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Query: UMLS:C0162275 (ketonuria)
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Four cases of diabetic ketoacidosis presenting with abdominal pain are reported. Case 1: a 14-year-old boy suffered from sudden onset of mid-abdominal pain, then migrating to the right lower quadrant. Nausea and vomiting occurred subsequently. Appendectomy was performed under the impression of acute appendicitis in an outside surgical clinic. The patient became comatose the next day and then was transferred to our hospital. Diabetic ketoacidosis was diagnosed after the detection of hyperglycemia, glycosuria, and ketonuria on the day of admission. Unfortunately, he expired on the same day in spite of vigorous resuscitation. Case 2: a 9-year-old boy complained of abdominal pain for 10 days. There was no specific finding in the physical examination. Diabetic ketoacidosis was confirmed four days later when conscious disturbance, dehydration, and tachypnea were noticed. Case 3: a 10-year-old girl presented with a history of intermittent abdominal pain for one month. The character of the abdominal pain was nonspecific. Glycosuria was detected in a pediatric clinic. Diabetic ketoacidosis was confirmed after her referral to our hospital. Case 4: a 5-year-old girl suffered from acute abdominal pain for four hours. She was found to have tachypnea, lethargy, and ill-looking. Diabetic ketoacidosis was diagnosed after serial examinations. The abdominal pain in diabetic ketoacidosis may lead the pediatrician into diagnostic error. Therefore, when a child presented with non-specific abdominal pain, a routine urine sugar should be checked in order not to miss the possibility of diabetic ketoacidosis.
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PMID:[Abdominal pain in diabetic ketoacidosis: report of four cases]. 212 98

Calcium hopantenate (HOPA) has been widely used as an activator of cerebral metabolism in Japan. However, several cases of acute encephalopathy during HOPA administration were recently reported, which were characterized by marked metabolic acidosis and hypoglycemia. The encephalopathy in these patients was named Reye-like syndrome because of the similarity to Reye's syndrome in children. The purposes of this presentation are to report on 5 patients with acute encephalopathy developing during HOPA administration, to summarize their symptoms and clinical courses, and to discuss the pathogenesis of metabolic acidosis and hypoglycemia. Initial characteristics of the clinical course in all patients were loss of appetite, nausea and vomiting, followed by unconsciousness. Laboratory examinations revealed marked metabolic acidosis, severe hypoglycemia, hyperlactacidemia, leukocytosis, ketonuria, and increased Ht and BUN. A few days after development of the initial symptoms, mild renal and liver dysfunction, and elevation of serum amylase were observed in all patients. Hyperlactacidemia was present in 4 in the initial period. Blood concentration of HOPA was 2.131 micrograms/ml in patient 1 (8-10 hours after final administration), and 10.7 micrograms/ml in patient 5 (24 hours after final administration). These values are extremely high, because usually HOPA concentration is almost negligible 7 hours after the drug is taken. As the pathogenesis of acute encephalopathy due to HOPA administration, the failure of fatty acid beta-oxidation has been proposed by some investigators. However, the serum concentrations of CoA, pantothenic acid and carnitine during the initial stage were not reduced in our patients. Furthermore, it is very difficult to explain the severe hypoglycemia in terms of the beta-oxidation theory.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Metabolic acidosis and hypoglycemia during calcium hopantenate administration--report on 5 patients]. 258 87

Hyperthyroidism is second to diabetes mellitus as the most common endocrinopathy in pregnancy. Inappropriate secretion of hCG is the most common cause of hyperthyroidism in the first part of gestation. In addition to hydatidiform mole and hyperemesis gravidarum, nonpathologic-conditions including multiple gestation, mild nausea and vomiting, and even normal pregnancies may present with transient undetectable or suppressed serum TSH values. The syndrome of transient hyperthyroidism of hyperemesis gravidarum is defined as severe nausea and vomiting, dehydration, ketonuria, and weight loss of more than 5% by 6 to 9 weeks of pregnancy. Thyroid tests are in the hyperthyroid range, and the abnormalities are related to the severity of symptoms. Tests normalize with resolution of the vomiting, and ATD therapy is not indicated. The natural history of Graves' disease in pregnancy is characterized by aggravation in the first trimester, amelioration in the second half, and recurrence in the year following delivery. ATD treatment is the therapy of choice in pregnancy. Either PTU or MMI may be used; the goal is to keep the FT4I in the upper limits of normal with the minimum dose of ATD. In approximately 30% of patients, ATDs may be discontinued in the last few weeks of gestation. Maternal, fetal, and neonatal complications are frequent when hyperthyroidism is not under control. Postpartum hyperthyroidism may be caused by an episode of silent thyroiditis or Graves' disease.
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PMID:Hyperthyroidism in pregnancy. 953 33

