Vascular Surgery
Trauma Surgery
General Surgery
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Acute Vascular Injury

Acute vascular injury encompasses traumatic damage to arteries or veins resulting from penetrating or blunt mechanisms. ... FRCS exam preparation.

Updated 17 Jan 2026
Reviewed 17 Jan 2026
57 min read
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MedVellum Editorial Team
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MedVellum Medical Education Platform

Clinical board

A visual summary of the highest-yield teaching signals on this page.

Urgent signals

Safety-critical features pulled from the topic metadata.

  • Active pulsatile bleeding
  • Hard signs: absent distal pulses, expanding hematoma, bruit/thrill
  • Acute limb ischemia (6 Ps)
  • Signs of compartment syndrome

Exam focus

Current exam surfaces linked to this topic.

  • FRCS

Linked comparisons

Differentials and adjacent topics worth opening next.

  • Acute Arterial Thrombosis
  • Arterial Embolism

Editorial and exam context

Reviewed by MedVellum Editorial Team · MedVellum Medical Education Platform

Credentials: MBBS, MRCP, Board Certified

FRCS
Clinical reference article

Acute Vascular Injury

1. Clinical Overview

Summary

Acute vascular injury encompasses traumatic damage to arteries or veins resulting from penetrating or blunt mechanisms. These injuries represent life- and limb-threatening emergencies requiring immediate recognition and intervention. The spectrum ranges from complete vessel transection with exsanguinating hemorrhage to subtle intimal injuries causing delayed thrombosis. Understanding the distinction between hard and soft signs of vascular injury is critical for appropriate triage and management decisions. [1,2]

Vascular injuries account for 3-5% of all civilian trauma cases but carry mortality rates of 5-15% depending on vessel location and injury severity. [3] Extremity vascular injuries are most common (70%), followed by neck (15%), thorax (10%), and abdomen (5%). [4] The "golden period" for limb salvage is traditionally considered 6 hours from injury to revascularization, though modern evidence suggests this varies by mechanism and associated soft tissue injury. [5]

The management paradigm has evolved significantly with the advent of endovascular techniques. However, open surgical repair remains the gold standard for most extremity injuries, while endovascular approaches have become first-line for selected truncal and neck injuries. [6,7] The fundamental principle remains unchanged: rapid control of hemorrhage, restoration of perfusion, and prevention of secondary complications including compartment syndrome.

Key Facts

  • Definition: Traumatic disruption of arterial or venous structures
  • Incidence: 3-5% of civilian trauma admissions, up to 30% in military trauma [3,4]
  • Mortality: 5-15% overall; up to 50% for aortic injuries [8]
  • Peak age: Bimodal - young adults (penetrating) and elderly (blunt)
  • Critical feature: Hard signs mandate immediate surgical intervention
  • Key investigation: Clinical assessment primary; CT angiography for stable patients with soft signs
  • First-line treatment: Hemorrhage control, resuscitation, urgent revascularization
  • Time-critical: 6-8 hour "golden period" for limb salvage (warm ischemia tolerance) [5]

Clinical Pearls

"Hard signs = operating theatre" — Presence of ANY hard sign (pulsatile bleeding, absent pulses, expanding hematoma, bruit/thrill, signs of ischemia) mandates immediate surgical exploration. No imaging required. These patients go directly from ED to OR. [1,9]

"The limb that looks dead may not be" — Initial assessment can be deceiving. A pulseless, pale limb may be salvageable if revascularized within the critical ischemia window. Conversely, a warm limb with pulses may harbor an intimal injury progressing to thrombosis. Serial examination is essential. [10]

"Pulse doesn't exclude injury" — Up to 15% of patients with significant arterial injuries maintain palpable distal pulses due to collateral flow or incomplete vessel disruption. High index of suspicion required for proximity injuries. [11,12]

"Compartment syndrome after vascular repair is the rule, not the exception" — Ischemia-reperfusion injury causes 10-25% incidence of compartment syndrome post-revascularization. Prophylactic fasciotomy should be strongly considered for ischemia > 6 hours, combined arteriovenous injuries, or high-energy mechanisms. [13,14]

"Repair vs ligation: Know your safe ligations" — Only specific vessels can be safely ligated: one forearm artery (if the other intact), one tibial artery (if other two intact), internal carotid (if circle of Willis intact), internal iliac. All other major vessels require repair. [15,16]

"ATLS approach saves lives" — Vascular injuries are managed within ATLS framework: control catastrophic hemorrhage even before airway, identify life-threatening bleeding in primary survey, definitive hemorrhage control in secondary survey or OR. [17]

Why This Matters Clinically

Vascular injuries are unforgiving. Missed diagnosis leads to exsanguination, thrombosis, or limb loss. Delayed treatment increases amputation rates from 5-10% (early treatment) to 40-50% (> 6 hours). [5,18] Recognition of hard signs, appropriate use of imaging to avoid delays, understanding of surgical decision-making (repair vs ligation, endovascular vs open), and vigilance for compartment syndrome distinguish competent from excellent trauma surgeons. This knowledge is essential for FRCS/FRACS trauma and vascular modules.


