Case Reports

Community‐associated methicillin‐resistant Staphylococcus aureus (MRSA) infection is an evolving disease that is changing medical practice. MRSA has become the most frequent cause of skin and soft‐tissue infections presenting to most emergency departments in the United States.1 In comparison with methicillin‐sensitive S. aureus, community‐associated MRSA is more likely to present as soft‐tissue abscesses or necrotizing pneumonia.2 In 2005 alone, 94,360 invasive MRSA infections were estimated to have occurred in the United States, most of which were associated with MRSA bacteremia.3 In the hospital, MRSA infections are associated with greater lengths of stay, higher mortality, and increased costs.3

We report a patient with persistent MRSA bacteremia due to a prostatic abscess. Prostatitis or prostatic abscess with MRSA has rarely been reported. Resolution of the bacteremia was achieved only after drainage of the abscess. This case highlights the importance of recognizing this clinical condition and draining any MRSA‐associated abscesses. In addition, the abscess‐forming characteristics of MRSA may suggest that the incidence of prostatic abscess due to this microbe is on the rise.

CASE REPORT

A 40‐year‐old human immunodeficiency viruspositive man presented with a 10‐day history of intermittent fever, urinary hesitancy, weak urinary stream, and intermittent abdominal pain relieved following urination. He denied dysuria, hematuria, chest pain, dyspnea, nausea, weight loss, diarrhea, or decreased functional status. His last CD4 count was 528/L on highly active antiretroviral therapy 1 year prior to presentation; however, he had run out of medications several months prior to presentation. His medical history was also significant for incision and drainage of skin abscesses with unknown microbiology several months prior to presentation. He currently used tobacco but denied illicit drug use. He was sexually abstinent for over a year prior to presentation but had a history of having unprotected sex with men.

On physical examination, his vital signs were as follows: temperature, 37.8C; blood pressure, 133/84 mm Hg; heart rate, 107 beats/minute; respiration rate, 16 breaths/minute; and oxygen saturation, 100% on room air. He was under no distress. His heart sound was tachycardic and regular with no murmur noted. Lung sounds were clear. Abdominal examination revealed no tenderness or organomegaly. His prostate was boggy, minimally tender, and slightly enlarged. The rest of his physical examination was normal. The white blood cell count was 7.5 10⁹/L with 79% neutrophils. The serum chemistry was normal. The prostate‐specific antigen level was 2.9 ng/mL. A repeat CD4 count was 140/L. Urinalysis revealed large leukocyte esterase, no nitrites, and 60 white blood cells per high‐power field. He was diagnosed with prostatitis and discharged on levofloxacin.

The subsequent day, he returned to the emergency department with an inability to void. A Foley catheter was placed with resolution of his symptoms. Later that day, blood cultures from his initial admission grew MRSA in 2 out of 4 bottles, and he was admitted to the hospital. A review of the prior urine culture showed no growth. Computed tomography (CT) of the abdomen and pelvis showed an enlarged prostate with multiple noncommunicating peripherally enhancing hypodensities consistent with prostatic abscesses (arrows in Figure 1). These abscesses were associated with periprostatic fat stranding, edematous seminal vesicles, diffuse urinary bladder wall thickening, and mild inguinal adenopathy. Therapy with intravenous vancomycin was initiated.

Figure 1

Over the next 6 days, the patient continued to have intermittent fevers. Blood cultures continued to grow MRSA. Gentamicin was added for possible synergy on hospital day 3 without improvement. A transesophageal echocardiogram was normal. On hospital day 6, repeat CT showed no change in the size of the prostatic abscesses but an increased capsular bulge along the right mid gland. The urology service was consulted. They performed bedside transperineal drainage of the largest abscess with transrectal ultrasound guidance. No indwelling drain was placed. A culture of the purulent drainage grew MRSA. Three days after the surgical drainage, the patient was afebrile, urinary symptoms had resolved, and serial blood cultures remained negative. He was discharged on hospital day 13 to complete a 4‐week course of intravenous vancomycin. The patient missed an appointment for follow‐up imaging.

DISCUSSION

We report a case of community‐associated MRSA bacteremia secondary to a prostatic abscess, as confirmed by cultures from serum and of the abscess. S. aureus bacteremia often stems from infections of the respiratory tract, skin, and soft tissues, endocarditis, or infections of indwelling devices.4S. aureus can then create embolic foci, including in the prostate, which can serve as sources of persistent bacteremia. However, new evidence suggests community‐associated MRSA might be sexually transmitted among men who have sex with men.5 An MRSA prostatic abscess could then potentially be related to an ascending urinary tract infection or translocation from the gastrointestinal tract.

