Editing Haemodialysis access (section)

== '''ACCESS FAILURE''' ==

=== Pathophysiology of mature access failure ===

* Flow limitation
** Limitation of flow by any mechanism results in recirculation of already dialysed blood to the dialysis machine, greatly reducing efficiency. This occurs when the afferent needle pulls blood that has just been returned to the patient via the efferent needle. 
** Mechanisms:
*** Stenosis/thrombosis at any point
*** Cannulation location - recirculation can occur due to inadequate separation of the needles.
*** Pseudoaneurysms caused by repeatedly puncturing the access at the same point - can result in infiltration and ulceration
* Conduit access limitation
** Vein too deep or too small
** Needs transposition or elevation of the vein conduit

=== Aetiology of access failure ===

* CVCs
** For tunnelled CVCs - failure usually results from thrombus or fibrin sheath formation
* '''Autogenous access'''
** '''Stenosis''' (secondary to intimal hyperplasia)
*** Arterial inflow stenosis - much less common cause of stenosis than venous outflow stenosis. Can similarly limit flow, but in this case both needles are distal to the stenosis. Common mechanism of failure of autogenous AV access, occasionally leading to complete collapse of the outflow vein during dialysis. Stenosis of the anastomosis is by far the most common location.
**** Juxta-anastomotic stenosis - occurs within the first 3-4cm of the AVF. More common in radiocephalic fistulas.
*** Stenosis of the autogenous access itself - in response to perturbed flow and repeated cannulation. Swing segment stenosis is more common in brachiobasilic fistulas.
*** Venous outflow stenosis - classic cause. More common in brachiocephalic fistulas.
**** Cephalic arch
**** Central vein stenosis
*** Arterial inflow stenosis
*** Intervention needs to happen before thrombosis occurs, as they may have limited patency after thrombectomy
** '''Thrombosis'''
*** Often associated with underlying compromise to endothelial surface, and there is therefore a high recurrence rate
*** Most commonly occurs as a result of venous outflow stenosis, but can also occur with pooling of blood in pseudoaneurysms or inadequate arterial inflow
* '''Prosthetic access'''
** Arterial inflow stenosis
** Venous outflow stenosis secondary to intimal hyperplasia at the venous anastomosis, secondary to turbulence (most common failure mode)
** Thrombosis
*** Occurs more frequently than in autogenous access
*** Flow rates less than 600-800mL/min predicts thrombosis in a prosthetic access

=== Assessing the access ===

* Assessing with dialysis measures - see above under 'access monitoring'
* '''Inspection'''
** Identify type of AVF
*** Anterior forearm - mostly radio-cephalic
*** Anterior upper arm - mostly brachiocephalic or if there is a scar medial, brachiobasilic (which is transposed if the fistula itself is more laterally)
** Inspect extremity and chest
*** Swelling/oedema - global increase in venous pressure
*** Aneurysms/pseudoaneurysms
*** Infection
**** Superficial infection associated with needle puncture sites
**** Deep infection - pain, swelling, erythema, fluctuance spreading outward in a circumferential manner. Requires surgery.
*** Ischaemia of the hand
** Arm elevation test
*** AVF should be distended at level of heart, and collapsed when elevated
*** If venous stenosis is present, the fistula (or, that part of the fistula distal to the stenosis) will remain distended
* '''Palpation'''
** Pulse. Normally the AVF should be easily compressible with little, if any, palpable pulse
*** Pulsatile AVF indicates downstream stenosis (unless an aneurysm/pseudoaneurysm is present), with degree of hyperpulsatility being proportional to severity of stenosis
*** Unusually weak pulse ('flat access') suggests an inflow lesion
** Thrill. Palpable vibration related to flow.
*** Normal thrill is diffuse, continuous, machinery-like sensation, which is most obvious at the arterial anastomosis.
*** Absent thrill means lack of flow - characteristic of thrombosed access.
*** An abnormal thrill, which is localised to the point of stenosis and might not be present in diastole, can be felt
*** Thrill can be felt subclavian with subclavian or cephalic arch stenosis.
** Pulse augmentation test.
*** First assess the pulse normally. Then occlude it using one finger, several cm above the anastomosis. The increase in the force of the pulse is assessed using the other hand.
*** The degree of pulse augmentation is directly proportional to the quality of the access inflow - if the inflow is good, it will augment well, and have a strong pulse after occlusion
*** If a hyperpulsatile AVF does not demonstrate augmentation with occlusion, it suggests the downstream stenosis is severe.
*** The degree of pulse augmentation can be graded from 0 to 3
* '''Auscultation'''
** Bruit. Auditory manifestation of a thrill, with the same basic implications.
*** Bruit over a well-functioning AVF has a low-pitched, soft, machinery-like rumbling sound, with both systolic and diastolic components.
*** Increasing resistance from a progressively stenotic lesion will result in the progressive loss of the diastolic component, until it becomes systolic only. The pitch will also become higher. The intensity of the bruit is highest at the point of stenosis.
* Continuous thrill should be present near the arterial anastomosis, and it should be detectable for several centimetres into the outflow vein. No pulse or thrill suggests it may be thrombosed or stenosed. USS can differentiate.
* Pseudoaneurysms of the access may result in pulsatility in the area of enlargement
* Inflow problem:
** Poor pulse augmentation within the access
* Outflow problem:
** Doesn't collapse on elevation
** Pulse - increased intensity, forceful
** Thrill - localised to site, accentuated, systolic only
** Bruit - localised to site, high pitched, systolic
** Check for collateral veins/oedema
** If a pulse is present near the venous outflow, then venous outflow stenosis is likely
** A thrill distal to an area of pulsatility generally suggests the location of the stenosis
** Access bleeding after removal of cannula - can result from high venous pressures - suggest either USS or venography

=== Investigating/planning ===

* USS can differentiate between thrombosed/stenosed access
* Thrombosis
** Determine the underlying cause of the thrombosis
** If you can't find a cause, probably assume it's a result of venous outflow stenosis

=== Revision of access ===

* Arterial anastomotic stenosis
** If >50% inflow stenosis in conjunction with clinical abnormality, UTD suggests percutaneous intervention first
* Venous outflow stenosis
** Below 2.7mm is considered stenosis and probably needs something done
** Endovascular (UTD says PTA first if >50% stenosis and any clinical abnormality)
*** Balloon angioplasty - insufflate for 2-3 minutes - appropriate for any significant venous stenosis, right up to central veins
*** Stenting - covered metal stent
** In practice, results of these two open techniques are fairly equivalent
*** Re-site with a venous interposition graft to bypass any stenosis
*** Patch angioplasty simply enlarges the area of stenosis, theoretically leading to a higher chance of recurrence
* Thrombosis in an autogenous access
** Open thrombectomy has controversial results, as 6-month primary and secondary patency rates were 51 and 69% respectively. Use a 4F balloon catheter for 6mm grafts. Then image the entire graft, looking for the underlying lesion. Repair anything you find.
** Percutaneous mechanical thrombectomy has good results
** UTD says endovascular thrombectomy first
** Contraindications to revision/salvage of thrombosed AVF
*** Infection
*** Right to left shunt
*** Chronic occlusion
* Thrombosis in a prosthetic access
** Balloon thrombectomy is tolerated quite well
* Multiple outflow vein branches
** If inhibiting maturation, can be ligated to maximise outflow
* Deep AV access
** Translocation or elevation

[[Category:Vascular]]