2. Epidemiology

Incidence & Prevalence

Civilian Trauma:

  • Overall vascular injury incidence: 3-5% of trauma admissions [3]
  • Penetrating mechanism: 10-15% develop vascular injury [4]
  • Blunt mechanism: 1-2% develop vascular injury [4]
  • Urban trauma centers: 200-300 vascular injuries per year at Level I centers [19]

Military Trauma:

  • Vascular injury incidence: 15-30% of combat casualties [20]
  • Extremity vascular injuries: 90% of military vascular trauma [20]

Anatomical Distribution:

  • Lower extremity: 40-50% [4]
  • Upper extremity: 20-30% [4]
  • Neck: 10-15% [4]
  • Thorax: 5-10% [8]
  • Abdomen: 5-10% [4]

Trend Analysis:

  • Increasing incidence of blunt vascular injuries with motor vehicle trauma [21]
  • Decreasing penetrating injuries in regions with strict weapon control [21]
  • Increasing proportion managed endovascularly (from less than 5% in 2000 to 25-35% in 2020) [6,7]

Demographics

FactorDetailsEvidence
AgeBimodal: peak 20-40 years (penetrating), second peak > 60 years (blunt)[21]
SexMale predominance 4:1 (reflects trauma patterns)[4]
EthnicityNo inherent predisposition; reflects trauma epidemiology[4]
GeographyHigher penetrating trauma in urban centers; higher blunt in rural areas[19]
OccupationIncreased in military, law enforcement, construction[20]
SocioeconomicInverse correlation with socioeconomic status (penetrating trauma)[21]

Risk Factors

Mechanism-Based Risk Factors:

MechanismVascular Injury RiskTypical VesselsEvidence
High-velocity gunshot40-60%Any in path[4]
Stab wound10-20%Superficial vessels preferentially[4]
Knee dislocation20-40% popliteal injuryPopliteal artery (fixed at two points)[22]
Posterior shoulder dislocation5-10% axillary injuryAxillary artery[23]
Supracondylar humerus fracture10-15% brachial injuryBrachial artery[24]
Open tibial fracture (Gustilo IIIc)20-30%Tibial vessels[5]
Pelvic fracture (Tile C)10-20% major bleedingInternal iliac, presacral venous plexus[25]

Patient Risk Factors for Poor Outcomes:

  • Age > 65 years: 3-fold increase in amputation risk [26]
  • Diabetes mellitus: impaired collateral flow, increased infection risk [26]
  • Peripheral vascular disease: pre-existing ischemia limits ischemic tolerance [26]
  • Smoking: impaired wound healing, increased thrombosis risk [26]
  • Anticoagulation: increased hemorrhage, complex reversal requirements [27]

Associated Injuries (Polytrauma Pattern)

Vascular injuries rarely occur in isolation:

  • Orthopedic injuries: 60-70% of extremity vascular injuries [5]
  • Nerve injuries: 30-40% (especially brachial plexus, peroneal nerve) [28]
  • Venous injuries: 50% have concomitant venous injury [29]
  • Visceral injuries: 40% in truncal vascular trauma [4]

3. Pathophysiology

Classification of Vascular Injuries

Multiple classification systems exist. The most clinically relevant is the descriptive anatomical classification:

By Vessel Wall Involvement

TypeDescriptionPathophysiologyClinical Significance
Intimal flap/tearInner lining disrupted, media intactTurbulent flow → thrombosis (hours to days)May have normal pulses initially; delayed presentation [10]
Laceration (partial)less than 50% circumference disruptedBleeding controlled by vasospasm/hematomaBleeding may recur; pseudoaneurysm risk [30]
Laceration (complete)> 50% circumference disruptedVessel retracts, ends spasmMay have LESS bleeding than partial (paradoxical) [31]
TransectionComplete vessel divisionComplete retraction, end artery spasmHard ischemia unless collaterals; may have less external bleeding [31]
ContusionVessel wall bruised, no breachVasospasm, thrombosis, delayed ruptureMay progress to thrombosis or pseudoaneurysm [32]
ThrombosisLuminal clot without breachSecondary to intimal injury, compression, or stasisIschemia without external signs [10]
Arteriovenous fistulaAbnormal arteriovenous connectionHigh-flow shunt; may cause high-output cardiac failureBruit, thrill, warm extremity despite inadequate flow [33]
PseudoaneurysmContained rupture, hematoma communicated with lumenPulsatile hematoma; rupture riskExpanding mass, bruit, delayed rupture [30]

By Hemorrhage Pattern

External Hemorrhage:

  • Pulsatile bleeding: arterial injury with skin breach
  • Continuous oozing: venous injury or small arterial injury
  • Volume loss dictates hemodynamic status

Contained Hemorrhage:

  • Hematoma: bleeding into tissue planes
  • Hemothorax: thoracic great vessel injury (can hold 2-3L per side)
  • Hemoperitoneum: abdominal vascular injury (entire blood volume can be lost)
  • Retroperitoneal hematoma: aortic, iliac, IVC injuries (several liters capacity)

Expanding Hematoma:

  • Active ongoing bleeding into contained space
  • Hard sign for vascular injury
  • Indicates failure of tamponade; requires urgent intervention

Molecular and Cellular Pathophysiology

Exam Detail: #### Acute Phase (0-6 hours): Injury and Thrombosis

Endothelial Disruption:

  1. Mechanical trauma exposes subendothelial collagen and von Willebrand factor (vWF)
  2. Platelet adhesion via GPIb-vWF interaction
  3. Platelet activation and aggregation (GPIIb/IIIa-fibrinogen binding)
  4. Coagulation cascade activation (tissue factor exposure)
  5. Thrombin generation and fibrin clot formation

Vasospasm:

  • Injured smooth muscle releases endothelin-1 and thromboxane A2
  • Loss of endothelial NO and prostacyclin
  • Intense vasoconstriction (protective in complete transection; harmful in partial injury)

Ischemic Phase (> 6 hours): Tissue Injury

Metabolic Derangement:

  • Anaerobic metabolism → lactic acidosis
  • ATP depletion → Na+/K+-ATPase failure → cellular edema
  • Calcium influx → mitochondrial damage → apoptosis initiation

Ischemia Tolerance by Tissue:

  • Nerve: 30 minutes (irreversible injury)
  • Muscle: 4-6 hours (irreversible injury, myonecrosis)
  • Skin: 12-24 hours (relatively tolerant)
  • Bone: days to weeks (very tolerant)

This explains the 6-hour "golden period" for limb salvage - based on irreversible muscle injury threshold. [5]

Reperfusion Phase: Ischemia-Reperfusion Injury

Oxygen Radical Generation:

  1. Xanthine oxidase pathway activated during ischemia
  2. Restoration of O2 → superoxide (O2-), hydrogen peroxide (H2O2), hydroxyl radical (OH•)
  3. Lipid peroxidation → membrane damage
  4. Protein oxidation → enzyme inactivation

Inflammatory Cascade:

  • Neutrophil activation and endothelial adhesion (selectins, ICAM-1)
  • Cytokine release (TNF-α, IL-1, IL-6)
  • Complement activation (C3a, C5a)
  • Increased capillary permeability → edema

Compartment Syndrome Mechanism:

  • Reperfusion edema increases compartment pressure
  • When pressure > capillary perfusion pressure (~30 mmHg), microvascular collapse
  • Creates vicious cycle: ischemia → edema → ↑ pressure → ischemia
  • Results in "second hit" ischemia despite patent macroscopic repair [13,14]

Systemic Effects:

  • Myoglobin release from muscle necrosis → myoglobinuric renal failure
  • Potassium release → hyperkalemic cardiac arrest
  • Acidosis → cardiovascular instability
  • Inflammatory mediators → systemic inflammatory response syndrome (SIRS), multi-organ dysfunction

Mechanism-Specific Injury Patterns

Penetrating Trauma

Low-Velocity (less than 600 m/s): Knife, Glass

  • Direct laceration only
  • Minimal surrounding tissue damage
  • Clean edges amenable to primary repair
  • Lower infection risk

High-Velocity (> 600 m/s): Gunshot

  • Primary missile track causes direct injury
  • Secondary blast effect causes cavitation injury (temporary cavity up to 30x bullet diameter)
  • Zone of injury extends well beyond visible wound
  • Thrombosis common in "stunned" vessels outside primary track [34]

Blast Injury

  • Primary: pressure wave causes shear injury to vessel walls
  • Secondary: fragment penetration (like low-velocity penetrating)
  • Tertiary: blunt trauma from body displacement
  • Quaternary: burns, inhalation injury

Blunt Trauma

Direct Vascular Compression/Crush

  • Vessel compressed between external force and bone
  • Intimal tear common (media relatively protected)
  • Thrombosis risk high [10]

Deceleration Injury

  • Occurs at points of vascular fixation (aortic isthmus, renal artery origins)
  • Shear forces cause transection or intimal tear
  • Classic: aortic transection at ligamentum arteriosum [35]

Stretch/Traction

  • Joint dislocation stretches tethered vessels
  • Knee dislocation → popliteal injury (fixed at adductor hiatus and soleus arch) [22]
  • Shoulder dislocation → axillary injury

Fracture-Associated

  • Bone fragments directly lacerate vessel
  • Displaced fracture compresses/kinks vessel
  • Classic associations:
    • Supracondylar humerus → brachial artery [24]
    • Tibial plateau → popliteal artery
    • Pelvic ring disruption → internal iliac vessels [25]

4. Clinical Presentation: Hard Signs vs Soft Signs

This is the most critical clinical distinction in vascular trauma. It determines immediate management pathway.

Hard Signs of Vascular Injury

Presence of ANY hard sign = immediate operative intervention (no imaging required) [1,9]

Hard SignMechanismSensitivitySpecificityClinical Notes
1. Active pulsatile bleedingArterial injury with skin breach100% (if present)100%Arterial = pulsatile, bright red; Venous = continuous, dark red [1]
2. Expanding hematomaOngoing bleeding into tissue95%98%Indicates failure of tamponade; measure serially [36]
3. Palpable thrillTurbulent arteriovenous flow90%99%Indicates AV fistula; may be subtle initially [33]
4. Audible bruitTurbulent flow (AVF or pseudoaneurysm)85%99%Use stethoscope; may not be present acutely in shock [33]
5. Absent distal pulsesArterial occlusion or transection85-95%85-90%Compare to contralateral; Doppler if impalpable [11,12]
6. Signs of acute ischemiaInadequate arterial perfusion95%95%"6 Ps" (see below); indicates less than 6 hours to salvage [5]

The "6 Ps" of Acute Limb Ischemia:

  1. Pain: severe, unremitting, out of proportion to exam
  2. Pallor: pale, white limb (vs pink normal)
  3. Pulselessness: absent distal pulses (Doppler signals absent)
  4. Paresthesias: numbness, tingling (indicates nerve ischemia - bad sign)
  5. Paralysis: inability to move (indicates muscle ischemia - very bad sign)
  6. Poikilothermia: cold to touch (compare to contralateral)

Key Point: Paresthesias and paralysis are late signs indicating advanced ischemia (> 4-6 hours). Their presence reduces salvage rates from 90% to 50%. [5,18]

Soft Signs of Vascular Injury

Soft signs indicate possible vascular injury. Require further investigation (typically CT angiography). [1,9,37]

Soft SignIncidence of Significant InjuryClinical ApproachEvidence
1. History of pulsatile bleeding (now stopped)5-10%CTA if hemodynamically stable; consider observation[37]
2. Diminished (but present) pulses10-15%Calculate ABI; if less than 0.9, obtain CTA[38]
3. Proximity to major vessel3-5%CTA vs observation (controversial)[39]
4. Peripheral nerve deficit15-20% (vascular) vs 80-85% (nerve only)CTA to rule out concomitant vascular injury[28]
5. Moderate, non-expanding hematoma5-8%Serial examination; CTA if expands or pulses change[36]
6. Injury trajectory near vessel3-5%CTA if high-energy mechanism[39]

Management Algorithm for Soft Signs:

SOFT SIGN PRESENT
        ↓
Hemodynamically stable? 
        ↓
    YES ↙     ↘ NO
        ↓           ↓
    Calculate ABI   Direct to OR
        ↓           ↓
   less than 0.9?   > 0.9?   Explore on clinical grounds
    ↓       ↓
   CTA    Observe with serial exams
    ↓       ↓
+ve  -ve   Discharge at 24h if stable
 ↓    ↓
 OR  Observe

