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Abstract: This patient is a young woman who came to the clinic due to abdominal pain, nausea and vomiting, and the suspected diagnosis of acute pancreatitis was also found to be difficult to correct elevated blood glucose and insulin deficiency, and it turned out that pancreatitis was only superficial, and the real culprit was ketoacidosis and dysfunction of the internal and external secretion of the pancreas caused by type 1 diabetes. After timely treatment, the condition has been controlled and all indicators are improving.
Basic information】Female, 30 years old
Type of disease】Type 1 diabetes mellitus
Hospital】Beijing Hospital
Date of consultation】September 2019
Treatment plan】Medication (lansoprazole enteric capsule, growth inhibitor for injection, reduced glutathione for injection, calcium gluconate injection, potassium chloride injection, sodium chloride injection, recombinant human insulin injection, menthol insulin injection, detergent insulin injection)
[Treatment period] 3 weeks of inpatient treatment, 2 months of outpatient follow-up
Treatment effect】The disease has been controlled, and all indicators are improving
I. Initial consultation
The patient was a 30-year-old female who came to the emergency room because of pain in the lower and middle abdomen for 3 days. The patient reported severe abdominal pain, accompanied by nausea, vomiting and low fever, and the temperature was 37.5℃. The patient was in good health and had no special medical history. On examination, the patient was clear, with acute painful face, poor skin elasticity, no significant abnormalities on cardiopulmonary auscultation, flat and soft abdomen, mild pressure pain and rebound pain in the middle and lower abdomen, and no palpable mass.
Emergency routine blood examination: white blood cell count: 16.13 × 10^9/L; neutrophil percentage: 87.9%; urine routine: glucose (++++), urinary ketone bodies (++++); blood gas analysis: PH: 7.09, partial pressure of carbon dioxide: 93 mmHg, residual alkali-22.3 mmol/L, bicarbonate: 5.7 mmol/L, glucose: 27.3 mmol/L, serum lipase: 995 U/L, serum amylase: 129 U/L, urinary amylase: 650 U/L; ECG showed sinus tachycardia; abdominal ultrasound, gynecologic ultrasound and appendiceal ultrasound showed no abnormality; CT examination of the whole abdomen (see below): 1, acute edematous pancreatitis changes; 2, punctate calcification foci in the right lobe of the liver. He was admitted to the hospital as “acute pancreatitis and ketoacidosis” in emergency.
Treatment history
The patient was admitted to the hospital for further laboratory tests, which showed that: calcitoninogen: 2.05ng/ml (0-0.10ng/ml); liver and kidney function, cardiac enzymes, blood lipids, blood calcium, thyroid function, and tumor markers were normal; fasting insulin: 0.5μU/ml; fasting C-peptide 0.03ng/ml; diabetic autoantibodies: insulin autoantibodies (IAA), pancreatic islet cell antibody (ICA) and glutamic acid decarboxylase antibody (GAD) were negative.
After admission, the patient was treated according to the principle of acute pancreatitis, fasting, lansoprazole enteric capsules for oral acid suppression and gastric protection, and intravenous growth inhibitor to inhibit pancreatic secretion and pancreatic enzyme activity. At the same time, injectable reduced glutathione, calcium gluconate injection, potassium chloride injection and sodium chloride injection were given to maintain electrolyte balance. At the same time, massive rehydration was given according to the principles of treatment of diabetic ketoacidosis, and small doses of recombinant human insulin injection were pumped intravenously to lower blood sugar.
On the second day after admission, blood gas analysis showed that the acidosis was corrected, and the glucose-lowering regimen was changed to intensive treatment with subcutaneous insulin injection (menthol insulin injection + dett insulin injection). On the 6th day of hospitalization, fasting C-peptide was <0.01ng/ml; on the 8th day, fasting C-peptide was <0.01ng/ml; on the 12th day of hospitalization, enhanced CT examination of the upper abdomen (see below) showed that the original "enlarged pancreas" was smaller than before and the peripancreatic exudate foci were absorbed. After 15 days of treatment, fasting blood glucose was 7.01 mmol/L and insulin was 7.89 μU/ml, 2h postprandial glucose was 13.29 mmol/L and insulin was 31.89 μU/ml, and C-peptide levels were <0.01 ng/mL at both time points, suggesting endogenous insulin deficiency. Combining the patient's medical history, clinical manifestations and laboratory findings, the patient was diagnosed with type 1 diabetes mellitus.
III. Treatment effect
After 21 days of hospitalization, the patient’s condition was effectively controlled, and he was discharged after resuming diabetic diet and stable glycemic control. The patient’s blood glucose was monitored as follows: 4.9-10.6 mmol/L before breakfast and 4.6-12.3 mmol/L 2h after meal, and the blood glucose was basically controlled within a certain range. In summary: the condition has been controlled and all indicators are improving.
IV. Notes
It is gratifying that the patient was diagnosed with type 1 diabetes and treated in time. After discharge from the hospital, the patient should closely monitor the blood glucose situation, and regularize three meals a day, reduce the intake of sugar in the diet, pay attention to avoid overeating, and not excessive diet or irregular diet.
And use insulin to control blood sugar according to the amount of food eaten. In addition, 20-30 minutes of moderate intensity aerobic exercise, such as jogging, brisk walking, etc., can be performed half an hour after meals every day, which is beneficial to lowering blood sugar.
V. Personal insight
Type 1 diabetes mellitus is common in Asian species. Patients in this article have an acute onset, and due to the destruction of pancreatic β-cells within a short period of time, it is easy to develop into more serious metabolic disorders and insulin deficiency, causing an acute rise in blood glucose and ketoacidosis, which can easily affect life safety if not treated promptly. Therefore, even though clinical imaging is currently advocated as an important diagnostic basis for pancreatitis, for mildly elevated pancreatic enzymes