A 50 year old man, who had a heart lung transplant 8 years earlier, presents to your ICU with pneumonia. Discuss the clinical issues specific to the heart lung transplant that will need consideration in your management of this patient.
a) Opportunistic infections - This can result in a wide range of opportunistic organisms causing infection including Pneumocystis, Aspergillus and CMV. It will therefore require early aggressive investigation and broad spectrum bacterial, fungal and possibly viral cover.
b) Immunosuppression : Ongoing immunosuppression will need to be carefully managed in consultation with the transplant unit
c) Cardiac issues- The transplanted heart is denervated. It is only responsive to directly acting drugs/hormones present in the circulation. Normal compensatory cardiac autonomic reflexes are not present and therefore the heart is more sensitive to directly acting drugs and less able to rapidly respond to changes in intravascular volume. This will clearly affect the ability to clinically assess a response to therapy and determine adequacy of therapy.
° Altered ECG /rhytm strip patterns
° Premature diffuse obliterative coronary atherosclerosis which results in impaired ventricular function
d) Respiratory issues - Impaired cough and clearance of secretions.
° Impaired lung function due to Obliterative Bronchiolitis ( a manifestation of chronic rejection)
° Bronchial or tracheal stenosis relating to the original anastomotic site.
e) Renal – altered renal function secondary to immunosuppressive drugs.
f) Altered adrenal function secondary to steroid use, need for steroid cover.
It is difficult to answer such a question intelligently without the experience of having worked in a cardiac transplant unit.
Fortunately, there are good papers.
This question benefits from a structured approach, and the systems-based structure provided by the college is as good as any. I will attempt to reorganise this question into a locally familiar alphabetic algorithm. For a broader overview of complications following heart-lung transplantation, and specifically sepsis in the heart-lung transplant recipient, there are dedicated chapter in the Required Reading section.
- This patient may require intubation;
- The risk of intubation in the immunocompromised patient must be weighed, as it places them at considerable risk of VAP.
- On the other hand, clearance of secretions may not be satisfactory, and effort of breathing may be so great that the cardiac reserve is exhausted (as these people tend to have a rather fixed cardiac output).
- Respiratory function will be impaired because of the pneumonia.
- The college also mentions obliterative bronchiolitis, which is a common feature of lung transplantation (it is a host vs graft chronic rejection syndrome)- in fact its the major cause of morbidity and mortality in long-term transplant patients. Obliterative bronchiolitis manifests as an obstructive respiratory disease, featuring an irreversible decrease in FEV1 which progressively worsens.
- Myocardial ischaemia: the myocardia of these people tend to also be subjected to chronic rejection, and the consequence of this looks like an accelerated rate of coronary vascular disease. This is a mixture of normal coronary athersclerosis and a uniquely transplant-associated distal obliterative disease, which looks totally different histologically. A seriously unfortunate feature of this unique obliterative process is the fact that collateral circulation doesn't seem to form, in contrast to normal atherosclerotic narrowing. The upshot of all this is the predisposition of relatively young hearts to relatively severe ischaemic heart disease.
- Increased responsiveness to infused inotropes: The denervated heart, in the absence of sympathetic stimulus, will grow vast numbers of catecholamine receptors. This is analogous to the skeletal muscle in the denervated legs of a spinal patient, which will overexpress acetylcholine receptors. Thus, inotropes will have an exaggerated effect on the transplanted heart.
- Insensitivity to normal autonomic stimuli: Severed from the autonomic nervous system, the heart will no longer respond normally to changes in blood pressure, posture, or volume. There will not be a compensatory tachycardia when the patient is hypovolemic.
Renal and electrolyte abnormalities:
- These patients like have been receiving steroids or cyclosporine-like drugs.
- The use of steroids will result in a hypernatremia, fluid retention, and hypokalemia.
- Alternatively, the barupt withdrawal of steroids may produce hyponatremia and hyperkalemia
- Renal function may be very poor, and drug clearance may be affected.
- Cyclosporine may also cause a distal renal tubular acidosis.
- In 60% of cases, pneumonia in the heart-lung trasplant recipient is due to an opportunistic pathogen.
- The pathogens are as follows:
- Moraxella catarrhalis
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.
Immunesuppression in the context of an acute infectious illness may have to be continued, because its cessation may result in catastrophic rejection.
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.