APACVS

April 8, 2018

Dejah R Judelson, MD

Assistant Professor of Surgery

Division of Vascular and Endovascular Surgery

University of Massachusetts Medical School

None

Understand the immediate management of◦ Paralysis due spinal cord ischemia

◦ Acute mesenteric ischemia

◦ Acute limb ischemia

◦ Access Site Complications

Be comfortable with evaluation of a peripheral vascular exam and change in exam

Post-operative patients are very tenuous

Without timely identification of a new problem → patients at higher risk for irreversible problems and death

Patients with vascular disease (and vascular complications) can decompensate quickly →high index of suspicion is paramount

Paralysis

Acute mesenteric ischemia

Acute limb Ischemia

Access Site Complications

Seen in the ICU after long aortic coverage (open TAAA repair, TEVAR)

Manifests as PARALYSIS◦ Proximal muscle group weakness → unable to lift

legs off the bed

Increased paralysis risk if:

◦ Previous aortic surgery

◦ Long length coverage

Artery of Adamkiewicz: T8-L1◦ Supplies lower 2/3 of spinal cord

via anterior spinal artery

Left vertebral artery◦ If left subclavian artery coverage is indicated → plan

for carotid-subclavian bypass

Hypogastric arteries◦ Avoid coiling/coverage of hypogastric arteries

Coverage of artery of Adamkiewicz (T8-L1)

Greater than 15cm descending thoracic aortic coverage

Coverage of L SCA

Coil embolization of hypogastric arteries

Biggest Risk: Spinal Cord Ischemia (SCI) Loss of costocervical collaterals from left vertebral and

subclavian arteries to anterior spinal artery

Paraplegia = Achilles Heel of TEVAR Ischemia of ventral horn (motor) of spinal cord

Spinal Cord Perfusion Pressure (SPP) = Mean Arterial Pressure (MAP) – Cerebrospinal Fluid Pressure (CSFP or ICP)

• Goals: • CPP >60-70 mmHg• MAP 80-90 mmHg • CSFP/ICP 10 cm H2O (13 cm H2O=10 mmHg)

CPP = MAP - ICP

Limited evidence

Strategies:◦ Maximize collateral

perfusion

◦ Maximize ischemic tolerance

CPP = MAP - ICP

1. Increasing MAP◦ Fluids (colloid >crystalloid)

◦ Inotropes

2. Decreasing CSFP/ICP◦ Spinal drainage

Maintain @ 10cm H20 (drain ~10cc/hr)

Avoid acute/large changes in CSF drainage to prevent brain herniation

3. Both!

CPP = MAP - ICP

Black arrow: “0” level with lumbar spine

Red arrow: level at which spinal fluid will overflow (usually 10cm H20)

White arrow: collection chamber to measure

• Spinal cord ischemia presents within 24 hours in 25% of patients•Remainder present > 24 hours post-op

• Drain maintained for 2-3 days following the procedure

• Remove drain with normal neurological exam and hemodynamic stability

Thiopental

Steroids

Naloxone

Hypothermia

Increase oxygen carrying capacity: Hct >30

Deficits can occur from immediate to 2weeks (median 3d); proximal LE muscles often first affected!

Exact mechanism unknown – “second hit” phenomenon

CSF drainage to achieve pressure <10, bedrest, MAP augmentation

Outcomes are better if CSF drain is in place at time of onset

Increase MAP: fluids, pressors◦ Goal MAP >90 (as high as >110 to regain normal

strength)

◦ Transfuse to Hct >30

Decrease ICP: drain spinal fluid, replace lumbar drain if needed◦ Limitation: can not place LD if patient has received

plavix

“….one of those conditions of which the diagnosis is impossible, the prognosis hopeless, and the treatment almost useless……"

Cokkinis, 1926

Mesenteric ischemia occurs when perfusion of visceral organs does not meet normal metabolic requirements

2 entities◦ acute (hours to days)

◦ chronic (weeks to years)

Elliott (1895): first case of AMI was diagnosed and treated successfully with intestinal resection and reanastomosis

Klass (1950): 1st modern SMA embolectomy

Mortality ~85%◦ High risk patients

◦ Delay in diagnosis

Failure to achieve postprandial hyperemic response◦ Inadequate O2 supply for metabolic processes (secretion,

absorption) and peristalsis◦ Decreased adenosine metabolism at cellular level

Failure of transport mechanisms

Inadequate muscle relaxation

◦ Malabsorption and abdominal pain (intestinal angina)

