Chapter 179 - Hemodialysis access - nonthrombotic complication Flashcards by Gary Yang

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

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Bleeding associated with ESRD

1) PUD
2) retroperitoneal spontaneous bleed
3) hemorrhagic transformation of stroke

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Causes of increased bleeding in ESRD

1) anemia
2) thrombocytopenia
3) acquired defects

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Uremia-induced platelet dysfunction

1) reduce GPIb (plt cannot adhere to subendothelium)

2) change GPIIb/IIIa (inhibit fibrinogen binding)

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Anemia causes platelet inhibition

Anemia –> increase NO activity –> vasodilation and plt inhibition

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Drugs that accumulate that can cause bleeding

1) beta-lactam antibiotics

2) oral anticoagulation (DOAC)

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Afib in CKD rate

20% have afib

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Percentage of herald bleed or access infection prior to fatal hemorrhage from access

40%

herald within 6 month

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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

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Platelet transfusion in bleeding in ESRD

immediate activity but last 45 hours

inactivated in uremic environment

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cryoprecipitate define

plasma derivative with

1) fibrinogen
2) vWF
3) factor VIII

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Maximum effect of cryoprecipitate and lasting duration

4-12 hours max, last 24 hr

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Complication with cryoprecipitate

1) anaphylaxis

2) hemolysis

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Protamine dose

1-1.5 mg/100 Units heparin

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Recombinant factor VIIa use in bleeding

Off label

risk of systemic thromboembolic complication

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Percentage of ESRD patients with HGB < 100

20%

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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

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Effect of estrogen for bleeding
onset
peak
duration

6 hours onset
peak 5-7 days
last 14 days

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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

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Most common access-related infection organism

Single organism Staphylococcus

Gram negative 25%

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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

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Centers for Disease control and prevention on risk factors associated with dialysis

1) catheter use
2) specific dialysis units
3) malnutrition (albumin < 35)

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Percentage of access loss due to infection

20%

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1 year infection rate for autogenous vs prosthetic

4.5% vs 19.7%

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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

Chapter 179 - Hemodialysis access - nonthrombotic complication Flashcards

(81 cards)