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a Division of Cardiac Surgery, University of Maryland Medical Center, Baltimore, Maryland
b Department of Pediatrics, University of Maryland Medical Center, Baltimore, Maryland
c Department of Pediatrics, University of New Mexico, Albuquerque, New Mexico
Accepted for publication July 25, 2008.
* Address correspondence to Dr Cardarelli, University of Maryland Medical Center, 22 S Greene St, Suite N4W94, Baltimore, MD 21201 (Email: mcard001{at}umaryland.edu).
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Abstract |
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Introduction |
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An 18-month-old woman diagnosed with hypoplastic left heart syndrome was admitted while extubated into the intensive care unit after completion of a lateral tunnel Fontan with a 5-mm fenestration. From her original diagnosis she had been palliated with a Sano procedure followed 6 months later by a bidirectional Glenn.
After a rapid surgical recovery with good peripheral saturations (86% to 92%) on postoperative day 10 while still on the ward due to poor feeding, she had bilateral pleural effusions develop and abdominal distension, requiring transfer to the intensive care unit, chest drainage, and placement of a central line (initial central venous pressure, 23 mm Hg). Treatment with gentamicin, cefepime hydrochloride, and Diflucan (fluconazole; Pfizer Inc, New York, NY) was started for a positive urine culture for Enterobacter or Candida Albicans. After 7 days, acute renal failure (BUN, 123 mg/dL and creatinine, 5.7 mg/dL) developed in the patient and she had significant metabolic acidosis and respiratory distress requiring reintubation and mechanical ventilation. A femoral hemodialysis catheter was placed, but due to hemodynamic instability, the original hemodialysis system was transformed into venous-venous hemofiltration. Although on hemofiltration, heparin therapy was found to be ineffective and a workup revealed anti-thrombin III deficiency. A venous duplex and a perfusion–ventilation scan was ordered for a drop in arterial blood saturations from 77.9 to 58.5, which resulted in a diagnosis of a deep venous thrombosis and a right pulmonary embolism. Treatment with tissue plasminogen activator was initiated, which effectively dissolved most of the thrombus. Fibrinolytic therapy was discontinued due to a life-threatening pericardial tamponade that required emergency needle-evacuation and an abnormal neurologic examination due to an intracranial hemorrhage. Lipase level peaked at 1,498 I/U with no attributable surgical cause found.
On postoperative day 43, a cardiac catheterization revealed elevated end-diastolic pressures. Therapy was initiated at this time to maximize afterload reduction and improve diuresis. Figure 1 shows a chart with the evolution of hemodynamic, weight, and inotropic score throughout admission.
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A third cardiac catheterization on postoperative day 90 revealed the development of a new set of collaterals, which were appropriately addressed. Inotropic and mechanical ventilation dependence prompted the decision to implant an assist device while entertaining the idea of a heart transplant, but never formally listing the patient. Approval from the insurance, Food and Drug Administration paperwork, and importation of the device delayed the process for more than 3 weeks to postoperative day 136.
The VAD inflow cannula was placed in the apex of the single ventricle, the outlet cannula in the ascending aorta, and a single, 25-cc pumping bladder was used. In the immediate postoperative period, vasopressin was added for hypotension, which was weaned during the course of 3 days. Diuretic therapy was resumed with the addition of Coreg (carvedilol; GlaxoSmithKline plc, London, UK). After the first 24 hours, a heparin drip was started and transitioned into sodium warfarin once the enteral feeds were resumed. International normalized ratios for clotting were checked daily, and low molecular heparin was added when nontherapeutic levels were suspected. Aspirin (Bayer, Leverkusen, Germany) and Dipyridamole (Rising Pharmaceuticals, Allendale, NJ) were administered daily.
Weekly echocardiograms suggested incomplete ventricular emptying with absence of clots in the inflow cannula. Three weeks into VAD support, the decision was made to exchange the bladder for a larger one (30 mL) at the bedside.
The patient's evolution continued to be assessed by weekly cardiac ultrasounds, daily coagulation profile, VAD bladder assessment to rule out clot formation, and overall patient clinical status and weight gain.
After 5 months of support, and with the VAD placed on standby for 5 minutes, a cardiac catheterization revealed a lower wedge (16 mm Hg) and pulmonary pressure (20 mm Hg). Confronted with the reality that our patient was never an ideal transplant candidate and after discussion with her parents, the decision was made to optimize her general status and move toward removal of the VAD.
After 179 days of cardiac support, she was taken to the operating room and the VAD was removed with the use of cardiopulmonary bypass through femoral cannulation. The outflow cannula site was primarily closed with reinforced sutures. Extended inotropic support was resumed for the following 41 days.
A newly formed thrombus extending into the inferior cava was discovered shortly after VAD removal and was treated with heparin and fibrinolytics. Ascites, secondary to portal hypertension, resulted in abdominal wound dehiscence at the skin site of cannula entry and exit. Temporary placement of a peritoneal drain relieved abdominal pressure, while allowing for wound healing until resolution of the thrombus and the ascites.
After resolution of the ascites, the patient was rapidly advanced toward tracheostomy decannulation. Failure to decannulate was due to a subglottic stenosis diagnosed by bronchoscopy, with the decision made to discharge her to a chronic care facility for further rehabilitation before going home. The cardiac ultrasound at the time of hospital discharge revealed moderate atrioventricular valve regurgitation and normal ventricular contractility. Medications at the time of discharge were diuretics and beta-blockers. She had spent 1 year and 8 days in the hospital, and 55 days had passed since VAD removal.
After a 3-month stay in a rehabilitation facility, the patient was sent home under a regime of tracheostomy collar oxygen, wheelchair bounded due to her original stroke, and on G-tube feeds. A cardiac ultrasound 6 months after discharge demonstrated a resolved valve insufficiency and good systolic function. Shortly after her last cardiology visit, she expired during her sleep. An autopsy revealed a dislodged tracheostomy tube as probable cause of death.
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Comment |
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Left ventricular remodeling has been the subject of numerous studies describing structural changes in response to chronic alterations in loading or unloading conditions [5]. Levin and colleagues [6] first described the anatomic and physiologic changes after long-term ventricular mechanical unloading in patients with idiopathic dilated cardiomyopathy and Frazier's group was the first to suggest that chronic mechanical support of failing ventricles had the potential to spare transplantation to a selected group of patients [7].
High pulmonary vascular resistance also seems to be amenable to significant involution with the help of mechanical support for the failing left ventricle. Adequate reduction of the pulmonary resistance can be expected within 3 to 6 months of implanting an left ventricular assist device in end-stage heart failure patients waiting for a heart transplant [8].
The use of the Berlin Heart (Berlin Heart AG) for a prolonged period of time seems to have effectively helped our patient. Although we speculate that chronic unloading led to ventricular remodeling, the true mechanism of recovery remains unknown and we have no further objective data to demonstrate our hypothesis. We believe that there has not been any study that has been published to date on single ventricles remodeling.
With a limited supply of hearts for children waiting for a transplant, temporary VAD support may provide the clinician with a dependable alternative for these patients.
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This article has been cited by other articles:
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  C. J. VanderPluym, I. M. Rebeyka, D. B. Ross, and H. Buchholz The use of ventricular assist devices in pediatric patients with univentricular hearts J. Thorac. Cardiovasc. Surg., February 1, 2011; 141(2): 588 - 590. [Full Text] [PDF]
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