20% mesenteric capillaries open at a given time →nl O2 consumption can be maintained with 20% of maximal blood flow

Prolonged ischemia →disruption of intestinal mucosal barrier → malabsorption and heme+stool

<1/1000 hospital admissions

Females 3:1 Males

Age 60s-70s

Mortality 24-96% (RR 3 in pts >60yr)

Thrombotic Causes

Non-thrombotic causes

ArterialEmbolization

Low flow states (NOMI)Cardiogenic ShockSepsisHypovolemiaVasoconstrictors

Arterial Thrombosis

Mechanical Strangulated HerniaAdhesive BandsIntussuception

MesentericVenous Thrombosis

Trauma

Aortic Dissection

Most common cause of AMI (40-50%): embolization to SMA

Most common source: intracardiac mural thrombus (thrombus in proximal aorta)

Emboli lodge just distal to middle colic artery due to high basal flow and parallel course to aorta◦ Ischemia pattern: spares the first portion of the small

intestine and the ascending colon

10-15% associated with concomitant emboli to additional source

Risk Factors: Afib (tachyarrhythmias), recent MI with WMA, low EF (cardiomyopathy, CHF), cardiac tumors, structural heart defect, ventricular aneurysm

25-30% AMI◦ Autopsy study: ~10% population has >50% stenosis

in 1+ mesenteric vessels

In-situ thrombosis at pre-existing atherosclerotic lesions◦ Present with acute on chronic symptoms

Low flow state → thrombosis

More proximal occlusion: no sparing of the proximal jejunum or right colic distribution because the SMA origin is almost uniformly occluded

< 10% AMI

SMV thrombosis most common, also can see thrombosis of the IMV, splenic or portal veins

Venous obstruction →edema and hemorrhage of intestinal wall → focal sloughing of mucosa → distension→ eventual infarction

Primary (25%) – idiopathic Secondary (75%) – hypercoagulable states, polycythemia vera,

recent surgery, malignancy, trauma, cirrhosis, pancreatitis, OCP, hepatic failure

Rare cause of AMI

Most common cause in the ICU

Occurs in patients without anatomic arterial or venous

obstruction during periods of low cardiac output

◦ Often with underlying 3 vessel atherosclerosis

Vasospasm

Causes: Cardiac failure, sepsis, administration of α-adrenergic

agents, hemodialysis, AI, cardiopulmonary bypass

Reyer, et al. Revascularization for Acute Mesenteric Ischemia, JVS 2012

Embolism Thrombosis Venous thrombosisSmoking 55% 90% 47%Hypertension 50% 45% 20%COPD 41% 30% 7%PUD 23% 55% 20%DM 18% 15% 7%Hyperlipidemia 18% 15% 0%Cancer 9% 10% 20%

Endean et al. Annals of Surgery June 2001Acute Mesenteric Ischemia: A Clinical Review. Oldenburg et al. Arch Intern

Med. 2004;164(10):1054-1062

Acute onset abdominal pain (100%)

Nausea (44%) and/or Vomiting

Diarrhea (35%)

Tachycardia with HR > 100 (33%)

Blood per rectum (16%)

Constipation (7%)

Late findings: fever, oliguria, dehydration, confusion, tachycardia, and shock

Park et al. Journal of Vascular Surgery March 2002

Bradbury AW, Brittenden J, McBride K, et al.: Mesenteric ischaemia: a multidisciplinary approach. Br J Surg. 82:1446-1459 1995

“Pain out of Proportion to exam”

Abdominal pain, nausea/vomiting, diarrhea, BRBPR

Vitals: tachycardic Labs: leukocytosis, metabolic acidosis,

hemoconcentration

If clinical suspicion of AMI, start therapeutic heparin gtt (bolus 80 units/kg and start gtt at 18 units/kg), fluid resuscitation, sepsis treatment

Order stat CTA abdomen/pelvis Vascular and general surgery consult: this is a

surgical emergency

Duplex Ultrasound

CT scan (CTA, CTV)

MR (MRA, MRV)

Angiography

Surgical Steel

Most invasive

Least invasive

Diagnosis

Intervention

Size of vessels

Calcification

Flow rates and directionality

Key: Patient must be FASTING

Limitations: bowel gas, body habitus, abdominal tenderness may limit patient cooperation

Best first line tool for most (non-emergent life threating disorders) → NOT useful in acute mesenteric ischemia

Abdominal plain films NORMAL in 25% AMI

Early findings: ileus

Advanced cases: pneumatosis, bowel wall edema (“thumbprinting”)

