A case study on hemolytic uremic syndrome- Leading to acute renal fail

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Jiguru Prasant et al / Int. J. of Allied Med. Sci. and Clin. Research Vol-31 2015 66-69 66 IJAMSCR |Volume 3 | Issue 1 | Jan-Mar- 2015 www.ijamscr.com Case study Medical research A case study on hemolytic uremic syndrome- Leading to acute renal failure Jiguru Prasant 1 Mohammad Kaleemullah Quraishi Amer Khan. Department of Doctor of Pharmacy Krishna Institute of Medical Sciences and Bharat Institute of Technology Pharmacy Hyderabad Telangana India. Corresponding author: Jiguru Prasant E-mail id: prashant7792gmail.com ABSTRACT A 65 yrs female patient was presented with complaints of vomiting loose stools pain fever high grade chills giddiness loss of appetite acute renal failure hemolytic anemia and thrombocytopenia She was diagnosed with Escherichia coli associated hemolytic-uremic syndrome and treated with plasmapheresis and other medications for 3 weeks. She recovered without sequelae. Keywords: Hemolytic uremic syndrome Atypical hemolytic uremic syndrome Acute kidney injury Shiga toxin- producing E.coli Complement factor H Therapeutic plasma exchange. INTRODUCTION Hemolytic uremic syndrome is a common cause of acute kidney injury. In children and adults hemolytic uremic syndrome is most commonly associated with gastrointestinal infections caused by Shiga toxin- producing Escherichia coli or other enteric organisms 13. Although less common atypical hemolytic uremic syndrome is triggered by multiple factors and portends a significantly worse prognosis with a high rate of recurrence. Infections of the gastrointestinal tract your stomach and intestines are the most common cause of this disorder. Toxins released during an intestinal bacterial infection can destroy the lining of small blood vessels in your stomach or intestines2. This in turn causes damage and destruction to blood cells as they circulate through the blood vessels. This destruction affects red blood cells RBC and platelets causing them to die prematurely. A buildup of these destroyed cells clogs the kidneys’ filtering system reducing the blood flow to the kidneys. Your kidneys are responsible for filtering out waste products and toxins so they can be eliminated from your body. The damage to your health and kidney function can be quite serious if left untreated or if complications arise. Kidney failure high blood pressure heart problems and stroke are all concerns if HUS advances without prompt treatment.45 CASE STUDY A 65 yrs female patient was presented with chief complaints of Vomiting since 2 daysseveral episodes/day Loose stools since 2daysseveral episodes/day Greenish Mucus Abdominal Pain since 3days Fever since 1 day High grade chills Giddiness on and off since 2 days Loss of appetite since 3days. Medical history: k/c/o Type 2DM- 9yrs on OHA’S Admitted with UTI in Feb. International Journal of Allied Medical Sciences and Clinical Research IJAMSCR

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Jiguru Prasant et al. / Int. J. of Allied Med. Sci. and Clin. Research Vol-31 2015 66-69 67 medication history: Tablet glybovin 25mg 3-0-1 Tablet metadose ipr 850 mg social history: mixed diet post-menopausal. Upon admission pulse rate was -110/min blood pressure was -90/60mm/hg respiratory rate was found to be -20/min and Temperature is -100F. Laboratory tests showed Urea: 97 mg/dL 8-35mg/dl Serum Creatine : 3.1 mg/dL 0.6-1.6mg/dl Na: 132 Meq/L 136-148Meq/LK:7Meq/L 3.5-5.0Meq/L Random blood Sugar: 331 mg/dL 60-50mg/dl Albumin: 4.0 g/dL 3.5-5g/dl hemoglobin: 10.6 g ESR: 620-20mm/hr platelet count 19000/mm3 Culture Test:- E.coli in blood was identified in the stool culture performed at the hospital where she was first admitted Peripheral blood smear showed polychromasia anisocytosis and schistocytes. Microangiopathic hemolytic anemia A diagnosis was made based on acute renal failure hemolytic anemia and thrombocytopenia and it was conformed as hemolytic uremic syndrome. She received hemodialysis for 10 days and plasma exchange and fresh frozen plasma for two weeks. The following medications was given in the stay of the hospital ivf ns 125ml/hr h.insulin-r sc ½ hr bf Table: 1 Treatment schedule Drug Dose ROA Frequency Inj optineuron 1amp IV STAT Inj ciprofloxacin 200mg IV BD Inj pantoprazole 40mg IV OD Inj ondansetron 4mg IV STAT Inj piperacillin + tazobactam 4.5mg + 2.25mg IV STAT Inj fursosemide 40mg IV STAT Inj. pheniramine 1amp IV STAT Inj paracetamol 1amp IV STAT Inj hydrocortisone 100mg IV STAT Inj haloperidol 2.5mg IV SOS Tab quetiapine 25mg PO HS Tab bisacodyl 10mg PO HS Syp kmac 10ml PO TID

