Post-prostate Biopsy Septic Shock Due to Extended-Spectrum Beta-Lactamase (ESBL)-Producing Escherichia coli: A Case Report

Abstract

Prostate biopsy is a commonly performed urological procedure, yet infectious complications, including sepsis and bacteremia, remain a significant and potentially life-threatening risk. We present a case of a 65-year-old male patient who developed urosepsis with Escherichia coli extended-spectrum beta-lactamase (ESBL)-producing bacteremia following a transrectal prostate biopsy. Despite an initially non-toxic appearance, the patient rapidly deteriorated, requiring vasopressor support and intensive care unit admission. Empiric therapy with vancomycin and ceftriaxone was initiated, and antibiotic coverage was escalated to meropenem upon identification of an ESBL-producing organism. He subsequently recovered and was discharged in stable condition. This case highlights the importance of early recognition of sepsis in post-procedural patients, the rising threat of ESBL-producing organisms in urological infections, and the need for vigilance even when initial presentations appear benign.

Introduction

Prostate biopsy is one of the most frequently performed urological procedures, typically indicated for elevated prostate-specific antigen levels or abnormal digital rectal examination findings. Complications encountered after transrectal biopsy are commonly minor and self-limiting, including mild hematuria, hematospermia, and transient rectal bleeding. However, major infectious complications - including sepsis, bacteremia, bacteriuria, and infection-related hospitalization - represent a significant and potentially life-threatening risk. A systematic review of 165 studies comprising 162,577 patients found a standardized prevalence of sepsis of 0.8% and infection-related hospitalization of 1.1% following transrectal prostate biopsy [1]. The transrectal approach carries an inherent risk of introducing rectal flora - most commonly Escherichia coli (E. coli) - into the urinary tract and bloodstream, with infection rates higher in regions where resistant organisms are more prevalent [2].

Of particular concern is the increasing prevalence of ESBL-producing organisms, which confer resistance to commonly used prophylactic and empiric antibiotic regimens, including fluoroquinolones and third-generation cephalosporins [3]. This resistance profile complicates management and necessitates escalation to carbapenem-class antibiotics [4]. Early identification of sepsis, appropriate resuscitation, and timely antimicrobial therapy are critical to improving outcomes in this population [5]. We present a case that underscores these challenges and illustrates the potential for rapid clinical deterioration following an otherwise uncomplicated outpatient procedure. While post-biopsy sepsis is not itself rare, this case is distinctive in its convergence of clinical challenges: an initially non-toxic presentation masking fulminant septic shock, ESBL-mediated resistance rendering empiric antibiotics ineffective, concurrent obstructive uropathy amplifying infectious severity, and the development of non-cardiogenic pulmonary edema in the presence of preserved cardiac function - a constellation that posed significant diagnostic complexity and underscores the limits of initial clinical reassurance in this setting.

Case presentation

A 65-year-old male patient with a past medical history significant for two prior ischemic strokes without residual neurological deficits, hypertension, and hyperlipidemia presented to the emergency department with complaints of hematuria and rigors beginning one day following a transrectal prostate biopsy. The biopsy had been performed on an outpatient basis due to an enlarged prostate, proceeded without reported complications, and the patient was discharged the same day. He reported visible blood in his urine but denied dysuria or difficulty voiding. He also endorsed diffuse, intermittent whole-body chills and shaking, though he was uncertain of their etiology and had not measured his temperature at home. He denied fever, abdominal pain, rectal bleeding, nausea, vomiting, chest pain, shortness of breath, diarrhea, dizziness, headache, or vision changes. He denied any personal history of malignancy, alcohol use, or illicit drug use. His daily medications included simvastatin and hydralazine, with reported compliance. He had no prior surgical history.

On presentation, vital signs were notable for a fever of 39.3°C, tachycardia with a heart rate of 116 beats per minute, blood pressure of 128/78 mmHg, respiratory rate of 20 breaths per minute, and oxygen saturation of 95% on room air. On physical examination, the patient was lying comfortably on a stretcher, in no acute distress, appearing pale but not overtly ill, with intermittent, diffuse shivering. Cardiovascular examination revealed tachycardia without murmurs, rubs, or gallops. Lungs were clear to auscultation bilaterally with no signs of respiratory distress. The abdomen was soft, non-distended, and non-tender throughout. Neurological examination was non-focal; the patient was alert and oriented to person, place, and time, with normal speech and no confusion. Given the clinical picture of fever, tachycardia, and a recent invasive genitourinary procedure, a full sepsis workup was initiated, including blood cultures and empiric broad-spectrum antibiotics - specifically vancomycin and ceftriaxone.