Beneficial to exclude other causes of abdominal pain (performation, SBO)

CTA: occlusion of 1+ mesenteric vessels (can be only SMA)◦ Preferred diagnostic test◦ Timing is key: CT with IV contrast is often non-

diagnostic

Pros:◦ High resolution → can visualize 2nd order branches◦ Diagnostic information on arterial and venous systems◦ Allows for operative planning◦ Exclude other causes of pain◦ Evidence of bowel compromise: pneumatosis, wall

thickening portal venous gas

Cons◦ PO contrast detracts from image quality◦ Renal damage from high contrast load◦ Hypersensitivity to iodinated contrast◦ Contrast can overestimate degree of stenosis

Impractical due to time constraints

Can overestimate degree of stenosis

May fail to show distal emboli, low-flow states, or vasculitis

More difficulty in identifying secondary signs, ieindurated fat or bowel wall thickening

Reported sensitivity of contrast-enhanced MRA of 100% and specificity of 87% to detect a > 50% visceral artery stenosis

ChronicAcute

Pros:◦ Often the gold standard in vascular

imaging◦ Has the potential to be both

diagnostic and therapeutic◦ Uses minimal contrast (<60 cc/case)

Cons◦ Invasive◦ Risk of access site complications◦ Doesn’t assess surrounding anatomy

(ie bowels)

Arteriography (Siegelman et al) diagnosis of vasospasm1. narrowing of the origins of

multiple branches of the SMA

2. alternate dilatation and narrowing of the intestinal branches—the “string of sausages” sign

3. spasm of the mesenteric arcades

4. impaired filling of the intramural vessels

Siegelman SS, Sprayregen S, Boley SJ: Angiographic diagnosis of mesenteric arterial vasoconstriction. Radiology. 112:533-542 1974

Initial resuscitation◦ Crystalloid◦ Correction of metabolic abnormalities (acidosis,

hyperkalemia)◦ Immediate monitoring: UOP (foley), continuous BP (A-

line)◦ Sepsis Treatment: Broad Spectrum Abx (target G- and

anaerobes)◦ Systemic Anticoagulation with IV Heparin

Special Consideration◦ Avoid vasopressors: low dose dopamine and epi

preferred (avoid pure alpha)◦ Large fluid sequestration: may require >15L in initial 24

hours

1. Preserve as much bowel and functionality as possible (optimize SB length)

2. Remove non-salvageable bowel

3. Prevent further bowel infarction

**Exploratory laparotomy = gold standard to determine viable bowel**

Angio: can be diagnostic and therapeutic TPA +/- plasty/stenting◦ Thrombolysis may take too long

May avoid synthetics in a possibly contaminated field

Does not eliminate need for direct visualization of threatened bowel

Increased risk of GI hemorrhage post reperfusion

More applicable in CMI

Open surgical exploration required for all threatened bowel

Revascularization should occur prior to bowel resection except in cases with frank necrosis, perforation, or peritoneal soilage◦ Bowel that appears severely ischemic may recover with

in-line flow

Exploratory laparotomy with vertical midline incision◦ Embolus: anterior approach at base of transverse

mesocolon◦ Bypass: lateral approach above 4th portion of duodenum

to facilitate retrograde bypass

Essential to assess after revascularization (allow 20-30 minutes if possible)

Visual inspection (color, motility)

Continuous Wave Doppler assessment

Fluorescien uptake

Surface oximetry

If viability is in question, second-look laparotomy is mandatory

Retrograde Open Mesenteric Stenting◦ SMA accessed at base of transverse mesocolon

◦ Patch angioplasty → retrograde stent at SMAorigin

◦ Useful for thrombotic events

Wyers MC, Powell RJ, Nolan BW, Cronenwett JL: Retrograde mesenteric stenting during laparotomy for acute occlusive mesenteric ischemia. J Vasc Surg. 45:269-275 2007

◦ 70 patients, 80% endovascular → 87% successful

◦ Open laparotomy: 69% of endovascular cases

◦ Endovascular: fewer cases of ARF and pulmonary failure, mortality 36% (compared to 50% with open or endofailure)

Peritonitis or Hypotension at presentation Intestinal necrosis at initial laparotomy

Edwards et al. Annals of Vascular Surgery January 2003

Renal insufficiency, age >70, metabolic acidosis, symptom duration and bowel resection in second-look operations associated with mortality