The vast majority of prostatitis cases prostatic abscesses are caused by Escherichia coli and other gram‐negative bacilli.6 Staphylococcus species are less common, and MRSA isolates have been described as a rare etiologic agent. Only four other case reports describing MRSA bacteremia associated with prostatitis or prostatic abscesses have been published.710 Both our patient and the three other case reports in the literature with prostatic abscesses and MRSA bacteremia required drainage of the abscess as well as antibiotics for resolution. The other reported cases involved drainage by transurethral resection of the prostate,79 whereas our case used transperineal drainage of the prostatic abscess via transrectal ultrasound guidance. In addition to intravenous antibiotics, drainage appears to be a key therapeutic measure for resolution of MRSA prostatic abscesses.

With the increasing incidence of community‐associated and healthcare‐associated MRSA infections, the incidence of prostatitis or prostatic abscesses secondary to MRSA may be increasing. MRSA seems to have a specific predilection for abscess formation in skin and soft‐tissue infections and pneumonia.2 Clinicians must be alert to a potentially higher frequency of MRSA as a cause of prostatic abscesses and prostatitis.

In the evaluation of a patient with persistent MRSA bacteremia, the potential for the prostate as a source of infection should be considered. Urinary symptoms may be subtle. Clinicians should have a low threshold for imaging studies such as CT to evaluate for a possible source of MRSA bacteremia. If a prostatic abscess is found, prompt surgical drainage or debridement is necessary for cure.

Community‐associated methicillin‐resistant Staphylococcus aureus (MRSA) infection is an evolving disease that is changing medical practice. MRSA has become the most frequent cause of skin and soft‐tissue infections presenting to most emergency departments in the United States.1 In comparison with methicillin‐sensitive S. aureus, community‐associated MRSA is more likely to present as soft‐tissue abscesses or necrotizing pneumonia.2 In 2005 alone, 94,360 invasive MRSA infections were estimated to have occurred in the United States, most of which were associated with MRSA bacteremia.3 In the hospital, MRSA infections are associated with greater lengths of stay, higher mortality, and increased costs.3

We report a patient with persistent MRSA bacteremia due to a prostatic abscess. Prostatitis or prostatic abscess with MRSA has rarely been reported. Resolution of the bacteremia was achieved only after drainage of the abscess. This case highlights the importance of recognizing this clinical condition and draining any MRSA‐associated abscesses. In addition, the abscess‐forming characteristics of MRSA may suggest that the incidence of prostatic abscess due to this microbe is on the rise.

CASE REPORT

A 40‐year‐old human immunodeficiency viruspositive man presented with a 10‐day history of intermittent fever, urinary hesitancy, weak urinary stream, and intermittent abdominal pain relieved following urination. He denied dysuria, hematuria, chest pain, dyspnea, nausea, weight loss, diarrhea, or decreased functional status. His last CD4 count was 528/L on highly active antiretroviral therapy 1 year prior to presentation; however, he had run out of medications several months prior to presentation. His medical history was also significant for incision and drainage of skin abscesses with unknown microbiology several months prior to presentation. He currently used tobacco but denied illicit drug use. He was sexually abstinent for over a year prior to presentation but had a history of having unprotected sex with men.

On physical examination, his vital signs were as follows: temperature, 37.8C; blood pressure, 133/84 mm Hg; heart rate, 107 beats/minute; respiration rate, 16 breaths/minute; and oxygen saturation, 100% on room air. He was under no distress. His heart sound was tachycardic and regular with no murmur noted. Lung sounds were clear. Abdominal examination revealed no tenderness or organomegaly. His prostate was boggy, minimally tender, and slightly enlarged. The rest of his physical examination was normal. The white blood cell count was 7.5 10⁹/L with 79% neutrophils. The serum chemistry was normal. The prostate‐specific antigen level was 2.9 ng/mL. A repeat CD4 count was 140/L. Urinalysis revealed large leukocyte esterase, no nitrites, and 60 white blood cells per high‐power field. He was diagnosed with prostatitis and discharged on levofloxacin.

The subsequent day, he returned to the emergency department with an inability to void. A Foley catheter was placed with resolution of his symptoms. Later that day, blood cultures from his initial admission grew MRSA in 2 out of 4 bottles, and he was admitted to the hospital. A review of the prior urine culture showed no growth. Computed tomography (CT) of the abdomen and pelvis showed an enlarged prostate with multiple noncommunicating peripherally enhancing hypodensities consistent with prostatic abscesses (arrows in Figure 1). These abscesses were associated with periprostatic fat stranding, edematous seminal vesicles, diffuse urinary bladder wall thickening, and mild inguinal adenopathy. Therapy with intravenous vancomycin was initiated.

