Left Ventricular Assist Devices: A Brief Overview

Bhargavi Gali MD

Department of Anesthesiology and Perioperative Medicine

Division of Critical Care Medicine

Mayo Clinic Minnesota

Rochester, MN, USA

Introduction

Second and third generation left ventricular assist devices (LVAD) have been increasingly utilized as both a bridge to transplantation and as destination therapy (in patients who are not considered transplant candidates) for advanced heart failure. Currently approximately 2500 LVADs are implanted yearly, with an estimated one year survival of >80% (1). Almost half of these patients undergo implantation as destination therapy. A recent systematic review and meta-analysis found no difference in one-year mortality between patients undergoing heart transplantation in comparison with patients undergoing LVAD placement (2).

Early LVADs were pulsatile pumps, but had multiple limitations including duration of device function, and requirement for a large external lead that increased risk of infection. Currently utilized second and third generation devices are continuous flow (first generation were pulsatile flow). Second generation devices have axial pumps (HeartMate II®). The third generation LVADs ((HeartMate III®), HVAD®) are also continuous flow, with centrifugal pumps, which are thought to decrease possibility of thrombus formation and increase pump duration in comparison to the second generation axial pumps. It is also felt that a lack of mechanical bearings contributes to this effect.

LVADs support circulation by either replacing or supplementing cardiac output. Blood is drained from the left ventricle with inflow cannula in the left ventricular apex to the pump, and blood is returned to the ascending aorta via the outflow cannula (3) (Figure 1).

Figure 1. Third generation Left Ventricular Assist Device. Heartware System ™. Continuous flow left ventricular assist device (LVAD) configuration. One of the third generation LVADs is the HeartWare System. With this device the inflow cannula is integrated into the pump. The pump is attached to the heart in the pericardial space, with the outflow cannula in the aorta. A driveline connects the device to the control unit. This control unit is attached to the two batteries. (Figure used with permission from Medtronic).

The device assists the left ventricle by the action of the axial (second generation) or centrifugal (third generation) pump that rotates at a very high speed and ejects the blood into the aorta via the outflow cannula. A tunneled driveline connects the pump to the external controller that operates the pump function. The controller connects to the power source via two cables, which can be battery or module-powered.

LVADs offload volume from the left ventricle, and decrease left ventricular work. Pulmonary pressures and the trans pulmonary gradients are also decreased by the reduced volume in the left ventricle (4). End organ perfusion is improved secondary to enhanced arterial blood pressure and micro perfusion.

There are four main parameters of pump function:

• Pump speed: the speed at which the LVAD rotors spin, and is programmed. Measured in RPM.
• Pump power: the wattage needed to maintain speed and flow, which is the energy needed to run the pump. Measured in Watts.
• Pump flow: estimate of the cardiac output, which is the blood returned to the ascending aorta, and is based on pump speed and power. Measure in L/min
• Pulsatility index (PI): a calculated value that indicates assistance the pump provides, in relation to intrinsic left ventricular A higher number indicates higher left ventricular contribution to pulsatile flow.

The cardiac output of currently utilized LVADs is directly related to pump speed and inversely related to the pressure gradient across the pump. As the pump speed is fixed, right ventricular failure can decrease the volume of blood transmitted to the pump and decrease LVAD flow (3, 4). With right ventricular failure, inotropic support may be needed to improve the LVAD pump flow. High afterload, such as may be seen with an increase in systemic vascular resistance can decrease pump flow.

Complications

Adverse events occur in more than 70% of LVAD patients in the first year (5). These complications include infections, bleeding, stroke, and LVAD thrombosis. More than 50% of patients are readmitted within the first 6 months after LVAD implantation (6).

Driveline infections are the most commonly reported LVAD infection, and are the most likely to respond to treatment (7). Pump pocket infections may require debridement plus/minus antibiotic bead placement. Bloodstream infections are less commonly reported, and more difficult to treat, and many patients are placed on chronic suppressive antibiotic therapy (7). There is a possible association between stroke and bloodstream infection, reported in some studies. Patients who were younger and had a higher body mass index were noted to have a higher incidence of LVAD infections.

