Chapter 179 - Hemodialysis access - nonthrombotic complication Flashcards
KDOQI 2006 listed access complications
1) bleeding
2) infection
3) aneurysm/pseudoaneurysm
4) seroma
5) access-related hand ischemia
6) venous hypertension
7) neuropathy
Cardiopulmonary not listed
Bleeding associated with ESRD
1) PUD
2) retroperitoneal spontaneous bleed
3) hemorrhagic transformation of stroke
Causes of increased bleeding in ESRD
1) anemia
2) thrombocytopenia
3) acquired defects
Uremia-induced platelet dysfunction
1) reduce GPIb (plt cannot adhere to subendothelium)
2) change GPIIb/IIIa (inhibit fibrinogen binding)
Anemia causes platelet inhibition
Anemia –> increase NO activity –> vasodilation and plt inhibition
Drugs that accumulate that can cause bleeding
1) beta-lactam antibiotics
2) oral anticoagulation (DOAC)
Afib in CKD rate
20% have afib
Percentage of herald bleed or access infection prior to fatal hemorrhage from access
40%
herald within 6 month
Desmopressin activity
1) synthetic ADH (arginine vasopressin) = 1-deasmino-8-D-arginine vasopressin
2) dose 0.3-0.4 mcg/kg iv or sc
3) rapid release of vWF and FVIII and decrease protein C activity
Platelet transfusion in bleeding in ESRD
immediate activity but last 45 hours
inactivated in uremic environment
cryoprecipitate define
plasma derivative with
1) fibrinogen
2) vWF
3) factor VIII
Maximum effect of cryoprecipitate and lasting duration
4-12 hours max, last 24 hr
Complication with cryoprecipitate
1) anaphylaxis
2) hemolysis
Protamine dose
1-1.5 mg/100 Units heparin
Recombinant factor VIIa use in bleeding
Off label
risk of systemic thromboembolic complication
Percentage of ESRD patients with HGB < 100
20%
Conjugated estrogen for prophylactic against bleeding
25-50 mg (0.6 mg/kg/d IV x 5 days)
1) vWF synthesis
2) reduce protein S
3) reduce NO
Effect of estrogen for bleeding
onset
peak
duration
6 hours onset
peak 5-7 days
last 14 days
Infection grade of AV access as per SVS
Grade 0: none
Grade 1: resolved with antibiotics
Grade 2: loss of AV access due to ligation, removal, bypass
Grade 3: loss of limb
Most common access-related infection organism
Single organism Staphylococcus
Gram negative 25%
Risk of infection of AV graft, tunneled catheter and temp catheter compared to autogenous AVF
AVG 2.2
Tunneled catheter 13.6
Temporary catheter 32.6
Centers for Disease control and prevention on risk factors associated with dialysis
1) catheter use
2) specific dialysis units
3) malnutrition (albumin < 35)
Percentage of access loss due to infection
20%
1 year infection rate for autogenous vs prosthetic
4.5% vs 19.7%
Risk factors for infection
1) repeated cannulation
2) cannulation technique (buttonhole)
3) poor hygiene
4) repeated hospitalization
5) duration of prosthetic AV access use
6) age
7) LE location
8) diabetes
Antibiotics in access infection
Vancomycin and gentamicin
If low MRSA then nafcillin, oxacillin or cefazolin
Antibiotic duration for autogenous infection
2-4 weeks
4-6 weeks if endograft exist
Recurrent infection rate in prosthetic infection salvage
20%
Rate of pseudoaneurysm in PTFE grafts
2-10%
usually in older grafts
Open revision of pseudoaneurysm in AV access
1) bypass
2) resection and interpositional repair
3) aneurysmorrhaphy
Endovascular repair of AV access pssudoaneurysm
Covered stent
concurrent treatment of outflow stenosis
cost ineffective
risk of infection and thrombosis
not justified to be done
Causes of true aneurysms in AV access
1) post-stenotic at arterial anastomosis
2) cannulation area
3) near vein junctions
4) near valves
Open repair of AV aneurysm
1) aneurysmorraphy
2) aneurysmectomy
Arterial inflow aneurysm associated with
1) renal transplant
2) immunosuppression
rare complication
Perigraft seroma grades
Grade 0: no collection
Grade 1: observed, resolved
Grade 2: involves aspiration or surgical drainage
Grade 3: results in loss of graft
Incidence of seroma with PTFE
< 2%
36% if gel coated PTFE - not to be used for dialysis
Location of seroma in AV access
near arterial anastomosis
Causes of seroma in AV access
1) immature fibroblast lining graft
2) immunologic reaction
3) graft damage
4) occult infection
Typical symptoms with seroma
1) appear within 1 month of creation
2) painless
3) enlarge over time
4) graft sweating can be seen
Treatment of AV access seroma and successes
1) Observation and aspiration 68-69%
2) cyst removal 72%
3) I&D 53%
4) Graft excision and cyst excision 100%
Infection after seroma attempted treatment different types
1) Aspiration 8% infection/thrombosis
2) Cyst removal 12% infection/thrombosis
3) I&D 7% infection/thrombosis
Access related hand ischemia first described by
1969 Storey et al
Rate of significant hand ischemia after wrist and brachial access creation
