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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abdominal pain is a frequent manifestation in patients presenting with Diabetic Ketoacidosis (DKA). Usually it is attributed to severe metabolic acidosis but it can be due to underlying abdominal pathologies (i.e., pancreatitis, appendicitis). We report a case of a 19-year-old female who presented with DKA and severe abdominal pain and was found on further examination to have underlying pancreatitis and visceral vein thrombosis. The patient improved with treatment for the mentioned co-morbidities, including anticoagulation.
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PMID:Diabetic ketoacidosis presenting with acute pancreatitis and visceral vein thrombosis. 2160 11

A 10-year-old girl presented with diabetic ketoacidosis, shock, and severe abdominal pain. She was found to have acute pancreatitis and acute kidney injury after shock resuscitation and severe persistent hypertriglyceridemia. The severe hypertriglyceridemia was treated with 1 course of plasmapheresis, which corrected the triglyceride level and was temporally associated with improvement of the abdominal pain and renal dysfunction. Diabetes is known to contribute to an elevated triglyceride level, especially in the setting of an underlying lipid disorder. However, no such disorders were found in this patient. To the best of our knowledge, this is the first report of a pediatric patient presenting with the triad of severe hypertriglyceridemia, diabetic ketoacidosis, and pancreatitis treated successfully with plasmapheresis.
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PMID:Plasmapheresis to treat hypertriglyceridemia in a child with diabetic ketoacidosis and pancreatitis. 2220 Nov 45

A 15-year-old female patient with known type 1 diabetes mellitus was referred because of abdominal pain. On admission, she was alert but dehydrated with marked Kussmaul breathing. Blood glucose was 414 mg/dL (23 mmol/L). Blood gas analysis revealed severe metabolic acidosis (pH: 6.99) with an elevated anion gap (29.8 mmol/L) and an increased base excess (-25.2 mmol/L). At the sixth hour of treatment with intravenous fluids and insulin, the patient became delirious. The delirium persisted despite the normalization of the acidosis and became difficult to manage. Brain imaging studies revealed neither brain edema nor other intracranial pathology. No evidence of intoxication could be found. The patient gradually regained consciousness and was diagnosed as a case of severe diabetic ketoacidosis (DKA) associated with infection. We were unable to find a similar case in the pediatric literature and thought that reporting this unusual case would be a contribution to the literature on DKA in children.
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PMID:Delirium in diabetic ketoacidosis: a case report. 2239 4

A 26-year-old male patient suffering from Type 1 diabetes mellitus got admitted with abdominal pain and high blood sugars. On further evaluation, he was found to have normal anion gap metabolic acidosis without ketonuria and urinary pH was alkaline. The patient was diagnosed as Type 1 renal tubular acidosis (RTA) (distal RTA) and was managed by alkali replacement in addition to control of blood sugars. The association of Type 1 RTA with Type 1 diabetes mellitus has been rarely reported in the literature. The association needs a different attention as diagnosis and management of diabetic ketoacidosis in such cases will be tricky. The case presented here is the first of its kind from our part of the world and second as far as English literature is concerned.
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PMID:Type 1 renal tubular acidosis in a patient of Type 1 diabetes mellitus: Is it coincidence or coexistence? 2270 29

New-onset diabetes mellitus after transplant is a well-recognized complication of tacrolimus immunosuppression and commonly occurs as a form of type 2 diabetes mellitus. However, tacrolimus-associated acute pancreatitis causing diabetic ketoacidosis has not been reported in heart transplant patients. We report a 22-year-old women hospitalized owing to diabetic ketoacidosis associated with acute pancreatitis 7 months after a heart transplant. Her immunosuppression included tacrolimus. She was admitted with complaints of polydipsia, anorexia, and abdominal pain of 3 days' duration. Her initial laboratory test revealed a toxic level of tacrolimus (> 30 ng/mL), severe hyperglycemia (39 mmol/L), severe metabolic acidosis (pH 6.9), and ketonuria, although diabetes mellitus had never been diagnosed. Serum amylase and lipase levels and abdominal computed tomography suggested the presence of acute pancreatitis. After correcting the diabetic ketoacidosis and getting the tacrolimus level to the normal range, she was discharged home. Three months later, insulin was replaced with oral hypoglycemic agents. Pancreatitis can present with diabetic ketoacidosis in the recipient of a heart transplant treated with tacrolimus. Clinicians should pay more attention to tacrolimus levels and the risk of pancreatitis.
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PMID:Diabetic ketoacidosis associated with acute pancreatitis in a heart transplant recipient treated with tacrolimus. 2307 84

