CASE REPORT
We describe a case of a 26-yr-old female with type I diabetes (T1DM) of more than 10-yr duration. This patient presented with severe abdominal pain started one day ago and had been performing continuous ambulatory peritoneal dialysis for one year. This patient had a history of tuberculosis which was cured already. Ten years ago when this patient was diagnosed with T1DM after showing polydipsia without obvious trigger, she was treated with insulin injection. One year ago this patient was hospitalized for uremia (late stage of chronic renal failure). Peritoneal dialysis catheter placement was performed and followed with regular peritoneal dialysis, after which this patient’s clinical evolution was favorable.
The patient was hospitalized because of a 24-hr history of durative blunt abdominal pain. The associated symptoms included mushy stool diarrhea, cloudy peritoneal dialysate fluid. The patient had no sign of dark stool, chills or fever. On physical examination the patient showed signs of moderate anemia-like paleness. The patient was alert, with vital signs in normal range which include temperature at 36.5℃, pulse rate at 80 bpm, respiratory rate at 20 bpm, blood pressure at 100/60 mmHg. The physical examination showed no jaundice-yellow with skin, sclera and mucous membranes, no swelling of superficial lymph nodes. The breath sounds are clear without obvious adventitious sounds like dry/moist rales. Abdominal swelling caused by accumulation of fluid was observed. There was no observation of hepatosplenomegaly, tenderness or rebound tenderness, as well as peripheral edema. The patient showed normal reflex action and no sign of pathological spread of reflexes.
The blood test results when hospitalized were as follows, leukocytes 11.8x109/L, hemoglobin 65 g/L, C-reactive protein (CRP) 140.94 mg/L, albumin 19.1 g/L, creatinine 528.0 μmol/L, blood glucose 15.0 mmol/L and potassium 2.58 mmol/L. The peritoneal fluid was cloudy, and the analysis of which showed leukocytes at 80% and nucleated cell count at 2.93x109/L. The suspected bacterial infection was treated with intravenous and peritoneal administration of cefazolin and levofloxacin lactate upon hospitalization. Measures were taken to adjust the levels of blood glucose and blood pressure, correct anemia, maintain the level of electrolytes and pH balance. On Oct 18th, the drug resistance result from culture of peritoneal dialysis fluid indicated the infection of Candida dubliniensis. Treatment was then switched to intravenous Fluconazole and intraperitoneal influx of antifungal medication. At the meantime, peritoneal dialysis catheters were removed and blood dialysis was performed. On Oct 25th, the abdominal pain got worse and the patient showed obvious tenderness and rebound tenderness, which indicated intestinal obstruction. The intake of water and food was forbidden and gastrointestinal decompression was performed. In addition to the antifungal medication, Piperacillin/Tazobactam was prescribed against the infection. At 12am of Oct 29th, the patient felt chest tightness and shortness of breath. The blood pressure was taken at 80/50 mmHg. The patient was in extremely low spirits. Obvious moist rales was noticed. Test of blood dialysis from Oct 27th read BNP>10000, CO2CP 6.4mmol/L, blood glucose 15mmol/L. Beside the supply of fluid, dopamine was given to correct the risk of shock. Dialysis was emergency performed against acidosis. The CRP level was measured again at 175 mg/L, calcitonin at 4.48, leukocytes count at 16.67 x 109/L. Again the abdominal pain got worse and the anti-infection reagent was switched to Meropenem. At the noon, CO2CP was read at 6.4 mmol/L, pH at 7.17. Dialysis was performed in the afternoon and again on Oct 30th. On Oct 31st, CO2CP was read at 9.7 mmol/L, blood glucose at 15 mmol/L (hypoglycemia). Multiple blood gas tests indicated metabolic acidosis whereas the level of lactic was normal. The blood glucose level was increased although not as significant as seen in DKA. No urine was available to measure the level of ketones and it is possible that urine ketones could be negative in DKA associated with chronic kidney disease (CKD). Other local hospitals did not have the ability to test the blood ketones either. So the dialysis fluid was used as urine to test for ketones, which showed positive. This patient was then diagnosed as ketoacidosis and CRRT was performed accordingly. The acidosis was following corrected and the blood sample was confirmed with ketoacidosis after sending out for test.