Diabetic ketoacidosis presenting with emphysematous pyelonephritis

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Journal of Diabetes and Its Complications 24 (2010) 214 – 216 WWW.JDCJOURNAL.COM

Diabetic ketoacidosis presenting with emphysematous pyelonephritis Yara M. Eid⁎, Mona M. Abdel Salam Department of Internal Medicine, Division of Endocrinology and Metabolism, Ain-Shams University Hospitals, Abbassieh, Cairo, Egypt Received 7 August 2008; accepted 22 December 2008

Abstract Mr. A.M.A. is 28-year-old Egyptian male patient who presented to the ER with diabetic ketoacidosis (DKA) and left loin pain of 3 weeks duration. The patient had a history of hospital admission 5 months earlier because of urinary tract infection and DKA. Workup of this clinical case revealed emphysematous pyelonephritis. © 2010 Published by Elsevier Inc. Keywords: Diabetic ketoacidosis; Necrotizing infection; Urinary tract infection; Emphysematous pyelonephritis; Sympathetic pleural effusion

1. Introduction We report the case of a patient with type 1 diabetes presenting with diabetic ketoacidosis (DKA) and an indolent course of emphysematous pyelonephritis. Emphysematous pyelonephritis is a rare condition that occurs almost exclusively in patients with diabetes mellitus (DM).The first case of gas-forming renal infection was reported in 1898. Since then, more than 200 cases have been reported in the literature. 2. Case presentation Mr. A.M.A. is 28-year-old Egyptian male patient. He is a known case of type 1 DM of 8 years duration. He presented to the ER with left loin pain of 3 weeks duration. The pain was localized, stabbing in character, and not relieved with nonnarcotic analgesics. The pain was associated with fever, vomiting, frequency of micturition, and dysuria.

Abbreviations: DKA, diabetic ketoacidosis; UTI, urinary tract infection; ABG, arterial blood gases; CBC, complete blood count; WBCs, white blood cells; Hb, hemoglobin; CT scan, computed tomography scan. ⁎ Corresponding author. Tel.: +20 24826715; fax: +20 24845647. E-mail address: [email protected] (Y.M. Eid). 1056-8727/08/$ – see front matter © 2010 Published by Elsevier Inc. doi:10.1016/j.jdiacomp.2008.12.010

Physical examination revealed a conscious patient with tachycardia, pallor, and temperature was 38°C. There was bilateral pedal edema and tender left renal angle. Lab revealed that he had DKA; his blood sugar was 606 mg/dl, his urine was +++ for acetone, and he had metabolic acidosis; ABG showed pH=7.18, PCO2=29 mmHg, PO2=135 mmHg, HCO 3 =10 mmol/l, Sat.=97%; and CBC showed WBCs=10×103 /ml, Hb=8.5 g/dl, platelets=152×10 3 /ml, serum creatinine=1.9 mg/dl, Na=118 mEq/l, K=3.0 mEq/l. The patient had a history of hospital admission 5 months earlier due to urinary tract infection (UTI) and DKA, and the condition was improved upon conventional treatment with insulin, fluids, and antibiotics. The patient was admitted to the ICU. DKA resolved, but most of the symptoms persisted including loin pain. Urine analysis revealed pus cells over 100; culture and sensitivity were done which revealed Escherichia coli and Methacillin resistant staph. aureus (MRSA) was isolated in culture upon which vancomycin was prescribed (dose adjusted according to renal function). During hospital course, the patient remained feverish with no improvement in his loin pain; in addition, the patient remained pale, and chest examination revealed stony dullness over left lung base. Chest X-ray was done and revealed moderate left-sided pleural effusion. Follow-up of laboratory investigations revealed persistence of UTI with pus cells over 100, anemia Hb was 8 g/dl,

Y.M. Eid, M.M.A. Salam / Journal of Diabetes and Its Complications 24 (2010) 214–216

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Fig. 1. CT scan showing left pyelonephritic kidney with large air fluid level.

serum creatinine remained 1.9 mg/dl, and protein creatinine ratio was 2.3. Imaging studies was performed, with the following results: •

Pelvi-abdominal ultrasonography showed mild hepatomegaly, acute pyelonephretic left kidney with multiple stones.

Fig. 3. CT scan showing sympathetic left pleural effusion with basal lung collapse.



Pelvi-abdominal computed tomography (CT) showed left pyelonephretic kidney with sympathetic left-sided pleural effusion. The left renal area shows an ill-defined mixed density lesion replacing most of renal tissue, showing large air fluid level with peripheral renal tissue (Fig. 1). The lesion shows surrounding fuzzy fat planes with thickening of fascia Gerota and Zuckerkandl and left lateral canal fascia. Picture highly suggestive of emphysematous pyelonephritis. Associated with sympathetic left pleural effusion with basal lung collapse (Figs. 2 and 3).

The urology department was consulted and nephrectomy was urgently recommended after doing renal scan which revealed split function of 95% for right kidney and 5% for the left. The patient was operated on, after which the patient's general condition improved, fever subsided, and blood sugar level normalized.

3. Discussion

Fig. 2. CT scan showing another cut of the left pyelonephritic kidney.

