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

Theoretically, absorption of an ingested dose of paraquat may be reduced by gastric lavage, induced emesis, whole-gut lavage or by the oral administration of absorbent substances. Animal experiments suggest that paraquat is absorbed poorly from the stomach and absorbed incompletely (less than 5%) from the small intestine over a 1-6 h period. Although gastric lavage would therefore seem a logical way to ameliorate the toxicity of an ingested dose of paraquat, peak plasma concentrations are attained rapidly and evidence for the efficacy of gastric lavage in man is poor. In 1977, a potent emetic (PP796) was added to liquid and solid formulations of paraquat because experiments in primates had demonstrated a fivefold reduction in toxicity. In man, ingestion of formulations containing an emetic is more likely to cause spontaneous vomiting within 30 min than non-emetic preparations. However, definite evidence of benefit, as judged by improved patient prognosis, has yet to be established. Gut lavage has been shown to remove only a small proportion of an ingested dose of paraquat. At the flow rates employed in man (75 ml/min), approximately 0.5-1.0 litres of lavage fluid/h may be absorbed across the intestinal wall. Since there is a theoretical risk of increasing paraquat absorption, the use of whole-gut lavage cannot be recommended. Bipyridilium herbicides are absorbed by soil and clay minerals, and montmorillonite in particular has been shown to be a strong binding agent in vitro. Accordingly, the use of Fuller's Earth (calcium montmorillonite) and Bentonite (sodium montmorillonite) for the treatment of poisoning has been investigated in animal models.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of paraquat poisoning in man: methods to prevent absorption. 354 86

A group of 28 Syrian children (19 males and 9 females; age ranging from 2.5 to 12 years) were diagnosed clinically and radiologically to have upper urinary tract stones. The commonest presentations were renal colic, vomiting, haematuria, pyrexia and vague abdominal pain. Family history of renal stones was present in 21% of cases. Haematological picture and chemical analysis of blood were within the normal limits for their age and sex. Urine analysis, however, showed significantly marked increase in the 24-hour excretions of calcium and uric acid. Microscopic examination showed haematuria and pyuria in 72% of the children with urolithiasis. Chemical analysis of removed stones revealed that most of them were mixed stones of calcium oxalate and urate or/and phosphate. Pure stones of calcium oxalate or calcium phosphate were less common. Radiologically, about 95% of all stones were demonstrated by plain X-ray, while 5% only after IVP.
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PMID:Some features of paediatric urolithiasis in a group of Syrian children. 358 9

To delineate the spectrum of clinical expressions of distal, type 1 renal tubular acidosis in children and to update progress in diagnosis, therapy, and prognosis, the medical records of 14 girls and 10 boys, seen over a 7 year period, who met the following criteria, were examined: persistent urinary pH more than 6, net acid excretion less than 70 microEq/min/1.73 m2, simultaneous serum total CO2 less than 17.5 mEq/1, and normal or mild impairment of the glomerular filtration rate. The mean age at diagnosis was 8 months. The presenting signs and symptoms were failure to thrive (50%), vomiting and/or diarrhea (37.5%), dehydration (12.5%), and poor feeding (8.3%). Mean values +/- SD of serum calcium (9.8 +/- 0.8 mg/dl), inorganic phosphate (5.6 +/- 0.8 mg/dl), and alkaline phosphatase (222.6 +/- 96.1 U/l) were normal. Hyperkalemia (serum potassium above 5.0 mEq/l) was present at diagnosis in 13 children. Type 4 renal tubular acidosis was ruled out by the inability to achieve a minimum urine pH. With a mean follow-up period of 28.1 +/- 25.3 months, after alkali therapy at 3.3-3.5 mEq/kg/day had been administered for at least 12 months, the growth parameters improved as follows: the percentile weight (mean +/- SD) increased from the initial 11.8 +/- 7.5 to the final 27.6 +/- 31.3 (p less than 0.003), and the length/height percentile increased from 11.5 +/- 7.3 to 29.7 +/- 24.2 (p less than 0.03). The relationship between urine calcium/creatinine ratio and serum total CO2 showed poor correlation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal tubular acidosis in children. Diagnosis, treatment and prognosis. 377 38

