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PostPosted: 30 Dec 2018 12:35 
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Joined: 21 Jul 2013 13:13
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Complications of haemodialysis
Most of the time we mention in our discussion about renal injury caused by the treatment of other ailments in the system with drugs like pain-killers and antibiotics. Also, in this forum last week I posted an article on chemotherapy induced renal injury. We should not forget the reverse also, namely, treatment of the renal diseases resulting in injury to the other systems in the body. In this forum earlier, I have mentioned about some of the cardiac events that are precipitated in the course of haemodialysis. Recently I had come across yet a few more complications which are likely to occur during the haemodialysis procedures.

It is stated that cardiovascular disease is the leading cause of the death in dialysis patients. Arteriovenous fistulas (AVFs) are associated with lower mortality and yet are viewed as the desired access option in most patients with advanced kidney disease needing dialysis. However, AVFs have significant and potentially deleterious effects on cardiac functions particularly in the setting of preexisting heart disease.
Since hemodynamic optimization is the corner stone of managing patients with ESRD as well as those with CHF, studying the hemodynamic effects of AVFs in patients with ESRD with and without CHF is a sensible thing.
Many studies investigated the impact of AVFs on echocardiographic indices of cardiac morphology and function. These studies consistently showed an increase in LV end-diastolic dimension (LVEDD), contractility, stroke volume and CO within 7–10 days after the surgical construction of AVF. Diastolic filling parameters were also impaired, indicative of worsening diastolic functions.
AVFs and coronary artery disease
https://www.sciencedirect.com/science/a ... 1415000449

Significant coronary artery disease (CAD) is found in 30–40% of ESRD patients on hemodialysis. The concern with AVFs in patients with CAD is three-fold: the potential to provoke silent subendocardial myocardial ischemia due to increased oxygen demand and/or decrease oxygen supply. The possible negative impact of AVFs on ipsilateral internal mammary artery (IMA) bypass graft, due to distal steal effect.

Right Ventricular Enlargement within Months of Arteriovenous Fistula Creation is reported:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4979398/
Surgically created arteriovenous fistulae (AVF) for hemodialysis can contribute to hemodynamic changes. We describe the cases of 2 male patients in whom new right ventricular enlargement developed after an AVF was created for hemodialysis. Patient 1 sustained high-output heart failure solely attributable to the AVF. After AVF banding and subsequent ligation, his heart failure and right ventricular enlargement resolved. In Patient 2, the AVF contributed to new-onset right ventricular enlargement, heart failure, and ascites. His severe pulmonary hypertension was caused by diastolic heart failure, diabetes mellitus, and obstructive sleep apnea. His right ventricular enlargement and heart failure symptoms did not improve after AVF ligation.

Pulmonary hypertension in dialysis patients.
https://www.ncbi.nlm.nih.gov/pubmed/23405977/

Pulmonary hypertension in end-stage renal disease patients is associated with significantly increased morbidity and mortality. The prevalence of pulmonary hypertension in dialysis patients is relatively high and varies in different studies from 17% to 49.53% depending on the mode of dialysis and other selection factors, such as the presence of other cardiovascular comorbidities. The etiopathogenic mechanisms that have been studied in relatively small studies mainly include arteriovenous fistula-induced increased cardiac output, which cannot be accomodated by, the spacious under normal conditions pulmonary circulation. Additionally, pulmonary vessels show signs of endothelial dysfunction, dysregulation of vascular tone due to an imbalance in vasoactive substances, and local as well as systemic inflammation. It is also believed that microbubbles escaping from the dialysis circuit can trigger vasoconstriction and vascular sclerosis. The non-specific therapeutic options that proved to be beneficial in pulmonary artery pressure reduction are endothelin inhibitors, phosphodiesterase inhibitor sildenafil, and vasodilatory prostaglandins in various forms. The specific modes of treatment are renal transplantation, size reduction or closure of high-flow arteriovenous fistulas, and transfer from hemodialysis to peritoneal dialysis-a modality that is associated with a lesser prevalence of pulmonary hypertension.

Lastly, I want to site the incidence of haemorrhagic strokes in dialysis patients.
It is stated that the risk of stroke is five times higher in dialysis patients than in the general population. Uremic patients are susceptible to hemorrhagic complications due to multiple reasons, namely, platelet dysfunction and low platelet count, heparin usage during haemodialysis and use of anticoagulants for thromboembolic risk coverage.

As I stated earlier in our forum the dialysis centres are coming up in an explosive manner. Most of the centres are managed by non-medical persons and even where medical men are available, they don’t have any monitoring facilities. I know many patients on dialysis are only based on the level of creatinine. I think it is absurd. If you take clinical picture and electrolytes levels particularly serum potassium, a sizable number of patients can be left alone with good quality of life.

UA Mohammed


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