Figure 1

Over the next 6 days, the patient continued to have intermittent fevers. Blood cultures continued to grow MRSA. Gentamicin was added for possible synergy on hospital day 3 without improvement. A transesophageal echocardiogram was normal. On hospital day 6, repeat CT showed no change in the size of the prostatic abscesses but an increased capsular bulge along the right mid gland. The urology service was consulted. They performed bedside transperineal drainage of the largest abscess with transrectal ultrasound guidance. No indwelling drain was placed. A culture of the purulent drainage grew MRSA. Three days after the surgical drainage, the patient was afebrile, urinary symptoms had resolved, and serial blood cultures remained negative. He was discharged on hospital day 13 to complete a 4‐week course of intravenous vancomycin. The patient missed an appointment for follow‐up imaging.

DISCUSSION

We report a case of community‐associated MRSA bacteremia secondary to a prostatic abscess, as confirmed by cultures from serum and of the abscess. S. aureus bacteremia often stems from infections of the respiratory tract, skin, and soft tissues, endocarditis, or infections of indwelling devices.4S. aureus can then create embolic foci, including in the prostate, which can serve as sources of persistent bacteremia. However, new evidence suggests community‐associated MRSA might be sexually transmitted among men who have sex with men.5 An MRSA prostatic abscess could then potentially be related to an ascending urinary tract infection or translocation from the gastrointestinal tract.

The vast majority of prostatitis cases prostatic abscesses are caused by Escherichia coli and other gram‐negative bacilli.6 Staphylococcus species are less common, and MRSA isolates have been described as a rare etiologic agent. Only four other case reports describing MRSA bacteremia associated with prostatitis or prostatic abscesses have been published.710 Both our patient and the three other case reports in the literature with prostatic abscesses and MRSA bacteremia required drainage of the abscess as well as antibiotics for resolution. The other reported cases involved drainage by transurethral resection of the prostate,79 whereas our case used transperineal drainage of the prostatic abscess via transrectal ultrasound guidance. In addition to intravenous antibiotics, drainage appears to be a key therapeutic measure for resolution of MRSA prostatic abscesses.

With the increasing incidence of community‐associated and healthcare‐associated MRSA infections, the incidence of prostatitis or prostatic abscesses secondary to MRSA may be increasing. MRSA seems to have a specific predilection for abscess formation in skin and soft‐tissue infections and pneumonia.2 Clinicians must be alert to a potentially higher frequency of MRSA as a cause of prostatic abscesses and prostatitis.

In the evaluation of a patient with persistent MRSA bacteremia, the potential for the prostate as a source of infection should be considered. Urinary symptoms may be subtle. Clinicians should have a low threshold for imaging studies such as CT to evaluate for a possible source of MRSA bacteremia. If a prostatic abscess is found, prompt surgical drainage or debridement is necessary for cure.

Community‐associated methicillin‐resistant Staphylococcus aureus (MRSA) infection is an evolving disease that is changing medical practice. MRSA has become the most frequent cause of skin and soft‐tissue infections presenting to most emergency departments in the United States.1 In comparison with methicillin‐sensitive S. aureus, community‐associated MRSA is more likely to present as soft‐tissue abscesses or necrotizing pneumonia.2 In 2005 alone, 94,360 invasive MRSA infections were estimated to have occurred in the United States, most of which were associated with MRSA bacteremia.3 In the hospital, MRSA infections are associated with greater lengths of stay, higher mortality, and increased costs.3

We report a patient with persistent MRSA bacteremia due to a prostatic abscess. Prostatitis or prostatic abscess with MRSA has rarely been reported. Resolution of the bacteremia was achieved only after drainage of the abscess. This case highlights the importance of recognizing this clinical condition and draining any MRSA‐associated abscesses. In addition, the abscess‐forming characteristics of MRSA may suggest that the incidence of prostatic abscess due to this microbe is on the rise.

CASE REPORT

A 40‐year‐old human immunodeficiency viruspositive man presented with a 10‐day history of intermittent fever, urinary hesitancy, weak urinary stream, and intermittent abdominal pain relieved following urination. He denied dysuria, hematuria, chest pain, dyspnea, nausea, weight loss, diarrhea, or decreased functional status. His last CD4 count was 528/L on highly active antiretroviral therapy 1 year prior to presentation; however, he had run out of medications several months prior to presentation. His medical history was also significant for incision and drainage of skin abscesses with unknown microbiology several months prior to presentation. He currently used tobacco but denied illicit drug use. He was sexually abstinent for over a year prior to presentation but had a history of having unprotected sex with men.