Ankle-Brachial Index (ABI) in Vascular Trauma

Technique:

  • Measure SBP in affected limb (ankle or wrist) using Doppler
  • Measure SBP in uninjured brachial artery
  • ABI = Affected limb SBP / Brachial SBP

Interpretation:

  • ABI ≥0.9: 95% NPV for significant arterial injury - safe to observe [38]
  • ABI less than 0.9: 85-90% sensitivity for arterial injury - obtain CTA [38]
  • ABI cannot be calculated if no Doppler signal: assume injury, obtain CTA or explore

Limitations:

  • Less accurate in hypotension (all pressures low)
  • Cannot detect venous injuries
  • Cannot detect intimal injuries with maintained flow
  • Operator-dependent

5. Clinical Examination: ATLS Approach

Vascular injuries are managed within the Advanced Trauma Life Support (ATLS) framework. [17]

Primary Survey: ABCs with Catastrophic Hemorrhage Control

(C)ABC Approach (ATLS 10th Edition): Modern ATLS places catastrophic hemorrhage control BEFORE airway. [17]

C - Catastrophic Hemorrhage:

  • External compressible hemorrhage: direct pressure (most effective)
  • External non-compressible junctional hemorrhage (groin, axilla, neck): hemostatic gauze + pressure
  • Extremity exsanguinating hemorrhage not controlled by pressure: tourniquet (2 inches above wound, tighten until bleeding stops)
  • Document tourniquet time (ischemia tolerance ~2 hours; up to 6 hours acceptable if life-saving) [40]

A - Airway with C-spine protection:

  • Assess and secure airway
  • In vascular neck trauma: establish airway BEFORE exploring hematoma (may lose airway if expanding)

B - Breathing:

  • Assess respiratory effort
  • Massive hemothorax (> 1500 mL or 1/3 blood volume): thoracic great vessel injury until proven otherwise [17]
  • Chest drain + prepare for thoracotomy

C - Circulation:

  • Two large-bore IVs (14-16G) in uninjured limbs
  • Bloods: FBC, coagulation, group & save / crossmatch (4-6 units if major hemorrhage)
  • Massive transfusion protocol if: SBP less than 90 mmHg despite 2L crystalloid, ongoing bleeding, positive FAST with hypotension [41]
  • Ratio 1:1:1 (RBC : FFP : Platelets) [41]

D - Disability:

  • GCS, pupils
  • Neurological deficit in injured limb? Document (may indicate nerve injury or ischemia)

E - Exposure:

  • Fully expose patient
  • Identify all wounds
  • Look for exit wounds (penetrating)
  • Log roll to examine back

Secondary Survey: Head-to-Toe Vascular Examination

For Each Anatomical Region:

1. Inspection

  • Wounds: entry/exit, proximity to vascular structures
  • Hematoma: size, expanding?, pulsatile?
  • Color: pallor, cyanosis, comparison to contralateral
  • Swelling: compartment tightness?

2. Palpation

  • Pulses: radial, ulnar, brachial, femoral, popliteal, dorsalis pedis, posterior tibial
  • Capillary refill: less than 2 seconds normal
  • Temperature: warm vs cool
  • Compartments: tense? (see compartment syndrome section)
  • Thrill: place hand over hematoma, feel for vibration (AVF)

3. Auscultation

  • Bruit: listen over hematoma and distal vessels (pseudoaneurysm, AVF)

4. Neurological

  • Sensory: light touch, pinprick in peripheral nerve distributions
  • Motor: test distal muscle groups
  • Peripheral nerves: especially median (ape hand), ulnar (claw hand), radial (wrist drop), peroneal (foot drop) [28]

Specific Examination Maneuvers

Allen Test (Hand Perfusion):

  • Occlude both radial and ulnar arteries
  • Ask patient to clench fist repeatedly (exsanguinate hand)
  • Release one artery
  • Normal: hand pinks up in less than 5 seconds
  • Interpretation: determines if one artery can be sacrificed

Doppler Examination:

  • If pulses impalpable: use handheld Doppler
  • Monophasic signal: partial occlusion or distal to injury
  • Triphasic signal: normal arterial flow
  • Absence: occlusion

Compartment Pressure Measurement:

  • Indication: high suspicion for compartment syndrome
  • Technique: needle manometry (Stryker device)
  • Interpretation:
    • "Absolute pressure > 30 mmHg: concerning"
    • "Delta pressure less than 30 mmHg (diastolic BP - compartment pressure): concerning [42]"
    • Clinical diagnosis trumps measurement

Documentation

Critical for medicolegal protection and continuity:

Example Documentation:

VASCULAR EXAMINATION - LEFT LOWER LIMB
Time: 14:30

Inspection: 3cm laceration medial mid-thigh, moderate hematoma (non-expanding, measured 5cm diameter), no active bleeding
Perfusion: Foot pale compared to right, delayed capillary refill (3 seconds)
Pulses: 
  - "Femoral: 2+ (normal)"
  - "Popliteal: 1+ (diminished)  "
  - "Dorsalis pedis: absent (Doppler: faint monophasic signal)"
  - "Posterior tibial: absent (Doppler: absent signal)"
Sensation: Decreased light touch over dorsum of foot
Motor: Unable to dorsiflex foot (power 2/5), plantarflexion weak (3/5)
Temperature: Cool to mid-calf
Compartments: Anterior compartment tense, tender

ASSESSMENT: HARD SIGNS present (absent DP/PT pulses, ischemic signs)
PLAN: Immediate OR for exploration + revascularization
Vascular surgery attending notified (Dr. Smith, 14:35)
Discussed with patient + family: limb-threatening injury, urgent surgery required
NPO, IV access x2, crossmatch 4 units, to OR within 30 minutes

6. Investigations

Clinical Assessment is Primary Investigation

For hard signs: NO imaging required. Imaging delays definitive treatment and worsens outcomes. [1,9,43]

Exception: Stable patient with hard sign in anatomically complex region where operative planning requires anatomical detail (e.g., Zone I neck injury, subclavian injury).