Age >70 and prolonged symptom duration = independent predictors of mortality

Kougias et al. Journal of Vascular Surgery. 2007

Typical patient◦ ICU on multiple pressors

◦ Marginal/poor cardiac reserve

◦ Underlying moderate to severe atherosclerosis

Treatment: supportive management, anticoagulation, antibiotics, intra-arterial infusion of vasodilators (PDE inhibitor: papaverine 30-60mg/hr x 24 hours)

Vasospasm Post vasodilator

Indications for OR (with general surgery):

pneumoperitoneum

peritonitis

→ no revascularization indicated

Treat the patient not the CT scan Up to 50% of patient who have had a recent laparoscopy will have

evidence of non-occlusive thrombus in the SMV

Treatment: Anticoagulation, bowel rest (NPO/TPN)

◦ Surgical interventions have poor outcomes and have gone out of favor

◦ Adjuncts include: thrombolysis, mechanical/aspiration/surgical thrombectomy, TIPS, liver transplant,

When vascular surgeons need a colonoscopy!

Open AAA repair

Endovascular repair of abdominal aortic aneurysm

Open Repair

◦ Causes: Ligation of IMA off aneurysm sac, rarely

reimplanted (if patent celiac, SMA)

Hypotension or hypoperfusion

EVAR

◦ Causes: Microembolization due to wire manipulation

Coil embolization of hypogastric arteries and exclusion of IMA

Watershed at risk: Sigmoid colon, splenic flexure

Symptoms: early BM → if guiac + need further workup ◦ Expect ileus of 2-3 days

◦ Bloody BM is VERY concerning

◦ Patients with epidural so often do not have pain

Diagnosis: Colonoscopy◦ Grade 1: patchy mucosal necrosis

◦ Grade 2: mucosal and muscularis involvement

◦ Grade 3: transmural necrosis, gangrene, and perforation

Treatment: Fluid resuscitation, antibiotics, bowel resection (if grade 3)

“Um… I think the patient has a cold leg

… No, I don’t think he has any pulses”

Due to of sudden inadequate arterial perfusion to an extremity.

Manifestations: loss of sensory and motor function of the affected extremity, gangrene leading to sepsis, as well as systemic acid–base disturbances and increased cardiopulmonary stress.

In the ICU: concomitant conditions such as myocardial infarction, hypercoagulable states, or hypotension requiring pharmacologic support play a role in both the etiology and disease progression

Revascularization can lead to ischemia–reperfusion injury impacting multiple organ systems and rhabdomyolysis as toxic by-products are reintroduced into the system circulation.

30-day mortality rates of 15% 5-year mortality rates of up to 50% Amputation rates range from 10% to 30%

Highest postoperative morbidity & mortality (except rAAA)

limb loss 24%, death 30%

Can be a manifestation of end of life

Irreversible ischemia at

6hr

Category Prognosis Sensory Loss Motor Deficit

Arterial Doppler

Venous Doppler

I: Viable No immediate Threat None None Audible Audible

IIA: Marginally Threatened

Salvageable if promptly treated

Minimal (toes) or none

None Inaudible

(often)

Audible

IIB: Immediately threatened

Salvageable if immediately revascularized

More than toes, rest pain

Mild/Moderate Inaudible

(usually)

Audible

III: Irreversible Major tissue loss, permanent nerve damage inevitable

Profound, anesthetic

Profound, paralysis (rigor)

Inaudible Inaudible

Modified from Ouriel K. Shortell CK, DeWeese JA, et al: A comparison of thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischemia. J Vasc Surg 19:1021-1030, 1994

Rutherford / SVS

Embolism Thrombosis Dissection Trauma Iatrogenic

Appropriate management is determined by(1) degree of ischemia(2) underlying etiology

Cardiac Origin Non-cardiac Origin

Atrial / ventricular◦ Atrial fibrillation◦ Mural thrombus (MI/LV

aneurysm)

Valvular disease◦ Rheumatic heart◦ Artificial valves

Endocarditis

Paradoxical (Patent Foramen Ovale)

Cardiac tumor

Atheroembolism Aortic mural thrombi◦ Hypercoaguable states◦ Ulceration

Aneurysm◦ Aortic◦ Peripheral

Other◦ Iatrogenic◦ Tumors◦ Air◦ Fat◦ Amniotic fluid

Embolism

Progression of chronic atherosclerotic disease◦ Plaque rupture and arterial

thrombosis

Low flow states◦ CHF◦ Hypotension◦ Vasoactive drugs

Hypercoagulable states

Bypass graft occlusion

Trauma/Iatrogenic (femoral access)