Initial laboratory evaluation revealed a pattern consistent with multi-organ dysfunction in the setting of septic shock, with results summarized in Table 1. Hematologic findings were notable for leukopenia and thrombocytopenia, suggestive of evolving sepsis-associated bone marrow suppression. The metabolic panel demonstrated early acute kidney injury with mildly elevated creatinine and blood urea nitrogen (BUN), as well as hypokalemia and hypophosphatemia, while hepatic transaminases remained preserved. Coagulation studies showed mild prolongation of the prothrombin time (PT) and international normalized ratio (INR), reflecting early coagulopathy. Cardiac biomarkers were markedly elevated, consistent with sepsis-related myocardial stress and possible early cardiomyopathy. Venous blood gas analysis demonstrated a compensated acid-base status; however, a markedly elevated lactate indicated significant occult tissue hypoperfusion despite the patient’s otherwise stable-appearing hemodynamics. Urinalysis was consistent with an infectious urological source, demonstrating moderate hematuria and leukocyte esterase.

Table 1. Initial laboratory results.

WBC = white blood cell count; BUN = blood urea nitrogen; AST = aspartate transaminase; ALT = alanine transaminase; PT = prothrombin time; aPTT = activated partial thromboplastin time; INR = international normalized ratio; BNP = B-type natriuretic peptide; VBG = venous blood gas; RBC = red blood cell

Laboratory test	Result	Reference range	Interpretation
Complete blood count (CBC)
White blood cell count (WBC)	2.2 ×10³/µL	4.2–9.1 ×10³/µL	↓↓ Markedly low
Hemoglobin	13.2 g/dL	13.7–17.5 g/dL	↓ Low
Platelet count	129 ×10³/µL	150–400 ×10³/µL	↓ Low
Relative neutrophils	89.5 %	34.0-67.9 %	↑ High
Absolute neutrophils	1.96 ×10³/µL	1.78-5.38 ×10³/µL	Normal
Basic metabolic panel
Sodium (Na⁺)	139 mEq/L	135–145 mEq/L	Normal
Potassium (K⁺)	3.4 mEq/L	3.5–5.3 mEq/L	↓ Low
Chloride (Cl-)	104 mEq/L	96-108 mEq/L	Normal
Phosphorus	0.7 mg/dL	2.7–4.5 mg/dL	↓↓ Markedly low
Magnesium	1.1 mEq/L	1.3-2.1 mEq/L	↓ Low
Creatinine	1.6 mg/dL	0.6–1.2 mg/dL	↑ High
Blood urea nitrogen (BUN)	21 mg/dL	8–23 mg/dL	↑ High
Hepatic function
Aspartate transaminase (AST)	32 U/L	8-33 U/L	Normal
Alanine transaminase (ALT)	29 U/L	4-36 U/L	Normal
Coagulation studies
Prothrombin time (PT)	15.2 seconds	11.0–13.5 seconds	↑ High
Activated partial thromboplastin time (aPTT)	28.7 seconds	23.2-31.6 seconds	Normal
International normalized ratio (INR)	1.46	0.8–1.1	↑ High
Cardiac biomarkers
Troponin	338 ng/L	<20 ng/L	↑↑ Markedly elevated
B-type natriuretic peptide (BNP)	174 pg/mL	<=100 pg/mL	↑ High
Venous blood gas (VBG)
pH	7.381	7.3–7.41	Normal
pCO2	39.7 mmHg	38–50 mmHg	Normal
Bicarbonate (HCO3⁻)	22.2 mEq/L	22–30 mEq/L	Normal
Lactate	5.0 mmol/L	0.5–2.2 mmol/L	↑↑ Markedly elevated
Urinalysis
White blood cell (leukocytes)	46/HPF	0-5/HPF	↑ High
Red blood cell (RBC)	>182/HPF	0-5/HPF	↑↑ Markedly elevated
Protein	100 mg/dL	Negative	↑ High
Nitrites	Negative	Negative	Normal
Leukocyte esterase	Moderate	Negative	↑ High

Twelve-lead electrocardiography demonstrated sinus tachycardia at 110 beats per minute with left axis deviation and right bundle branch block, with a corrected QT interval (QTc) of 449 milliseconds; no ischemic ST-segment or T-wave changes were identified, further supporting a non-ischemic etiology for the elevated cardiac biomarkers (Figure 1).

Figure 1. Twelve-lead electrocardiogram demonstrating sinus tachycardia at 110 beats per minute with left axis deviation and right bundle branch block.

No ischemic ST-segment or T-wave changes are identified. QTc interval is 449 milliseconds.

Chest radiograph revealed mild pulmonary edema with perihilar airspace opacities and cardiomegaly, raising early concern for cardiogenic pulmonary edema; however, given the clinical context of recent genitourinary instrumentation and systemic inflammatory response, an infectious etiology was felt to be the more likely unifying diagnosis (Figure 2). The perihilar opacities were interpreted as more consistent with non-cardiogenic pulmonary edema in the setting of sepsis than a primary cardiac process, given the absence of overt clinical features of left heart failure.