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Jiguru Prasant et al / Int. J. of Allied Med. Sci. and Clin. Research Vol-31 2015 66-69 68 After day 16 three successive stool specimens resulted negative results for Escherichia coli. After the treatment platelet count increased to 1 lakh hemoglobin raised to 14.5 g albumin to normal range urea to 34mg/dl k value to 4.0 meq/l and serum creatinine 1.2mg/dl. On hospital day 18 she was discharged and received follow-up care as an outpatient. DISCUSSION The patient in this case presented with gastroenteritis symptoms with severe systemic upset. So the etiologic agent causing HUS this time is probably due to enteric pathogen and the most likely candidate is E. Coli 6.The patho types of intestinal pathogenic Escherichia coli are classified as follows : Shiga toxin-producing Escherichia coli STEC/entero - hemorrhagic Escherichia coli EHEC enterotoxigenic Escherichia coli ETEC entero pathogenic Escherichia coli EPEC enteroinvasive Escherichia coli EIEC entero aggregative Escherichia coli EAEC and diffusely adherent Escherichia coli DAEC. STEC/EHEC strains can cause hemorrhagic colitis and Hemolytic uremic syndrome HUS. EHEC has since been documented as the cause of both large outbreaks and sporadic infections in the United States and around the world. Several large outbreaks resulted from the consumption of undercooked ground beef and other foods 7. Our patient frequently ate fast food particularly Chinese noodles. We could not exclude the possibility that EHEC was transmitted by contaminated food consumed by our patient. However we did not investigate the origins of the EHEC infection Hemorrhagic colitis associated with EHEC and others is characterized by grossly bloody diarrhea often with remarkably little fever or inflammatory exudate in the stool. Although the diarrheal illnesses have been self-limiting a significant number of children and adults have subsequently developed a potentially fatal hemolytic uremic syndrome or thrombotic thrombocytopenic purpura8. The clinical manifestations of post- diarrheal HUS include renal failure microangiopathic hemolytic anemia and thrombocytopenia. Several studies reported that the culture rate of EHEC was 2 to 51 in post- diarrheal HUS. HUS complicates 10 of bloody diarrhea induced by EHEC. Some estimate that EHEC causes at least 70 of post-diarrheal HUS in the India and that 80 of these are caused by EHEC and the other 20 by a different serotype of EHEC. However EHEC infections are rare in patients with post-diarrheal HUS and the majorities are caused by non EHEC. The use of antimotility agents in children under 10 years of age or in elderly patients should be avoided as it increases the risk of HUS with EHEC infections. The incubation period has usually been 3 to 5 days after bloody diarrhea but HUS infrequently develops no prodromal symptom 9. Although the illness is usually self-limited the mortality rate is 3 to 5 in young children and 30 of patients with HUS develop permanent renal failure hypertension or neurologic sequelae. Thrombocytopenia occurs as a consequence of platelet consumption and hemolytic anemia results from intravascular fibrin deposition increased red blood cell fragility and fragmentation. Plasma exchange which removes the plasma with the shiga- like toxin and its breakdown products may decrease the effects of the toxin. Plamapheresis may not be necessary in mild cases if water and electrolyte balance are well maintained. Fresh frozen plasma can be administered to the patient to replace the loss of plasma proteins and coagulation factors.10 CONCLUSION This case highlights the clinical challenges in diagnosing and managing patients with hemolytic uremic syndrome. Because of similarity in symptoms differentiating Shiga toxin-producing Escherichia coli associated hemolytic uremic syndrome and atypical hemolytic uremic syndrome can be challenging. However because of the increased morbidity and mortality of atypical hemolytic uremic syndrome early detection and initiation of therapy are critical. Providers must have a heightened suspicion in order to initiate supportive care or disease directed therapy in the case of atypical hemolytic uremic syndrome.