Dissection◦ Aortic◦ Branch arteries

(renal/mesenteric/extremity) Trauma fibrodysplasia

Acu

Embolism ThrombosisArrhythmia No arrhythmia

Sudden onset Sudden or slower onset

Severe signs and symptoms Less severe signs and symptoms

No history of claudication, rest pain History of claudication, rest pain

No risk factors for peripheral vascular disease*

Risk factors for peripheral vascular disease

Normal contralateral pulse exam Abnormal contralateral pulse exam

No Physical findings of chronic limb ischemia

Physical findings of chronic limb ischemia†

*Cardiac disease, prior myocardial infarction, hyperlipidemia, stroke, family history, history of

smoking, diabetes, etc.

†Absence of extremity pulses, diminished hair growth, thin skin, thick nails, ulcersCITC Seminars in Vascular Surgery

Heparin (bolus 80units/kg, gtt at 18units/kg)◦ Reduces propagation of embolus or thrombus both

proximally and distally◦ Reduces risk of metachronous embolism

Supportive Measures◦ Resuscitation (especially before contrast agents)◦ Analgesia

OR versus Imaging

Acute Limb Ischemia:Initial Management

Embolism:OPERATING ROOM◦ Fogarty catheter

◦ Fasciotomies

Thrombosis: OPERATING ROOM◦ Fogarty catheter

◦ Bypass/endarterectomy

◦ Fasciotomies

Acute Limb Ischemia:Treatment: Rutherford IIb/III (threatened limb)

Catheter directed thrombolysis - tPA

Acute Limb IschemiaTreatment: Rutherford IIa

Absolute contraindications

1. Established cerebrovascular event (excluding TIA within previous 2 months)

2. Active bleeding diasthesis

3. Recent gastrointestinal bleeding (within previous 10 months)

4. Intracranial trauma within previous 3 months

Relative contraindications

1. Cardiopulmonary resusitation within previous 10 days

2. Major nonvascular surgery or trauma within previous 10 days

3. Uncontrolled hypertension (systolic >180mmHg or diastolic >110mmHg)

4. Puncture of non compressible vessel

5. Intracranial tumor

6. Recent eye surgery

Minor contraindications

1. Hepatic failure, particularly those with coagulopathy

2. Bacterial endocarditis

3. Pregnancy

4. Active diabetic proliferative retinopathy

Lysis

Initiated

Reimage

Angiojet

Worsening Ischemia at

any point.

(LYSIS ABORTED)

Terminate Lysis

12-24 hrs

None or

minimal

change

Lyse 12-24

hrs and

reimage

Lyse 12-

24hrs and

reimage

Terminate

Lysis

Near resolution

with small amount

of residual clot

burden

Complete Resolution

From Schanzer et al, Acute

Limb Ischemia, Endovascular

Peripheral Interventions,

2012.

Acute Limb Ischemia: Thrombolysis

Initiation of Therapy Initial dose of tPA is 0.5-4.0 mg/min

Selective infusion at site of occlusion based on angiogram (systemic therapy needed infrequently)

A NON-therapeutic heparin gtt is usually administered via the sheath (to maintain sheath and access vessel patency); usual dose is 500 units/hr, NOT to reach a therapeutic PTT, do not titrate up!

Monitoring of thrombolytic therapy Check fibrinogen levels Q4hr.

Fibrinogen <100 or drop by >50%: systemic lytic state and an increased risk for hemorrhage. STOP LYSIS

Angiograms are typically performed on a daily basis, not to exceed 72 hrs.

PTT should be monitored Q4hr (not to be therapeutic, goal typically <40)

Acute Limb Ischemia: Thrombolysis

1% RISK OF INTRACRANIAL HEMORRHAGE Stop lysis and heparin IMMEDIATELY if

Mental Status Change/change in Neurologic Exam

Nausea: don’t give Zofran! New somnolence New onset headache: never just give Tylenol!

Immediately stop thrombolysis/heparin gtt May give protamine or FFP (not very effective) STAT Head CT

Depends on:

-Degree of ischemia-Comorbid conditions- Etiology of the event

Acidosis

Hyperkalemia

Systemic inflammatorystate

Myoglobinuria/ARF

Compartment syndrome

Fluid resuscitation

Cardiac stabilization◦ Insulin/D50

◦ Calcium

◦ Albuterol

Dialysis

Fasciotomies

Know your exam!◦ Did the patient have palpable or dopplerable

pulses… this matters!

