Cases reported "Diabetic Ketoacidosis"

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1/25. Severe diabetic ketoacidosis: the need for large doses of insulin.

    A 21-year-old female with Type 1 diabetes mellitus (DM) presented in ketoacidosis. She received intravenous normal saline and insulin at 6 U/h and 1.26% sodium bicarbonate solution. After the blood glucose had fallen to 9.5 mmol/l, the saline infusion was changed to 5% glucose solution and the insulin infusion rate to 2 to 3 U/h. The next day the patient became more drowsy (glasgow coma scale 13/15, later falling to 4/15). Computed tomography (CT) scan suggested cerebral oedema and the patient was treated with dexamethasone and mannitol. She remained critically ill for 48 h, eventually making a full recovery. insulin was given at rates of 8 to 14 U/h, with 10% or 20% glucose infusion to maintain the blood glucose above 5 mmol/l; despite this it was not until the fifth day that her serum bicarbonate became normal. textbooks usually advise starting insulin at 6 U/h and reducing the infusion rate to 1-4 U/h when the blood glucose falls below a certain level. In this case, even with high rates of insulin infusion, it took 5 days before the patient's serum bicarbonate returned to normal. Thus, in severe diabetic ketoacidosis (DKA), protocols should advise that the insulin infusion be continued at high dose (4 to 6 U/h or more), with appropriate glucose infusion to prevent hypoglycaemia, until the serum bicarbonate is normal or nearly so.
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2/25. Painful swelling of the thigh in a diabetic patient: diabetic muscle infarction.

    A 44-year-old woman with a 5-year history of poorly controlled Type 1 diabetes mellitus presented with a painful, firm and warm swelling in her right thigh. pain was severe but the patient was not febrile, and had no history of trauma or abnormal exercise. Laboratory tests showed ketoacidosis, major inflammation (erythrocyte sedimentation rate (ESR) = 83 mm/h), normal white blood cell count and normal creatine kinase level. Plain radiographs were normal, and there were no signs of thrombophlebitis at Doppler ultrasound. magnetic resonance imaging (MRI) showed diffuse enlargement and an oedematous pattern of the adductors, vastus medialis, vastus intermedius and sartorius of the right thigh. The patient's symptoms improved dramatically, making biopsy unnecessary, and a diagnosis of diabetic muscular infarction was reached. Idiopathic muscular infarction is a rare and specific complication of diabetes mellitus, typically presenting as a severely painful mass in a lower limb, with high ESR. The diabetes involved is generally poorly controlled longstanding Type 1 diabetes with established microangiopathy. Differential diagnoses include deep vein thrombosis, acute exertional compartment syndrome, muscle rupture, soft tissue abscess, haematoma, sarcoma, inflammatory or calcifying myositis and pyomyositis. In fact, physician awareness should allow early diagnosis on the basis of clinical presentation, routine laboratory tests and MRI, thereby avoiding biopsy and its potential complications as well as unnecessary investigations. rest, symptomatic pain relief and adequate control of diabetes usually ensure progressive total recovery within a few weeks. Recurrences may occur in the same or contralateral limb.
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3/25. Bilateral basal ganglion haemorrhage in diabetic ketoacidotic coma: case report.

    We report bilateral oedema and haemorrhagic transformation in the basal ganglia of a 59-year old woman with severe diabetic ketoacidosis. Lack of cerebral vascular autoregulation, followed by blood-brain barrier disruption due to the so-called breakthrough mechanism is presumed to be the cause.
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4/25. The care of students with insulin-treated diabetes mellitus living in university accommodation: scope for improvement?

    Concern has been expressed about the welfare of young adults with Type 1 diabetes mellitus who leave home to attend university or college for tertiary education. This has been highlighted by the local experience in Edinburgh of two male students with Type 1 diabetes, both of whom died from metabolic complications of diabetes during their first term at universities distant from their homes. One student died following the development of cerebral oedema secondary to diabetic ketoacidosis, which was probably precipitated by prolonged coma after an episode of severe hypoglycaemia. Another student, who was found 'dead in bed', had a history of previous severe hypoglycaemia. At a Fatal Accident Inquiry in Edinburgh, held following the death of the first student, recommendations were made to improve the care and personal safety of students with diabetes living in university accommodation. Despite the report being circulated to all Scottish universities, the second student died within three years of the inquiry. Further efforts to protect the welfare of students with Type 1 diabetes who are attending centres for tertiary education away from their home environment may require the more active participation by diabetes healthcare professionals.
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ranking = 1
keywords = coma
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5/25. guillain-barre syndrome occurring in two women after ketoacidosic comatose state disclosing an insulin-dependent diabetes mellitus.

    We report two women who presented with a guillain-barre syndrome just after a ketoacidosic comatose state disclosing an insulin-dependent diabetes mellitus. One had characteristic clinical signs and the other had major motor involvement. At neurophysiologic investigations, one had typical demyelinating neuropathy whereas the second had mainly axonal degeneration. At ultrastructural examination of a peripheral nerve biopsy, features of macrophage-associated demyelination were present in both nerve specimens, thus confirming the diagnosis of acute inflammatory demyelinating polyneuropathy, i.e., guillain-barre syndrome. Prominent axonal involvement was also present in the motor nerves of the second patient. insulin therapy had to be permanently continued and these two cases are quite different from the transient diabetes sometimes observed in certain cases of guillain-barre syndrome. Both the latter and insulin-dependent diabetes mellitus probably have auto-immune mechanisms. It is likely that in our two patients both auto-immune diseases were triggered by a common event. Such cases of guillain-barre syndrome have to be distinguished from other acute diabetic neuropathies.
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keywords = coma
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6/25. diabetic ketoacidosis associated with guillain-barre syndrome with autonomic dysfunction.

