Cholera is gastroenteritis caused by Vibrio cholerae. It presents with vomiting, severe secretory diarrhoea, and dehydration. It presents as watery, rice-water stools with a fishy odour. It can cause severe complications with severe electrolyte imbalances such as hyponatraemia, hypernatraemia, and hypokalaemia and oligoanuric acute kidney injury (AKI) due to acute tubular necrosis (ATN). Case 1: A 19-year-old arrived few days back from Bangladish was admitted with altered mental status, vomiting and diarrhea, His labs on admission showed creatinine 713 micromol/L, urea 21.6 mmol/L, bicarbonate 13 mmol sodium 148 mmol/L, potassium 3.6 mmol/L, chloride 109 mmol/L. WBC 28 x 109, Hb 154 g/L , lactate was normal,urine analysis showed positive leucocyte esterase, negative nitrates, positive blood, WBCs 756 cells/microL, RBCs 12,759 cells/microL, PH 6.5, specific gravity 1.019 with granular casts, procalcitonin 813 ng/dL. Urine albumin was > 400 mg/L. On day 3 of admission creatinine peaked to 1,104 micromol/L, urea 38mmol/L, he became anuric with development of pulmonary edema, he received 2 short sessions of hemodialysis. Stool PCR showed positive Vibrio,Enteroaggregative E.coli (EAEC), Enteropathogenic E.coli (EPEC), Enterotoxigenic E. coli (ETEC) lt/ st, Shigella/ Enteroinvasive E. coli (EIEC) Norovirus, Sapovirus, C.diff, and campylobacter. During hospitalization patient was afebrile and maintained his blood pressure, he received intravenous fluids for resuscitation and completed a course of ceftriaxone, azithromycin and doxycycline. Creatinine on discharge was 110microcol/L, urea 6.4 mmol/L. Case 2: 47 years old male patient previously healthy, arrived from Bangladesh 2 days prior to admission, presented with uncountable episodes of watery diarrhea associated with central abdominal pain, nausea, and vomiting. Patient was severely dehydrated, anuric, labs in ED showed creatinine 456 micromol/L , bicarbonate 11 mmol/L , urea 10.8 mmol/L, no hyperkalemia, Albumin 55g/L ( normal range 32-52), venous PH 7.16, hemoglobin 180 g/L , WBCs 17.7 x109. repeated labs within 12 hours showed worsening acidosis despite starting sodium bicarbonate intravenous boluses and infusion. Venous PH 7.04, patient was initiated on hemodialysis via temporary dialysis line due to refractory worsening acidosis,. Peak creatinine reached 635 micromol/L and bicarbonate 9 mmol/L, protein creatinine ration 2 g/g. He received 2 short session of hemodialysis with aggressive fluid resuscitation, urine output in day was 1.4 L, on day 10 of hospitalization, creatinine continue to improve and reached 94 micromol/L and patient was discharged home. His stool PCR was negative for Campylobacter (jejuni, coli and upsalien ), Clostridium difficile (toxin A/ B), Plesiomonas shigelloides, salmonella, Yersinia enterocolitica,Vibrio (parahaemolyticus, vulnificus, and Vibrio cholerae), EAEC, EPEC, ETEC all were not detected. He completed 1 week course of Ceftriaxone, Metronidazole, and Azithromycin. The cause of his traveler diarrhea was not known but the patient responded well to supportive measures, hemodialysis and antibiotics. Both patients were discharged home with improving renal function. Traveler diarrhea from endemic areas can be due to multiple pathogens. supportive treatment including vigorous hydration and initiation of hemodialysis may be required in sever cases of AKI.
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Oct 1, 2022
Shams Tasnim + 3