Check femoral, popliteal, DP, PT pulses

◦ What does the “normal” side have – people are symmetric!

Start therapeutic heparin drip with a bolus

Call vascular surgery and consider imaging (usually CT angiogram)

If the limb is non-viable → make sure it isn’t making the patient worse

Amputations often can wait for the patient’s clinical picture to improve

If acidosis is worsening with no other etiology → may need to proceed with urgent amputation to save the patient (cryo amp if too unstable for the OR)

“all bleeding stops eventually”

-said every vascular surgeon

Multifactorial

Bleeding varices in ESLD

Spontaneous: DIC

Post-procedure:◦ Tamponade

◦ Hemothorax

◦ Access Site Complications

IABP

TAVR

Diagnostic angiogram

Brachial/axillary arterial line

Iatrogenic arterial line

Critical to know what size sheath was in your patients◦ IABP: 7.5-8Fr

◦ TAVR access sheath: 16-18Fr

◦ Cardiac cath: 4Fr (groin, diagnostic) or 6Fr (radial)

Expanding hematoma◦ Slow ooze

◦ Pulsatile bleed

Arteriovenous fistula

Pseudoaneurysm

Retroperitoneal bleed

Usually due to inadequate pressure hold or patient not compliant with appropriate bed rest

Management:◦ Re-hold pressure based on size of the sheath

5min per French

NO PEAKING!

6 hours bed rest once completed

◦ Consider groin duplex

Usually due to inadequate pressure hold or patient not compliant with appropriate bed rest

Within an hour of sheath pull

Management:◦ Re-hold pressure based on size of the sheath

5min per French

NO PEAKING!

6 hours bed rest once completed

Usually due to inadequate pressure hold or patient not compliant with appropriate bed rest

Often several hours after sheath pull

Management:◦ Hold immediate pressure and call vascular

◦ If patient stable → CTA angiogram◦ If patient unstable or rapidly expanding hematoma → OR emergently for repair Make sure patient has up to date type and cross

Abnormal connection between an artery and a vein

Access site complication: needle goes through vein into artery

Typically occurs hours to days after procedure

Patients complain of enlarging hematoma in groin

Diagnosis◦ Pulsatile mass in groin

◦ Audible bruit, palpable thrill

◦ Groin duplex

Treatment◦ Operative ligation

Not a true aneurysm

Doesn’t contain all levels of arterial wall

Essentially a hematoma contained by the surrounding tissues with a small hole in the blood vessel

Expanding hematoma after percutaneous access (days to weeks)

Occasionally pulsatile

Risk factors:◦ Anti-platelet agents

◦ Anticoagulation

◦ Female gender

◦ obesity

Arterial Duplex◦ Identifies normal vessel

◦ Neck of pseudoaneurysm

◦ Body of aneurysm

◦ Classic “ying yang” sign on color flow

90F POD#2 s/p TAVR via R CFA (Perclosed) with 6Fr sheath in L CFA (Angiosealed)

Started anticoagulation → slowing expanding hematoma

Thrombin injection◦ If long narrow neck (length >=2x width)

◦ No overlying skin changes

◦ Preferred for patients that can not come off anticoagulation/anti-platelets → also increases risk of failure

Open repair◦ Overlying skin changes

◦ Failed thrombin injection

Monitor pulses after thrombin injection◦ Risk of native vessel thrombosis and embolization

Repeat duplex day after thrombin injection

Can either be immediate (during procedure) or delayed (night after procedure) diagnosis

Causes:◦ High stick (external iliac artery)

◦ Injured or ruptured iliac artery

Calcific vessels

Large sheaths

Flank pain

Dropping hematocrit

Groin hematoma (especially if stick through inguinal ligament)

Often a delayed diagnosis → high index of suspicion

CT angiogram of abdomen and pelvis◦ Make sure radiology gets delayed images as well!

◦ Often difficult to identify location of bleed but does confirm there is a bleed

RP space is limited – often these bleed can tamponade themselves off◦ Fluid and blood resuscitation

◦ Close monitoring

Operative◦ Diagnostic angiogram from CONTRALATERAL side

◦ Identify location of bleed

◦ Repair: covered stent, open repair

Brachial sheath has limited space

Median nerve runs medial to brachial artery

Even a small hematoma in brachial sheath can cause neurologic damage◦ Numbness or paresthesias in fingers

Early operative hematoma evacuation preserves neurologic function

High index of suspicion!

Thank You