Cases reported "Starvation"

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1/7. The refeeding syndrome and hypophosphatemia.

    The refeeding syndrome is an underappreciated entity characterized by acute electrolyte derangements--notably hypophosphatemia--that occur during nutritional repletion of patients with significant suboptimal caloric intake. Adverse effects of hypophosphatemia include cardiac failure, muscle weakness, immune dysfunction, and death. hypokalemia and hypomagnesemia commonly complicate refeeding syndrome as well; however, this report briefly reviews the clinical manifestations of refeeding-induced hypophosphatemia.
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2/7. Estimation of caloric deficit in a fatal case of starvation resulting from child neglect.

    We report the case of a 3-year-20-day-old girl who died of starvation as a result of severe neglect. Her body weight had been 12 kg 70 days before her death, but was only 5 kg at the time of autopsy. From information supplied by her parents to police, we calculated her daily caloric intake and estimated the factors for physical activity. The daily recommended dietary allowance for the victim was calculated from 700 kcal/ day x the appropriate factor for physical activity. In the absence of enough food, body fat (7.2 kcal/g body fat) and protein (4 kcal/g protein) would have been used to compensate until death. The calculated body weight at the time of death was around 5 kg. The statements of the parents therefore appear to be true.
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3/7. Deaths due to hunger strike: post-mortem findings.

    hunger strike is described as voluntary refusal of food and/or fluids. Prolonged starvation may produce many adverse events including even death in rare circumstances. Here, we present three fatal cases (all males, 25-38 years) died from hunger strike. In all corpses, obvious muscle wasting with reduced subcutaneous and internal fat deposits, and atrophy in some organs were demonstrated at autopsy. The extraordinary long starvation period before death could presumably be linked to the thiamine uptake in this period, which had been discontinued by all subjects before the death occurred. Prolonged caloric deficiency with subsequent complications such as multiple organ failure, severe sepsis and ventricular fibrillation could account as major causes of death in these subjects. The competence of the physicians working with hunger strikers about the processes and potential problems is of great importance since they have to acknowledge about them to their patients.
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4/7. Spontaneous hypoglycemia in end-stage renal failure.

    Five men with end-stage renal failure had spontaneous hypoglycemia during lengthy hospitalizations. Four were cachectic, and all five had weight loss and poor caloric intake. malnutrition were seen also in some of the ten previous case reports of hypoglycemia in renal failure. Impaired renal gluconeogenesis may allow hypoglycemia in such patients.
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5/7. infanticide by starvation: calculation of caloric deficit to determine degree of deprivation.

    A review of medical records and autopsy examination of a six-week-old male revealed the cause of death to be severe malnutrition with dehydration. Weight and caloric deficits were calculated to determine the degree of deprivation, which could be expressed as an interval of days for clear courtroom presentation. These calculations may be useful for quantifying the degree of malnutrition in a variety of child abuse cases.
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6/7. serum lipids during starvation in obesity.

    The HDL-cholesterol level was found to decrease during the first week of therapeutic starvation in hyperlipoproteinaemic (hypertriglyceridaemic), diabetic (non-insulin dependent) patients. The possible causes of the finding are discussed, and the view is expressed that the fall in HDL given no cause for discontinuing the caloric restriction or starvation as the therapeutic measures in obesity.
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7/7. hypophosphatemia and neurological changes secondary to oral caloric intake: a variant of hyperalimentation syndrome.

    Previous reports have described a syndrome of paresthesias, weakness, seizures and hypophosphatemia in patients and animals receiving intravenous hyperalimentation. In this report we describe a group of five patients who developed this syndrome while on oral caloric intake and three patients who received only modest amounts of hyperalimentation therapy. As an experimental corollary, studies were performed in starved and normal dogs with calories infused via an intragastric catheter. The serum inorganic phosphorus (Pi) fell slightly in normal animals from 4.8-2.5 mg. %. In the starved dogs with diarrhea or vomiting the Pi fell gradually from 4.8-1.6. In starved dogs without gastrointestinal symptoms the Pi fell precipitously from 3.7-1.4 mg % on the first day of infusion and remained at that level. Approximately 50% of the starved animals developed the neurological syndrome; none of the normal animals had neurological symptoms.
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