Nausea and vomiting are both common in early pregnancy. Most cases are mild and do not require treatment. However, persistent vomiting and severe nausea can progress to hyperemesis if the woman is unable to maintain adequate hydration, and fluid and electrolyte as well as nutritional status are jeopardised. Hyperemesis gravidarum is a diagnosis of exclusion, characterised by prolonged and severe nausea and vomiting, dehydration, ketosis and bodyweight loss. Investigation may show hyponatraemia, hypokalaemia, a low serum urea level, metabolic hypochloraemic alkalosis and ketonuria. The haematocrit is raised and the specific gravity of the urine is increased. There may be associated liver function test abnormalities and abnormal thyroid function tests, with biochemical thyrotoxicosis with raised free thyroxine levels and/or suppressed thyroid-stimulating hormone levels. The pathophysiology of hyperemesis is poorly understood. Various hormonal, mechanical and psychological factors have been implicated. Studies have demonstrated a direct relationship between the severity of hyperemesis, the degree of biochemical hyperthyroidism and the levels of human chorionic gonadotrophin (hCG). Management of hyperemesis should include hospitalisation, intravenous fluid and electrolyte replacement, thiamine (vitamin B1) supplementation, use of conventional antiemetics and psychological support. Most patients improve spontaneously with the help of the above measures without long term sequelae. Conventionally, antiemetics are not usually prescribed, especially before 12 weeks gestation, except for women with hyperemesis. This reluctance relates to fears which are often unfounded concerning the teratogenic effects of antiemetics. Severe hyperemesis, refractory to conventional management with intravenous fluids and antiemetics is a rare, miserable and disabling condition, associated with multiple hospital admissions, time away from work and the family, and psychological morbidity. If inadequately or inappropriately treated, it may cause Wernicke's encephalopathy, central pontine myelinolysis and death. In extreme cases, women may request, or their obstetricians recommend, termination of the pregnancy. There are uncontrolled data supporting a beneficial effect of corticosteroids in these women, and a randomised placebo-controlled trial is currently in progress.
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PMID:Treatment of nausea and vomiting in pregnancy. When should it be treated and what can be safely taken? 970 51

A 5-year-old boy presented with abdominal pain, nausea and vomiting of blood. Twelve hours after admission, "diabetic ketoacidosis" was diagnosed on the basis of elevated glycaemia, glycosuria, ketonuria and a low bicarbonate blood level, which led to treatment with fluids and regular insulin infusion. Over a 36-hour period, insulin was progressively decreased and finally stopped because of the rapid fall and normalization of blood glucose concentration. Drug poisoning was suspected on the basis of persistent tachycardia in the absence of other signs of dehydration. Salicylate intoxication was excluded, and theophylline was finally incriminated. This compound, used by adults in the child's home, had caused accidental theophylline poisoning, mimicking diabetic ketoacidosis. Pre-diabetic immune markers were repeatedly negative, and no diabetes has developed after four years of follow-up. Thus, the transient increase in blood glucose was not related to a pre-diabetic status. A diagnosis of masked theophylline poisoning should be considered in similar situations involving a rapid decrease of insulin requirements.
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PMID:Theophylline intoxication mimicking diabetic ketoacidosis in a child. 1063 77

Hyperemesis gravidarum affects up to 2% of pregnancies and is characterized by severe nausea and vomiting persisting beyond the 14th week of gestation with weight loss, dehydration, electrolyte imbalance and ketonuria. We present the case of a woman with severe, refractory hyperemesis gravidarum in whom treatment with a percutaneous endoscopic gastrostomy with a jejunal extension allowed improvement of symptoms, reversal of maternal weight loss and the delivery of a healthy infant. Review of the literature reveals only one other paper describing this treatment. In all three cases successful outcomes for both mothers and children are described. We propose that percutaneous endoscopic gastrostomy with a jejunal extension is a safe, effective and relatively cheap intervention for severe, refractory hyperemesis gravidarum.
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PMID:Percutaneous endoscopic gastrostomy with a jejunal port for severe hyperemesis gravidarum. 1531 22

