketoalkalosis. 45 54


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