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Saudi Journal of Kidney Diseases and Transplantation
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LETTER TO THE EDITOR Table of Contents   
Year : 2009  |  Volume : 20  |  Issue : 5  |  Page : 846-847
The impact of diagnostic delay on the course of septic shock caused by extended-spectrum-beta­ lactamase-producing Escherichiacoli

1 Department of Urology, Emergency Center and Clinic of Surgery, Prishtina, Kosova
2 National Institute of Public Health of Kosova, and Medical School, Prishtina University, Prishtina, Kosova
3 Infectious Disease Clinic, and Department of Pathology, University Clinical Center of Kosova, Prishtina, Kosova
4 Department of Pathology, University Clinical Center of Kosova, Prishtina, Kosova

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Date of Web Publication2-Sep-2009

How to cite this article:
Gashi M, Raka L, Ahmeti S, Gashi S, Dika A, Gashi G. The impact of diagnostic delay on the course of septic shock caused by extended-spectrum-beta­ lactamase-producing Escherichiacoli. Saudi J Kidney Dis Transpl 2009;20:846-7

How to cite this URL:
Gashi M, Raka L, Ahmeti S, Gashi S, Dika A, Gashi G. The impact of diagnostic delay on the course of septic shock caused by extended-spectrum-beta­ lactamase-producing Escherichiacoli. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2022 Aug 18];20:846-7. Available from: https://www.sjkdt.org/text.asp?2009/20/5/846/55375
To the Editor,

Sepsis is a systemic response to infection and is generally associated with multi-organ dys­function. It is often lethal, killing 20-50% of severely affected patients, mainly due to asso­ciated complications. The mortality rate increa­ses with age. [1],[2] Major factors for decreasing mortality rate are: early diagnosis of septic shock, reducing systemic over-response to in­fection, source control and supportive care. In the past, the largely predominating cause of sepsis was gram-negative bacteria (70-80%). With the development of new antimicrobial agents, the incidence of gram-negative sepsis has declined over the years. By the year 2000, the situation had been completely reversed; gram-positive bacteria caused 52.1% cases of sepsis, gram-negative organisms accounted for 37.6%, mixed infections for 4.7%, anaerobes for 1.0%, and fungi for 4.6%. [3],[4] The rise of fungi as a cause for sepsis is due to the increasing num­ber of immuno-compromised patients. Treatment of septic shock should be directed towards eradication of infection and administering ade­quate life-supporting measures.

The aim of this presentation is to highlight the impact of delay in diagnosis on the outcome of shock caused by gram negative bacteria. A 59­year-old male from Peja, Kosova, was admitted on March 2, 2006 at the Emergency Centre of the University Clinical Center of Kosova (UCCK). He presented with altered sensorium and pain in the left lumbar area. Patient was referred from the regional hospital to UCCK, which is tertiary-care hospital, with clinical diagnosis of hypovolemic shock and urosepsis. From the referral letter, it was gathered that the hemodynamic status of patient was unstable with arterial pressure of 40/0 mmHg, pulse 92/min and normal electrocardiogram (EKG). He had been treated with ciprofloxacin. The patient was diagnosed nine months earlier to have nephroli­thiasis in the right kidney. Extra-corporeal Shock Wave Lithotripsy (ESWL) was performed fo­llowed by placement of a double-J catheter in the right ureter.

An admission to our center, the patient was febrile (39.3°C), dyspneic with impaired senso­rium. The skin was cold and pale. His vital signs showed a respiratory rate of 30/min, blood pressure of 60/20 mmHg, oxygen saturation of 89%, pulse rate of 120/min and urine volume of 20 mL/hour. The EKG and chest X-ray were normal.

After admission to the department of emer­gency medicine, the patient was managed with oxygen administration, intravenous fluids and dopamine (14 µg/kg/min) until stabilization of arterial pressure was achieved. With a provi­sional diagnosis of urosepsis, the patient was treated with intravenous antibiotics (metronida­zole 500 mg q 6 h and cefotaxime 1 gram, every four hours).