On physical examination, his vital signs were as follows: temperature, 37.8C; blood pressure, 133/84 mm Hg; heart rate, 107 beats/minute; respiration rate, 16 breaths/minute; and oxygen saturation, 100% on room air. He was under no distress. His heart sound was tachycardic and regular with no murmur noted. Lung sounds were clear. Abdominal examination revealed no tenderness or organomegaly. His prostate was boggy, minimally tender, and slightly enlarged. The rest of his physical examination was normal. The white blood cell count was 7.5 10⁹/L with 79% neutrophils. The serum chemistry was normal. The prostate‐specific antigen level was 2.9 ng/mL. A repeat CD4 count was 140/L. Urinalysis revealed large leukocyte esterase, no nitrites, and 60 white blood cells per high‐power field. He was diagnosed with prostatitis and discharged on levofloxacin.

The subsequent day, he returned to the emergency department with an inability to void. A Foley catheter was placed with resolution of his symptoms. Later that day, blood cultures from his initial admission grew MRSA in 2 out of 4 bottles, and he was admitted to the hospital. A review of the prior urine culture showed no growth. Computed tomography (CT) of the abdomen and pelvis showed an enlarged prostate with multiple noncommunicating peripherally enhancing hypodensities consistent with prostatic abscesses (arrows in Figure 1). These abscesses were associated with periprostatic fat stranding, edematous seminal vesicles, diffuse urinary bladder wall thickening, and mild inguinal adenopathy. Therapy with intravenous vancomycin was initiated.

Figure 1

Over the next 6 days, the patient continued to have intermittent fevers. Blood cultures continued to grow MRSA. Gentamicin was added for possible synergy on hospital day 3 without improvement. A transesophageal echocardiogram was normal. On hospital day 6, repeat CT showed no change in the size of the prostatic abscesses but an increased capsular bulge along the right mid gland. The urology service was consulted. They performed bedside transperineal drainage of the largest abscess with transrectal ultrasound guidance. No indwelling drain was placed. A culture of the purulent drainage grew MRSA. Three days after the surgical drainage, the patient was afebrile, urinary symptoms had resolved, and serial blood cultures remained negative. He was discharged on hospital day 13 to complete a 4‐week course of intravenous vancomycin. The patient missed an appointment for follow‐up imaging.

DISCUSSION

We report a case of community‐associated MRSA bacteremia secondary to a prostatic abscess, as confirmed by cultures from serum and of the abscess. S. aureus bacteremia often stems from infections of the respiratory tract, skin, and soft tissues, endocarditis, or infections of indwelling devices.4S. aureus can then create embolic foci, including in the prostate, which can serve as sources of persistent bacteremia. However, new evidence suggests community‐associated MRSA might be sexually transmitted among men who have sex with men.5 An MRSA prostatic abscess could then potentially be related to an ascending urinary tract infection or translocation from the gastrointestinal tract.

The vast majority of prostatitis cases prostatic abscesses are caused by Escherichia coli and other gram‐negative bacilli.6 Staphylococcus species are less common, and MRSA isolates have been described as a rare etiologic agent. Only four other case reports describing MRSA bacteremia associated with prostatitis or prostatic abscesses have been published.710 Both our patient and the three other case reports in the literature with prostatic abscesses and MRSA bacteremia required drainage of the abscess as well as antibiotics for resolution. The other reported cases involved drainage by transurethral resection of the prostate,79 whereas our case used transperineal drainage of the prostatic abscess via transrectal ultrasound guidance. In addition to intravenous antibiotics, drainage appears to be a key therapeutic measure for resolution of MRSA prostatic abscesses.

With the increasing incidence of community‐associated and healthcare‐associated MRSA infections, the incidence of prostatitis or prostatic abscesses secondary to MRSA may be increasing. MRSA seems to have a specific predilection for abscess formation in skin and soft‐tissue infections and pneumonia.2 Clinicians must be alert to a potentially higher frequency of MRSA as a cause of prostatic abscesses and prostatitis.

In the evaluation of a patient with persistent MRSA bacteremia, the potential for the prostate as a source of infection should be considered. Urinary symptoms may be subtle. Clinicians should have a low threshold for imaging studies such as CT to evaluate for a possible source of MRSA bacteremia. If a prostatic abscess is found, prompt surgical drainage or debridement is necessary for cure.