Figure 2. Posteroanterior (panel A) and lateral (panel B) chest radiographs demonstrating mild pulmonary edema with perihilar airspace opacities (red arrows) and cardiomegaly (green arrow).

Despite these initial workup findings, the patient's clinical status deteriorated during his emergency department course, with the development of progressive hypoxia without overt respiratory distress. Bedside point-of-care ultrasound (POCUS) was promptly performed. Echocardiographic evaluation excluded cardiac tamponade, demonstrating no pericardial effusion, and argued against acute coronary syndrome (ACS) as the primary driver, with grossly preserved left ventricular systolic function, normal right ventricular size and function, no interventricular septal flattening, and no sonographic features of right ventricular strain - findings collectively inconsistent with massive pulmonary embolism or cardiogenic shock. Bilateral thoracic ultrasound was performed and revealed normal lung sliding, absence of B-lines, and no pleural effusions, corroborating the non-cardiogenic interpretation of the radiographic opacities and excluding pneumothorax at the bedside.

Given persistent hypoxia and tachycardia despite these reassuring findings, pulmonary embolism remained on the differential; CT angiography of the chest was subsequently obtained and confirmed no thromboembolic disease, while also demonstrating dependent bibasilar consolidations consistent with atelectasis or early consolidation - and critically, no pulmonary edema and no pleural effusions - further reinforcing the non-cardiogenic etiology of the radiographic opacities. CT of the abdomen and pelvis demonstrated mild bilateral hydronephrosis and hydroureter without obstructing nephrolithiasis, excluding obstructive nephrolithiasis as a contributing etiology while supporting an ascending inflammatory or infectious process affecting the upper urinary tract; importantly, no periprostatic or pelvic fluid collection, rim-enhancing lesion, fistulous tract, or free air in the bladder was identified, effectively ruling out periprostatic abscess and rectovesical fistula as complications of the recent biopsy (Figure 3). 

Figure 3. Axial CT images of the abdomen and pelvis.

Panels A and B demonstrate mild bilateral hydronephrosis and hydroureter (red arrows) without obstructing nephrolithiasis. Panels C and D reveal an enlarged prostate gland (green arrows) contributing to obstructive uropathy. No periprostatic fluid collection or abscess was identified.

Stable hemoglobin with no hemorrhagic collection on CT argued against significant hemorrhagic biopsy complications despite the visible hematuria. Given the markedly elevated lactate, evolving cytopenias, and the clinical trajectory strongly suggesting imminent decompensation, stress-dose corticosteroids were administered at this juncture - prior to frank hemodynamic collapse - as a pre-emptive measure to blunt the anticipated inflammatory surge and support vascular tone. He eventually became increasingly hypotensive, necessitating central venous access and initiation of two vasopressors. He was subsequently transferred to the medical intensive care unit with a working diagnosis of urosepsis, supported by the systematic exclusion of alternative etiologies and the clinical context of recent transrectal prostate biopsy with obstructive uropathy contributing to the severity of the infectious process.

During admission, urine and blood cultures subsequently yielded ESBL-producing E. coli, confirming urological bacteremia. Given that the ESBL phenotype confers resistance to ceftriaxone and other third-generation cephalosporins, antibiotic therapy was escalated to meropenem in accordance with the organism’s resistance profile. Following appropriate resuscitation and antibiotic escalation, the patient demonstrated rapid clinical improvement. Oxygen saturation normalized, vasopressor support was successfully weaned, and he was downgraded from the intensive care unit within 24 hours of admission. Serial lactate measurements confirmed resolution of hyperlactatemia, and renal function trended toward baseline. The patient completed a two-week course of intravenous antibiotics and was subsequently discharged home with oral antibiotics to finish a four-week course, in stable condition.

Discussion

This case illustrates several clinically important lessons regarding post-procedural urosepsis caused by ESBL-producing E. coli following prostate biopsy. First, it underscores the nature of sepsis presentations in which patients may appear deceptively well despite harboring significant physiological compromise. This patient was alert, oriented, not ill appearing, and in no acute distress - yet his markedly elevated lactate of 5.0 mmol/L and developing cytopenias signaled a serious underlying process that would soon manifest as frank septic shock [5].

Transrectal prostate biopsy carries an inherent risk of introducing rectal flora into the bloodstream. Traditionally, fluoroquinolone prophylaxis has been the standard of care; however, the increasing prevalence of fluoroquinolone-resistant and ESBL-producing organisms has significantly complicated this approach [3]. ESBL-producing E. coli hydrolyzes beta-lactam antibiotics, rendering penicillins and cephalosporins ineffective and necessitating carbapenem therapy, as was required in this case [4]. The emergence of ESBL organisms in community-acquired urological infections is a growing public health concern, and clinicians must maintain a high index of suspicion, particularly in patients who fail to respond to first-line empiric regimens [2].

