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Year : 2014  |  Volume : 41  |  Issue : 2  |  Page : 140-142

Raised cardiac enzymes in sepsis with renal failure: An encompassing umbrella or a masquerader?

1 Department of Internal Medicine, Princess Durru Shehvar Children's and General Hospital, Hyderabad, India
2 Department of Nephrology, Medwin Hospital, Hyderabad, India

Date of Web Publication20-May-2014

Correspondence Address:
Dilip Gude
Department of Internal Medicine, Princess Durru Shehvar Children's and General Hospital, Hyderabad
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Source of Support: Princess Durru Shehvar Children’s and General Hospital Hyderabad, AP, India, Conflict of Interest: None

DOI: 10.4103/0974-5009.132869

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Elevation of cardiac enzymes and troponins particularly in settings of sepsis and renal failure may cloud the diagnostic picture of acute coronary syndrome in many cases. Interpretation of such elevated enzymes thus warrants caution. It necessitates adequate awareness amongst clinicians, of conditions with such elevation in the absence of myocardial ischemia/infarction as well as those that harbinger false positives. We discuss one such case that posed a diagnostic dilemma and review the pertinent literature.

Keywords: Renal failure, sepsis, troponins

How to cite this article:
Gude D, Zubair MA, Abbas A, Jha R, Mohiuddin H. Raised cardiac enzymes in sepsis with renal failure: An encompassing umbrella or a masquerader?. J Sci Soc 2014;41:140-2

How to cite this URL:
Gude D, Zubair MA, Abbas A, Jha R, Mohiuddin H. Raised cardiac enzymes in sepsis with renal failure: An encompassing umbrella or a masquerader?. J Sci Soc [serial online] 2014 [cited 2021 Jul 29];41:140-2. Available from: https://www.jscisociety.com/text.asp?2014/41/2/140/132869

  Introduction Top

A number of conditions other than acute myocardial infarction (AMI) have been known to cause elevations in cardiac enzymes and troponins. In such conditions, it is of paramount importance to rule out the associated myocardial injury, if any. The situation demands a keen eye in the assessment of the significance of elevated cardiac enzymes. We exemplify with a case that presented with sepsis and renal failure sporting elevated cardiac enzymes and normal coronaries.

  Case Report Top

A 45-year-old female, non-diabetic, non-hypertensive presented with 2 day history of watery diarrhea associated with pain in the abdomen. Physical examination revealed sunken eyes, dry tongue, loss of skin turgor and cold clammy extremities. Blood pressure (BP) was 70/50 mm of Hg in right upper limb; heart rate 110/min; respiratory rate was 28/min. Cardiorespiratory exam was unremarkable except for tachycardia. Abdominal exam revealed increased bowel sounds and no tenderness. Complete blood picture demonstrated Hemoglobin-12.9 g%, Total white blood cell count (TWBC)-38,900/mm 3 , platelets-6,50,000/mm 3 . Renal function tests showed urea-44 mg/dl and creatinine-2.8 mg/dl; Serum electrolytes showed Na-124 mEq, K-5.4 mEq, and Cl-100 m Eq. Blood cultures were sent for analysis and patient was started on meropenem 1 g 8 th h and linezolid 600 mg 12 th h. Twelve lead Electrocardiogram (ECG) showed non-specific ST changes (ST depression in lead I and AVL and T wave inversions in AVF and V1). Cardiac enzymes were raised (CK-MB 129 IU/L) and troponin-T was raised at 0.2 ng/ml (normal value < 0.01 ng/ml) and troponin-I was 0.8 ng/ml (normal value <0.1 ng/ml) respectively. Lactate dehydrogenase (LDH) was 3,354 IU/L and Aspartate aminotransaminase-1150 IU/L. There was no urine output for the first 24 h. Arterial blood gas analysis showed PH of 7.06 and HCO 3 at 8.6 mmol/L. Her acute physiology and chronic health evaluation (APACHE) II score at admission was 23-signifying about 40% non-operative mortality. Blood cultures grew Klebsiella oxytoca sensitive to meropenem, which was then continued for a total of 7 days. A provisional diagnosis of acute gastroenteritis with severe dehydration, lactic acidosis and pre-renal failure with probable non-ST elevation myocardial infarction was made.