Eight days prior to admission to our hospital, a 50‐year‐old morbidly obese patient presented to his primary care clinic, complaining of weakness, dizziness, and symptoms consistent with paroxysmal nocturnal dyspnea. He had a history of diabetes mellitus type 2, hypertension, chronic renal insufficiency with baseline creatinine in the range of 2.0 mg/dL, and atrial fibrillation on warfarin (10 mg/day). He was given diuretics and sent home. Two days later, the patient presented to a rural emergency department, complaining of leg pain and swelling. He was given cephalexin for cellulitis and discharged home. The evening prior to admission to our hospital, the patient developed sharp left‐sided chest pain, orthopnea, and worsening dyspnea. He again presented to the rural emergency department and was found to have a blood pressure of 60/40 mm Hg. He was admitted and given boluses of intravenous fluids and a dose of ceftriaxone. Laboratory studies at that time demonstrated the following: sodium, 130 mEq/L; potassium, 6.5 mEq/L; CO₂, 21 mEq/L; blood urea nitrogen (BUN), 105 mg/dL; creatinine, 5.5 mg/dL; alkaline phosphatase, 330 IU/L; aspartate aminotransferase (AST), 507 IU/L; and alanine aminotransferase (ALT), 145 IU/L. The following morning, he was oliguric, and his liver transaminases had increased to an AST level of 1862 IU/L and an ALT level of 1055 IU/L. At this point, he was transferred to our hospital for hemodialysis with a diagnosis of acute oliguric renal failure.

On admission to our hospital, the patient was afebrile, had a blood pressure of 112/80 mm Hg, and was hypoxic with an O₂ saturation of 93% on 4 L of oxygen by nasal cannula. His weight was 201 kg. He was alert and cooperative. Heart sounds were distant but had a regular rate and rhythm without murmurs, rubs, or gallops. No jugular venous pulsations were appreciated. He had decreased lung sounds throughout both lung fields. His abdomen was morbidly obese and nontender. Extremities demonstrated chronic venous stasis changes with multiple superficial ulcers and bilateral pitting edema.

In light of the elevated liver function tests reported by the referring hospital, these studies were repeated on arrival, revealing an AST level of 4780 IU/L and an ALT level of 1876 IU/L. Other initial laboratory studies demonstrated a BUN level of 116 mg/dL, a creatinine level of 6 mg/dL, a potassium level of 7.2 mEq/L, negative cardiac enzymes, and an international normalized ratio greater than 9.0. A urinalysis could not be performed because the patient was anuric. An electrocardiogram demonstrated a normal sinus rhythm with a right bundle branch block and nonspecific ST segment and T wave changes. There was no prior electrocardiogram available for comparison. Blood acetaminophen level and infectious hepatitis panels were negative.

Within 1 hour of admission, the patient became hypotensive, with his systolic blood pressure decreasing into the 70s. Over the next 24 hours, the patient was treated with intravenous fluids and pressors (neosynephrine) but remained hypotensive, with his systolic blood pressure in the range of 64 to 80 mm Hg.

At 14 hours after admission, liver function tests were repeated and revealed further elevation of his transaminases (AST, 5135 IU/L; ALT, 2468 IU/L). The diagnosis of shock liver was entertained. A portable chest X‐ray (CXR) demonstrated an enlarged cardiac silhouette suggestive of cardiomegaly or pericardial effusion. No prior CXR was available for comparison. An echocardiogram showed probable effusion but was not diagnostic secondary to his body habitus and poor windows. A computed tomography (CT) scan confirmed a large pericardial effusion. This finding, in combination with diminished heart sounds and hypotension, presented a clinical picture consistent with cardiac tamponade. The patient underwent a subxiphoid pericardial window, and 1.5 L of bloody effusion was removed. Intraoperatively, his systolic blood pressure immediately improved from 95 to 135 mm Hg. Urine output increased from 0 to 80 mL/hour in the first hour. Five days later, his creatinine returned to his baseline of 1.9 mg/dL, and other laboratory values had decreased: AST, 306 IU/L; ALT, 520 IU/L; alkaline phosphatase, 122 IU/L; and BUN, 86 mg/dL.

DISCUSSION

Acute renal failure (ARF) is a common condition, with an incidence of 1% on admission to the hospital; 70% of these cases are due to prerenal causes.1 Among patients already in the hospital, prerenal azotemia is responsible for 21% to 39% of cases of ARF.2, 3 Prerenal ARF is most commonly caused by hypotension, which may be cardiogenic, hypovolemic, septic, or due to vasodilatation. Adrenal insufficiency and other etiologies should also be considered. In our patient, chronic renal failure and superimposed hypotension contributed to acute oliguric renal failure. In searching for the etiology of his hypotension, we concentrated on cardiogenic causes in view of his enlarged cardiac silhouette.

In considering the cardiogenic causes of hypotension, we did not initially focus on tamponade. Although oliguria with renal failure is recognized as a complication of cardiac tamponade, relatively little has been written about ARF as the presenting problem in tamponade. The literature is limited to a few case reports, such as those described by Queffeulou et al.4 and Saklayen et al.5 In our patient, the diagnosis of tamponade was made more difficult by the patient's large size, which made the interpretation of physical findings such as heart sounds more difficult and compromised the quality of essential imaging studies.