The presence of bilateral hydronephrosis on imaging, along with bacteremia and urosepsis, suggests an ascending infection with possible obstructive uropathy contributing to the clinical picture. The elevated troponin and BNP are consistent with myocardial stress in severe sepsis, reflecting either demand ischemia or early sepsis-induced cardiomyopathy - both recognized complications that often improve with treatment of the underlying infection [6,7]. Although bedside echocardiography demonstrated preserved left ventricular systolic function, the discordance with elevated biomarkers (troponin 338 ng/L, BNP 174 pg/mL) suggests subclinical myocardial dysfunction not fully captured by qualitative POCUS, a pattern described in early sepsis-related cardiac involvement.

Pulmonary findings further clarified the clinical picture. While the chest radiograph showed perihilar opacities concerning for cardiogenic pulmonary edema, CT angiography instead demonstrated dependent bibasilar consolidations, cardiomegaly, and no evidence of pulmonary edema or pleural effusions. In conjunction with preserved systolic function and absence of B-lines on thoracic ultrasound, these findings support a non-cardiogenic process. In sepsis, such findings are best explained by inflammatory injury to the alveolar-capillary barrier with increased permeability rather than elevated hydrostatic pressures, indicating that the patient’s respiratory abnormalities were driven by systemic infection rather than primary cardiac dysfunction [8].

The mortality burden of E. coli bacteremia is substantial and warrants emphasis. A multinational population-based cohort study spanning Finland, Sweden, and Canada found a 30-day case fatality risk of 14.1% in third-generation cephalosporin-resistant E. coli bloodstream infections, compared to lower rates in susceptible strains. Patients aged 70 or older experienced an 11.4% 30-day case fatality risk versus 6.6% in those younger than 70 years of age, and hospital-onset infections carried a markedly higher 30-day mortality of 17.7% compared to 7.8% in community-onset cases [9]. In the emergency department setting specifically, ESBL E. coli bacteremia, elevated serum lactate, and vasopressor requirement have all been identified as independent predictors of 28-day mortality - all features present in this case [10]. This underscores the importance of early recognition and aggressive management, as delayed appropriate antibiotic therapy in ESBL bacteremia is a key modifiable driver of mortality.

The rapid clinical recovery following antibiotic escalation and supportive care reinforces the importance of source control, early broad-spectrum coverage in undifferentiated sepsis, and timely transition to targeted therapy once culture data are available. This case also highlights the value of the elevated lactate as an early marker of occult hypoperfusion, even in the absence of overt hemodynamic instability at presentation [11].

Of note, stress-dose corticosteroids were administered in anticipation of clinical deterioration rather than after vasopressor escalation - deviating from the standard Surviving Sepsis Campaign (SSC) recommendation to initiate hydrocortisone only once norepinephrine requirements reach ≥0.25 mcg/kg/min for at least four hours [11]. This pre-emptive approach is supported by emerging evidence: a 2024 meta-analysis of 3,063 patients found that early hydrocortisone initiation was associated with lower ICU and in-hospital mortality compared to later administration [12], and a 2023 prospective study found that hydrocortisone initiated within three hours reduced time to vasopressor discontinuation from 37 to 25 hours compared to later initiation, with more patients achieving shock reversal [13]. In this patient, a lactate of 5.0 mmol/L with evolving cytopenias signaled imminent decompensation despite preserved blood pressure, providing physiologic justification for early intervention. Anticipatory corticosteroid use in patients demonstrating clear markers of impending septic shock may represent a clinically rational strategy worthy of further investigation.

Conclusions

This case underscores that a reassuring bedside appearance does not exclude severe underlying pathology. Patients who seem stable can still have elevated lactate, multi-organ dysfunction, and rapidly progressing bacteremia requiring vasopressors within hours. In post-procedural febrile patients, complacency is dangerous.

Four key lessons follow. First, check lactate early and interpret it independently of blood pressure, as occult hypoperfusion may precede hemodynamic collapse. Second, after genitourinary procedures, ESBL organisms should be considered when empiric antibiotics are started; lack of improvement warrants prompt reassessment and escalation to carbapenems. Third, a systematic bedside approach - POCUS, serial lactates, and broad imaging - is essential to rule out alternative diagnoses and guide care. Fourth, when a patient presents with compelling biochemical and clinical evidence of impending septic shock - including hyperlactatemia, evolving cytopenias, and an established infectious source - waiting for formal hemodynamic collapse before initiating corticosteroids may forfeit a critical therapeutic window; early recognition of physiological deterioration, even before vasopressor thresholds are met, should prompt consideration of pre-emptive stress-dose corticosteroids as part of a proactive resuscitation strategy. Recognizing and acting on the gap between clinical appearance and physiological compromise - and doing so before the patient forces your hand - is critical to improving outcomes.