Heart failure is an alarming global public health issue impacting approximately twenty-six million individuals internationally. According to Chung (3 pp1), 6.5 million people are from the US out of these estimates. It has been determined that people with refractory American Heart Association Stage D tend to utilize Cardiac transplantation as the most effective therapy for their issue. Nevertheless, cardiac transplantation has significantly been restricted due to the limited supply of donor hearts, resulting in a surge in the utilization of left ventricular assist devices (LVAD) for destination therapy (DT) and bridge to transplant (BTT). Chung (8-14 pp1) cites that Individuals ineligible for cardiac transplantation have gotten to an instance where they undergo permanent implantation of an LVAD whenever they have this health issue. This paper will examine why patients with LVADs are at more risk of getting internal bleeding, specifically GI bleeding. The report will then assess the kind of patients at higher risk for GI bleeding and the treatments that can be utilized to manage the bleeding.
Patients with LVAD have a higher risk of GI bleeding due to many factors. Among the techniques used to describe the higher chances of GI bleeding is the occurrence of a non-pulsatile blood flow leading to endothelial dysfunction. Chung (23 pp4) stated that this is more prevalent in CF- LVADs and less common in patients with PF- LVADs. It was determined that patients treated with CF- LVADs lost physiologic pulsatility, attributed to the preexisting cardiac contractions in such patients. The issue leads to a narrowing of pulse pressure of the artery resulting in a decline in the size of the opening of the aorta.
The other technique brought up by Chung (48-51 pp4) is acquired von Willebrand disease caused by surging degradation of von Willebrand factor, which ultimately causes massive bleeding. Studies have often depicted that vWF has a crucial purpose in the angiogenesis regulation. This is because lack of VWF results in an increase in cytokines and endothelial cells, which results in a high rate of angiogenesis and ultimately leads to arteriovenous malformations. GI bleeding is in other instances associated with the declined number of high-molecular-weight multimers because of the LVAD device’s mechanical forces. The occurrence results in ineffective platelet aggregation and thrombosis. Further studies reveal that GI bleeding in LVAD patients may also result from a genetic predisposition.
The other factor that can cause GI bleeding in LVAD patients is impaired platelet aggregation. The platelet impairment is caused by increased platelet sensitivity to shear stress. Most LVAD recipients ended up having impaired platelet aggregation, which became normal once the heart transplant had been conducted. The LVAD implantation often activates the fibrinolytic in patients undergoing LVAD. The activation of fibrinolysis results from pre-existing state inflammation. In most cases, post-LVAD placement episodes are prevalent in the first year. The fibrinogen levels tend to peak after a month and later return to normal one year after LVAD implantation. Letsou et al. (10-11 pp 107) argue that most bleeding occurrences in LVAD patients relate to AVMs and are often not life-threatening. However, when the bleeding is brisk, it has a minimal chance of being related to an AVM, and the patient requires an emergent scope to rule out the possibilities of GI bleeding. Most bleeding occurrences often become solved in an average of four days. They primarily need four packed red blood cell units to be resolved.
GI bleeding is a severe complication resulting from LVAD implantation. It has a likelihood of causing hemodynamic instability and ultimately hemorrhagic shock that might cause death. Managing GI bleeding after LVAD implantation needs rapid evaluation since it is somehow challenging to manage anticoagulation in such patients due to the risk of bleeding and pump thrombosis (Weiskopf, Nicolosi & Pagel pp 565). The management strategy is built upon considerations such as the availability of therapeutic options, coexisting coronary artery disease, the severity of bleeding, and patient hemodynamics. Medical personnel plays a vital role in assessing these patients since they are at increased risk of undergoing GI bleeding. Moreover, risk stratification is needed for these patients since they are also at risk of readmissions and reoccurrence. It is also worth considering LVAD thrombosis as a differential in patients with minimal bleeding who are still witnessing a drop in hemoglobin levels.
LVAD management in outpatients is often done using antithrombosis. Besides aspirin, warfarin can also be used as an anticoagulant for such patients (Weiskopf, Nicolosi & Pagel pp 569). However, LVAD patients with GI bleeding need a comprehensive and multi-disciplinary approach. There is a need to perform a detailed examination and history of these patients. Besides, it is also worth conducting a hemodynamic resuscitation and initial assessment. NSAID used LVAD as a factor that leads to GI bleeding. Therefore, they need to check for their use in patient history. When carrying out the physical examination, it is essential to include the cardiology team’s LVAD assessment function. An assessment of intensive care admission should follow this Dalia et al., (15-18 pp 1007). Investigations need to entail d-dimer levels, fibrinogen, INR, hepatic and metabolic panels, and complete blood count. Nevertheless, the cardiology department should discuss withholding anticoagulation and antiplatelet therapy. The main issue that needs to be taken into account is the likelihood of developing thrombosis in the coming days.
