Pauwaa, Sunil; Raghuvir, Rashmi; Kurien, Sudha; Tatooles, Antone J.; Pappas, Pat S.; Bhat, Geetha
From the Center for Heart Transplant and Assist Devices, Advocate Christ Medical Center, Oak Lawn, Illinois.
Submitted for consideration September 2010; accepted for publication in revised form December 2010.
Reprint Requests: Geetha Bhat, PhD, MD, Center for Heart Transplant and Assist Devices, Advocate Christ Medical Center, POB Suite 407, 4400 W. 95th Street, Oak Lawn, IL 60453. E-mail: firstname.lastname@example.org.
Device infection remains a significant cause of morbidity and mortality in patients with mechanical assist devices. Fungal infections represent a virulent pathogen occurring in up to 3% of left ventricular assist device (LVAD) patients.1 Diagnosing infection in a LVAD is challenging, especially when these infections involve the pump apparatus or the inflow or outflow grafts, which are difficult to image. Transthoracic (TTE) and transesophageal echocardiography (TEE) are useful; however, the data on their use in evaluating LVAD malfunction are limited, especially with regard to continuous axial flow devices.2,3 This report presents two cases in which unique TEE findings suggest obstruction in two patients with continuous axial-flow HeartMate II (HMII) LVADs.
A 55-year-old African American woman with a history of HMII LVAD presented with severe left arm, wrist, and elbow pain. Vital signs, laboratory analysis, and venous and arterial studies were normal.
Three days after admission, blood cultures grew Candida parapsilosis, and the patient was placed on intravenous (IV) caspofungin. TEE demonstrated no vegetations, mild continuous aortic insufficiency (AI) during systole and diastole, and an aortic valve (AV) remaining closed the entire time.
On hospital day 9, the patient's LVAD displayed multiple red heart alarms; however, LVAD flows and pulsatility index (PI) remained normal, and there were no changes in pump speed or power. The patient was upgraded to status 1A for cardiac transplant because of infection. Repeat blood cultures grew Candida parapsilosis despite IV antifungal therapy.
Repeat TEE demonstrated no evidence of vegetations or left ventricular apical thrombus and good flow at the level of the LVAD inflow cannula. This time moderate AI was seen; however, it would intermittently disappear altogether and then worsen again with temporal variation in the width of the vena contracta (Figures 1 and 2). Again, the AV remained closed throughout systole and diastole. Furthermore, the TEE probe repeatedly over-heated throughout the study. Postprocedure evaluation of the TEE probe demonstrated normal function and no mechanical cause for the overheating.
Within 12 hours of TEE, the patient demonstrated worsening mental status, nausea, and vomiting. Emergent computed tomography (CT) of the head demonstrated a large intraparenchymal hemorrhage. Postmortem analysis of the patient's LVAD revealed a large fungal vegetation on the LVAD rotor (Figure 3).
A 58-year-old Indian man with a HMII LVAD had two red heart alarms 3 days apart. Power connections were confirmed to be secure, the system controller was replaced, and the alarms resolved. In clinic, the system controller showed multiple episodes of “no flow” state.
On admission, the patient was asymptomatic with normal vital signs and LVAD parameters. On physical examination, the LVAD driveline demonstrated dark brown drainage with an exposed device pocket draining purulent fluid. Laboratory tests were normal. TTE demonstrated a closed AV, no vegetations, and mild continuous AI.
The patient remained afebrile; however, the LVAD intermittently showed speed drops and power surges. Forty-eight hours later, blood cultures grew Candida albicans and the patient's peripherally inserted central catheter (PICC) line was removed; this later grew Candida albicans. Gated CT angiography of the chest and abdomen revealed no evidence of filling defects within the inflow or outflow tract to suggest obstruction. Plans were made to take the patient to the operating room.
Preoperative TEE demonstrated an AV remaining closed throughout the cardiac cycle with moderate intermittent AI, which was present continuously for several beats and then completely absent for several beats. This represented a change from his prior TTE that demonstrated mild continuous AI present during systole and diastole. LVAD parameters were stable throughout.
