Skip to main content
Indian Journal of Anaesthesia logoLink to Indian Journal of Anaesthesia
letter
. 2021 Mar 20;65(Suppl 1):S53–S55. doi: 10.4103/ija.IJA_833_20

Unanticipated severe pulmonary hypertension in a patient undergoing living donor liver transplant - Role of milrinone and transesophageal echocardiography

Gaurav Sindwani 1,, Mahesh K Arora 1, Achal Dhir 2, Viniyendra Pamecha 1
PMCID: PMC7993036  PMID: 33814593

Sir,

Liver transplantation is a definitive treatment for end-stage liver disease patients.[1] These patients can have cardiomyopathy, coronary artery disease, hepato-pulmonary syndrome and porto-pulmonary hypertension.[2] Despite a screening echocardiography, patients with severe pulmonary artery hypertension (PAH) may go unrecognised until the time of surgery resulting in case cancellation with grave consequences. Here we report a case where combining transesophageal echocardiography (TEE) to pulmonary artery catheterisation helped establish the aetiology of severe PAH in a liver transplant patient. Further, the reversibility of raised pulmonary artery pressure (PAP) with milrinone injection helped in deciding to proceed with the surgery.

A 51-year-old man, weighing 64 kg, was posted for living donor liver transplantation. Model for end stage liver disease score was 27. His preoperative echocardiogram, done 2 months ago, showed mildly dilated left atrium, mild aortic regurgitation (AR) with normal ejection fraction. Abnormal pre-operative laboratory findings were: Hb – 7 gm dl-1, Platelets – 42,000 μl-1, International Normalised Ratio (INR) – 1.95, and serum albumin – 2 gm dl-1. All standard American Society of Anesthesiologists (ASA) monitors were instituted. Anaesthesia was induced as per institutional protocol. Pulmonary artery catheter (PAC) was placed. To our surprise, PAP was 84/38 (55) mm Hg, pulmonary capillary wedge pressure was 28 mm Hg and calculated pulmonary vascular resistance was 370 dynes sec cm-5. Donor surgery was immediately stopped. TEE probe inserted, revealed moderate AR with vegetation, moderate mitral regurgitation (MR), mild tricuspid regurgitation, mildly dilated left atrium, and moderate diastolic dysfunction (pseudonormal pattern) [Figure 1]. The points for discussion at this stage were PAH and endocarditis. Since there were no signs of active endocarditis, it was managed conservatively. For PAH, injection furosemide 60 mg i.v was given in increments. After sometime, PAP came down to 68/32 (45) mm Hg. Injection milrinone 1 mg i.v bolus was also given which further decreased PAP to 55/25 (36) mm Hg [Table 1]. Milrinone infusion was started at 0.2 μg kg-1 min-1 and the surgery was resumed. Intraoperative blood loss was 5240 mL. A total of 14 units of packed red blood cell, 8 units of fresh frozen plasma, and 10 units of cryoprecipitates were administered. Reperfusion went uneventful. Milrinone infusion was stopped 1 h after the reperfusion due to the increasing haemodynamic instability. The patient was transferred to the ICU for elective mechanical ventilation. In ICU, his mean PAP remained moderately raised (35–40 mm Hg). The patient was extubated on postoperative day one. Immunosupression was started from postoperative day one (methylprednisolone 80 mg, tacrolimus 1mg amd mycophenolate mofetil 250 mg). Cardiology consultation was obtained and patient was advised conservative management. The patient got discharged after 28 days.

Figure 1.

Figure 1

(a) – Four chamber view. (b)– Arrow is showing the pleural effusion on left side. (c) – Arrow is showing the mitral regurgitation. (d) – Arrow is showing the aortic regurgitation

Table 1.

Haemodynamic variables during the surgery

Liver Transplant stages Time (minutes) H.R (bpm) SBP (mm Hg) DBP (mm Hg) MAP (mm Hg) PAP Systolic (mm Hg) PAP Diastolic (mm Hg) PAP Mean (mm Hg) CVP (mm Hg)
Dissection phase 60 84 94 42 63 84 38 55 25
90 85 94 47 67 82 37 52 24
120 86 94 48 67 78 38 52 23
150 83 103 44 65 82 38 53 24
180 80 105 38 64 68 32 45 18
210 81 101 38 61 55 25 36 14
240 82 107 35 62 56 24 35 13
270 85 102 36 62 48 24 33 12
300 88 98 39 63 49 20 32 12
Anhepatic phase 330 89 96 41 64 51 21 33 10
360 93 92 43 64 55 24 35 10
390 92 98 42 65 47 21 31 11
420 90 101 39 62 46 22 32 10
Post Reperfusion phase 450 95 100 35 60 48 25 34 10
480 98 108 40 65 48 25 35 11
510 93 111 43 69 53 26 38 12
540 92 110 40 67 55 25 38 13
570 91 94 38 61 57 26 39 13
600 94 100 36 61 55 24 37 12
660 93 104 38 64 56 26 38 12
720 92 103 39 62 58 26 39 13

H.R: Heart rate, SBP: Systolic blood pressure, DBP: Diastolic blood pressure, MAP: Mean arterial pressure, PAP: Pulmonary artery pressure, CVP: Central venous pressure, bpm: Beats per minute

Our patient had mixed high PAP pathology: precapillary due to high cardiac output and anemia, capillary due to portopulmonary hypertension and post-capillary due to AR, MR and volume over load. Milrinone is a phosphodiesterase-3 enzyme inhibitor, which causes systemic and pulmonary vascular dilatation.[3] We have used milrinone for the following reasons:(1) To prevent and treat right ventricle dysfunction which may ensue during reperfusion phase.(2) Our patient had diastolic heart failure and milrinone does improve lucitropy and relaxation properties of the heart. On one side proceeding with the surgery in a patient with high PAP can be associated with adverse outcomes, while on the other hand, case cancellation may not be an option where live donor liver surgery has already progressed.[4] We took a decision to proceed with the surgery based on the following reasons: (1) moderate left heart pathology,(2) normal right ventricular function on TEE,(3) reversibility of high pulmonary artery pressure with injection milirinone,(4) progressed donor surgery. To conclude, severe PAH rarely is diagnosed on the operating table. Our report highlights the complementary roles of pulmonary artery catheter and TEE in diagnosis and decision-making. Demonstration of reversibility of high PAP with milrinone injection is an important indication of feasibility for liver transplant. Proper management improves the patient outcome and avoids unnecessary case cancellation.

Declaration of patient consent

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

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

REFERENCES

  • 1.Samuel D, Coilly A. Management of patients with liver diseases on the waiting list for transplantation: A major impact to the success of liver transplantation. BMC Med. 2018;16:113. doi: 10.1186/s12916-018-1110-y. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.Bozbas SS, Bozbas H. Portopulmonary hypertension in liver transplant candidates. World J Gastroenterol. 2016;22:2024–9. doi: 10.3748/wjg.v22.i6.2024. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Swamy MC, Mukherjee A, Rao LL, Pandith S. Anaesthetic management of a patient with severe pulmonary arterial hypertension for renal transplantation. Indian J Anaesth. 2017;61:167–9. doi: 10.4103/0019-5049.199854. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Singh SA, Ashraf H, Subramanian R, Krishnan GA, Pandey V, Gupta S. Living donor liver transplantation in a patient with severe portopulmonary hypertension. Indian J Anaesth. 2020;64:153–5. doi: 10.4103/ija.IJA_512_19. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from Indian Journal of Anaesthesia are provided here courtesy of Wolters Kluwer -- Medknow Publications

RESOURCES