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Year : 2021  |  Volume : 15  |  Issue : 4  |  Page : 343-345

Hypoxemia with stress cardiomyopathy following liver transplant: Is there a role for nitric oxide? - A case report

Department of Anaesthesia and Critical Care, Amrita Institute of Medical Sciences, Amrita Vishwa Vidyapeetham, Kochi, Kerala, India

Date of Submission02-Jun-2020
Date of Decision22-Nov-2020
Date of Acceptance12-Dec-2020
Date of Web Publication30-Dec-2021

Correspondence Address:
Dr. Anandajith P Kartha
Department of Anaesthesia and Critical Care, Amrita Institute of Medical Sciences, Amrita Vishwa Vidyapeetham, Kochi - 682 041, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijot.ijot_52_20

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Patients with liver disease can have varied cardiac manifestations including pulmonary arteriovenous dilatation. The stress of surgery associated with catecholamine surges can also potentiate stress-related changes. We report management of hypoxemia in a patient who underwent liver transplantation. Although her preoperative oxygenation (SpO2 97%) measured 2 weeks earlier was normal, she manifested hypoxemia on the day of surgery and cardiovascular failure perioperatively. Postoperative investigations revealed a stress cardiomyopathy. The cause of persistent and refractory hypoxemia was uncertain in the context of normal preoperative tests. However, she responded immediately to inhaled nitric oxide, suggesting a correction of ventilation perfusion dynamics. We wish to highlight a possible role of nitric oxide in postoperative liver transplant patients with refractory hypoxemia of uncertain etiology.

Keywords: Hypoxia, liver transplantation, nitric oxide, Takotsubo cardiomyopathy

How to cite this article:
Sawant A, Kartha AP, Kesavan R, Kumar LK. Hypoxemia with stress cardiomyopathy following liver transplant: Is there a role for nitric oxide? - A case report. Indian J Transplant 2021;15:343-5

How to cite this URL:
Sawant A, Kartha AP, Kesavan R, Kumar LK. Hypoxemia with stress cardiomyopathy following liver transplant: Is there a role for nitric oxide? - A case report. Indian J Transplant [serial online] 2021 [cited 2022 Aug 10];15:343-5. Available from: https://www.ijtonline.in/text.asp?2021/15/4/343/334434

  Introduction Top

Liver transplantation surgery is accompanied by hemodynamic changes following perfusion of a newly grafted liver. Extreme stress with catecholamine surges is known to potentiate stress cardiomyopathy (SCM) or Takotsubo cardiomyopathy associated with liver transplant has been reported.[1],[2],[3] We report SCM with severe hypoxemia successfully managed with inhaled nitric oxide and supportive care following living donor liver transplantation.

  Case Report Top

A 65-year-old woman with early hepatocellular carcinoma presented for living donor liver transplantation. Her model for end-stage liver disease score was 28, and she did not have other associated illnesses. Her preoperative cardiac evaluation revealed normal electrocardiogram [ECG, [Figure 1]a], and a transthoracic echocardiogram showed an ejection fraction of 65% with a right ventricular systolic pressure of 40 mmHg and good left ventricular (LV) systolic function. She was negative for inducible ischemia on dobutamine stress echocardiography.
Figure 1: (a) Preoperative electrocardiogram. (b) Postoperative electrocardiogram showing changes in inferior and chest leads

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As her saturation in room air at preliminary evaluation 2 weeks earlier was 98%, further evaluation for hepatopulmonary syndrome (HPS) was not performed even though echocardiography suggested the presence of pulmonary arteriovenous fistula. However, on arrival to the operating suite, her saturation had dropped to 90% on room air and corresponding blood gas showed a PaO2 of 49.8%. Her heart rate was 96/min, blood pressure was 126/64 mmHg, and chest was clear on auscultation with no evidence of respiratory distress. As she was asymptomatic, combined specialty discussions were undertaken and a decision to proceed with the surgery was made.

Two hours after the start of surgery, she developed increase in peak airway pressures with fall in saturation accompanied by changes on the ECG. Saturation improved with diuretics and application of positive end expiratory pressure. Noradrenaline and a small dose of vasopressin were added for maintenance of the blood pressure given the background of vasodilatory cirrhotic state. As the patient remained stable on supports, it was decided to proceed with the transplant surgery. The cardiac biomarkers sent from the operating room; troponin I – 13.5 ng/ml and creatine kinase (CK MB - 113 and CK – 371 IU/L) were suggestive of a coronary event. However, the rest of the surgery progressed uneventfully with minimal hemodynamic changes at reperfusion, and the patient was shifted to the postoperative ICU for further management.