Gastrointestinal bleeding is a major cause of nonsurgical bleeding, reported in almost 30% of patients after LVAD placement (1). Patients may develop acquired von Willebrand factor deficiency secondary to high shear forces in the LVAD that lead to breakdown of von Willebrand protein (6). Antithrombotic therapy is commonly instituted after LVAD implantation which also increases risk of bleeding. A high incidence of arteriovenous malformations is reported in these patients, although the etiology is not clear. Transfusion, holding antithrombotic therapy, and identifying possible sources are included in the standard approach to management.

There is a high risk of both ischemic and hemorrhagic strokes in the first year after LVAD placement (8). Surgical closure of the aortic valve and off-axis positioning of the cannulas have been suggested as altering shear forces, increasing thrombotic risk, and thus risk of stroke.  Post-surgical risks may include pump thrombosis, infections, supratherapeutic INR, and poorly controlled hypertension. Early diagnosis has led to consideration of interventions such as thrombectomy (8).

LVAD thrombosis can occur on either cannula (inflow or outflow) or the pump. Typically patients receive ongoing anticoagulation, commonly with warfarin, and antiplatelet agents, and often aspirin. Heartmate II® may have higher rate of thrombosis than HVAD or Heart Mate 3, although this is under debate (6). Thrombotic complications range in severity from asymptomatic increase in lactate dehydrogenase or plasma-free hemoglobin, to triggering of LVAD alarms, up to development of heart failure. The inflow and outflow cannulas and pump can be the site of thrombosis. Management typically involves revising the antithrombotic management. If there is no improvement or worsening, replacement of LVAD may be indicated. There is limited evidence to suggest that systemic thrombolysis may be of benefit in treating pump thrombosis, particularly in regards to the HVAD, though better data would be useful

Procedural Management

When a patient with an LVAD requires non cardiac surgery, optimal management includes having an on-site VAD technician, and close involvement of VAD cardiology and cardiac surgery in consultation. Anticoagulation will often be transitioned to heparin infusion prior to elective procedures (9). Suction events (LV wall is sucked into the inflow cannula) can occur secondary to under filled left heart, and this can become more apparent perioperatively. This can also decrease right heart contractility by moving the interventricular septum to the left, and thus decrease cardiac output. Management often involves fluid bolus. Suction events can lead to decreased flow, left ventricular damage, and ventricular arrhythmias. Hemodynamic management can be challenging with non-pulsatile flow, and placement of an arterial line can facilitate optimal management. Postoperative care in a monitored setting is beneficial in case of further volume related events and to watch for bleeding.

Emergent Complications

Arrhythmias occur in many patients after LVAD implantation. Atrial arrhythmias are reported in up to half of LVAD patients, and ventricular arrhythmias in 22-59% (10, 11).  Loss of AV synchrony can lead to decreased LV filling and subsequent RV failure. Rhythm or rate control with rapid atrial arrhythmias is necessary to decrease development of heart failure. Ventricular arrhythmias may be hemodynamically tolerated for some time secondary to the LVAD support (6).  If there is concern that the inflow cannula is touching the LV septum, as may occur with severe hypovolemia, echocardiography can help determine if volume resuscitation should be the initial step in treating ventricular arrhythmia.

If cardiac arrest occurs, the first step of cardiopulmonary resuscitation in patients with LVAD is assessment of appropriate perfusion via physical examination (12). If perfusion is poor or absent, assessment of LVAD function should take place. If the LVAD is not functioning appropriately, checking for connections and power is the next step. If unable to confirm function or restart LVAD, chest compressions are indicated by most recent guidelines from the American Heart Association. There is always concern of dislodgement of LVAD cannula or bleeding during these situations.

Conclusion

Currently implanted LVADS are continuous flow, and provide support via a parallel path from the left ventricle to the aorta. As the number of patients with LVADs increase all medical providers should have a basic understanding of the function and common complications associated with these devices. This will enhance the ability to initiate appropriate care.