Laboratory Investigations

TestPurposeExpected FindingInterpretation
Full Blood CountAssess blood lossHb may be normal acutely (hemodilution takes hours)Repeat q4-6h; trend more useful than single value
Coagulation (PT/APTT)Identify coagulopathyProlonged in massive transfusion, hypothermiaCorrect to PT less than 18s, APTT less than 45s [41]
FibrinogenMarker of consumptive coagulopathyless than 1.5 g/L: criticalMaintain > 1.5 g/L with cryoprecipitate [41]
LactateTissue perfusion markerElevated in shock/ischemiaNormal less than 2 mmol/L; > 4 = severe shock
Base excessMetabolic acidosis markerNegative in ischemia/shock< -6 = significant acidosis
Creatine kinase (CK)Muscle damage markerMarkedly elevated in rhabdomyolysis> 5000 U/L: risk myoglobinuric renal failure [44]
MyoglobinMuscle breakdown productElevated in reperfusionRisk renal failure; ensure urine output > 100 mL/h
TroponinMyocardial injuryMay be elevated in severe ischemia-reperfusionDifferentiate cardiac vs demand ischemia
Group & Save / CrossmatchBlood product readiness-Crossmatch 4-6 units for major vascular injury

Imaging

Plain Radiography

Indications:

  • All trauma patients (trauma series: chest, pelvis, C-spine)
  • Identify fractures associated with vascular injury
  • Identify retained foreign bodies (bullets, fragments)

Findings Suggestive of Vascular Injury:

  • Mediastinal widening > 8 cm (thoracic aortic injury)
  • Fractures at high-risk sites (supracondylar humerus, knee dislocation)
  • Trajectory of penetrating object near vessels

Limitations:

  • Cannot directly visualize vessels
  • Low sensitivity for vascular injury

CT Angiography (CTA)

Gold standard imaging modality for stable patients with soft signs. [37,45]

Indications:

  • Soft signs present + hemodynamically stable
  • Stable patient with hard sign in complex anatomy (operative planning)
  • Penetrating neck trauma (Zone II/III) without hard signs [46]
  • Blunt cerebrovascular injury screening (BCVI) [47]
  • Post-operative assessment of repair

Protocol:

  • Arterial phase contrast-enhanced CT (100 mL contrast, 4 mL/s injection)
  • Thin slice (0.625-1.25 mm) with 3D reconstruction
  • "Run-off" imaging to distal vessels

Findings:

  • Contrast extravasation: active bleeding (arterial "blush")
  • Vessel occlusion: abrupt cut-off, absent distal flow
  • Pseudoaneurysm: contrast-filled outpouching
  • Dissection/intimal flap: linear filling defect
  • AV fistula: early venous filling

Performance:

  • Sensitivity: 95-98% [45]
  • Specificity: 95-99% [45]
  • NPV: 98-99% (excellent rule-out tool) [45]

Limitations:

  • Requires stable patient (cannot be used in shock)
  • Contrast allergy (rare absolute contraindication in emergency)
  • Renal impairment (acceptable risk in limb-threatening emergency)
  • Cannot assess functional perfusion (ABI superior for this)

Catheter Angiography (Digital Subtraction Angiography, DSA)

Indications (diagnostic):

  • CTA equivocal
  • Inability to obtain CTA (contrast allergy, equipment failure)
  • Complex injuries requiring detailed vascular roadmap

Indications (therapeutic):

  • Endovascular treatment planned (see management section)

Advantages:

  • Gold standard for vascular anatomy
  • Therapeutic capability

Disadvantages:

  • Invasive
  • Requires specialist (interventional radiologist/vascular surgeon)
  • Time-consuming (delays definitive treatment)
  • Complications: access site hematoma (5%), pseudoaneurysm (1%), dissection (less than 1%)

Modern Role: Largely replaced by CTA for diagnosis; reserved for endovascular intervention.

Doppler Ultrasound

Indications:

  • Bedside assessment of pulses (handheld Doppler)
  • Duplex ultrasound: assessment of pseudoaneurysm, AVF in delayed presentation
  • Post-operative surveillance

Advantages:

  • Portable, no radiation, no contrast
  • Real-time assessment
  • Can assess flow dynamics (waveforms)

Disadvantages:

  • Operator-dependent
  • Limited in acute trauma (hematoma, swelling obscures view)
  • Cannot assess deep vessels well (thorax, abdomen)

Role in Acute Trauma: Limited to bedside Doppler for pulse assessment and ABI calculation.

Blunt Cerebrovascular Injury (BCVI) Screening

Special consideration for blunt neck trauma. [47,68]

Screening Indications (Denver Criteria):

Signs/Symptoms:

  • Arterial hemorrhage from neck/nose/mouth
  • Cervical bruit in patient less than 50 years
  • Expanding cervical hematoma
  • Focal neurological deficit inconsistent with head CT
  • Neurological deficit inconsistent with head CT
  • Stroke on CT or MRI

High-Risk Injury Patterns:

  • High-energy mechanism with:
    • Le Fort II or III fractures
    • Cervical spine fracture (especially C1-3)
    • Basilar skull fracture with carotid canal involvement
    • Diffuse axonal injury with GCS less than 6

Screening Modality: CTA neck (sensitivity 97%, specificity 100%) [47,68]

Emerging Practice: Universal screening for high-risk blunt trauma (GCS less than 8, high-energy mechanism) identifies 2-3% BCVI incidence; early detection allows antithrombotic therapy reducing stroke risk. [68]


7. Acute Management: ATLS Framework

Pre-Hospital Care

Principles:

