The Case Study section of Insulin concludes with questions about the case being presented. A summary of the responses we receive for each case study will appear in the next issue along with a new case study (and its accompanying questions).
October 2007
Chief Complaint: The patient was a 16-year-old, obese black male who presented to the local emergency department where he was described as being in “acute distress.”
History of Present Illness: Two weeks before admission, the patient had noted polyuria, nocturia, weight loss (despite being constantly hungry), and little energy. Two days before admission, he developed headaches, generalized abdominal pain, nausea, and vomiting. He was taken by his mother to the local emergency department. Although the patient was in acute distress, he was able to respond appropriately to questioning.
Social History: The patient is currently in 11th grade and doing fairly well in school. He is a member of the high school football team.
Medical History: The patient had no significant medical history. Family history revealed that the patient’s mother had developed diabetes mellitus (DM) before 25 years of age. There was a strong family history of DM on the maternal side of the family.
Physical Exam: At admission, the patient’s temperature was 98.8°F; heart rate was 140 beats/min; respiratory rate was 30 breaths/min; and blood pressure was 150/80 mm Hg. His body mass index was 32 kg/m2. His physical examination revealed clear lungs and, except for tachycardia and systolic hypertension, a normal cardiovascular evaluation. There was no rebound or point tenderness on abdominal examination. The remainder of his examination was normal. Results of his chest radiograph were also normal.
At the outside hospital, immediate treatment included bolus IV fluids (3 L over ~3 hours) followed by replacement fluids (normal saline with 40-mEq/L potassium at ~150 mL/h), insulin drip (4 U/h [0.025 U/kg/h] that was increased to 8 U/h), and bicarbonate given over 3 hours (dose not recorded). Unfortunately, the patient’s mental status deteriorated, with increasing confusion and lethargy, persistent acidosis (carbon dioxide, <10 mEq/L; pH, 7.04), rising creatinine (to 5.9 mg/dL), oliguria, and hypotension. His pupillary responses were not recorded. He was intubated, hyperventilated, and received IV mannitol. Shortly thereafter, he was transferred to the university hospital.
Despite appropriate fluid management and insulin therapy, the patient’s acidosis and poor mental status persisted while at the university hospital. Twelve hours after admission, increasing respiratory distress was noted. His chest radiograph displayed a right upper lobe consolidation, and he developed nonoliguric renal failure. On hospital day 5, bronchoalveolar lavage revealed a “fungus,” and he was begun on appropriate antifungal therapy. Results of his sinus computerized tomography (CT) scan were negative, but his lung CT scan displayed cavitation in the right lung. On hospital day 7, the patient’s right upper and middle lobes were surgically resected. In the operating room and the recovery room, the patient
was hypotensive (cardiac output, <5 L/min), severely acidotic (lactic acid, 13.9 mmol/L), oligouric, and hyperkalemic. He suffered 4 cardiopulmonary arrests. Cardiopulmonary resuscitation was ultimately unsuccessful.
Lab Results: On admission to the emergency department, laboratory studies revealed the following: sodium, 131 mEq/L (low); potassium, 4.9 mEq/L; chloride, 103 mEq/L; pH, 7.27; serum carbon dioxide, 8 mEq/L (low); creatinine, 1.5 mg/dL (increased); and blood urea nitrogen, 11 mg/dL. His glucose level was elevated at 521 mg/dL, and his lactic acid level was normal at 1.2 mmol/L (reference interval, <1.5 mmol/L). The urine was strongly positive for ketones.
On admission to the university hospital, the following additional laboratory test results were obtained: β-hydroxybutyrate, 442.7 mg/dL (reference interval, 0.2–2.8 mg/dL); amylase, 316 U/L (reference interval, 0–65 U/L); lipase, 1045 U/L (reference interval, 7–60 U/L); triglycerides, 585 mg/dL (target level, <125 mg/dL); and glycosylated hemoglobin, 12.7% (reference interval, <6.1%).
After the patient’s death, the following data were obtained from previously drawn samples: islet cell autoantibodies, negative; glutamic acid decarboxylase autoantibodies, negative; IA-2 autoantibodies, negative; and human leukocyte antigen (HLA) type, HLA-DQB1*0602 and HLA-DQB1*0301.
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