Laboratory investigations revealed a signifi­cantly elevated leukocyte count of 24.200/µL (91.5% polymorphonuclear cells), erythrocyte count of 4 × 10 12 , hemoglobin level of 12.4 g/dL, hematocrit of 36% and C-reactive protein (CRP) level of 20.1 mg/dL. Serum glucose was 9.5 mmol/L, creatinine was 225 µmol/L and urea was 10.4 mmol/L. Serum electrolyte profile showed serum calcium (Ca ++ ) of 1.03 mmol/L, potassium (K + ) of 2.7 mmol/L and sodium (Na + ) of 131 mmol/L. Microscopy of sedimented urine showed 8-10 leukocytes, up to 25 erythrocytes per field (×400) and bacteria.

After two days in the intensive care, the pa­tient was transferred to the Urology Department. Physical examination, CT scan of the abdomen and pelvis, and complete metabolic evaluation revealed a left lower pole renal calculus. Urine and blood culture grew E. coli with an extended­spectrum-beta-lactamase-producer (ESBL) phe­notype, confirmed using the CLSI method. [5] The organism was resistant to piperacillin-tazobac­tam, fluoroquinolones and co-trimoxazole. It was sensitive to imipenem and amikacin, and mode­rately sensitive to gentamycin and tobramycin. The patient was treated with intravenous mero­penem, given at 1 g twice daily, for a total of 15 days. The leukocyte count was back to normal levels (8,100/µL); the CRP level came down to 12.9 mg/dL; and the body temperature was 37.3°C.

After stabilization of the general condition, on the 18 th day of hospital stay, the patient under­went percutaneous nephrolithotomy and a double-J catheter was placed in the left ureter. Three weeks after intervention, the patient was discharged from the hospital in good condition.

The empirical treatment with ciprofloxacin administered initially in a county hospital was not effective, since the pathogen turned out to be resistant to fluoroquinolones and cephalos­porins. Adequate initial pharmacological therapy is a critical step in decreasing the mortality rate of patients with severe sepsis and septic shock. Rapid clinical sampling and identification of the causative microorganisms with the use of appro­priate antimicrobials is another key treatment strategy. [6] This was proved in our case, where adequate treatment avoided fatal outcome.

In conclusion, our case highlights the possi­bility that diagnostic delay in patients with uropathogenic ESBL E. coli can be virulent and can lead to severe shock. Success of treatment is determined by immediate intervention and initiation of appropriate therapy.

   References Top

1.Martin GS, Mannino DM, Eaton S, et al. The epidemiology of sepsis in the United States from 1979 through 2000. N Engl J Med 2003; 348:1546-54.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Angus DC, Wax RS. Epidemiology of sepsis: an update. Crit Care Med 2001;29(suppl):S109­-16.  Back to cited text no. 2    
3.The International Sepsis Forum. Guidelines for the management of severe sepsis and septic shock. Intensive Care Med 2001;27(suppl 1): S1-134.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Sessler CN, Shepherd W. New concepts in sepsis. Curr Opin Crit Care 2002;8:465-72.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Clinical and Laboratory Standards Institute. Per­formance standards for antimicrobial disk tests; Approved Standards, 9 th ed. CLSI Document M2- A9, Vol. 26 No 1. Wayne PA: 2006.  Back to cited text no. 5    
6.Dellinger RP, Carlet JM, Masur H, et al. Sur­viving Sepsis Campaign Management Guidelines Committee. Surviving Sepsis Campaign guide­lines for management of severe sepsis and septic shock. Crit Care Med 2004;32:858-73.  Back to cited text no. 6    

Correspondence Address:
Lul Raka
National Institute of Public Health of Kosova, Medical School, Prishtina University, Prishtina, Kosova

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Source of Support: None, Conflict of Interest: None

PMID: 19736487

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