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.