Brachial 4-8%
Wrist 1-2%
10% will get some tingling that are self limiting
80% will have reduced flow but most asymp
Grades of hand ischemia
Grade 0: no symptom
Grade 1: mild - cool extremity, flow augmentation with access occlusion
Grade 2 moderate - intermitted ischemia during dialysis
Grade 3 severe - ischemic pain at rest, tissue loss
Definition of ARHI
locoregional hypoperfusion secondary to inadequate arterial compensation
failure to increase CO and vasodilate hand vascular bed
Risk factors for ARHI
1) PAD
2) DM (hyperglycemia reduces shear-induced vasodilation)
3) CAD
4) brachial-based access
5) female
6) history of steal
7) multiple previous procedures
Digital brachial index likely to develop steal
< 1.0
Timing of onset of ARHI
Weeks to months
< 24hr is rare and usually with prosthetic
Differential of ARHI
1) carpal tunnel syndrome
2) venous hypertension
3) ischemic monomelic neuropathy
Diagnostic testing to support ARHI
1) digital pressure measurement
2) photoplethysmography
3) pulse oximetry
4) color duplex ultrasound
5) angiography
all performed with/without access compression
Goal of treating ARHI
1) symptom resolution
2) access preservation
ARHI treatment options
1) banding
2) RUDI
3) PAI
4) DRIL
5) angioplasty
6) ligation
Banding key points
1) patency 1 year 38-84%
2) symptom resolution 86-100%
3) maintain access > 700 ml/min
MILLER technique
Minimally invasive limited ligation endoluminal-assisted revision
1) 4-5 mm balloon placed and inflated
2) small incision made near anastamosis to tie knot around the balloon
Revision using distal inflow first described
Minion 2005
someone actually described previously
RUDI key points
1) ligation of fistula at arterial anast
2) new inflow from more distal artery
3) translocation of a vein branch or bypass
RUDI patency of fistula and clinical improvement
84% secondary patency 1 year
90% clinical improvement
Proximalization of arterial inflow first described by
Zanow
PAI key points
1) ligate AV anastomosis
2) PTFE 4-5 mm from more proximal inflow
PAI resolution and patency
86% symptom resolution
Patency 87% 12 months
Distal revascularization-interval ligation first described by
Schanzer 1988
DRIL key points
1) bypass inflow from proximal to access and terminate distal to access
2) ligate artery distal to access
3) locate origin of bypass 7-10 cm above inflow anastomosis to avoid pressure sink
DRIL access and bypass patencies
access patency 83%
bypass patency 90-100%
1 year
Distal radial artery ligation key points
1) retrograde flow from palmar arch results in palmar arch steal syndrome (PASS)
2) evaluate patency of ulnar artery and palmar arch prior to ligation
High flow ARHI definition and treatment preference
Autogenous > 800 ml/min
Prosthetic > 1200 ml/min
more likely to have adequate inflow
Therefore banding and RUDI ok
Low flow states require revasc: DRIL, PAI, angioplasty
Rate of central stenosis in failing AV access
17-26%
KDOQI mandates venography in this patient population prior to access creation
Previous subclavian lines
Open treatment for venous hypertension and central stenosis
1) GSV spiral graft
2) prosthetic bypass
3) jugular turndown to ipsilateral subclavian vein
Endo treatment for venous hypertension central stenosis:
elastic vs non-elastic lesions
Elastic: stent
non-eastic: dont stent? balloon only
Neuropathy grades after AV ccess
Grade 0: asymptomatic
Grade 1: mild - intermittent changes (pain, paresthesia, sensory deficit)
Grade 2: moderate - persistent sensory change
Grade 3: severe - motor loss and muscle wasting
Neuropathy category in CKD
1) systemic disease neuropathy: progressive and gradual
2) mononeuropathies: compression, compartment syndrome and entrapment
3) ischemic monomelic neuropathy: acutely after AV access
Systemic disease neuropathy in CKD
1) diabetes 46% of CKD
2) uremic polyneuropathy 50-70% of CKD
Compressive mononeuropathies rate in HD patients
10x more
increases with time on HD
50% at 10 years
Etiology of compressive mononeuropathy
venous HTN and congestion –> median nerve compression and chronic irritation –> carpal ligament thickening
Ischemic monomelic neuropathy rate of occurence
0.5%
Define IMN
Acute vascular compromise of neurologic structures
Risk factors of IMN
1) older
2) diabetic
3) preexisting peripheral neuropathy
4) PAD
5) brachial-based access ONLY or proximal
Findings with IMN
1) warm palpable pulse
2) audible signal in radial and ulnar
3) pain out of proportion
4) digital pressure index > 0.3
rate of CHF with HD patients
1/3
Access flow/cardiac output ratio higher than this suggest risk of high output cardiac failure
> 0.3
Coronary steal syndrome
IMA CABG on same side as AV access
28% develop signs of malperfusion on HD