A-13-year-old girl presented with diabetic ketoacidosis with convincing clinical signs of parotitis (fever, drooling of saliva, inability to swallow with development of bilateral parotid swelling) and pancreatitis (fever, abdominal pain and vomiting), along with high serum amylase and positive mumps IgM titer. This suggests that mumps virus may have been the causative factor, probably as a result of concomitant involvement of the pancreas.
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PMID:Diabetic ketoacidosis following mumps. 2325 2

Diabetic ketoacidosis (DKA) is characterized by excessive production of organic acids leading to a low blood pH. Rarely, because of other complicating factors blood pH may be in the alkalemic range and the term diabetic ketoalkalosis has been coined to describe this condition. So far, less than 30 such cases have been reported in the literature. We report a 34-year-old woman who received methylprednisolone pulse therapy for the treatment of pancreas transplant rejection. Thereafter, she developed vomiting and abdominal pain. Her laboratory data showed high blood sugar, hypokalemia, alkalemic pH, elevated plasma anion gap, and significant ketonemia. She responded well to the treatment of DKA. It was concluded that an alkalemic pH does not rule out the presence of ongoing DKA. In suspected cases, changes in plasma anion gap and bicarbonate and the presence of ketonemia should be noted.
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PMID:Diabetic ketoalkalosis after steroid pulse therapy in a patient with pancreas transplant rejection. 2339 Mar 35

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as information on the importance of medication compliance.
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PMID:Diabetic ketoacidosis: evaluation and treatment. 2354 50

Ketoacidosis is a metabolic condition that occurs as a result of an insufficient amount of insulin. The lack of insulin results in an increased release of glucose from the liver and an excess of ketone bodies as a result of the breakdown of adipose tissue. This occurs when carbohydrates are unable to be properly processed for needed energy requirements during cellular metabolism. Ketoacidosis is commonly linked to diabetes mellitus. Diabetes mellitus is a condition where the body is unable to produce the proper amount of insulin or is unable to effectively respond to insulin stimulation. Excessive alcohol use can damage the pancreas, reducing insulin secretion. Other conditions such as pneumonia or urinary tract infections can trigger the release of counter-regulatory hormones that may contribute to the decrease in insulin's activity and secretion. Symptoms of diabetic ketoacidosis often include nausea and vomiting, increased thirst and urine production, hyperglycemia, abdominal pain, shortness of breath, confusion, headache, general weakness, fatigue and increased heart rate. If left untreated, diabetic ketoacidosis can lead to more serious complications including circulatory collapse, decreased blood potassium levels, infection and cerebral edema. The following case study presents a complex condition of ketoacidosis associated with a bacterial infection compounded by the patient's history of alcohol abuse.
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PMID:Alcohol induced diabetic ketoacidosis exacerbated by an acute respiratory infection with Klebsiella pneumoniae. 2377 71

A healthy 18-year-old girl presented to a local emergency room with 48 h of abdominal pain and vomiting. A radiological and biochemical diagnosis of moderate acute pancreatitis was made. Bloodwork demonstrated prominent hypertriglyceridaemia (HTG) of 19.5 mmol/L (severe HTG: 11.2-22.4), detectable urine ketones and a random blood glucose of 13 mmol/L dropping to 10.5 mmol/L on repeat (normal random <11). Ketone levels were deemed consistent with fasting ketosis after 48 h of vomiting. There was no known history of diabetes in the patient. Management included aggressive rehydration and pain control, yet the patient rapidly decompensated into shock requiring intensive care unit support. Blood gases revealed severe metabolic acidosis (pH 6.99) and unsuspected underlying diabetic ketoacidosis was diagnosed. The HTG gradually resolved following intravenous fluids and insulin infusion with slower correction of the metabolic acidosis. Importantly, her glycated haemoglobin was 12%, indicating the silent presence of chronic glucose elevations.
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PMID:Acute pancreatitis and severe hypertriglyceridaemia masking unsuspected underlying diabetic ketoacidosis. 2400 72


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