His rising transaminases suggested shock liver and eventually provided the key to the patient's diagnosis. In light of his worsening liver function tests, chest pain, shortness of breath, and cardiomegaly on CXR, we focused on a cardiac etiology. An echocardiogram, which often can be used to identify pericardial effusion and hence tamponade, was nondiagnostic because of the patient's obesity. Despite the concerns regarding the weight limits of the examination table, the diagnosis was finally established with a CT scan.

In our patient, no definite cause for his bloody pericardial effusion was found. Cardiac enzymes were negative, and this helped rule out ischemia. Nothing indicative of a neoplasm was seen on the CT of his chest. Blood cultures were negative. Viral studies were not performed, and the effusion was not sent for special studies. He may have had an underlying pericarditis secondary to his chronic kidney disease or a viral syndrome that, combined with his anticoagulation treatment, resulted in a bloody effusion.

In addition to illustrating the difficulties in properly diagnosing acutely ill morbidly obese patients, this report also demonstrates that in patients with shock liver and ARF, pericardial tamponade may be the culprit. If preliminary studies including CXR and echocardiogram are equivocal and sufficient suspicion remains, then a CT is warranted.

Eight days prior to admission to our hospital, a 50‐year‐old morbidly obese patient presented to his primary care clinic, complaining of weakness, dizziness, and symptoms consistent with paroxysmal nocturnal dyspnea. He had a history of diabetes mellitus type 2, hypertension, chronic renal insufficiency with baseline creatinine in the range of 2.0 mg/dL, and atrial fibrillation on warfarin (10 mg/day). He was given diuretics and sent home. Two days later, the patient presented to a rural emergency department, complaining of leg pain and swelling. He was given cephalexin for cellulitis and discharged home. The evening prior to admission to our hospital, the patient developed sharp left‐sided chest pain, orthopnea, and worsening dyspnea. He again presented to the rural emergency department and was found to have a blood pressure of 60/40 mm Hg. He was admitted and given boluses of intravenous fluids and a dose of ceftriaxone. Laboratory studies at that time demonstrated the following: sodium, 130 mEq/L; potassium, 6.5 mEq/L; CO₂, 21 mEq/L; blood urea nitrogen (BUN), 105 mg/dL; creatinine, 5.5 mg/dL; alkaline phosphatase, 330 IU/L; aspartate aminotransferase (AST), 507 IU/L; and alanine aminotransferase (ALT), 145 IU/L. The following morning, he was oliguric, and his liver transaminases had increased to an AST level of 1862 IU/L and an ALT level of 1055 IU/L. At this point, he was transferred to our hospital for hemodialysis with a diagnosis of acute oliguric renal failure.

On admission to our hospital, the patient was afebrile, had a blood pressure of 112/80 mm Hg, and was hypoxic with an O₂ saturation of 93% on 4 L of oxygen by nasal cannula. His weight was 201 kg. He was alert and cooperative. Heart sounds were distant but had a regular rate and rhythm without murmurs, rubs, or gallops. No jugular venous pulsations were appreciated. He had decreased lung sounds throughout both lung fields. His abdomen was morbidly obese and nontender. Extremities demonstrated chronic venous stasis changes with multiple superficial ulcers and bilateral pitting edema.

In light of the elevated liver function tests reported by the referring hospital, these studies were repeated on arrival, revealing an AST level of 4780 IU/L and an ALT level of 1876 IU/L. Other initial laboratory studies demonstrated a BUN level of 116 mg/dL, a creatinine level of 6 mg/dL, a potassium level of 7.2 mEq/L, negative cardiac enzymes, and an international normalized ratio greater than 9.0. A urinalysis could not be performed because the patient was anuric. An electrocardiogram demonstrated a normal sinus rhythm with a right bundle branch block and nonspecific ST segment and T wave changes. There was no prior electrocardiogram available for comparison. Blood acetaminophen level and infectious hepatitis panels were negative.

Within 1 hour of admission, the patient became hypotensive, with his systolic blood pressure decreasing into the 70s. Over the next 24 hours, the patient was treated with intravenous fluids and pressors (neosynephrine) but remained hypotensive, with his systolic blood pressure in the range of 64 to 80 mm Hg.

