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

Pituitary apoplexy indicates pituitary adenoma hemorrhage, which could result in acute pituitary insufficiency and mortality. The typical symptoms are headache, visual disturbance, nausea, vomiting, altered mental status, and panhypopituitarism. However, cortisol-induced hyperglycemia and acute delirium could be an initial presentation of a pituitary adenoma hemorrhage with stormy release of the adrenocorticotrophic hormone. A 28-year-old woman presented with severe vomiting, irritable state, and delusion. She had medical history of irregular menstrual cycles and marked body weight gain after her second childbirth 8 years ago. She was diagnosed of diabetic ketoacidosis 2 days before this visiting at local medical department. On physical examination, Cushing appearance without definite neurological deficit was disclosed. Further blood tests revealed high blood sugar, cortisol, and adrenocorticotrophic hormone levels without evidence of diabetic ketoacidosis. The brain computed tomography and magnetic resonance imaging showed pituitary macroadenoma and pituitary hemorrhage. Cushing disease with pituitary apoplexy was then diagnosed. Conservative management with delayed neurosurgery was applied. The patient became clear with normalized cortisol and blood sugar levels soon after. Follow-up computed tomography scan of the brain revealed no progression of tumor bleeding or mass effect. To our knowledge, pituitary apoplexy associated with cortisol-induced hyperglycemia and acute delirium has never been reported before. This case reminds us of pituitary apoplexy and its rare manifestations.
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PMID:Pituitary apoplexy associated with cortisol-induced hyperglycemia and acute delirium. 1909 Dec 87

We report two type 1 diabetic patients with diabetic ketoacidosis accompanied by alkalaemia. Twenty-three cases have been reported to date, and the main causes for alkalaemia were vomiting, alkali ingestion, and diuretics use. Our report indicated that poorly controlled diabetic patients who already had autonomic neuropathy are at risk.
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PMID:Two cases of type 1 diabetic women with diabetic ketoacidosis presenting as alkalaemia. 1911 32

In this report, the authors describe a unique presentation of ventriculomegaly in the setting of diabetic ketoacidosis (DKA). A 15-year-old male, with a history of shunt placement for hydrocephalus and repair of a myelomeningocele, presented to the emergency room with DKA and was found to have ventriculomegaly. At the time of presentation, the patient had a 24- to 48-hour history of lethargy, nausea, vomiting, fever (102.2 degrees F), and polydipsia. A computed tomographic (CT) scan of the head indicated increased ventricular size compared with previous studies, thus prompting a neurosurgical evaluation. Blood glucose level at admission was found to be 1,551 mg/dl, bicarbonate level was 9 mmol/l, and pH was 7.08. The patient was treated for DKA; his fever, lethargy, nausea, and vomiting subsequently resolved. A repeat CT scan obtained 24 h after admission revealed a return of the ventricular system to its baseline size. On the basis of radiographic and laboratory evaluations, the authors hypothesize that the transient ventriculomegaly was directly related to extreme hyperglycemia.
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PMID:Transient ventriculomegaly in an adolescent presenting with shunted hydrocephalus, diabetic ketoacidosis, and hyperglycemia. 1912 93

Diabetic ketoacidosis (DKA) is an important medical emergency and may cause electrocardiogram (ECG) changes mimicking myocardial infarction. In the literature, hyperkalemia-associated ST-segment elevations have been defined in DKA; it has been demonstrated that these changes resolve completely after the treatment of hyperkalemia. We aimed to present a case with DKA in whom ST-segment elevation in inferior derivations was observed, but serum potassium level (4.4 mEq/L) was normal. The patient was admitted to the emergency department with complaints of nausea, bloody vomiting, and epigastric pain. Intravenous 0.9% saline, soluble insulin, and proton pump inhibitor were begun. Because of bloody vomiting, antiaggregant and anticoagulant therapy was not administered and coronary angiography was not considered at the beginning. Two hours after the beginning of the treatment, the blood glucose level dramatically decreased (from 712 to 263 mg/dL), and the metabolic acidosis view in arterial blood gas sample was improved. The repeated ECG depicted complete ST segment resolution. Transthoracic echocardiogram determined normal ventricular wall motion. Cardiac biomarkers remained in normal limits in the follow-up period. Coronary angiography performed 3 days after hospital admission was evaluated as normal. The patient recovered uneventfully, and gastrointestinal tract bleeding did not repeat. The ECG was repeated, and ST segments in izoelectric line were observed.
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PMID:Acute inferior pseudoinfarction pattern in a patient with normokalemia and diabetic ketoacidosis. 1937 49