References

1. Kirklin JK, Pagani FD, Kormos RL, et al. Eighth annual INTERMACS report: Special focus on framing the impact of adverse events. J Heart Lung Transplant. 2017 Oct;36(10):1080-6. [CrossRef] [PubMed]
2. Theochari CA, Michalopoulos G, Oikonomou EK, et al. Heart transplantation versus left ventricular assist devices as destination therapy or bridge to transplantation for 1-year mortality: a systematic review and meta-analysis. Annals of Cardiothoracic Surgery. 2017;7(1):3-11. [CrossRef] [PubMed]
3. Lim HS, Howell N, Ranasinghe A. The physiology of continuous-flow left ventricular assist devices. J Card Fail. 2017;23(2):169-80. [CrossRef] [PubMed]
4. Roberts SM, Hovord DG, Kodavatiganti R, Sathishkumar S. Ventricular assist devices and non-cardiac surgery. BMC Anesthesiology. 2015;15(1):185. [CrossRef] [PubMed]
5. Miller LW, Rogers JG. Evolution of left ventricular assist device therapy for advanced heart failure: a review. JAMA Cardiol. 2018 Jul 1;3(7):650-8. [CrossRef] [PubMed]
6. DeVore AD, Patel PA, Patel CB. Medical management of patients with a left ventricular assist device for the non-left ventricular assist device specialist. JACC Heart Fail. 2017 Sep;5(9):621-31. [CrossRef] [PubMed]
7. O'Horo JC, Abu Saleh OM, Stulak JM, Wilhelm MP, Baddour LM, Rizwan Sohail M. Left ventricular assist device infections: a systematic review. ASAIO J. 2018 May/Jun;64(3):287-294. [CrossRef] [PubMed]
8. Goodwin K, Kluis A, Alexy T, John R, Voeller R. Neurological complications associated with left ventricular assist device therapy. pert Rev Cardiovasc Ther. 2018 Dec;16(12):909-17. [CrossRef] [PubMed]
9. Barbara DW, Wetzel DR, Pulido JN, et al. The perioperative management of patients with left ventricular assist devices undergoing noncardiac surgery. Mayo Clinic Proceedings. 2013;88(7):674-82. [CrossRef] [PubMed]
10. Enriquez AD, Calenda B, Gandhi PU, Nair AP, Anyanwu AC, Pinney SP. Clinical impact of atrial fibrillation in patients with the heartmate ii left ventricular assist device. J Am Coll Cardiol. 2014 Nov 4;64(18):1883-90. [CrossRef] [PubMed]
11. Nakahara S, Chien C, Gelow J, et al. Ventricular arrhythmias after left ventricular assist device. Circ Arrhythm Electrophysiol. 2013 Jun;6(3):648-54. [CrossRef] [PubMed]
12. Peberdy MA, Gluck JA, Ornato JP, et al. Cardiopulmonary resuscitation in adults and children with mechanical circulatory support: a scientific statement from the American Heart Association. Circulation. 2017;135(24):e1115-e34.`[CrossRef] [PubMed]

Cite as: Gali B. Left ventricular assist devices: a brief overview. Southwest J Pulm Crit Care. 2019;19(2):68-72. doi: https://doi.org/10.13175/swjpcc039-19 PDF 

May 2018 Critical Care Case of the Month

Lacey Gagnon APRN, CNP
Theo Loftsgard APRN, CNP

Department of Anesthesiology and Critical Care

Mayo Clinic Minnesota

Rochester, MN USA

Chief Complaint

Shortness of breath

History of Present Illness

The patient is a 44-year-old woman who was admitted with a history of “pericarditis”. She has a several years history of progressive shortness of breath, abdominal distention and lower extremity edema.

Past Medical History, Social History and Family History

She has a history of obesity, poorly controlled type 2 diabetes, uterine fibroids and hypertension. She does not smoke but does have 1-2 alcoholic beverages per day. Family history is noncontributory.

Physical Examination

• Vital signs: pulse 96 beats/min, blood pressure 110/85 mm Hg, temperature 37° C, respirations 18 breaths/min.
• Neck: there is jugular venous distention with a positive hepatojugular reflux.
• Lungs: rales at both bases.
• Heart: regular rhythm without murmur.
• Abdomen: Distended. Shifting dullness is present.
• Extremities: 2-3 pretibial pitting edema.

Chest Radiography

Chest x-ray shows a small right pleural effusion with mild vascular congestion at the bases. Heart size is normal.

Which of the following should be performed?

1. Abdominal CT scan
2. Echocardiography
3. Thoracic CT scan
4. 1 and 3
5. All of the above

Cite as: Gagnon L, Loftsgard T. May 2018 critical care case of the month. Southwest J Pulm Crit Care. 2018;16(5):245-51. doi: https://doi.org/10.13175/swjpcc048-18 PDF 

January 2018 Critical Care Case of the Month

Theodore Loftsgard, APRN, ACNP 

Department of Anesthesiology and Critical Care

Mayo Clinic Minnesota

Rochester, MN USA

History of Present Illness

The patient is a 51-year-old woman admitted with a long history of progressive shortness of breath.  She has a long history of “heart problems”. She uses supplemental oxygen at 1 LPM by nasal cannula.