  1. Hemorrhage control: Direct pressure > tourniquet if pressure fails
  2. Rapid extrication and transport ("scoop and run" for penetrating trauma to torso)
  3. DO NOT remove impaled objects (may be tamponading injury)
  4. Fluid resuscitation: Permissive hypotension (SBP 80-90 mmHg) until hemorrhage controlled [48]
  5. Notification: Pre-alert trauma team (allows mobilization of vascular surgeon, blood products, OR)

Tourniquet Use: [40]

  • Indication: Life-threatening extremity hemorrhage not controlled by direct pressure
  • Placement: 2 inches (5 cm) proximal to wound, over single bone if possible
  • Tightness: Until distal pulses/bleeding cease
  • Documentation: TIME applied (ischemia clock starts)
  • DO NOT release until definitive hemorrhage control in OR

Hemostatic Dressings:

  • Indication: Junctional hemorrhage (groin, axilla, neck) not controlled by pressure alone
  • Agents: Combat Gauze (kaolin), Celox (chitosan), QuikClot
  • Technique: Pack wound tightly, apply pressure x 3 minutes

Emergency Department Management

Immediate Actions (Simultaneous)

1. Team Activation

  • Trauma team leader
  • Vascular surgeon (for hard signs)
  • Anesthesia (for OR/massive transfusion)
  • Blood bank (massive transfusion protocol)
  • OR team (prepare emergency OR)

2. Hemorrhage Control

  • External bleeding:

    • Direct pressure (most effective)
    • "If tourniquet in place: leave until OR (do NOT release in ED - may cause sudden cardiovascular collapse)"
    • "If no tourniquet: apply direct pressure, consider hemostatic dressing"
    • DO NOT clamp vessels blindly (may injure nerves)
  • Internal bleeding:

    • "Massive hemothorax: chest drain + prepare for thoracotomy"
    • "Hemoperitoneum: prepare for laparotomy"
    • "Pelvic hemorrhage: pelvic binder, consider REBOA (see below)"

3. Resuscitation

Damage Control Resuscitation (DCR) Principles: [41,48]

PrincipleTargetEvidence
Permissive hypotensionSBP 80-90 mmHg until hemorrhage controlledReduced mortality vs aggressive resuscitation [48]
Hemostatic resuscitation1:1:1 ratio (RBC:FFP:Platelets)Reduced coagulopathy, improved survival [41]
Avoid crystalloid overloadMinimize crystalloid (causes dilutional coagulopathy)Improved outcomes [41]
Early tranexamic acid1g IV over 10 min, then 1g over 8h (within 3h injury)15% mortality reduction [49]
Prevent "lethal triad"Avoid hypothermia (less than 35°C), acidosis (pH less than 7.2), coagulopathy (PT > 18s)Each worsens others (vicious cycle) [50]

Massive Transfusion Protocol (MTP): [41]

  • Trigger: SBP less than 90 despite 2L crystalloid, or clinical judgment (exsanguinating hemorrhage)
  • Ratio: 1:1:1:1 (6 units RBC : 6 units FFP : 1 platelet pack : 10 units cryoprecipitate per "round")
  • Targets:
    • Hb > 70 g/L (> 90 g/L if ongoing ischemia)
    • PT less than 18 seconds
    • APTT less than 45 seconds
    • Fibrinogen > 1.5 g/L
    • Platelets > 75 x10⁹/L (> 100 if ongoing bleeding)
    • Calcium > 1.1 mmol/L (citrate in blood products chelates calcium)

Tranexamic Acid (TXA): [49]

  • Dose: 1 g IV over 10 minutes, then 1 g IV over 8 hours
  • Timing: Within 3 hours of injury (no benefit after 3h, possible harm)
  • Mechanism: Inhibits fibrinolysis
  • Evidence: CRASH-2 trial showed 15% mortality reduction [49]

4. Assessment

  • Primary survey (ABCDE)
  • Identify hard vs soft signs
  • Calculate ABI if soft signs

5. Decision: OR vs Imaging vs Observation

DECISION ALGORITHM
        ↓
   HARD SIGNS?
        ↓
    YES ↙  ↘ NO
       ↓       ↓
      OR    SOFT SIGNS?
            ↓
        YES ↙  ↘ NO
           ↓       ↓
  Hemodynamically   Observe
     stable?        (admit 24h)
       ↓
   YES ↙  ↘ NO
      ↓       ↓
     CTA      OR
      ↓
  Injury?
      ↓
  YES ↙  ↘ NO
     ↓       ↓
    OR    Observe

Adjuncts: REBOA (Resuscitative Endovascular Balloon Occlusion of the Aorta)

Emerging technique for non-compressible torso hemorrhage. [51,65,66]

UK-REBOA Trial (2023): Landmark RCT showed REBOA use in ED for exsanguinating trauma was safe and feasible; mortality 54% (REBOA) vs 56% (standard care), suggesting potential benefit in selected cases. [65]

Indications:

  • Exsanguinating hemorrhage from:
    • "Zone I: Infradiaphragmatic aorta, celiac, SMA (balloon in Zone I - descending thoracic aorta)"
    • "Zone III: Infrarenal aorta, iliac vessels (balloon in Zone I or III)"
  • Bridge to definitive control (OR or angioembolization)
  • SBP less than 60 mmHg despite resuscitation

Contraindications:

  • Thoracic aortic injury (may exacerbate)
  • Severe peripheral vascular disease (cannot pass catheter)

Technique:

  • Common femoral artery access (percutaneous or cutdown)
  • 7Fr sheath + guidewire + balloon catheter
  • Position under fluoroscopy (or estimate based on external landmarks)
  • Inflate balloon to occlude aorta (30-40 mL)
  • Confirm proximal BP rise, distal pulse loss

Complications:

  • Limb ischemia (100% below balloon)
  • Balloon rupture
  • Aortic injury
  • Visceral ischemia

Time Limit:

  • Zone I occlusion: Maximum 30 minutes (visceral ischemia)
  • Zone III occlusion: Maximum 60 minutes (limb ischemia)
  • Must achieve definitive hemorrhage control rapidly