At 14 hours after admission, liver function tests were repeated and revealed further elevation of his transaminases (AST, 5135 IU/L; ALT, 2468 IU/L). The diagnosis of shock liver was entertained. A portable chest X‐ray (CXR) demonstrated an enlarged cardiac silhouette suggestive of cardiomegaly or pericardial effusion. No prior CXR was available for comparison. An echocardiogram showed probable effusion but was not diagnostic secondary to his body habitus and poor windows. A computed tomography (CT) scan confirmed a large pericardial effusion. This finding, in combination with diminished heart sounds and hypotension, presented a clinical picture consistent with cardiac tamponade. The patient underwent a subxiphoid pericardial window, and 1.5 L of bloody effusion was removed. Intraoperatively, his systolic blood pressure immediately improved from 95 to 135 mm Hg. Urine output increased from 0 to 80 mL/hour in the first hour. Five days later, his creatinine returned to his baseline of 1.9 mg/dL, and other laboratory values had decreased: AST, 306 IU/L; ALT, 520 IU/L; alkaline phosphatase, 122 IU/L; and BUN, 86 mg/dL.

DISCUSSION

Acute renal failure (ARF) is a common condition, with an incidence of 1% on admission to the hospital; 70% of these cases are due to prerenal causes.1 Among patients already in the hospital, prerenal azotemia is responsible for 21% to 39% of cases of ARF.2, 3 Prerenal ARF is most commonly caused by hypotension, which may be cardiogenic, hypovolemic, septic, or due to vasodilatation. Adrenal insufficiency and other etiologies should also be considered. In our patient, chronic renal failure and superimposed hypotension contributed to acute oliguric renal failure. In searching for the etiology of his hypotension, we concentrated on cardiogenic causes in view of his enlarged cardiac silhouette.

In considering the cardiogenic causes of hypotension, we did not initially focus on tamponade. Although oliguria with renal failure is recognized as a complication of cardiac tamponade, relatively little has been written about ARF as the presenting problem in tamponade. The literature is limited to a few case reports, such as those described by Queffeulou et al.4 and Saklayen et al.5 In our patient, the diagnosis of tamponade was made more difficult by the patient's large size, which made the interpretation of physical findings such as heart sounds more difficult and compromised the quality of essential imaging studies.

His rising transaminases suggested shock liver and eventually provided the key to the patient's diagnosis. In light of his worsening liver function tests, chest pain, shortness of breath, and cardiomegaly on CXR, we focused on a cardiac etiology. An echocardiogram, which often can be used to identify pericardial effusion and hence tamponade, was nondiagnostic because of the patient's obesity. Despite the concerns regarding the weight limits of the examination table, the diagnosis was finally established with a CT scan.

In our patient, no definite cause for his bloody pericardial effusion was found. Cardiac enzymes were negative, and this helped rule out ischemia. Nothing indicative of a neoplasm was seen on the CT of his chest. Blood cultures were negative. Viral studies were not performed, and the effusion was not sent for special studies. He may have had an underlying pericarditis secondary to his chronic kidney disease or a viral syndrome that, combined with his anticoagulation treatment, resulted in a bloody effusion.

In addition to illustrating the difficulties in properly diagnosing acutely ill morbidly obese patients, this report also demonstrates that in patients with shock liver and ARF, pericardial tamponade may be the culprit. If preliminary studies including CXR and echocardiogram are equivocal and sufficient suspicion remains, then a CT is warranted.

Eight days prior to admission to our hospital, a 50‐year‐old morbidly obese patient presented to his primary care clinic, complaining of weakness, dizziness, and symptoms consistent with paroxysmal nocturnal dyspnea. He had a history of diabetes mellitus type 2, hypertension, chronic renal insufficiency with baseline creatinine in the range of 2.0 mg/dL, and atrial fibrillation on warfarin (10 mg/day). He was given diuretics and sent home. Two days later, the patient presented to a rural emergency department, complaining of leg pain and swelling. He was given cephalexin for cellulitis and discharged home. The evening prior to admission to our hospital, the patient developed sharp left‐sided chest pain, orthopnea, and worsening dyspnea. He again presented to the rural emergency department and was found to have a blood pressure of 60/40 mm Hg. He was admitted and given boluses of intravenous fluids and a dose of ceftriaxone. Laboratory studies at that time demonstrated the following: sodium, 130 mEq/L; potassium, 6.5 mEq/L; CO₂, 21 mEq/L; blood urea nitrogen (BUN), 105 mg/dL; creatinine, 5.5 mg/dL; alkaline phosphatase, 330 IU/L; aspartate aminotransferase (AST), 507 IU/L; and alanine aminotransferase (ALT), 145 IU/L. The following morning, he was oliguric, and his liver transaminases had increased to an AST level of 1862 IU/L and an ALT level of 1055 IU/L. At this point, he was transferred to our hospital for hemodialysis with a diagnosis of acute oliguric renal failure.

