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Anesthetizing a Patient with Escalating Cardiac Enzyme Levels for Urgent Noncardiac Surgery

Clinical and Ethical Concerns

Ramarapu, Srikiran MD

doi: 10.1213/XAA.0000000000000168
Case Reports: Case Report

An 81-year-old man with a history of villous adenoma of the duodenum was admitted with new-onset jaundice, abdominal pain, and pruritus, which raised concerns about disease progression and hepatobiliary obstruction. The patient had refused surgical resection of tumor on initial diagnosis 2 years earlier and opted out of it again at the current presentation because of his significant comorbidities. While discussing treatment options with his family, he developed symptoms suggesting myocardial infarction. Therefore, before anesthetizing this patient with escalating cardiac enzyme levels for an urgent noncardiac procedure, it was important to attend to the dynamics of the decision-making process.

From the Department of Anesthesiology, The University of Oklahoma College of Medicine, Oklahoma City, Oklahoma.

Accepted for publication January 31, 2015.

Funding: None.

The author declares no conflicts of interest.

Address correspondence to Srikiran Ramarapu, MD, Department of Anesthesiology, The University of Oklahoma College of Medicine, 750 N.E. 13th St., Suite 200, Oklahoma City, OK 73104. Address e-mail to

Elevated cardiac enzyme levels almost always signal an adverse cardiac event. The situation demands particular attention if the patient requires an urgent noncardiac procedure. We report an interesting case in which various clinical and ethical questions had to be addressed to produce an optimal outcome.

The patient gave written consent for the use of his medical information in this report.

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An 81-year-old man with a history of villous adenoma of the duodenum was admitted with new-onset jaundice, abdominal pain, decreased appetite, pruritus, and weight loss, which raised concerns about disease progression and hepatobiliary obstruction. On initial evaluation, his total bilirubin level was 25 mg/dL, and his liver enzyme levels were elevated, suggesting cholestasis. Abdominal computed tomography showed marked biliary obstruction at the ampulla/pancreatic head; the morphology of the distal duct suggested malignant stricture. His medical history was significant for hypertension, 2-vessel coronary artery disease (CAD), atrial fibrillation, sick sinus syndrome, moderate aortic stenosis, aortic insufficiency, peripheral vascular disease, chronic obstructive pulmonary disease, benign prostatic hypertrophy, depression, and Crohn disease. His surgical history was significant for endovascular repair of an infrarenal abdominal aortic aneurysm, placement of a permanent pacemaker, endoscopic retrograde cholangiopancreatography, and multiple repairs of anal fistula. The patient had refused surgical resection of tumor on initial diagnosis 2 years earlier, and he opted out of it again during the current presentation because of his significant comorbidities.

During the time the patient was discussing treatment options with his family, he developed hypotension and fever. He was transferred to the intensive care unit to be treated for possible sepsis and ascending cholangitis. He required norepinephrine administered at a rate of 2 μg/min for 6 hours, and then was able to maintain hemodynamic stability while receiving IV fluids and antibiotic therapy. A 12-lead electrocardiogram showed minimal ST changes, but his cardiac enzyme levels were now significantly elevated: His troponin-I and creatine kinase-MB (CK-MB) levels had risen to 7.99 and 76.2 ng/mL, respectively. Bedside transthoracic echocardiography showed moderate to severe aortic stenosis, moderate aortic insufficiency, moderate mitral regurgitation, left ventricular hypertrophy, and an estimated left ventricular ejection fraction of 55% to 60%. Although no diagnostic regional wall motion abnormality was identified, the possibility of acute coronary syndrome (ACS) could not be completely excluded on the basis of this study.

Given the rapid rise of the patient’s cardiac enzyme levels, a diagnosis of non–ST-segment elevation myocardial infarction (NSTEMI) was made and an ACS protocol was initiated. A sliding-scale insulin regimen was started to maintain blood glucose between 110 and 180 mg/dL. After 24 hours, his troponin-I and CK-MB levels had decreased to 5.77 and 16.3 ng/mL, respectively. The patient refused further aggressive treatment to optimize his cardiac condition and requested placement of a biliary stent for palliation.