Evidence: Promising in case series and RCT data; UK-REBOA trial shows feasibility though mortality benefit remains modest. [51,65,66]


8. Definitive Management: Surgical Principles

Timing: The "Golden Period"

Traditional Teaching: 6-hour window for limb salvage [5]

Modern Evidence: More nuanced [5,18]

  • Warm ischemia tolerance:
    • "Nerve: 30 minutes"
    • "Muscle: 4-6 hours"
    • "Skin: 12-24 hours"
  • Factors shortening window:
    • Complete ischemia (vs partial flow via collaterals)
    • High-energy mechanism (additional soft tissue injury)
    • Shock/hypotension (compounds ischemia)
    • Concomitant venous injury (impairs collateral flow)
  • Factors extending window:
    • Partial perfusion maintained
    • Good collaterals (young, non-PAD patient)
    • Low-energy mechanism

Key Principle: Don't watch the clock, treat the limb. However, every hour delay increases amputation risk. [18]

Damage Control Surgery vs Definitive Repair

Damage Control Surgery (DCS) Indications: [50]

  • Hemodynamic instability despite resuscitation (SBP less than 90 mmHg)
  • Hypothermia (less than 35°C)
  • Acidosis (pH less than 7.2, lactate > 5)
  • Coagulopathy (clinical bleeding, PT > 18s)
  • Massive transfusion (> 10 units RBC)
  • Multiple injuries requiring lengthy repair

DCS Principles:

  1. Control hemorrhage: Ligate or shunt vessel
  2. Prevent contamination: Control GI/GU injuries
  3. Abbreviate surgery: Get to ICU in less than 90 minutes
  4. Resuscitate in ICU: Warm, correct coagulopathy, optimize
  5. Return to OR: Definitive repair when stable (24-48h later)

Temporary Vascular Shunt:

  • Indication: Restore perfusion temporarily during DCS
  • Technique: Insert sterile tubing (chest tube, commercial shunt) into proximal and distal vessel, secure with vessel loops
  • Duration: Up to 24-48 hours tolerated
  • Definitive repair when stable [52]

Open Surgical Repair: Standard of Care for Extremity Injuries

Pre-Operative Preparation

Antibiotics:

  • Cefazolin 2g IV (or vancomycin if MRSA risk)
  • Within 1 hour of incision
  • Redose q4h if surgery > 4 hours

Positioning:

  • Full limb prep (allows access to entire extremity for vein harvest)
  • Contralateral limb also prepped (potential vein donor)

Anesthesia:

  • General anesthesia preferred (allows muscle relaxation, airway control)
  • Regional possible for distal extremity

Operative Steps

1. Proximal and Distal Control

  • Expose vessel proximal and distal to injury
  • Obtain control before entering hematoma (prevents "losing the field")
  • Use vessel loops or soft clamps

2. Exploration and Debridement

  • Open hematoma
  • Identify injury extent
  • Debride non-viable vessel: Intima must be intact (if damaged, thrombosis certain)
    • "Look for: Intimal flap, discoloration, lack of bleeding from vessel wall (non-viable)"
    • Excise back to healthy, bleeding edges

3. Assess Repair Options

Decision: Primary Repair vs Interposition Graft vs Ligation

Primary Repair

Indications:

  • Clean laceration
  • less than 2 cm gap after debridement
  • No tension on repair

Technique:

  • 6-0 or 7-0 polypropylene (Prolene) suture
  • Interrupted or continuous
  • Everting edges (intima-to-intima)
  • Assess flow after repair (palpable pulse, Doppler signal, back-bleeding)

Advantages:

  • No foreign material
  • Best long-term patency

Disadvantages:

  • Only suitable for short defects

Interposition Graft

Indications:

  • Gap > 2 cm
  • Tension on primary repair
  • Extensive debridement required

Graft Choice:

Graft TypeAdvantagesDisadvantagesPreferred Use
Autologous veinBest patency (90% at 5y), no foreign material, resistant to infectionRequires harvest time, size mismatch possibleFirst choice for all extremity repairs [53]
Synthetic (PTFE, Dacron)Immediately available, no harvest, size varietyLower patency (60-70% at 5y), infection riskAcceptable for large vessels (aorta, iliac); avoid in contaminated wounds [53]
Cadaveric vein allograftNo harvest, good size matchLimited availability, cost, immunogenicityRarely used

Harvest Sites for Vein Graft:

  1. Greater saphenous vein (GSV): First choice (3-6 mm diameter)
    • Harvest from medial leg/thigh
    • Reversed orientation (valves)
  2. Basilic vein: Upper extremity alternative
  3. Contralateral limb: If ipsilateral insufficient

Technique:

  • Spatulate ends (prevents stenosis)
  • End-to-end anastomosis with 6-0/7-0 Prolene
  • Ensure no tension
  • Ensure graft not twisted
  • Check flow (pulse, Doppler, on-table angiogram if available)

Completion Assessment:

  • Palpable pulse
  • Doppler signal (triphasic = good)
  • Restore perfusion (pink, warm extremity)
  • Consider on-table angiography if concern

Ligation: Know Your Safe Ligations [15,16]

Critical Decision: Which vessels can be safely ligated?

Safe to Ligate (if Other Criteria Met):

VesselConditionsEvidence
One forearm artery (radial OR ulnar)Other artery intact + Allen test normal95% limb salvage [15]
One tibial vessel (AT, PT, or peroneal)Other TWO arteries intact90% limb salvage [16]
Internal iliac arteryContralateral iliac intact, external iliac intactTolerated (may have claudication, sexual dysfunction)
Internal carotid arteryCircle of Willis intact (assess with pre-op CTA if possible)30-40% stroke risk; only if absolutely necessary [54]

NEVER ligate (ALWAYS repair or bypass):

  • Brachial artery (only vessel to forearm)
  • Superficial femoral / popliteal artery (only vessel to lower leg)
  • Common femoral artery
  • Common carotid artery
  • Aorta
  • Subclavian / axillary artery
  • Superior mesenteric artery
  • Renal artery
  • External iliac artery

Indications for Ligation (instead of repair):

  • Damage control surgery (temporary; plan for reconstruction)
  • Small vessel, good collaterals
  • Contaminated wound + no autologous conduit available (risk infected graft)
  • Distal vessel with poor runoff

Venous Injury Management [29,64]

Controversy: Repair vs ligate?