Past Medical History, Social History and Family History

She also has several comorbidities including renal failure with two renal transplants and a history of relatively recent RSV and CMV pneumonia. She is a life-long nonsmoker. Her family history is noncontributory.

Physical Examination

• Vital signs: Blood pressure 145/80 mm Hg, heart rate 59 beats/min, respiratory rate 18, T 37.0º C, SpO2 91% of 1 LPM.
• Lungs: Clear.
• Heart: Regular rhythm with G 3/6 systolic ejection murmur at the base.
• Abdomen: unremarkable.
• Extremities: no edema

Which of the following should be performed? (Click on the correct answer to proceed to the second of seven pages)

1. Brain naturetic peptide (BNP)
2. Chest x-ray
3. Echocardiogram
4. Electrocardiogram
5. All of the above

Cite as: Loftsgard T. January 2018 critical care case of the month. Southwest J Pulm Crit Care. 2018;16(1):1-7. doi: https://doi.org/10.13175/swjpcc155-17 PDF

March 2017 Critical Care Case of the Month

Kyle J. Henry, MD

Banner University Medical Center Phoenix

Phoenix, AZ USA

History of Present Illness

A 50-year-old man presented to the emergency room via private vehicle complaining of 5 days of intermittent chest and right upper quadrant pain. Associated with the pain he had nausea, cough, shortness of breath, lower extremity edema, and palpitations. 

Past Medical History, Social History, and Family History

He had a history of hypertension and diabetes mellitus but was on no medications and had not seen a provider in years. He was disabled from his job as a construction worker. He had smoked a pack per day for 30 years. He was a heavy daily ethanol consumer. He had an extensive family history of diabetes.

Physical Examination

• Vitals: T 36.4 C, pulse 106/min and regular, blood pressure 96/69 mm Hg, respiratory rate 19 breaths/min, SpO2 98% on room air
• Lungs: clear
• Heart: regular rhythm without murmur.
• Abdomen: mild RUQ tenderness
• Extremities: No edema noted.

Electrocardiogram

His electrocardiogram is show in Figure 1.

Figure 1. Admission electrocardiogram.

Which of the following are true regarding the electrocardiogram? (Click on the correct answer to proceed to the second of seven pages)

1. The lack of Q waves in V2 and V3 excludes an anteroseptal myocardial infarction
2. The S1Q3T3 patter is diagnostic of a pulmonary embolism
3. There are nonspecific ST and T wave changes
4. 1 and 3
5. All of the above

Cite as: Henry KJ. March 2017 critical care case of the month. Southwest J Pulm Crit Care. 2017;14(3):94-102. doi: https://doi.org/10.13175/swjpcc021-17 PDF

Ultrasound for Critical Care Physicians: A Pericardial Effusion of Uncertain Significance

Brandon Murguia  M.D.

Department of Medicine

University of New Mexico School of Medicine

Albuquerque, NM USA

A 75-year-old woman with known systolic congestive heart failure (ejection fraction of 40%), chronic atrial fibrillation on rivaroxaban oral anticoagulation, morbid obesity, and chronic kidney disease stage 3, was transferred to the Medical Intensive Care Unit for acute hypoxic respiratory failure thought to be secondary to worsening pneumonia.

She had presented to the emergency department 3 days prior with shortness of breath, malaise, left-sided chest pain, and mildly-productive cough over a period of 4 days. She had mild tachycardia on presentation, but was normotensive without tachypnea, hypoxia, or fever. Routine labs were remarkable for a leukocytosis of 15,000 cells/μL. Cardiac biomarkers were normal, and electrocardiogram demonstrated atrial fibrillation with rapid ventricular rate of 114 bpm. Chest x-ray revealed cardiomegaly and left lower lobe consolidation consistent with bacterial pneumonia. Patient was admitted to the floor for intravenous antibiotics, cardiac monitoring, and judicious isotonic fluids if needed.

On night 2 of hospitalization, the patient developed respiratory distress with tachypnea, pulse oximetry of 80-85%, and increased ventricular response into the 140 bpm range. The patient remained normotensive. A portable anterior-posterior chest x-ray showed cardiomegaly and now complete opacification of the left lower lobe. She was transferred to the MICU for suspected worsening pneumonia and congestive heart failure.