In situations where the cause of hypokalemia is not obvious, measurement of urinary potassium excretion and blood pressure and assessment of acid-base balance are often helpful. A random urine potassium-creatinine ratio (K/C) less than 1.5 suggests poor intake, gastrointestinal losses, or a shift of potassium into cells. If hypokalemia is associated with paralysis, we should consider hyperthyroidism, familial or sporadic periodic paralysis. Metabolic acidosis with a urine K/C ratio less than 1.5 suggests lower gastrointestinal losses due to diarrhea or laxative abuse. Metabolic acidosis with K/C ratio of 1.5 higher is often due to diabetic ketoacidosis or type 1 or type 2 distal renal tubular acidosis. Metabolic alkalosis with a K/C ratio less than 1.5 and a normal blood pressure is often due to surreptitious vomiting. Metabolic alkalosis with a higher K/C ratio and a normal blood pressure suggests diuretic use, Bartter syndrome, or Gitelman syndrome. Metabolic alkalosis with a high urine K/C ratio and hypertension suggests primary hyperaldosteronism, Cushing syndrome, congenital adrenal hyperplasia, renal artery stenosis, apparent mineralocorticoid excess, or Liddle syndrome. Hypomagnesemia can lead to increased urinary potassium losses and hypokalemia. The differential rests upon measurement of blood magnesium, aldosterone and renin levels, diuretic screen in urine, response to spironolactone and amiloride, measurement of plasma cortisol level and the urinary cortisol-cortisone ratio, and genetic testing.
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PMID:Diagnosis of hypokalemia: a problem-solving approach to clinical cases. 1937 23

An 18-year-old male with type 1 diabetes mellitus presented to the emergency department after one day of lethargy and vomiting. Physical examination revealed a dehydrated male with tachycardia and Kussmaul's respiration. There was subcutaneous emphysema in both supraclavicular regions. Chest auscultation revealed a positive Hamman's sign. Laboratory investigation was significant for metabolic acidosis with venous blood pH 7.08. Plasma glucose was 1438 mg/dl; ketones were present in the urine. Chest X-ray showed subcutaneous emphysema and pneumomediastinum, which resolved spontaneously within 72 hours of initiation of treatment for diabetic ketoacidosis.Pneumomediastinum is an uncommon complication of diabetic ketoacidosis. Recognizing that severe diabetic ketoacidosis may cause pneumomediastinum allows for expedient management.
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PMID:Diabetic ketoacidosis with pneumomediastinum: a case report. 1991 51

Acute esophageal necrosis (AEN), commonly referred to as "black esophagus", is a rare clinical entity arising from a combination of ischemic insult seen in hemodynamic compromise and low-flow states, corrosive injury from gastric contents in the setting of esophago-gastroparesis and gastric outlet obstruction, and decreased function of mucosal barrier systems and reparative mechanisms present in malnourished and debilitated physical states. AEN may arise in the setting of multiorgan dysfunction, hypoperfusion, vasculopathy, sepsis, diabetic ketoacidosis, alcohol intoxication, gastric volvulus, traumatic transection of the thoracic aorta, thromboembolic phenomena, and malignancy. Clinical presentation is remarkable for upper gastrointestinal bleeding. Notable symptoms may include epigastric/abdominal pain, vomiting, dysphagia, fever, nausea, and syncope. Associated laboratory findings may reflect anemia and leukocytosis. The hallmark of this syndrome is the development of diffuse circumferential black mucosal discoloration in the distal esophagus that may extend proximally to involve variable length of the organ. Classic "black esophagus" abruptly stops at the gastroesophageal junction. Biopsy is recommended but not required for the diagnosis. Histologically, necrotic debris, absence of viable squamous epithelium, and necrosis of esophageal mucosa, with possible involvement of submucosa and muscularis propria, are present. Classification of the disease spectrum is best described by a staging system. Treatment is directed at correcting coexisting clinical conditions, restoring hemodynamic stability, nil-per-os restriction, supportive red blood cell transfusion, and intravenous acid suppression with proton pump inhibitors. Complications include perforation with mediastinal infection/abscess, esophageal stricture and stenosis, superinfection, and death. A high mortality of 32% seen in the setting of AEN syndrome is usually related to the underlying medical co-morbidities and diseases.
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PMID:Black esophagus: acute esophageal necrosis syndrome. 2061 76