Mild to Moderate Bleeding
According to Dalia et al. (2-5 pp 1001), most GI bleeding experienced by LVAD patients are extremely dangerous but they still cause recurrent hospitalizations and a surge in morbidity. However, it is necessary to conduct an endoscopy and stop the anticoagulation in patients with moderate and mild bleeding. The treatment and diagnosis of GI bleeding are mostly made using an endoscopy. However, the endoscopy sometimes yields false-negative results, and it is non-diagnostic in more than sixty percent of the patients. Once the cause of bleeding is determined and tackled effectively, warfarin with a minimal INR goal should replace aspirin. Balancing thromboembolism and bleeding with outpatient follow-ups is an issue that needs to be decided by patients and physicians. The main problem that needs to be considered is the individualized risk factors to Dalia et al. (6-17 pp 1002). When GI bleeding occurs, anticoagulation is held for 2-4 weeks may increase the risks of thromboembolic events. In such patients, colonoscopy after bowel preparation and the occult belt are used to diagnose the primary cause of the GI bleed. A push enteroscopy is required in instances of suspected small intestinal angiodysplastic lesions. Push enteroscopy often minimizes the risks of future readmission and rebleeding.
Once colonoscopy fails to reveal the cause, the other best step is carrying out an esophagogastroduodenoscopy. According to Letsou et al. (pp 106), patients with GI bleeding need to undergo endoscopy within a day, preceded by optimizing hemodynamic parameters through resuscitative efforts. Once these two measures fail, video capsule endoscopy needs to be conducted. Nevertheless, video capsule leads to a more extended hospital stay for the patient, and the video capsule is also not therapeutic.
Rapid resuscitative efforts need to be deployed in patients with profuse bleeding or hemodynamically unstable ones. The main aim of doing these activities is to help maintain hemodynamic stability. Fluid resuscitation also needs to be initiated in these patients, and all the antiplatelet and anticoagulant drug needs to be stopped. Similarly, Chung (47 pp 1845) asserted that it is also necessary to obtain immediate consults from concerned specialists and gastroenterologists. In severe bleeding scenarios, vitamin K needs to be administered to the patient. Nevertheless, after the patient is stabilized, it is necessary to restart warfarin immediately. Sometimes restarting warfarin becomes challenging because of excess vitamin K in the blood. The intention to reverse anticoagulation should be first discussed with the LVAD team, and a review of the patient’s hemodynamic status and PT/INR should follow before administering vitamin k.
Patients with a higher risk for GI bleeding
GI bleeding is common in terminally ill patients who need LVAD therapy and intensive support. Nevertheless, life-threatening bleeding is minimized with the utilization of Heartmate and Novacoor, which are pulsatile ventricular assist systems. Chung (17-96 pp 1847) cites that GI bleeding wasn’t included as being a vital issue in the two most recent HeartMate pulsatile LVAD reviews. However, aortic stenosis also has an association with GI bleeding. This issue was first brought into the limelight by Herde in 1958.
Similarly, Schwartz also reported that GI bleeding had an association with aortic stenosis. Soon after, more reports with similar observations came up. Some of the perfect instances of the studies with these findings include Boley et al., 1979. Although GI bleeding correlates with aortic stenosis, some studies still question it. Imperiale and Ransohoff conducted a methodologic and quantitative literature analysis in 1998. They asserted that the studies’ issues include non-comparable demographic groups, non-comparable diagnostic examination, and non-blinded data collection. Imperiale and Ranshoff further claimed that most studies paid attention to the association between chronic GI bleeding and aortic stenosis, not angiodysplasia. The study concluded that a careful literature review didn’t support the relation between aortic stenosis and GI bleeding, and they called for a need to have other controlled studies.
In conclusion, LVAD plays a vital role in providing mechanical support to terminal-stage heart failure patients. LVAD can be a definitive treatment and a bridge to cardiac transplants. Nevertheless, certain complications are linked with LVAD placement, and GI bleeding is the most common of them all. GI bleeding requires transfusion therapy, but they are rarely therapy. GI bleeding is prevalent in terminally ill patients and patients with aortic stenosis. There are various GI bleeding causes, including deficiency of the Willebrand factor and unstable dynamics. The management of mild and moderate GI bleeding is done by conducting an endoscopy and stopping the anticoagulation. In other instances, colonoscopy after bowel preparation and the occult belt is used to diagnose the primary cause of the GI bleed. In severe GI bleeding, Fluid resuscitation needs to be initiated in patients, and all the antiplatelet and anticoagulant drugs must be stopped.
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