Upon arrival to the intensive care unit, vital signs were unchanged and high-flow nasal cannula was started at 6 liters per minute. A focused point-of-care cardiac ultrasound (PCU) was done, limited in quality by patient body habitus, but nonetheless demonstrating the clear presence of a moderate pericardial effusion on subcostal long axis view.

Figure 1: Subcostal long axis view of the heart.

What should be done next regarding this pericardial effusion? (Click on the correct answer for the answer and explanation)

1. Observe, this is not significant.
2. Additional echocardiographic imaging /evaluation.
3. Immediate pericardiocentesis.
4. Fluid challenge.

Cite as: Murguia B. Ultrasound for critical care physicians: a pericardial effusion of uncertain significance. Southwest J Pulm Crit Care. 2016;13(5):261-5. doi: https://doi.org/10.13175/swjpcc127-16 PDF

September 2015 Critical Care Case of the Month: If You Don't Look, You Won't Find

Robert A. Raschke, MD

Banner University Medical Center

Phoenix, AZ

 History of Present Illness

A 55-year-old woman was transferred from Mexico emergently for acute cardiomyopathy. On the day of admission, she went for a 45-min “exercise” walk and cleaned her house. While taking a shower, she suffered an acute onset of dyspnea with nausea and vomiting and possibly a small amount of hematemesis. She appeared seriously ill to her husband, who took her blood pressure (198/?) and pulse (90) and rushed her to a local medical facility.  There, she was found to have severe pulmonary edema, and a troponin of 11.  Her echo showed inferior wall motion abnormality with an ejection fraction of 35%.  However, coronary catheterization showed normal coronaries.  She was treated with oxygen, furosemide, labetolol and enoxaparin and transferred emergently to Banner-University Medical Center. 

Past Medical History, Family History and Social History

The patient reported intermittent "spells" since May. These typically occurred upon  lying down in bed and were characterized by her as a feeling of “numbness” or tingling  which ascends from her chest to her head associated with palpitations and a feeling of  “desperation”, typically relieved after a few minutes upon getting up out of bed.

She had a history of hypertension and had been on losartan but this was discontinued a few months previously because of the onset of orthostatic dizziness. She also has a history of hypothyroidism and is taking synthroid. She was treated three times in the last 6 month for amoebiasis. She is a medical missionary to La Paz, Mexico and has recently traveled to Bolivia and Guatemala.

Review of Systems

She has had some night sweats, coughing with deep inspiration, and some slight hemoptysis. She did have a headache one month previously at 7000 ft elevation while in Guatemala.

Physical Examination

• She appears in moderate distress. Her vital signs are normal other than a mild tachycardia.  
• She does have rales on auscultation of her lungs.
• The remainder of the physical examination was unremarkable.

Radiography

A portable chest radiograph is performed (Figure 1).

Figure 1. Admission portable chest radiograph.

Laboratory evaluation

Her CBC shows a normal hemoglobin and hematocrit but with an elevated white blood cell count of 26,500 cells/mcL with a left shift. Admission electrolytes and blood sugar are within normal limits.

What additional procedures/testing are indicated? (Click on the correct answer to proceed to the second of four panels)

1. Blood cultures
2. Echocardiogram
3. Electrocardiogram
4. NT-pro-brain natriuretic peptide (NT-pro-BNP)
5. All of the above

Reference as: Raschke RA. September 2015 critical care case of the month: if you don't look, you won't find. Southwest J Pulm Crit Care. 2015;11(3):97-102. doi: http://dx.doi.org/10.13175/swjpcc113-15 PDF 

Analysis of a Fatal Left Ventricular Assist Device Infection: A Case Report and Discussion

Neal Stuart Gerstein, MD FASE¹

Henry G. Chou, MD²

Andrew Lewis Dixon, MD¹

¹Department of Anesthesiology & Critical Care Medicine

University of New Mexico

Albuquerque, NM

²Department of Anesthesiology

Cedars-Sinai Medical Center

Los Angeles, CA

Introduction

Left ventricular assist device (VAD) therapy is an increasingly utilized treatment as a bridge to heart transplantation or as long-term destination therapy. Recent reports show there is a 22% - 32% incidence of VAD-associated infections with staphylococci and nosocomial gram-negative bacilli being the most common causative organisms (1,2). These organisms are often found in intensive care units, where they have the highest proportion of resistance, thus exposing already critically ill patients to the possibility of resistant organism VAD-associated infections (3). Mortality rates exceed 60% when sepsis develops in a patient with a continuous flow left VAD and infection is the number one cause of death in those awaiting cardiac transplantation (4,5). With continued left VAD use clinicians will likely see multidrug-resistant (MDR) or even pandrug-resistant organism VAD-associated infections. Clinicians need to be prepared to manage such an intimidating entity.