After 48 hours, he developed acute kidney injury, along with gram-negative bacteremia and lactic and metabolic acidosis. His platelet count rapidly decreased by more than 50%. Heparin-induced thrombocytopenia was suspected. However, a heparin-induced platelet antibody was negative. The cardiologist opined that the patient would benefit from early percutaneous coronary intervention (PCI) for his CAD, but stent deployment would necessitate uninterrupted clopidogrel administration for at least 1 month, potentially increasing the risk of bleeding associated with subsequent invasive procedures. The gastroenterologist suggested that the patient would benefit from early endoscopic retrograde cholangiopancreatography and placement of a biliary stent before PCI.

After a discussion among the patient, gastroenterologist, interventional radiologist, cardiologist, intensivist, oncologist, and anesthesiologist, the patient gave informed consent to undergo endoscopic placement of a biliary stent as a palliative procedure under general anesthesia. He tolerated the procedure uneventfully, but because of the severely distorted anatomy of his duodenum/ampulla, stent placement was unsuccessful. Later, a percutaneous biliary drain was successfully placed by the interventional radiologist without complications. The patient declined any further interventions and opted for palliative care.

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At the patient’s index presentation, several issues required immediate attention. First, we needed to determine whether he was really having an acute coronary event, as suggested by his escalating cardiac enzyme levels and history of CAD. Troponin I is a well-established, specific, and sensitive marker of myocardial injury, with both diagnostic and prognostic value. It permits early identification of patients at increased risk of death from ACS.1 In addition, this patient’s CK-MB values were elevated. Both peak CK-MB and peak troponin I levels are independently associated with in-hospital mortality among patients with acute myocardial infarction.2 However, this event coincided with the onset of fever, indicating sepsis and ascending cholangitis. Using additional biomarkers of NSTEMI may have helped us to better differentiate between cardiac and noncardiac reasons for the patient’s elevated troponin I level.

Second, we needed to ascertain whether the elevation in the patient’s cardiac enzyme levels might have a noncardiac cause. Troponin-I elevation occurs in 60% to 75% of patients with acute liver failure, and its cause is probably multifactorial.3 Troponin-I elevation observed in a patient with acute liver failure may therefore not represent true myocardial injury and may be better viewed as a marker of metabolic stress. It has been postulated that intracellular pathways may be triggered in critically ill patients, resulting in degradation of free troponin to lower-molecular-weight fragments, which are released because of increased cell membrane permeability. Patients with troponin I levels higher than 3.0 ng/mL have a poor prognosis.4 An unexpectedly high troponin level may also be a false-positive result. Chimeric monoclonal antibodies used in the treatment of Crohn disease (infliximab) can potentially cause such false positives.5–8 In addition, a case report by Maghamiour and Safaie9 showed that high CK-MB and lactate dehydrogenase levels in the absence of myocardial injury or infarction could occur in patients with liver disease.

Third, we had to determine whether this patient would benefit from urgent left heart catheterization and management of his CAD. New-onset NSTEMI in a patient with known CAD would be a good indication for early PCI. A previous study by Azarbal et al.10 showed the safety and feasibility of PCI in a small cohort of patients with end-stage liver disease and hemodynamically significant CAD, the majority of whom had significant thrombocytopenia. However, any coronary intervention would require uninterrupted anticoagulation, which potentially increases the risk of bleeding during all subsequent invasive procedures.

Fourth, we had to select appropriate invasive monitoring techniques and vasopressor drugs to use during the procedure. The patient had a thrombolysis in myocardial infarction score of 5 and an estimated 26% risk at 14 days of all-cause mortality, new or recurrent myocardial infarction, or severe recurrent ischemia requiring urgent revascularization.11 His preexisting moderate to severe aortic stenosis, pacemaker dependence for sick sinus syndrome, and recent NSTEMI necessitated the use of invasive arterial and central venous pressure monitoring to optimize the anesthetic management. Transesophageal echocardiography could give more information about new regional wall motion abnormalities, valvular function, and ejection fraction. Norepinephrine, which acts on both alpha and beta adrenergic receptors, was probably the most appropriate vasopressor to use.

Fifth, we needed to determine whether the patient really wanted to have biliary stent placement as part of palliative care, which required stopping heparin infusion during the procedure. Ethical concerns emerged when the patient refused management of his coronary disease after initiating an ACS protocol. It was difficult to select the optimal time of the biliary stent procedure in view of the patient’s reluctance to continue his cardiac care.