Hyperemesis gravidarum is defined as severe nausea and vomiting during the first trimester of pregnancy. It is characterized by dehydration, electrolyte imbalance, ketonuria and weight loss of more than 5% of body weight and it usually requires hospitalization. Traditionally, total parenteral nutrition has been used when patients with hyperemesis gravidarum fail to respond to conservative measures, including dietary manipulation and antiemetics. Total parenteral nutrition has been shown to be an effective method of nutritional support during pregnancy but it is expensive and has potentially serious complications. Peripheral parenteral nutrition reduces the risk of complications, but caloric intake is limited. A small number of investigators have suggested using enteral nutrition as an alternative to total parenteral nutrition. Herein we report two cases of hyperemesis gravidarum successfully treated with an effective regimen of peripheral parenteral nutrition.
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PMID:Peripheral parenteral nutrition in protracted hyperemesis gravidarum--report of two cases and a literature review. 1872 Sep 39

Nausea and vomiting occur in up to 80% of normal pregnancies. Hyperemesis gravidarum, resulting in dehydration and ketonuria, is a more severe, disabling and potentially life threatening condition affecting up to 1.5% of pregnancies. Treatment is supportive with intravenous rehydration, antiemetics and correction of vitamin deficiency to minimize complications. There are good safety data to support the use of antihistamines, phenothiazines and metoclopromide in hyperemesis gravidarum, though trials of efficacy are lacking and there is little evidence on which to chose the optimum therapy. This review discusses the diagnosis and management of hyperemesis gravidarum and the prevention, recognition and treatment of the serious complications of Wernicke encephalopathy, osmotic demyelination syndrome and thromboembolism.
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PMID:Management strategies for hyperemesis. 1926 46

Although nausea and vomiting are common symptoms in early pregnancy, hyperemesis gravidarum (HG) is a rare complication of the first trimester of pregnancy. This condition is defined as intractable vomiting occurring before 20 weeks of gestation, with fluid and electrolyte disturbance, significant weight loss, and ketonuria, leading to hospitalization in the absence of other cause than pregnancy. Some biological disturbances found in HG, such as hyperthyroidism and hepatic cytolysis, which are correlated with the importance of vomiting, are without severe clinical consequences, but may represent diagnostic pitfalls. The aetiology is unknown, but human chorionic gonadotropin hormones likely play the first role. Psychological disturbance is currently seen as the result of the burden and stress of HG rather than a causal factor. Maternal outcome may be severe in the absence of treatment, but pregnancy outcome seems good, as far as the condition has been adequately controlled. The management of HG includes IV rehydration, thiamine supplementation, antiemetic drugs (doxylamine, metoclopramide and chlorpromazine being the first-line choices), and in severe cases, nasogastric or parenteral nutrition. A psychological support is often necessary.
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PMID:[Hyperemesis gravidarum: a rare but potentially severe complication of the first trimester of pregnancy]. 2062 88

We report a case of starvation-induced metabolic ketoacidosis in a previously healthy 29-year-old, nulliparous woman at 32 weeks of gestation. She was admitted to hospital with mild preeclampsia associated with persistent nausea and vomiting that progressed to severe preeclampsia requiring urgent control of hypertension before caesarean delivery. Prolonged and severe vomiting limited oral caloric intake and led to starvation ketoacidosis, characterised by ketonuria and a raised anion gap metabolic acidosis that required intensive care support. Despite significant metabolic derangement the patient appeared clinically well. Intravascular volume was replenished. Fluid restriction used as part of our preeclampsia treatment regimen delayed the therapeutic administration of sufficient dextrose, which rapidly corrected her metabolic derangement when commenced after delivery. Electrolyte supplementation was given to prevent re-feeding syndrome. Both mother and baby were discharged without sequelae.
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PMID:Acute starvation in pregnancy: a cause of severe metabolic acidosis. 2131 80


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