In a 26-year-old patient admitted to the emergency ward with acute abdomen, all the symptoms--nausea, vomiting, indeterminate abdominal pain, constipation, renal failure, polyuria and polydipsia--could be explained by calcium intoxication syndrome. Investigation revealed generalized sarcoidosis. Under medical treatment with prednisone all the pathologic findings rapidly regressed. The pathogenesis of hypercalcemia in sarcoidosis, and particularly the disorder of vitamin D metabolism with raised levels of 1,25-dihydroxycholecalciferol, are discussed.
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PMID:[Acute hypercalcemia syndrome in sarcoidosis]. 384 Sep 13

Hypercalcaemia can be caused by many disorders, but is most commonly due to primary hyperparathyroidism in outpatients, and to malignant disease in hospital inpatients. When mild (less than 3 mmol/L) it does not cause symptoms, but can have long term effects such as renal calculi. It is important that the aetiology of the hypercalcaemia be established, as it can reflect serious disease. In most patients the correct diagnosis can be suspected from clinical history and examination, and confirmed by laboratory tests and x-rays. The most difficult diagnostic problem is the patient with negative clinical findings, mild hypercalcaemia and mild renal impairment, when the parathyroid hormone level is normal or slightly elevated. When hypercalcaemia is severe (greater than 3.5 mmol/L), it can cause vomiting, polyuria, dehydration and renal impairment, and is then an important therapeutic problem. Therapy includes treatment of the cause, such as radiotherapy for malignant disease or surgery for primary hyperparathyroidism. In addition, it is usually necessary to treat the hypercalcaemia itself, and the initial step is always rehydration. If the plasma calcium concentration remains high, drug treatment must be added, the most effective and reliable agent being intravenous mithramycin. Aminohydroxypropylidene diphosphonate (APD), though less studied, may be equally useful in this situation. Glucocorticoids are not always effective, and phosphate may cause renal damage, particularly when given intravenously. For long term treatment of malignant hypercalcaemia, oral glucocorticoids and phosphate are often effective, and can be given in combination. When primary hyperparathyroidism cannot be corrected surgically, the hypercalcaemia (and hypercalciuria) are probably best treated with a low calcium diet and cellulose phosphate, a regimen also effective for the hypercalcaemia of sarcoidosis.
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PMID:Hypercalcaemia. What does it signify? 394 Aug 49

Unexpected differences in clinical and biochemical findings in two brothers occupationally exposed to the same source of lead for dissimilar lengths of time are presented. Only the brother with the shorter period of lead exposure was anemic and afflicted by nausea, vomiting, abdominal colic and arthralgia. His urinary PBG output yielded the high orders of magnitude found in acute intermittent porphyria in relapse. Prior to administration of a single dose of EDTA (1 g of the calcium disodium salt given intravenously in 325 mL 0.15 mol/L NaCl), his blood lead levels averaged 3.6 mumol/L. The amount of chelatable lead retrieved from his urine, 31 mumol/day, was more than twice that found in his asymptomatic counterpart who was exposed to lead for 13 months and whose pre-EDTA blood lead levels averaged 4.0 mumol/L. Not only the activity of delta-aminolaevulinic acid dehydratase, but also that of uroporphyrinogen I synthetase, was markedly inhibited by lead in red cells of both brothers. These activities were restored to normal levels in vitro by addition to the assay system of zinc and dithiothreitol. This ruled out a coexisting genetic deficiency of either enzyme. The anemia of the symptomatic brother with the shorter period of lead exposure was alleviated by folic acid, 15 mg/day. The differences in findings between the two brothers point to differential susceptibility to lead and illustrate the extent to which symptomatic lead poisoning may mimic biochemical and clinical features of the acute porphyrias.
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PMID:Occupational lead exposure: studies in two brothers showing differential susceptibility to lead. 401 20