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Jiguru Prasant et al. / Int. J. of Allied Med. Sci. and Clin. Research Vol-31 2015 66-69 69 REFERENCES 1 Scheiring J Andreoli SP Zimmerhackl LB: Treatment and outcome of Shiga-toxin-associated hemolytic uremia syndrome HUS. Pediatr Nephrol 2008 23:1749–1760. 2 Michael M Elliott EJ Ridley GF Hodson EM Craig JC: Interventions for haemolytic uraemic syndrome and thrombotic thrombocytopenic purpura. Cochrane Rev 2009. doi:10.1002/14651858.CD003595.pub2. http://thecochranereviewlibrary.com 3 Legendre CM Licht C Greenbaum LA Babu S Bedrosian C Bingham C Cohen DH Delmas Y Douglas K Eitner F Feldkamp T Fougue DFurman RR Gaber O Herthelius M Hourmant M Karpman D Lebranchu Y Mariat C Menne J Moulin B Nurnberger J Ogawa M Remuzzi GRichard T Sberro- Soussari R Severino B Sheerin NS Trivelli A Zimmerhackl LB et al: Terminal Complement inhibitor eculizumab in atypical Hemolytic-Uremia Syndrome. N Engl J Med 2013 368:2169–2181. 4 Noris M Giuseppe R: Atypical hemolytic uremic syndrome. N Engl J Med 2009 361:1676–1687. 5 Gould LH Bopp C Strockbine N Atkinson R Baselski V Body B Carey R Crandall C Hurd S Kaplan R Neill M Shea S Somsel P Tobin-D’Angelo M Griffin PM Gener-Smith P: Recommendations for diagnosis of Shiga Toxin producing Escherichia coli infections by clinical laboratories. MMWR 2009 58:1–14. 6 Fremeaux-Bacchi V Fkahouri F Garnier A Bienaime’ F Drgaon-Durey M-A Ngo S Moulin B Servais A Provot F Rostaing L Burtey S Niaudet P Deschenes G Lebrachu Y Zuber J Loirat C: Genetics and outcome of atypical hemolytic uremic syndrome: A nationwide French series comparing children and adults. Clin J Am Soc Nephrol 2013 8:554–562. 7 Hofer J Janecke AR Zimmerhackl LB Riedl M Rosales A Giner T Cortina G Haindl CJ Petzelberger B Pawlik M Jeller V Vester U Gadner B van Husen M Moritz ML Wurzner R Jungraithmayr T German-Austrian HUS Study Group: Complement factor H-related protein 1 deficiency and factor H antibodies in pediatric patients with atypical hemolytic uremic syndrome. Clin J Am Soc Nephrol 2013 8:407–415. 8 Caprioli J Castelletti F Bucchioni S Bettinaglio P Bresin E Pianette G Gamba S Brioschi S Daina E Remuzzi G Noris M International registry of Recurrent and Familial HUS/TTP: Complement factor H mutations and gene polymorphisms in haemolytic uraemic syndrome: the C-257T the A2089G and the G2881T polymorphisms are strongly associated with the disease. Human Molecular Genetics 2003 12:3385–3395. 9 Kavanagh D Goodship T: Genetics and complement in atypical HUS. Pediatr Nephrol 2010 25:2431– 2442. 10 Bresin E Rurali E Caprioli J Sanchez-Corral P Fremeaux-Bacchi Vde Cordoba R Pinto S Goodship THJ Alberti M Ribes D Valoti E Remuzzi G Noris M on behalf of the European Working Party on Complement Genetics in Renal Disease: Combined complement gene mutations in atypical hemolytic uremic syndrome influence clinical phenotype. J Am Soc Nephrol 2013 24:475–486.

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