Emphysematous pyelonephritis (EPN) has been defined as a necrotizing infection of the renal parenchyma and its surrounding areas that results in the presence of gas in the renal parenchyma, collecting system, or perinephric tissue (Michaeli, Mogle, Perlberg, Heiman, & Caine, 1984). It was first described by Kelly and Mac Cullum in 1898 and later

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Y.M. Eid, M.M.A. Salam / Journal of Diabetes and Its Complications 24 (2010) 214–216

diagnosed as EPN by Schultz and Klorfe in 1962 (Jong, Huang, Lan, Wang, & Chen, 1998). It is a rare life-threatening suppurative necrotizing infection of the renal parenchyma and perirenal tissue producing abscess with intrarenal gas, vasculitis, intravascular hemolysis, thrombosis with infarction, papillary necrosis, and glomerular sclerosis (Whan, Lo, Bullard, Chang, & Lee, 1998). It is almost always associated with DM, and in those who are nondiabetic, it is associated with ureteric obstruction, renal failure, and immunosuppression, as contributing factors. In most diabetic patients, the diabetes is uncontrolled, with high levels of glycosylated hemoglobin or high levels of blood sugar (Pontin, Barnes, Joffe, & Kahn, 1995). Causative organism is E. coli in majority of the cases, followed by Klebsiella pneumoniae, Proteus, and Pseudomonas. Rarely, fungi such as Cryptococcus or Candida can be the causative factors. True gas-producing organisms like clostridia have never been isolated (Palynasalo, Hellstrom, Siniluoto, & Leinonen, 1989). Four factors have been involved in the pathogenesis of EPN, including gas-forming bacteria, high tissue glucose level, impaired tissue perfusion, and a defective immune response (such as DM). The most common clinical manifestations of EPN (i.e., fever, flank pain, and pyuria) were nonspecific and not different from the classic triad of upper UTI other than EPN. Thrombocytopenia, acute renal function impairment, disturbance of consciousness, and shock can be the initial presentations, especially in severe cases. Diabetic ketoacidosis is an uncommon presentation; only few cases of DKA and EPN have been reported in the literature (Jain, Agarwal, & Chaturvedi, 2000). The finding of gas within renal structures is pathognomonic of EPN (McDermid, Watterson, & Van Eden, 1999). The spectrum of EPN varies from extensive necrosis with streaky or mottled gas to localized infection with bubbly and loculated gas formation (Ramanathan, Nguyen, Khan, & Musher, 2006). According to radiological findings and CT scans, EPN can be classified as follows: Class 1—gas confined to the collecting system Class 2—gas confined to the renal parenchyma alone Class 3A—perinephric extension of gas or abscess Class 3B—Extension of gas beyond the Gerota fascia Class 4—bilateral EPN or EPN in a solitary kidney (Huang and Tseng, 2000). Here, in our case, the patient was Class 3A according to his CT scans.

Patients with EPN Class 3A, 3B, and 4 should be treated with aggressive medical management and prompt surgical intervention. Shock, altered sensorium, and thrombocytopenia at the time of presentation were associated with poor prognosis (Aswathaman et al., 2008). Medical management alone could be successful in Class 1 and Class 2 EPN; also, trials have been made with percutaneous drainage and parental antibiotics in Classes 3A, 3B, and 4 in the absence of risk factors (altered consciousness, thrombocytopenia, shock, and acute renal failure) (Aswathaman et al., 2008). In our case, a trial of conservative treatment was done, yet the patient's condition did not improve; in addition, access to percutaneous drainage or internal stenting was not available, and so nephrectomy was considered after stabilization of the patient's general condition was achieved. Saving nephrons and the patient's life should be weighed based on the clinical situation, response to treatment, and available facilities. Acknowledgment We would like to acknowledge Professor Dr Muhammed Hisham Al-Gayar for his valuable assistance in revising this work. References Aswathaman, K., Gopalakrishnan, G., Gnanaraj, L., Chacko, N. K., Kekre, N. S., & Devasia, A. (2008). Emphysematous. Pyelonephritis: Outcome of conservative management. Urology, 71, 1007−1009. Huang, J. J., & Tseng, C. C. (2000). Emphysematous pyelonephritis clinicoradiologic classification, management, prognosis and pathogenesis. Archives of Internal Medicine, 160, 797−805. Jain, S. K., Agarwal, N., & Chaturvedi, S. K. (2000). Emphysematous pyelonephritis: A rare presentation. Journal of Postgraduate Medicine, 46, 31−32. Jong, I. C., Huang, J. J., Lan, R. R., Wang, M. C., & Chen, K. W. (1998). Emphysematous pyelonephritis in two diabetic patients with complete uterine prolapse and cystocele. Nephrology, Dialysis, Transplantation, 13, 3214−3217. McDermid, K. P., Watterson, J., & Van Eden, S. F. (1999). Emphysematous pyelonephritis: A case report and review of literature. Diabetes Research and Clinical Practice, 44, 71−75. Michaeli, J., Mogle, P., Perlberg, S., Heiman, S., & Caine, M. (1984). Emphysematous pyelonephritis. Journal of Urology, 131, 203−208. Palynasalo, M., Hellstrom, P., Siniluoto, T., & Leinonen, A. (1989). Emphysematous pyelonephritis. Acta Radiolgica, 30, 311−315. Pontin, A. R., Barnes, R. D., Joffe, J., & Kahn, D. (1995). Emphysematous pyelonephritis in diabetic patients. British Journal of Urology, 75(1), 71−74. Ramanathan, V., Nguyen, P. T., Khan, A., & Musher, D. (2006). Successful medical management of recurrent emphysematous pyelonephritis. Urology, 67, 623.e11−623.e13. Whan, Y. L., Lo, S. K., Bullard, M. J., Chang, P. L., & Lee, T. Y. (1998). Predictors of outcome in emphysematous pyelonephritis. Journal of Urology, 159, 369−373.

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