Anticoagulation with aspirin, clopidogrel and low-molecular weight heparin was started. Right sub clavian central venous access was gained (initial central venous pressure being 1 cm), and aggressive rehydration and inotropic support were given. BP improved to 110/70 mmHg in the next 12-16 h. 2D Echocardiogram showed no abnormality with left ventricular function being normal (EF of 68%) and no regional wall motion abnormalities. Serial CK-MB values showed a decreasing trend and the troponin assays were negative the next day.

Hemodynamic improvement was followed by clinical improvement over the subsequent 2-3 days. Anuria improved mildly to an output of 350 and 700 ml per day over the next two days while creatinine worsened to 3.4 mg/dl and 5.5 mg/dl over 2 days. Patient underwent hemodialysis due to the worsening azotemia. ECG changes reverted to normal and 2D echo repeated after 4 days was normal. Patient underwent coronary angiography a month later and was found to have normal coronaries. At a last follow-up two months later her creatinine remained at a baseline of 2.2 mg/dl.

  Discussion Top

Elevated troponin levels are found in acute pulmonary embolism, acute pericarditis, acute or severe heart failure, myocarditis, sepsis and/or shock, and renal failure. Erroneous elevation of cardiac enzymes (false positive) have been reported in literature due to heterophilic antibodies, rheumatoid factor, fibrin clots and micro particles and/or analyzer malfunction. [1] Especially in end-stage renal disease (ESRD) false positive elevations of serum cardiac troponin-T cTnT are seen in about 82% with significantly high levels. [2] On the other hand, cTnI is known to have lesser false positive rate in diagnosing myocardial injury in renal failure. Left ventricular hypertrophy, endothelial dysfunction, loss of membrane integrity with leakage of the free cytosolic troponin pool, stretch-mediated troponin release, and impaired renal excretion are hypothesized to cause troponin elevations (with or without myocardial infarction). [3] Studies show that elevated troponin levels in asymptomatic patients with ESRD are highly predictive of all-cause mortality and highly prognostic for both short-term and long-term outcomes. Renal failure is also known to cause elevations in CK-MB without evidence of myocardial injury. [4]

Although extensive literature is lacking on elevation of cardiac enzymes and troponins in acute kidney injury (as opposed to chronic), our case is a classic example of raised cardiac enzymes and troponins (along with ECG changes) with no evidence of myocardial infarction. The conditions causing false positives were ruled out in our case (specific lack of rheumatoid factor, hemolysis, equipment malfunction, etc.). Septic shock and renal failure are probably the culprits for the elevated cardiac enzymes and troponins raising false alarms for acute coronary syndrome.

Infections may act on plaque vulnerability through systemic inflammation and especially in the presence of pre-disposing factors; heighten the risk for coronary events. Apart from inflammation, infections may precipitate acute coronary events via hypotension (in septic shock), hyperocagulable states, quantitative/qualitative platelet dysfunction, etc. A study showed that patients with three or more risk-factors had a relative risk for myocardial infarction after gastroenteritis of 2.08. [5] Ischemia and reperfusion injury of the myocardium in sepsis may be triggered by the cardiac myocytotoxic local and circulating mediators (e.g., cytokines or reactive oxygen species), myocardial injury from bacterial endotoxins and dysfunction of the microcirculation. A case of febrile viral gastroenteritis (documented Coxsackie B2 virus infection) with acute posterior myocardial infarction related to a right coronary artery thrombosis was reported. [6] Coxsackie B2 myocarditis was believed to have triggered a coronary artery spasm and subsequent thrombosis. Myocarditis was less likely in our case given the normal findings of 2D Echo. A study on 1196 patients showed that there is a significant correlation of the distribution of AMI to acute systemic infections cases. [7] Gastroenteritis and the resultant sepsis (secondary to Klebsiella oxytoca) in our patient definitely placed her at high-risk for AMI and convoluted the presentation.