On admission to our hospital, the patient was afebrile, had a blood pressure of 112/80 mm Hg, and was hypoxic with an O₂ saturation of 93% on 4 L of oxygen by nasal cannula. His weight was 201 kg. He was alert and cooperative. Heart sounds were distant but had a regular rate and rhythm without murmurs, rubs, or gallops. No jugular venous pulsations were appreciated. He had decreased lung sounds throughout both lung fields. His abdomen was morbidly obese and nontender. Extremities demonstrated chronic venous stasis changes with multiple superficial ulcers and bilateral pitting edema.

In light of the elevated liver function tests reported by the referring hospital, these studies were repeated on arrival, revealing an AST level of 4780 IU/L and an ALT level of 1876 IU/L. Other initial laboratory studies demonstrated a BUN level of 116 mg/dL, a creatinine level of 6 mg/dL, a potassium level of 7.2 mEq/L, negative cardiac enzymes, and an international normalized ratio greater than 9.0. A urinalysis could not be performed because the patient was anuric. An electrocardiogram demonstrated a normal sinus rhythm with a right bundle branch block and nonspecific ST segment and T wave changes. There was no prior electrocardiogram available for comparison. Blood acetaminophen level and infectious hepatitis panels were negative.

Within 1 hour of admission, the patient became hypotensive, with his systolic blood pressure decreasing into the 70s. Over the next 24 hours, the patient was treated with intravenous fluids and pressors (neosynephrine) but remained hypotensive, with his systolic blood pressure in the range of 64 to 80 mm Hg.

At 14 hours after admission, liver function tests were repeated and revealed further elevation of his transaminases (AST, 5135 IU/L; ALT, 2468 IU/L). The diagnosis of shock liver was entertained. A portable chest X‐ray (CXR) demonstrated an enlarged cardiac silhouette suggestive of cardiomegaly or pericardial effusion. No prior CXR was available for comparison. An echocardiogram showed probable effusion but was not diagnostic secondary to his body habitus and poor windows. A computed tomography (CT) scan confirmed a large pericardial effusion. This finding, in combination with diminished heart sounds and hypotension, presented a clinical picture consistent with cardiac tamponade. The patient underwent a subxiphoid pericardial window, and 1.5 L of bloody effusion was removed. Intraoperatively, his systolic blood pressure immediately improved from 95 to 135 mm Hg. Urine output increased from 0 to 80 mL/hour in the first hour. Five days later, his creatinine returned to his baseline of 1.9 mg/dL, and other laboratory values had decreased: AST, 306 IU/L; ALT, 520 IU/L; alkaline phosphatase, 122 IU/L; and BUN, 86 mg/dL.

DISCUSSION

Acute renal failure (ARF) is a common condition, with an incidence of 1% on admission to the hospital; 70% of these cases are due to prerenal causes.1 Among patients already in the hospital, prerenal azotemia is responsible for 21% to 39% of cases of ARF.2, 3 Prerenal ARF is most commonly caused by hypotension, which may be cardiogenic, hypovolemic, septic, or due to vasodilatation. Adrenal insufficiency and other etiologies should also be considered. In our patient, chronic renal failure and superimposed hypotension contributed to acute oliguric renal failure. In searching for the etiology of his hypotension, we concentrated on cardiogenic causes in view of his enlarged cardiac silhouette.

In considering the cardiogenic causes of hypotension, we did not initially focus on tamponade. Although oliguria with renal failure is recognized as a complication of cardiac tamponade, relatively little has been written about ARF as the presenting problem in tamponade. The literature is limited to a few case reports, such as those described by Queffeulou et al.4 and Saklayen et al.5 In our patient, the diagnosis of tamponade was made more difficult by the patient's large size, which made the interpretation of physical findings such as heart sounds more difficult and compromised the quality of essential imaging studies.

His rising transaminases suggested shock liver and eventually provided the key to the patient's diagnosis. In light of his worsening liver function tests, chest pain, shortness of breath, and cardiomegaly on CXR, we focused on a cardiac etiology. An echocardiogram, which often can be used to identify pericardial effusion and hence tamponade, was nondiagnostic because of the patient's obesity. Despite the concerns regarding the weight limits of the examination table, the diagnosis was finally established with a CT scan.

In our patient, no definite cause for his bloody pericardial effusion was found. Cardiac enzymes were negative, and this helped rule out ischemia. Nothing indicative of a neoplasm was seen on the CT of his chest. Blood cultures were negative. Viral studies were not performed, and the effusion was not sent for special studies. He may have had an underlying pericarditis secondary to his chronic kidney disease or a viral syndrome that, combined with his anticoagulation treatment, resulted in a bloody effusion.

In addition to illustrating the difficulties in properly diagnosing acutely ill morbidly obese patients, this report also demonstrates that in patients with shock liver and ARF, pericardial tamponade may be the culprit. If preliminary studies including CXR and echocardiogram are equivocal and sufficient suspicion remains, then a CT is warranted.