The "limy bile" is uncommon in adults and very exceptional in childhood. The authors report a new case of a 7 years old girl. The review of the literature since Churchman's description (1911) allowed to collect eleven other cases of children, less than fifteen old. The usual sexual distribution in biliary diseases with female predominance is not true for them: eight boys for four girls. The youngest was three years and six months old. All but one have presented mainly right upper abdominal pain and vomiting. The diagnosis was made by an abdominal plain film showing a spontaneous visualization of the gallbladder which contained a material made of carbonate of calcium. One was an operative detection. All presented a stone of neck of gallbladder or cystic duct. The origin of "limy bile" is unknown. Nine children have been operated (cholecystectomy) with good result. Spontaneous disappearance of "limy bile" was noted in three cases. It was marked by acute abdominal pain, inconstant jaundice or pancreatic reaction. No surgical care was brought with nor further problems or recurrence.
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PMID:[The calcium bile syndrome in children]. 404 61

The main purpose of this study was to evaluate the effectiveness of an oral fluid therapy alone or combined with parenteral administration of a 5% dextrose solution to attenuate the clinical signs and the pathophysiological consequences of transmissible gastroenteritis in neonatal piglets. Eighteen two day old conventional piglets were infected with transmissible gastroenteritis virus while six others were used as controls (Group 1). At the onset of diarrhea, infected piglets were divided into three groups of six (Groups 2, 3 and 4). Piglets in group 2 were not treated and were fed a milk replacer ad libitum. Piglets in group 3 were removed from the milk replacer and placed on an oral glucose-glycine-electrolyte solution ad libitum. Those in group 4 were placed on oral fluid therapy and received a 5% dextrose solution intraperitoneally at the rate of 25 mL/kg of body weight once a day. Blood samples were collected in heparin within minutes after the infected piglets became comatose and from the controls at four or five days of age. The following variables were measured: packed red cell volume, blood pH, total plasma protein and bicarbonate, blood urea nitrogen, and plasma glucose, creatinine, chloride, inorganic phosphorus, sodium, potassium, magnesium and calcium. Vomiting and diarrhea appeared 12 to 24 hours postinoculation in the infected piglets. There was a sudden and rapid progression into a comatose and moribund state one or two days later whether the infected piglets were treated or not.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fluid therapy trials in neonatal piglets infected with transmissible gastroenteritis virus. 407 36

Thirteen patients with hypercalcaemia due to carcinoma received inorganic phosphate, orally or intravenously, as palliative treatment for their high serum calcium levels. The serum calcium promptly fell in all patients fully treated, and there was a striking clinical improvement in most patients. The blood urea was usually unchanged or became nearer to normal, while the serum phosphate altered variably. Only two of the eight patients who were studied at necropsy had microscopical nephrocalcinosis; corneal calcification was evident in both before phosphate treatment was started.This oral inorganic phosphate (1 gramme thrice daily) is a safe and effective means of treating hypercalcaemia due to carcinoma. An intravenous infusion of 1 gramme over eight hours may sometimes be required initially for patients who are vomiting.
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PMID:Phosphate treatment of hypercalcaemia due to carcinoma. 417 70

In three patients with thyrotoxicosis and with symptomatic hypercalcaemia antithyroid therapy restored the plasma calcium concentration to normal, though initially in one case intravenous and oral neutral phosphate solution were required to curtail intractable vomiting.Nine cases have been recorded in which the plasma calcium concentration returned to normal after antithyroid treatment was started; all but one became normocalcaemic within eight weeks. It is suggested that in hypercalcaemic thyrotoxicosis a second pathological condition should be considered only if the plasma calcium concentration fails to return to normal within eight weeks.
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PMID:Symptomatic hypercalcaemia in thyrotoxicosis. 542 53


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