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.
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Copyright © 2011 by the American Society for Artificial Internal Organs
6. Otto C. Textbook of Clinical Echocardiography
, 4th ed. Pennsylvania, Saunders, 2009, pp. 309.