We describe an acute onset of diabetes mellitus during third trimester of pregnancy revealed by ketoacidosis, complicated by fetal death, which could evoke fulminant type 1 diabetes, a novel subtype of type 1 diabetes first described in Japan and rarely described in Caucasian people. Diagnosis of diabetic ketoacidosis could be made on simple signs as abdominal pain, vomiting or ketone bodies on urinary multistix. Capillary glycaemic control is necessary to distinguish fast from ketoacidosis. The treatment of this severe imbalance must be initiated in emergency.
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PMID:[Ketoacidosis complicated by fetal death revealing fulminant diabetes during the third trimester of pregnancy]. 2062 14

This study describes the profile of 100 cases of diabetic ketoacidosis (DKA) at a teaching hospital in 1 Benghazi, Libyan Arab Jamahiriya. DKA was more frequent in young women with type 1 diabetes and mostly due to preventable causes, e.g., disrupted insulin treatment and/or infection. DKA also occurred in type 2 diabetics, with a higher mortality rate, as they were older patients with co-morbidity. Polyurea, fatigue, abdominal pain and vomiting were the most common clinical features, while coma was rarer. A high number of cases were first presentations of type 1 diabetes; hence this diagnosis should be considered in all patients with acute abdomen or decreased level of consciousness. The reasons for high mortality rate in this study (10%) were multifactorial.
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PMID:Profile of diabetic ketoacidosis at a teaching hospital in Benghazi, Libyan Arab Jamahiriya. 2079 43

Methylmalonic acidemia (MMA) is an inherited organic acidemia usually present with recurrent episodes of acute illness. A typical episode is ushered in with ketonuria and vomiting, followed by acidosis, dehydration, and lethargy, leading, in the absence of aggressive treatment, to coma and death. We report an infant with MMA presented with diabetes symptoms. A 13-month-old girl complained of polydipsia, diuresis, and loss of weight. She had clinical signs of diabetic ketoacidosis such as dehydration, deep sighing respiration, smell of ketones, lethargy, and vomiting. Laboratory analysis showed hyperglycemia with acidosis and ketonuria. She was treated with parenteral fluid, electrolyte, and insulin infusion. Two days after her discharge, after having a meal rich in protein, she was brought unconscious with hepatomegaly, severe acidosis, ketonuria, and mild hyperammonemia. The absence of hyperglycemia and the presence of neurologic findings suggested organic acidemia. MMA was diagnosed because of methylmalonic aciduria and elevated C3 carnitine esters. Cranial magnetic resonance imaging (MRI) showed increased uptake of radiocontrast material in the basal ganglia bilaterally. A homozygous mutation in exon 4 of the MMAA gene was found in mutation analysis and confirmed the diagnosis of cblA-deficient MMA. Neurologic regression was improved with treatment of low-protein diet, vitamin B12, and l-carnitine. In patients born to consanguineous parents who admit during infancy with severe acidosis refractory to treatment, organic acidemias should be kept in mind, even they have high blood glucose. The definitive diagnosis is important because it may allow a specific treatment and a favorable evolution to prevent the sequelae.
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PMID:Methylmalonic acidemia mimicking diabetic ketoacidosis in an infant. 2154 77


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