Finally, we needed to know why the patient wanted to have a general anesthetic during placement of the biliary stent. An earlier endoscopic retrograde cholangiopancreatography was unsuccessful under sedation due to limited sedation provided by the gastroenterology team. Therefore, the patient was unhappy with the technique and requested a general anesthetic. However, general anesthesia could have significantly increased his risk, especially after the onset of NSTEMI and sepsis. Teh et al.12 found that American Society of Anesthesiologists class significantly predicted increased mortality and morbidity among patients with cirrhosis who underwent major abdominal, orthopedic, or cardiovascular surgery; in this study, American Society of Anesthesiologists class V was the strongest predictor of postoperative mortality at 7 days.

Due to his comorbidities, the patient was at high risk for a perioperative cardiac event, even before his troponin level had increased, whether general anesthesia or another technique was selected. When NSTEMI is suspected, baseline and serial estimation of troponin I level, in combination with other biomarkers (e.g., CK-MB levels), is a reasonable approach to differentiate cardiac from noncardiac causes of elevation of cardiac enzymes (e.g., significant liver disease, peripheral vascular disease, or Crohn disease).

In conclusion, the dynamics of the decision-making processes were extremely important in this patient with NSTEMI, since the risk of perioperative death was potentially high. Such issues are paramount in geriatric medicine. Indeed, we have superb anesthetic drugs and surgical techniques, but we need to listen to the wishes of our patients.

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1. Cardinale D, Sandri MT, Colombo A, Colombo N, Boeri M, Lamantia G, Civelli M, Peccatori F, Martinelli G, Fiorentini C, Cipolla CM. Prognostic value of troponin I in cardiac risk stratification of cancer patients undergoing high-dose chemotherapy. Circulation. 2004;109:2749–54
2. Chin CT, Wang TY, Li S, Wiviott SD, deLemos JA, Kontos MC, Peterson ED, Roe MT. Comparison of the prognostic value of peak creatine kinase-MB and troponin levels among patients with acute myocardial infarction: a report from the Acute Coronary Treatment and Intervention Outcomes Network Registry-get with the guidelines. Clin Cardiol. 2012;35:424–9
3. Jaber S, Paugam-Burtz C. Acute liver failure and elevated troponin-I: controversial results and significance? Crit Care. 2013;17:102
4. Parekh NK, Hynan LS, De Lemos J, Lee WMAcute Liver Failure Study Group. Acute Liver Failure Study Group. . Elevated troponin I levels in acute liver failure: is myocardial injury an integral part of acute liver failure? Hepatology. 2007;45:1489–95
5. Kricka LJ. Human anti-animal antibody interferences in immunological assays. Clin Chem. 1999;45:942–56
6. Fitzmaurice TF, Brown C, Rifai N, Wu AH, Yeo KT. False increase of cardiac troponin I with heterophilic antibodies. Clin Chem. 1998;44:2212–4
7. Targan SR, Hanauer SB, van Deventer SJ, Mayer L, Present DH, Braakman T, DeWoody KL, Schaible TF, Rutgeerts PJ. A short-term study of chimeric monoclonal antibody cA2 to tumor necrosis alpha for Crohn’s disease. N Engl J Med. 1997;337:1029–36
8. Present DH, Rutgeerts P, Targan S, Hanauer SB, Mayer L, van Hogezand RA, Podolsky DK, Sands BE, Braakman T, DeWoody KL, Schaible TF, van Deventer SJ. Infliximab for the treatment of fistulas in patients with Crohn’s disease. N Engl J Med. 1999;340:1398–405
9. Maghamiour N, Safaie N. High creatine kinase (CK)-MB and lactate dehydrogenase in the absence of myocardial injury or infarction: a case report. J Cardiovasc Thorac Res. 2014;6:69–70
10. Azarbal B, Poommipanit P, Arbit B, Hage A, Patel J, Kittleson M, Kar S, Kaldas FM, Busuttil RW. Feasibility and safety of percutaneous coronary intervention in patients with end-stage liver disease referred for liver transplantation. Liver Transpl. 2011;17:809–13
11. Antman EM, Cohen M, Bernink PJ, McCabe CH, Horacek T, Papuchis G, Mautner B, Corbalan R, Radley D, Braunwald E. The TIMI risk score for unstable angina/non-ST elevation MI: a method for prognostication and therapeutic decision making. JAMA. 2000;284:835–42
12. Teh SH, Nagorney DM, Stevens SR, Offord KP, Therneau TM, Plevak DJ, Talwalkar JA, Kim WR, Kamath PS. Risk factors for mortality after surgery in patients with cirrhosis. Gastroenterology. 2007;132:1261–9
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