Published literature confirms previous instances of elevated of cardiac troponin in critically ill sepsis patients without demonstrable myocardial infarction. Streptococcus pneumoniae infection was the cause of sepsis in 41% of TnI-positive patients in one study, whereas Gram-negative bacteria were incriminated in 63% of cases in another study. [8],[9] Elevations of troponin in sepsis appear to correlate with severity of the disease process (degree of hypotension and APACHE II score). [9],[10],[11] This holds true in our case as the high levels of troponins reflected her severe hypotension and high APACHE II score of 23 at admission.

  Conclusion Top

We advocate utmost caution in interpreting the raised cardiac enzymes in the presence of renal failure erroneously triggering a diagnosis of myocardial infarction/acute coronary syndrome. Administering unwarranted and aggressive anticoagulation in the presence of pre-existing coagulation dysfunction (thrombocytopenia, defective platelet function in azotemia/uremia etc.) may contribute to the overall morbidity/mortality. Conversely, early treatment of acute coronary event is warranted to limit overall morbidity. For diagnosing myocardial damage among patients with sepsis and/or renal failure (as in our case) serial measurements of cTnI in conjunction with other modalities such as serial echocardiography combined with frequent meticulous assessment of the over-all clinical picture would ensure appropriate tailoring of therapy to ensure a good outcome.

  Acknowledgments Top

We thank our colleagues and staff of the department of Internal medicine for their perpetual support.

  References Top

1.Roongsritong C, Warraich I, Bradley C. Common causes of troponin elevations in the absence of acute myocardial infarction: Incidence and clinical significance. Chest 2004;125:1877-84.  Back to cited text no. 1
2.Apple FS, Murakami MM, Pearce LA, Herzog CA. Predictive value of cardiac troponin I and T for subsequent death in end-stage renal disease. Circulation 2002;106:2941-5.  Back to cited text no. 2
3.White HD. Pathobiology of troponin elevations: Do elevations occur with myocardial ischemia as well as necrosis? J Am Coll Cardiol 2011;57:2406-8.  Back to cited text no. 3
4.Mannem SR, Ehtesham M, Praveen K, Gupta V. Elevated ck-mb without myocardial infarction. Sci Med 2009;1(2). Retrieved from http://scientificmedicineonline.org/index.php?journal=smo&page=article&op=viewFile&path%5B%5D=35&path%5B%5D=30   Back to cited text no. 4
5.Baylin A, Hernandez-Diaz S, Siles X, Kabagambe EK, Campos H. Triggers of nonfatal myocardial infarction in Costa Rica: Heavy physical exertion, sexual activity, and infection. Ann Epidemiol 2007;17:112-8.  Back to cited text no. 5
6.Liapounova NA, Mouquet F, Ennezat PV. Acute myocardial infarction spurred by myopericarditis in a young female patient: Coxsackie B2 to blame. Acta Cardiol 2011;66:79-81.  Back to cited text no. 6
7.Moschos N, Christoforaki M, Antonatos P. Seasonal distribution of acute myocardial infarction and its relation to acute infections in a mild climate. Int J Cardiol 2004;93:39-44.  Back to cited text no. 7
8.Ammann P, Fehr T, Minder EI, Günter C, Bertel O. Elevation of troponin I in sepsis and septic shock. Intensive Care Med 2001;27:965-9.  Back to cited text no. 8
9.ver Elst KM, Spapen HD, Nguyen DN, Garbar C, Huyghens LP, Gorus FK. Cardiac troponins I and T are biological markers of left ventricular dysfunction in septic shock. Clin Chem 2000;46:650-7.  Back to cited text no. 9
10.Spies C, Haude V, Fitzner R, Schröder K, Overbeck M, Runkel N, et al. Serum cardiac troponin T as a prognostic marker in early sepsis. Chest 1998;113:1055-63.  Back to cited text no. 10
11.Arlati S, Brenna S, Prencipe L, Marocchi A, Casella GP, Lanzani M, et al. Myocardial necrosis in ICU patients with acute non-cardiac disease: A prospective study. Intensive Care Med 2000;26:31-7.  Back to cited text no. 11


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