Case Report

We report a case of a 25 year-old male with a pandrug-resistant Pseudomonas aeruginosa VAD-associated infection. The patient’s medical history is significant for a diagnosis of idiopathic dilated cardiomyopathy refractory to maximal medical therapy requiring implantation of a HeartMate II (Thoratec Co., Pleasanton, CA, USA) continuous flow left VAD (Figure 1).

Figure 1. HeartMate II^® left VAD schematic (reprinted with the permission of Thoratec Co., Pleasanton, CA, USA).

His course was complicated with multiple hospital admissions for recurrent VAD-associated infections and numerous episodes of P. aeruginosa bacteremia that had been treated with a multitude of antipseudomonal antibiotics. He presented to our hospital for management of severe volume overload in the setting of VAD-associated infections. Transesophageal echocardiography demonstrated a left ventricular ejection fraction of 24% with severe left and right ventricular dilatation. Chest x-ray revealed cardiomegaly and multiple devices including the left VAD (Figure 2).

Figure 2. Chest X-ray demonstrating an enlarged cardiac silhouette, the HeartMate II axial pump (*) with inflow (down arrow, ↓) and outflow (up arrow, ↑) cannulas, biventricular pacer with leads in right atrium (A), coronary sinus (B), and right ventricle (C) (dashed arrows).

Blood cultures revealed MDR P. aeruginosa; except for showing intermediate sensitivity to tobramycin there was resistance to all antimicrobials tested. In vitro synergy testing revealed modest bacterial inhibition when only colistin, fosfomycin, imipenem, and tobramycin were combined. After maximizing medical therapy, multiple left VAD pocket washings and implantation of tobramycin beads followed. Intraoperative findings included an encapsulated infection around the driveline and obvious infection of the left VAD pocket. Repeat blood cultures showed P. aeruginosa had developed resistance to all antimicrobials including tobramycin. Subsequently the left VAD was explanted and the patient was transitioned to an extracorporeal membrane oxygenator (ECMO) in attempt to clear the infection. He was then transitioned to a TandemHeart (CardiacAssist Inc., Pittsburgh, PA, USA), a percutaneous LVAD, as he was not dependent on ECMO for oxygenation. He was able to clear the bacteremia after removal of the infected HeartMate II while on colistin, fosfomycin, tobramycin, azithromycin and rifampin, but was not able to clear the remaining left VAD pocket infection, which again spread systemically. Despite maximal medical and surgical interventions, he died from profound septic shock and multisystem organ failure. To date this is the first known case of a pandrug-resistant P. aeruginosa VAD-associated infection reported in the literature.

Discussion

P. aeruginosa organisms have intrinsic resistance to numerous broad spectrum antibiotics, and can easily develop acquired resistance to most if not all available antimicrobial agents (3). Risk factors for the development of pandrug-resistant P. aeruginosa include previous treatment with antipseudomonal antibiotics and prolonged treatment times. Given our patient had multiple P. aeruginosa infections, treated with multiple rounds of antipseudomonal antibiotics, it is not surprising that pandrug-resistance developed. Few therapeutic options are available for treatment and no new agents are available to evade the known resistance mechanisms. Treatment can be optimized using synergistic combination therapy, which may be the only medical management option in patients with pandrug-resistant P. aeruginosa infections. Some have suggested that rifampin in combination with colistin may be a promising approach (3). Some experts recommend in vitro synergy testing when an organism is resistant to currently recommended antibiotic regimens (6,7). However, a recent review of antibiotic therapy for gram-negative infections describes the utility of in vitro synergy testing equivocal in the context of Pseudomonas infection (8). We managed our patient with combination therapy; however, not until pandrug-resistant P. aeruginosa was isolated did we introduce rifampin in combination with colistin.

