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A 54-Year-Old Woman With Poorly Controlled Diabetes and Refractory CystitisWoman With Poorly Controlled Diabetes and Cystitis FREE TO VIEW

Whittney A. Warren, DO; Jared T. Hagaman, MD, FCCP
Author and Funding Information

From the Wright State University Boonshoft School of Medicine (Drs Warren and Hagaman); Wright-Patterson Medical Center (Dr Warren); Pulmonary and Critical Care Consultants of Dayton (Dr Hagaman); and the Miami Valley Hospital (Dr Hagaman), Dayton, OH.

Correspondence to: Whittney A. Warren, DO, Department of Internal Medicine, Wright State University Boonshoft School of Medicine, PO Box 927, Dayton, OH 45401-0927; e-mail: Whittney.Warren@gmail.com


This case has been presented in poster form at the Ohio American College of Physicians Scientific Meeting, October 10-11, 2013, Columbus, OH.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;146(1):e24-e27. doi:10.1378/chest.13-2680
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A 54-year-old woman presented to the ED complaining of dysuria. Following basic diagnostic testing, she received a diagnosis of cystitis and was discharged with ciprofloxacin. Urine cultures later grew pan-susceptible Escherichia coli. Three days later, she returned, complaining of progressively worsening shortness of breath and confusion. The patient’s medical history was significant for poorly controlled type 2 diabetes mellitus. She had no significant history of kidney disease prior to presentation.

Physical Examination Findings

The patient was afebrile with a BP of 150/59 mm Hg. She had a Kussmaul respiratory pattern at a rate of 12 breaths/min and an oxygen saturation of 96%. She had altered mental status and was in moderate distress. Examination revealed dry mucous membranes, bilaterally diminished breath sounds, irregularly irregular heart rhythm, and marked left-sided abdominal tenderness.

Diagnostic Studies

The patient’s hemoglobin level was 13.8 g/dL, her WBC count was 10,300/μL with 12% bands, and platelet count was 28,000/μL. Her blood sodium level was 132 mM/L, potassium level was 4.4 mM/L, chloride level was 97 mM/L, bicarbonate level was 16 mM/L, blood urea nitrogen was 57 mg/dL, and creatinine level was 3.5 mg/dL. Her blood glucose level was 425 mg/dL; urinalysis results were positive for leukocyte esterase, pyuria, and ketones. The serum β-hydroxybutyrate level was elevated, lactic acid level was 3.2 mM/L. The patient’s arterial pH was 7.06, CO2 level was 62.1 mm Hg, and oxygen level was 140 mm Hg on 80% fraction of inspired oxygen. Subsequent blood and urine cultures grew E coli resistant to fluoroquinolones.

Findings on an abdominal radiograph were unremarkable. Chest radiograph revealed bilateral pulmonary edema. ECG showed atrial fibrillation. Abdominal ultrasound revealed no evidence of hydronephrosis or parenchymal abnormality of the right kidney; the left kidney was unable to be visualized. An abdominal CT scan was ordered for further evaluation (Figs 1, 2).

Figure Jump LinkFigure 1. CT scan of abdomen, transverse view. Printed with written consent from the patient.Grahic Jump Location
Figure Jump LinkFigure 2. CT scan of abdomen, coronal view. Printed with written consent from the patient.Grahic Jump Location
What is the diagnosis?
Diagnosis: Emphysematous pyelonephritis

Nearly 95% of cases of emphysematous pyelonephritis (EPN) occur in patients with uncontrolled diabetes mellitus. EPN predominantly affects women, with a 1:6 male to female ratio. Patients with diabetes have 60% increased risk for urinary tract infection (UTI); approximately 80% of these involve the upper urinary tract.

EPN is a rare infection involving gas-forming organisms in the renal collecting system, parenchyma, or tissues surrounding the kidney. This necrotizing infection is facilitated by high blood glucose level, poor host renovascular supply, and impaired host immunity. Poorly controlled diabetes is a major risk factor for EPN. Approximately 40% to 50% of patients with EPN experience concurrent urinary tract obstruction, though this finding does not increase mortality. The most common causative organism, E coli, is a facultative anaerobe. Metabolism of glucose and lactate leads to formation of CO2 and hydrogen gas causing renal parenchyma destruction. Klebsiella, Proteus, and polymicrobial infections have also been described as pathogens. Multiple studies have suggested that patients with diabetes have higher risk for infection, with drug-resistant organisms increasing the risk for developing EPN via treatment of initial cystitis with ineffective antibiotic therapy.