Although the initial plan was to explore and debride the LVAD driveline and pocket, a decision was made to replace the LVAD based on the TEE findings. This was out of concern for a mobile obstructive thrombus functioning like a ball valve and causing intermittent variation in flow and hence in the patient's AI. On removal of the device, a large vegetation was found within the inflow cannula of the LVAD (Figure 4). Postoperative TEE demonstrated a closed AV with mild, continuous AI present during systole and diastole.
LVAD infections can be difficult to diagnose. Despite positive blood cultures, the exact source of infection can remain unclear. Device infection may involve the percutaneous driveline, device pocket, or internal components of the device. Differentiating the etiology of an infection is crucial, because each of these sources warrants a different therapeutic approach.
AI is a significant finding complicating LVAD function. Patients with AI before LVAD usually demonstrate continuous AI with every beat during systole and diastole after LVAD.4,5 A change in this pattern of AI in a patient with LVAD can therefore theoretically provide insight on LVAD function.
The HMII has system-provided parameters of speed, power, PI, and flow that give information about device function. Red heart alarms indicate that pump flow is <2.5 L/min, the percutaneous lead is disconnected, or the pump is not working properly.
In both our cases, the patients had recurrent red heart alarms. In patient 1, the TEE probe repeatedly overheated despite proper probe function and optimal probe parameters. We speculate that this was secondary to passive transfer of heat generated by the obstructive vegetation on the LVAD rotor. The TEE did not demonstrate vegetations but the change in the pattern of AI suggested an obstruction. Both patients had bulky fungal vegetations within the LVAD that were likely mobile and may have functioned as a ball valve resulting in intermittent subtle changes in flow. In both cases, we theorize that a vegetation causing a ball-valve effect may have caused intermittent obstruction leading first to a decrease in flow through the LVAD during the obstruction and afterward to an increase in flow through the LVAD once the obstruction was relieved thereby increasing the AI. The obstruction was apparently not enough to completely impede flow through the LVAD and thus did not result in ejection through the AV. The obstruction was enough to alter the effective regurgitant volume (ERV) of the AI seen on Doppler examination of the AV. Otto6 states that the ERV in patients with moderate AI is 30–60 ml/beat. Although color Doppler is sensitive to detecting such subtle alterations in flow, we suspect that this change in flow is not sufficient to register a significant alteration in the flow computed by the LVAD, which explains the lack of a significant change in the LVAD parameters. The experience from the TEE findings in the first patient enabled us to make the decision to change the surgical approach in the second case, possibly averting a major catastrophe.
A single previous case report on echocardiographic diagnosis of axial flow pump malfunction provided a number of findings suggestive of pump thrombosis and obstruction.3 These findings included pulsatile, low-velocity retrograde flow at the inflow cannula in the left ventricular apex via color and pulsed wave Doppler, and thrombotic material detected on TEE at the apical orifice of the inflow cannula. These were not noted in our patients.
Usually red heart alarms in the context of a power surge suggest an obstruction. Our experience illustrates that intermittent variation of AI may also suggest obstruction, functioning as a mobile ball valve, intermittently reducing flow through the LVAD and consequently through the AV. Coupled with the right clinical scenario, this could represent an emergent situation demanding prompt action.
1. Bagdasarian NG, Malani AN, Pagani FD, Malani PN: Fungemia associated with left ventricular assist device support. J Card Surg
24: 763–765, 2009.
2. Horton S, Khodaverdian R, Chatelain P, et al
: Left ventricular assist device malfunction: An approach to diagnosis by echocardiography. J Am Coll Cardiol
45: 1435–1440, 2005.
3. Catena E, Milazzo F, Montorsi E, et al
: Left ventricular support by axial flow pump: The echocardiographic approach to device malfunction. J Am Soc Echocardiogr
18: 1422e7–1422e13, 2005.
4. Bryant AS, Holman WL, Nanda NC, et al
: Native aortic valve insufficiency in patients with left ventricular assist devices. Ann Thorac Surg
81: e6–e8, 2006.
5. Samuels LE, Thomas MP, Holmes EC, et al
: Insufficiency of the native aortic valve and left ventricular assist system inflow valve after support with an implantable left ventricular assist system: signs, symptoms, and concerns. J Thorac Cardiovasc Surg
122: 380–381, 2001.
6. Otto C. Textbook of Clinical Echocardiography
, 4th ed. Pennsylvania, Saunders, 2009, pp. 309.