    A 37-year-old woman was admitted in a comatose state, after exhibiting fever and diarrhea. diabetic ketoacidosis was diagnosed due to an increased blood glucose level (672 mg/dl), metabolic acidosis, and positive urinary ketone bodies. On the fifth hospital day, despite recovery from the critical state of ketoacidosis, the patient suffered from dysphagia, hypesthesia and motor weakness, followed by respiratory failure. cerebrospinal fluid analysis was suggestive of guillain-barre syndrome (GBS). Autonomic dysfunction was manifested as tachycardia and mild hypertension in the acute stage. Marked orthostatic hypotension persisted long after paresis was improved, indicating an atypical clinical course of GBS.
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keywords = coma
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7/25. Reversible amnesia in a Type 1 diabetic patient and bilateral hippocampal lesions on magnetic resonance imaging (MRI).

    AIMS: Intensive insulin therapy of Type 1 diabetes limits its chronic complications, but is associated with an increased risk of severe hypoglycaemia and its neuroglycopenic consequences. methods: Case report. RESULTS: A 24-year-old male with 15 years' history of Type 1 diabetes, who was missing for 48 h, was found at home in ketoacidosis coma. intensive care permitted a rapid improvement revealing an unexpected severe anterograde amnesia, confirmed by neuropsychological testing. MRI performed 4 days after admission showed abnormal bilateral hyperintensity signals on T2-weighted images in the hippocampus. Three months later, the patient had nearly completely recovered and resumed work. MR images and neuropsychological testing returned to normal. CONCLUSIONS: The most likely course of events favours an initial prolonged hypoglycaemic coma following insulin overdose. The hippocampal injury may be a result of hypoglycaemia. Neuropsychological testing and MRI abnormalities were completely reversible. This case underlines the potential risks of intensive insulin therapy.
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ranking = 2
keywords = coma
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8/25. Diabetic keto-acidotic (DKA) coma following olanzapine initiation in a previously euglycaemic woman and successful continued therapy with olanzapine.

    We report the case of a euglycaemic woman whose glucose control rapidly decompensated following olanzapine initiation leading to diabetic coma. Hyperglycaemia has been associated with chronic psychotic disorders and antipsychotics for many years. However, it is unusual to see such rapid and life-threatening changes associated with treatment. The case highlights that changes in antipsychotic treatment may be associated with large changes in glucose tolerance, and that it is possible to continue antipsychotic treatment with appropriate diabetic care.
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ranking = 5
keywords = coma
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9/25. Profound hypokalemia in diabetic ketoacidosis: a therapeutic challenge.

    OBJECTIVE: To describe profound hypokalemia in a comatose patient with diabetic ketoacidosis. methods: We present a case report, review the mechanisms for the occurrence of hypokalemia in diabetic ketoacidosis, and discuss its management in the setting of hyperglycemia and hyperosmolality. RESULTS: A 22-year-old woman with a history of type 1 diabetes mellitus was admitted in a comatose state. Laboratory tests revealed a blood glucose level of 747 mg/dL, serum potassium of 1.9 mEq/L, pH of 6.8, and calculated effective serum osmolality of 320 mOsm/kg. She was intubated and resuscitated with intravenously administered fluids. Intravenous administration of vasopressors was necessary for stabilization of the blood pressure. Intravenous infusion of insulin was initiated to control the hyperglycemia, and repletion of total body potassium stores was undertaken. A total of 660 mEq of potassium was administered intravenously during the first 12.5 hours. Despite such aggressive initial repletion of potassium, the patient required 40 to 80 mEq of potassium daily for the next 8 days to increase the serum potassium concentration to normal. CONCLUSION: Profound hypokalemia, an uncommon initial manifestation in patients with diabetic ketoacidosis, is indicative of severe total body potassium deficiency. Under such circumstances, aggressive potassium repletion in a comatose patient must be undertaken during correction of other metabolic abnormalities, including hyperglycemia and hyperosmolality. Intravenously administered insulin should be withheld until the serum potassium concentration is (3)3.3 mEq/L.
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ranking = 3
keywords = coma
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10/25. The use of continuous hemodiafiltration in a patient with diabetic ketoacidosis.

    A variety of fatal complications are associated with diabetes mellitus. Among these, diabetic ketoacidosis (DKA) figures largely in fatalities in young diabetics. Although hyperosmotic diuresis in DKA causes extreme fluid loss, acute renal failure is less common than expected in DKA. We treated a case of severe DKA with associated coma, acute respiratory failure, and acute renal failure in a 24-year-old man who had been diagnosed with type 1 diabetes mellitus at age 19. The comatose patient had been intubated before transfer to our hospital for intensive care. Despite infusion with isotonic saline and insulin, metabolic acidosis was refractory. On day 2, urine output decreased and pulmonary congestion developed, so we started continuous veno-venous hemodiafiltration (CVVHDF), which was effective against the metabolic acidosis; urine output increased gradually. CVVHDF was withdrawn on day 7, and the patient's renal function recovered completely. He was discharged from the intensive care unit (ICU) on day 14.
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ranking = 2
keywords = coma
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