Patients with EPN often present with acute renal failure in addition to symptoms of pyelonephritis, such as fever, pyuria, and abdominal pain; less than one-half will present with flank pain. Many patients presenting with EPN will have acid-base disturbances and hyperglycemia. Shock and sepsis may be the initial presentation in patients with severe EPN. In one study, the majority of patients presenting with EPN were also found to have thrombocytopenia, which may be a predictor of impending shock. Patients with diabetes and sepsis secondary to UTI frequently lack localizing symptoms of genitourinary tract infection, making the diagnosis even more difficult. Evidence of UTI with the tetrad of diabetes, acute renal failure, thrombocytopenia, and altered level of consciousness on presentation should raise a high level of suspicion for EPN.

The diagnosis of EPN should be considered in patients presenting with UTI and severe systemic symptoms or persistent fever despite antibiotic therapy. One review suggested that in patients exhibiting cystitis and fever for > 3 days, papillary necrosis, renal abscess, or EPN should be strongly considered. Differentiation of EPN from pyelonephritis is clinically difficult and rests on abdominal imaging. Appropriate imaging after confirmation of UTI is key to early diagnosis. Abdominal radiographs reportedly reveal EPN in only 33% to 65% of patients; ultrasound is marginally better, detecting 65% of EPN. Abdominal CT scan without contrast is the preferred method for early diagnosis, as the majority of patients presenting with EPN have acute renal failure and are unable to tolerate contrasted studies. In addition to superior diagnostic capabilities, abdominal CT imaging also facilitates classification guiding treatment decisions, and providing prognostic information.

Initial treatment of EPN involves resuscitation and antibiotic coverage directed at common pathogens, predominantly gram-negative bacilli. Further therapy is dictated by radiologic classification on abdominal CT scan. Class 1 and 2 EPN are defined by gas in the collecting system and gas in the parenchyma, respectively. Gas in the perinephric or pararenal space characterizes class 3 EPN. Gas in a solitary kidney or gas in bilateral kidneys is representative of class 4 EPN. Medical management plus percutaneous drainage is recommended for patients categorized as having class 1, 2, low-risk class 3, and class 4 EPN. Patients with high-risk class 3 EPN and patients who have failed medical management with percutaneous drainage undergo nephrectomy. Patients are deemed high risk if presenting with at least two of the following: shock, diabetes, altered consciousness, thrombocytopenia, or acute renal failure. Early detection of EPN is strongly advocated to avoid the potential of nephrectomy.

Mortality for EPN is approximately 21%, emphasizing the importance of early diagnosis and definitive treatment. Poor prognostic indicators include altered sensorium on presentation, renal failure, proteinuria, shock, and thrombocytopenia.

Clinical Course

The patient presented with symptoms of acute pyelonephritis with renal failure in the setting of diabetic ketoacidosis after a failed trial of outpatient antibiotic therapy. On repeat presentation to the ED, antibiotic therapy was broadened to cover multidrug-resistant pathogens. Her condition declined despite these measures, and she developed severe sepsis with shock, requiring vasopressors and mechanical ventilation. Failure to respond to prior antibiotic therapy and lack of clinical improvement prompted a CT scan of the abdomen early in the course of admission. Severe EPN with liquefaction of the left kidney was found. Gaseous dissection through the retroperitoneal fascia and involvement of the adjacent omentum and mesentery with associated pneumoperitoneum was also observed (high-risk class 3 EPN). The patient was taken for emergency nephrectomy and was found to have frank polymicrobial exudate with minimal residual renal parenchyma. Subsequently, she had dramatic clinical improvement with antibiotic therapy and was discharged after a 3-week hospital stay with near-complete recovery of renal function.

  • 1. Strongly consider local antibiotic resistance in patients with diabetes mellitus. This population is more likely to have UTIs from resistant organisms and appropriate antibiotic therapy early in the course of disease can decrease the risk of pyelonephritis and EPN.

  • 2. Expect diabetic patients presenting with cystitis to have upper UTI. Acute renal failure, thrombocytopenia, and altered consciousness increase the likelihood of EPN.

