Address of correspondence:
Alexandros Briasoulis
Section of Heart Failure and Transplant, Division of Cardiovascular
Diseases
University of Iowa Hospitals and Clinics,
200 Hawkins Dr, Iowa City, IA 52242
Office: 319-678-8418
Fax: 319-353-6343
E-mail:
alexbriasoulis@gmail.com
Abstract: Outflow cannula occlusion is an infrequent
complication occurring among recipients of continuous flow left
ventricular assist devices (LVAD). Hereby, we present a case of
intrinsic and extrinsic outflow cannula obstruction resulting in
cardiogenic shock and multiorgan failure.
Data availability : upon request by Editors
International Review Board approval : Waived, as this is a
single case report
Informed consent : This is a case report, informed consent was
not obtained as the patient did not survival to hospital discharge.
Case Description: A 66 year old Caucasian male with medical
history of emphysema, ischemic cardiomyopathy and stage D heart failure
status post HeartMate 3 LVAD implantation as destination therapy
eighteen months before the index admission for fever and shortness of
breath. His international normalized ratio was in therapeutic range
between 2 and 3 on admission. Despite early symptomatic improvement of
the respiratory symptoms with intravenous diuresis and antibiotics on
the fifth day of this hospital stay he developed low flow alarms,
decreased power but stable LVAD speed (5600 rpm) (Figure A). A bedside
echo showed persistent aortic valve opening in spite of increasing speed
to 6000rpm. Outflow cannula obstruction was suspected and a CT scan of
the chest was performed which revealed an irregular circumferential
hypodensity in the outflow cannula of the left ventricular assist device
consistent with thrombus or extrinsic compression from material between
the outflow and the bend relief material, without evidence of acute
kinking of the outflow graft (Figures B-D). Of note, a previous CT
angiography of abdomen did not reveal evidence of outflow graft
occlusion (Figure E). The became became hypotensive and was intubated
because of altered mentation and worsening respiratory distress. He was
resuscitated with infusion of norepinephrine and dobutamine. The lactate
dehydrogenase (LDH) and plasma free hemoglobin were not elevated. The
patient was started intravenous anticoagulation with intravenous heparin
in anticipation of surgical intervention. However, in the first 48 hours
of initiation of intravenous anticoagulation, he developed diffuse
alveolar hemorrhage diagnosed with a CT chest and confirmed by
bronchoscopy. His overall condition progressed rapidly to multiorgan
failure (acute kidney and liver injury). His hemodynamics at the time
suggested cardiogenic shock with Fick and thermodiluation cardiac index
of <1.8 l/minute/m2, mixed venous
saturations <40%, and elevated pulmonary capillary wedge
pressure over 20 mmHg and central venous pressure of 14mmHg. After
meeting with family of the patient, the decision of the
multi-disciplinary team was to proceed with comfort care measures and
hospice on the basis of deteriorating multi-organ function, low
likelihood of lung function recovery in the context of acute on chronic
lung disease, and poor candidacy for cardiac surgery.
Autopsy exam revealed instrinsic and extrinsic outflow graft
obstruction. The extrinsic obstruction consisted of fibrinous tissue
between the woven polyester tube and the bend relief (Figures F-N).