A recent review of VAD-associated infections showed the majority were managed without surgical intervention; only 13% required surgical debridement and only in cases of severe infection and/or failed conservative treatment was left VAD explantation required. Since this case there has been a proposed algorithm for management of VAD-associated infections (2); our management, though prior to published guidelines, was in step with the algorithm. Of note, there was no discussion of explanting an left VAD to ECMO to aid in clearing a resistant infection. We felt this was a rational option given our inability to clear the infection. It is unclear as to exactly why our patient was never able to fully clear his infection. Given the patient’s other pre-existing extensive cardiac hardware (i.e. implanted pacer), it is possible that he remained colonized even after maximal surgical and medical therapy. Though speculative, it is possible that removing all foreign material may have allowed for complete infection clearance.

Aside from aggressive medical and surgical management, systolic heart failure with VAD-associated infections may be effectively managed with heart transplantation (9). Our consensus was that this option was neither in the best interest of the patient nor the best use of available resources given the severity of his condition.

Conclusion

Clinicians will continue to see VAD-associated infections with resistant organisms. To minimize adverse outcomes, including VAD-associated infection, prudent patient selection and timing of VAD placement is paramount, as VAD’s placed in critically ill patients have been consistently associated with adverse outcomes (10).

References

1. Gordon RJ, Weinberg AD, Pagani FD, Slaughter MS, Pappas PS, Naka Y, Goldstein DJ, Dembitsky WP, Giacalone JC, Ferrante J, Ascheim DD, Moskowitz AJ, Rose EA, Gelijns AC, Lowy FD. Prospective, multicenter study of ventricular assist device infections. Circulation. 2013;127:691-702. [CrossRef] [PubMed]
2. Nienaber JJ, Kusne S, Riaz T, Walker RC, Baddour LM, Wright AJ, Park SJ, Vikram HR, Keating MR, Arabia FA, Lahr BD, Sohail MR. Clinical manifestations and management of left ventricular assist device-associated infections. Clin Infect Dis. 2013;57:1438-48. [CrossRef] [PubMed]
3. Zavascki AP, Carvalhaes CG, Picao RC, Gales AC. Multidrug-resistant Pseudomonas aeruginosa and Acinetobacter baumannii: resistance mechanisms and implications for therapy. Expert Rev Anti Infect Ther. 2010;8:71-93. [CrossRef] [PubMed]
4. Topkara VK, Kondareddy S, Malik F, Wang IW, Mann DL, Ewald GA, Moazami N. Infectious complications in patients with left ventricular assist device: etiology and outcomes in the continuous-flow era. Ann Thorac Surg. 2010;90:1270-7. [CrossRef] [PubMed]
5. Bartoli CR, Demarest CT, Khalpey Z, Takayama H, Naka Y. Current management of left ventricular assist device erosion. J Card Surg. 2013;28:776-82. [CrossRef] [PubMed]
6. Balaji V, Jeremiah SS, Baliga PR. Polymyxins: Antimicrobial susceptibility concerns and therapeutic options. Indian J Med Microbiol. 2011;29:230-42. [CrossRef] [PubMed]
7. Martis N, Leroy S, Blanc V. Colistin in multi-drug resistant Pseudomonas aeruginosa blood-stream infections: a narrative review for the clinician. J Infect. 2014;69:1-12. [CrossRef] [PubMed]
8. Tamma PD, Cosgrove SE, Maragakis LL. Combination therapy for treatment of infections with gram-negative bacteria. Clin Microbiol Rev. 2012;25:450-70. [CrossRef] [PubMed]
9. Prendergast TW, Todd BA, Beyer AJ, 3rd, Furukawa S, Eisen HJ, Addonizio VP, Browne BJ, Jeevanandam V. Management of left ventricular assist device infection with heart transplantation. Ann Thorac Surg. 1997;64:142-7. [CrossRef] [PubMed]
10. Lietz K, Long JW, Kfoury AG, Slaughter MS, Silver MA, Milano CA, Rogers JG, Naka Y, Mancini D, Miller LW. Outcomes of left ventricular assist device implantation as destination therapy in the post-REMATCH era: implications for patient selection. Circulation. 2007;116:497-505. [CrossRef] [PubMed] 

Reference as: Gerstein NS, Chou HG, Dixon AL. Analysis of a fatal left ventricular assist device infection: a case report and discussion. Southwest J Pulm Crit Care. 2015;10:16-20. doi: http://dx.doi.org/10.13175/swjpcc139-14 PDF