  • 3. Treat EPN based on radiographic classification. Class 1, 2, low-risk class 3, and class 4 EPN benefit from trial of percutaneous drainage with medical management; high-risk class 3 EPN requires emergent nephrectomy.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Other contributions:CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.

Wan YL, Lee TY, Bullard MJ, Tsai CC. Acute gas-producing bacterial renal infection: correlation between imaging findings and clinical outcome. Radiology. 1996;198(2):433-438. [PubMed]
 
Huang JJ, Tseng CC. Emphysematous pyelonephritis: clinicoradiological classification, management, prognosis, and pathogenesis. Arch Intern Med. 2000;160(6):797-805. [CrossRef] [PubMed]
 
Nicolle LE. Urinary tract infection in diabetes. Curr Opin Infect Dis. 2005;18(1):49-53. [CrossRef] [PubMed]
 
Falagas ME, Alexiou VG, Giannopoulou KP, Siempos II. Risk factors for mortality in patients with emphysematous pyelonephritis: a meta-analysis. J Urol. 2007;178(3 pt 1):880-885. [CrossRef] [PubMed]
 
Somani BK, Nabi G, Thorpe P, Hussey J, Cook J, N’Dow J; ABACUS Research Group. Is percutaneous drainage the new gold standard in the management of emphysematous pyelonephritis? Evidence from a systematic review. J Urol. 2008;179(5):1844-1849. [CrossRef] [PubMed]
 
Pontin AR, Barnes RD. Current management of emphysematous pyelonephritis. Nat Rev Urol. 2009;6(5):272-279. [CrossRef] [PubMed]
 
Ubee SS, McGlynn L, Fordham M. Emphysematous pyelonephritis. BJU Int. 2011;107(9):1474-1478. [CrossRef] [PubMed]
 
Julka S. Genitourinary infection in diabetes. Indian J Endocrinol Metab. 2013;17(suppl 1):S83-S87. [CrossRef] [PubMed]
 
Sharma PK, Sharma R, Vijay MK, Tiwari P, Goel A, Kundu AK. Emphysematous pyelonephritis: Our experience with conservative management in 14 cases. Urol Ann. 2013;5(3):157-162. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1. CT scan of abdomen, transverse view. Printed with written consent from the patient.Grahic Jump Location
Figure Jump LinkFigure 2. CT scan of abdomen, coronal view. Printed with written consent from the patient.Grahic Jump Location

Tables

Suggested Readings

Wan YL, Lee TY, Bullard MJ, Tsai CC. Acute gas-producing bacterial renal infection: correlation between imaging findings and clinical outcome. Radiology. 1996;198(2):433-438. [PubMed]
 
Huang JJ, Tseng CC. Emphysematous pyelonephritis: clinicoradiological classification, management, prognosis, and pathogenesis. Arch Intern Med. 2000;160(6):797-805. [CrossRef] [PubMed]
 
Nicolle LE. Urinary tract infection in diabetes. Curr Opin Infect Dis. 2005;18(1):49-53. [CrossRef] [PubMed]
 
Falagas ME, Alexiou VG, Giannopoulou KP, Siempos II. Risk factors for mortality in patients with emphysematous pyelonephritis: a meta-analysis. J Urol. 2007;178(3 pt 1):880-885. [CrossRef] [PubMed]
 
Somani BK, Nabi G, Thorpe P, Hussey J, Cook J, N’Dow J; ABACUS Research Group. Is percutaneous drainage the new gold standard in the management of emphysematous pyelonephritis? Evidence from a systematic review. J Urol. 2008;179(5):1844-1849. [CrossRef] [PubMed]
 
Pontin AR, Barnes RD. Current management of emphysematous pyelonephritis. Nat Rev Urol. 2009;6(5):272-279. [CrossRef] [PubMed]
 
Ubee SS, McGlynn L, Fordham M. Emphysematous pyelonephritis. BJU Int. 2011;107(9):1474-1478. [CrossRef] [PubMed]
 
Julka S. Genitourinary infection in diabetes. Indian J Endocrinol Metab. 2013;17(suppl 1):S83-S87. [CrossRef] [PubMed]
 
Sharma PK, Sharma R, Vijay MK, Tiwari P, Goel A, Kundu AK. Emphysematous pyelonephritis: Our experience with conservative management in 14 cases. Urol Ann. 2013;5(3):157-162. [CrossRef] [PubMed]
 
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