Heart-lung transplantation is a fairly specialised area, which makes it all the more surprising that so far two ten-mark CICM fellowship questions have asked for detailed answers about it. Question 28 from the second paper of 2016 and the identical Question 22 from the first paper of 2009 have asked the candidates to discuss the peculiarities of managing a heart-lung transplant recipient who turns up to your ICU with community-acquired pneumonia.
The bewildering array of physiological curiosities which result from the transplantation of virtually the entire thoracic contents are discussed at greater length in the Required Reading section for Cardiothoracic Intensive Care. This section focuses on the infectious complications of such a transplant. Much of the information summarised below is derived from the published experience of the Stanford University Medical Center. The specific local chapters are:
The Stanford people found the following distribution of cases:
Apart from the fact that the donated lung tends to get various pneumonias (that is discussed later) there are specific organ-transplant-related infectious complications to consider.
The heart is generally not a major problem, but the lung is the organ transplant which is most prone to infection. This is because of several features:
This is a situation where the transplanted organ acts as the vehicle of infection.
One may get some advanced warning about this if the laboratory finds something untoward in the actual transport fluid in which the organ was stored. Typically, this tends to result in mediastinitis, and case reports of this complication suggest that the prognosis may be poor.
In these patients, pneumonia is the most common infection, and also the most common cause of death.
Note how weirdly the range of bugs is arrayed. The community pathogens are fairly bog-standard, but the Stanford people found that gram-negatives dominated the hospital-acquired infectious lung flora. In 60% of cases, pneumonia in the heart-lung trasplant recipient is due to some sort of an opportunistic pathogen, and these tend to occur in chronological order (eg. CMV first, then Pneumocystis, then Nocardia).
Aspergillus, though common, is less common than you think - because there are still active neutrophils around with tacrolimus and mycophenolate (i.e. the immunesuppression is not as profound as it would be with some sort of bone marrow failure).
Cisneros, J. M., et al. "Pneumonia after heart transplantation: a multiinstitutional study." Clinical infectious diseases 27.2 (1998): 324-331.
Reichenspurner, Hermann, et al. "Stanford experience with obliterative bronchiolitis after lung and heart-lung transplantation." The Annals of thoracic surgery 62.5 (1996): 1467-1473.
Gao, Shao-Zhou, et al. "Accelerated coronary vascular disease in the heart transplant patient: coronary arteriographic findings." Journal of the American College of Cardiology 12.2 (1988): 334-340.
Yusuf, S. A. L. I. M., et al. "Increased sensitivity of the denervated transplanted human heart to isoprenaline both before and after beta-adrenergic blockade."Circulation 75.4 (1987): 696-704.
Kramer, Mordechai R., et al. "Infectious complications in heart-lung transplantation: analysis of 200 episodes." Archives of internal medicine 153.17 (1993): 2010-2016.
Montoya, Jose G., et al. "Infectious complications among 620 consecutive heart transplant patients at Stanford University Medical Center." Clinical infectious diseases 33.5 (2001): 629-640.
Pektok, Erman, et al. "Sepsis and mediastinitis after heart transplantation: donor-transmitted Klebsiella infection." TURK GOGUS KALP DAMAR CERRAHISI DERGISI-TURKISH JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY 22.1 (2014): 145-148.
Dudau, Daniela, et al. "Incidence of nosocomial pneumonia and risk of recurrence after antimicrobial therapy in critically ill lung and heart–lung transplant patients." Clinical transplantation 28.1 (2014): 27-36.