An investigation into the mechanisms, consequences and moderators of intradialytic hypotension in paediatric haemodialysis.
Doctoral thesis, UCL (University College London).
The relationship between hypertension and cardiovascular morbidity has long been recognised. However evidence is mounting implicating hypotension and not hypertension as the predominant risk factor for mortality. I demonstrated a 20-30% prevalence of intradialytic symptoms and hypotension in children during conventional, 4 hour haemodialysis (HD) sessions. The declining blood pressure (BP) was originally believed to be caused by ultrafiltration (UF) and priming of the HD circuit due to loss of fluid from the intravascular space. However data, largely in adults, challenged this hypothesis leading to a new consensus that intradialytic hypotension has a multifactorial aetiology. The uraemic milieu triggers a series of events that alters the cardiovascular compensatory responses to haemodynamic stresses, however the extent to which these physiological responses are impaired and their consequences are unknown and poorly understood. At first I corroborated adult findings that a poor correlation existed between relative blood volume changes and intradialytic hypotension in children, supporting the theory that fluid removal alone was not responsible for cardiovascular decompensation during HD and this assumption was a gross oversimplification of the underlying problem. Using a traditional method (endocardial wall motion) and a novel method (Speckle tracking 2-dimensional strain) I then measured the regional left ventricular (LV) function in children (aged 2 to 17 years) at the start of dialysis and again during peak stress at the end of HD. I found rising cardiac troponin I levels in 25% of the cohort and reduced regional LV function in all the children examined. The level of dysfunction significantly correlated with actual BP, the degree of intradialytic BP fall and UF volumes. What remains unclear however is whether the fall in BP was the cause or effect of the ischaemic cardiac injury. Finally I investigated dialysis methods for abrogating intradialytic morbidy in children treated with four hour HD sessions. A step sodium profile from 148mmol/l to 138mmol/l, prophylactic mannitol and sequential dialysis were successful, to variable degrees in attenuating intradialytic symptoms or hypotensive episodes. Intradialytic midodrine was exclusively used in one patient resistant to all other forms of therapy and was found to be the most efficacious in supporting the BP and preventing hypotension.
|Title:||An investigation into the mechanisms, consequences and moderators of intradialytic hypotension in paediatric haemodialysis|
|Open access status:||An open access version is available from UCL Discovery|
|Additional information:||Published articles in the appendices have been removed for copyright reasons|
|UCL classification:||UCL > School of Life and Medical Sciences > Faculty of Population Health Sciences > Institute of Child Health|
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