ECG [Figure 1]b and echocardiogram [Figure 2] immediately after surgery revealed basal hyperkinesia and apical ballooning consistent with SCM. There was no pericardial effusion or an increase in the right ventricular pressures. A contrast echo to document fistula was not performed due to risks for embolization at a critical state. She was electively ventilated in view of her cardiac status and supports tapered gradually.
Figure 2: Echo with apical ballooning and basal hyperkinesia

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Despite an improvement in blood pressure, her saturation began to fall even at an inspired concentration of 100% oxygen. Administration of inhaled nitric oxide at 0.2 L/min showed a dramatic response with the improvement in oxygenation, and the patient weaned off nitric oxide gradually over 84 h. Her LV function showed a slow but progressive recovery; however, she remained tachypneic needing ventilatory assistance that mandated an elective tracheostomy and intermittent ventilatory support. Her postoperative course was complicated by acute kidney injury and Gram-negative septicemia but was discharged in a stable state on the 68th postoperative day.

  Discussion Top

Our patient had features suggestive of SCM even before the major surgical stress had occurred. The confounding finding in her was the occurrence of hypoxemia as a new finding despite an earlier evaluation with normal oxygenation. We had interpreted this as a manifestation of HPS associated with liver disease[4] as there were no symptoms or signs of pulmonary edema or LV dysfunction. The decrease in oxygenation before the start of surgery and increasing airway pressures were probably due to an LV dysfunction that should have been evaluated and surgery deferred.

Posttransplantation hypoxemia in patients with HPS is precipitated by hypoxemic pulmonary vasoconstriction (HPV) that alters the existing balance of ventilation perfusion (V-Q). Despite its vasodilatory effect, nitric oxide is beneficial in altering the V-Q mismatch and improving saturation.[5],[6]

The characteristic echocardiographic finding in SCM is apical hypokinesia and ballooning with basal hypercontractility and regional wall motion abnormality extending beyond the territory of one coronary artery[7] that was seen in our patient. Despite the maintenance of mean arterial pressure above 65 mmHg monitored in the femoral artery, our patient developed rise in hepatic enzymes and elevation of urea and creatinine consistent with hypoperfusion of vital organs. Blood cultures sent were sterile. The fall in saturation occurred at a time when blood pressures had picked up and hemodynamics stable which implied pulmonary V-Q mismatch as a possible etiology. Echocardiography revealed only a modest increase in the right ventricular pressure and no evidence of LV dysfunction that could account for this desaturation. Inhalational nitric oxide can potentiate the cardiac dysfunction in heart failure and induce pulmonary edema,[8] and the dramatic response to nitric oxide suggested an improvement from pulmonary vascular dilatation and decrease in pulmonary vascular resistance. The slow recovery from surgery was accounted for by her age, background sarcopenia, and perioperative events.

  Conclusion Top

Hypoxemia following liver transplant is multifactorial and is exaggerated by V-Q mismatch due to HPV. We wish to highlight upon the possible role of nitric oxide for resistant hypoxemia in altering this mismatch and facilitating early recovery.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Bedanova H, Orban M, Nemec P. Postoperative left ventricular apical ballooning: Transient Takotsubo cardiomyopathy following orthotopic liver transplantation. Am J Case Rep 2013;14:494-7.  Back to cited text no. 1
Jophlin LL, Koch DG. Takutsubo cardiomyopathy after acute liver failure. Hepatology 2015;61:1430-1.  Back to cited text no. 2
Tachotti Pires LJ, Cardoso Curiati MN, Vissoci Reiche F, Silvestre OM, Mangini S, Carballo Afonso R, et al. Stress-induced cardiomyopathy (Takotsubo cardiomyopathy) after liver transplantation-report of two cases. Transplant Proc 2012;44:2497-500.  Back to cited text no. 3
Rodríguez-Roisin R, Krowka MJ. Hepatopulmonary syndrome – A liver-induced lung vascular disorder. N Engl J Med 2008;358:2378-87.  Back to cited text no. 4
Krowka MJ, Fallon MB, Kawut SM, Fuhrmann V, Heimbach JK, Ramsay MA, et al. International liver transplant society practice guidelines: Diagnosis and management of hepatopulmonary syndrome and portopulmonary hypertension. Transplantation 2016;100:1440-52.  Back to cited text no. 5
Nayyar D, Man HS, Granton J, Lilly LB, Gupta S. Proposed management algorithm for severe hypoxemia after liver transplantation in the hepatopulmonary syndrome. Am J Transplant 2015;15:903-13.  Back to cited text no. 6
Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, et al. Clinical features and outcomes of Takotsubo (Stress) cardiomyopathy. N Engl J Med 2015;373:929-38.  Back to cited text no. 7
Natori S, Hasebe N, Jin YT, Matsusaka T, Ido A, Matsuhashi H, et al. Inhaled nitric oxide modifies left ventricular diastolic stress in the presence of vasoactive agents in heart failure. Am J Respir Crit Care Med 2003;167:895-901.  Back to cited text no. 8


  [Figure 1], [Figure 2]


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