Article, Emergency Medicine

Urosepsis-induced takotsubo

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American Journal of Emergency Medicine

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Urosepsis-induced takotsubo?,??

Abstract

Urinary tract infections are vigorously encountered by emergency department physicians with a wide continuum of presentation ranging from simple cystitis to severe sepsis and septic shock. Nevertheless, there are scant data in the literature reporting on urosepsis-induced takotsubo cardiomyopathy (TC). The high preva- lence of UTI admissions and the occasional seriousness of TC warrant the awareness of this complication. We present a case of urosepsis that was complicated by acute heart failure due to TC.

A 42-year-old woman with a medical history of hypertension and dyslipidemia who recently completed a course of ciprofloxacin for urinary tract infection presented to the emergency department (ED) with suprapubic and flank pain, fever, chills, rigors, nausea, and vomiting. Her vital signs were significant for a heart rate of 150 beats per minute, blood pressure of 110/80 mm Hg, temperature of 35.2?C, and oxygen saturation of 97% on room air. On physical examination, she was having rigors, suprapubic and right costovertebral angle tenderness, and no clinical signs of heart failure. urine analysis showed evidence of UTI, and computed tomographic scan of the abdomen revealed Perinephric stranding surrounding the right kidney con- forming to acute pyelonephritis. Laboratory workup showed a white blood cell count of 37,000 [normal (N) 4.8-10.8], hemoglobin 16.5 g/dL (N 12-15), platelet count 470,000/mm3 (N 150,000-450,000), lactic acid 6.4 mmol/L (N 0.36-2), blood urea nitrogen 23 mg/dL (N 6-24), creatinine 1.63 mg/dL (N 0.4-1), and bicarbonate level 21 mmol/L (N 22-32). Interestingly, serum troponin I was 6.78 ng/mL (N b 0.06), creatine kinase (CK) 251 IU/L (N 20-220), CK-myocardial band 21.5 (N b 5.9), and B-type natriuretic peptide was 2547 pg/mL (N 0-178). An electrocardiogram (ECG) showed sinus tachycardia without signs of ischemia (Fig. A).

Because of absence of chest pain and ischemic ECG changes, it was thought that this Troponin elevation represent Non-ST-segment elevation myocardial infarction type II due to demand ischemia from urosepsis. Moreover, she had recently had an exercise stress test that was normal. The patient was managed with broad spectrum antibiotics, hydration in addition to aspirin, ? blocker, and heparin infusion. Twelve hours after admission, the patient became hypoxic with signs of clinical overload requiring a non-rebreather mask and intravenous diuresis to maintain her oxygen saturation above 90%. On the second hospital day, she started experiencing episodes of chest pain for which repeat ECG revealed widespread deep T-wave inversion with prolongation of corrected QT (QTc) interval raising

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suspicion for takotsubo cardiomyopathy (TC) (Fig. B). Her echocar- diogram showed a dilated Left ventricle with severely reduced ejection fraction to 30%, apical, and anteroseptal hypokinesis. To rule out occlusive coronary artery disease (CAD), coronary angiography was performed showing normal coronaries. The patient has been maintained on antifailure measures including furosemide, metopro- lol, lisinopril in addition to aspirin. Follow-up ECG 1 week later showed resolution of T-wave inversion (Fig. C), and repeat echocar- diogram confirmed recovery of LV function.

Urinary tract infection is estimated to account for 2.7 million ED visits yearly of which 16.7% get admitted to the hospital for further management [1]. The occurrence of TC triggered by UTI has been rarely reported. Interestingly, both reported cases occurred in elderly males after prostatic biopsy in 1 case, and prostatitis in a second case. Karvouniaris et al [2] reported a case of pyelonephritis caused by Escherichia coli producing extended spectrum ?-lacta- mase after a transrectal Prostate biopsy that had been performed 6 days earlier. Santoro et al [3] reported a case of urosepsis caused by Staphylococcus gallinarum in a 63-year-old male thought to have Acute prostatitis. Both cases responded well to antibiotics and levosimendan infusion (for hemodynamic support) and were successfully discharged from the hospital. There are another 2 reported cases of urosepsis with a picture of TC; however, the significantly Elevated blood pressure in both cases prompted further workup that confirmed the diagnosis of pheochromocytoma [4,5]. Although TC is estimated to account for 2% of patients presenting with acute coronary syndrome [6], it is now being increasingly recognized due to improved awareness with this clinicopathologic entity. Despite a favorable course in most cases of TC with recovery of the LV function within 4 to 6 weeks, complications occur in 18.9% of the cases, and mortality rate is 3.2% [7]. Reported complications include–but are not limited to– cardiogenic shock, stroke from an LV thrombus [8], arrhythmia- induced cardiac arrest [9], cardiac tamponade [10], and Cardiac rupture [11]. This highlights the importance of early recognition of the disorder through awareness of the ECG features that raise suspicion for TC [12] to decrease morbidity and mortality. In the presented case, TC was strongly suspected for several reasons: a recent normal cardiac stress test, the presence of underlying stressor (urosepsis), ECG evolution to widespread deep T-wave inversion with prolongation of the QTc interval, modest troponin elevation, and an echocardiogram showing severe LV dysfunction in the presence of normal coronaries. Takotsubo cardiomyopathy is therefore a possible complication of urosepsis and should be suspected when LV dysfunction, elevated cardiac biomarkers, and suspicious ECG changes are present. In this instance, a coronary angiogram is still mandatory to rule out occlusive CAD of which consequences can be fatal if missed.

0735-6757/(C) 2014

image of Fig

Fig. Evolution of ECG changes in a case of urosepsis-induced takotsubo. Electrocardiogram on admission showing sinus tachycardia (A); ECG 24 hours later (coinciding with chest pain and pulmonary edema) showing widespread T-wave inversion and prolongation of QTc calculated as 479 milliseconds (B); ECG 1 week later (after resolution of symptoms) showing resolution of T-wave inversion and QTc prolongation (C).

Hesham R. Omar, MD Internal Medicine Department Mercy Medical Center

Clinton, IA, USA E-mail address: [email protected]

Devanand Mangar, MD

Tampa General Hospital

Tampa, FL, USA

Enrico M. Camporesi, MD

Molecular Pharmacology and Physiology

Tampa General Hospital

Tampa, FL, USA

http://dx.doi.org/10.1016/j.ajem.2014.01.036

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