Historical Context: Vietnam War data showed venous ligation alone had poor outcomes; modern approach favors selective repair. [64]

Evidence: [29,64]

  • Major veins (common femoral, popliteal, axillary): Repair if possible (reduces edema, improves arterial graft patency, lowers amputation risk)
  • Minor veins (lesser saphenous, basilic, cephalic): Ligate (acceptable)
  • Damage control situation: Ligate (can reconstruct later if needed)
  • Combined arteriovenous injury with prolonged ischemia: Repair both (venous repair reduces compartment syndrome risk)

Technique if repairing:

  • Lateral venorrhaphy (partial injury): Repair with 5-0 Prolene
  • Vein patch (if primary closure narrows lumen > 50%)
  • Interposition graft (if > 2 cm defect): PTFE acceptable (lower pressure than arterial)

Sequelae of venous ligation:

  • Edema (common, usually resolves)
  • Post-thrombotic syndrome (chronic venous insufficiency): 20-30%
  • Compartment syndrome: Increased risk

Endovascular Management: Growing Role [6,7]

Paradigm Shift: Endovascular first-line for selected injuries.

Indications for Endovascular Management

Preferred Over Open:

  • Thoracic aortic injury (TEVAR = thoracic endovascular aortic repair) [6]
  • Subclavian / axillary artery injury (difficult surgical exposure) [7]
  • Internal iliac artery hemorrhage (embolization) [25]
  • Pelvic venous hemorrhage (embolization) [25]

Alternative to Open (Operator/Center-Dependent):

  • Common/external iliac artery injury (covered stent)
  • Superficial femoral artery injury (covered stent) - controversial [7]
  • Pseudoaneurysm (thrombin injection, covered stent, or coil embolization)
  • Hemorrhage not amenable to surgery (e.g., deep pelvic)

Contraindications:

  • Hemodynamic instability (no time for endovascular)
  • Lack of equipment/expertise
  • Injuries requiring exploration anyway (orthopedic fixation, debridement)

Techniques

1. Covered Stent (Stent Graft)

  • Indication: Arterial laceration, pseudoaneurysm, short-segment occlusion
  • Device: PTFE-covered self-expanding stent (e.g., Viabahn, Gore)
  • Technique: Femoral access, wire across lesion, deploy stent to exclude injury
  • Advantages: Rapid, avoids open surgery, useful in hostile anatomy
  • Disadvantages:
    • Long-term patency uncertain in small vessels (70-80% at 1 year) [7]
    • Requires antiplatelet therapy (increases bleeding risk in polytrauma)
    • Cannot address concomitant injuries (bone, nerve, soft tissue)

2. Angioembolization

  • Indication: Hemorrhage from vessels that can be sacrificed
    • Internal iliac branches
    • Pelvic venous plexus
    • Muscular branches
    • Solid organ injuries (liver, spleen, kidney)
  • Technique: Catheterize bleeding vessel, deploy coils or particles to occlude
  • Advantages: No incision, can target inaccessible vessels
  • Disadvantages:
    • Requires stable patient
    • Risk of non-target embolization
    • Ischemia risk

3. TEVAR (Thoracic Endovascular Aortic Repair)

  • Indication: Blunt thoracic aortic injury (BTAI) [6]
    • "Historically: 80% mortality with conservative management"
    • "With TEVAR: 90% survival [6]"
  • Technique: Femoral access, deploy covered stent across aortic injury (usually at isthmus)
  • Timing: Urgent for hemodynamically unstable; within 24h for stable [6]
  • Advantages: Lower mortality than open repair (5% vs 20%) [6]
  • Disadvantages: Requires sizing (CTA), may cover left subclavian (revascularize if symptomatic)

Evidence:

  • TEVAR for BTAI: Multiple series show 90-95% survival, 95-98% patency [6]
  • Covered stents for extremity: Less robust data; 70-80% patency at 1 year [7,67]
  • Embolization for pelvic hemorrhage: 85% success rate [25]
  • Endovascular management of iatrogenic injury: 95% technical success, lower morbidity than open conversion [67]

Repair vs Endovascular: Decision Framework

Injury LocationFirst-LineSecond-LineEvidence
Thoracic aortaTEVAROpen (if unsuitable anatomy)Level I [6]
Subclavian/AxillaryEndovascular (covered stent)Open (if not amenable)Level II [7]
BrachialOpen repairEndovascular (selected cases)Level I [53]
Forearm (radial/ulnar)Repair if both injured; ligate if one intact-Level II [15]
Iliac (common/external)Endovascular vs Open (equivalent)-Level II [7]
Femoral (common/superficial)Open repairEndovascular (controversial)Level I [53]
PoplitealOpen repair-Level I [22]
Tibial vesselsRepair at least one; ligate if two intact-Level II [16]

9. Post-Operative Management and Complications

Immediate Post-Operative Care

ICU Admission Indications:

  • Hemodynamic instability
  • Massive transfusion (> 10 units)
  • Reperfusion of prolonged ischemia (> 6 hours)
  • High risk of compartment syndrome
  • Associated major injuries

Monitoring:

  • Hourly pulse checks (Doppler if impalpable)
  • Hourly compartment assessment (clinical)
  • Perfusion markers: color, temperature, capillary refill
  • Urine output > 0.5 mL/kg/h (myoglobin clearance if reperfusion injury)
  • Serial lactate (trend to normalization)
  • Coagulation parameters (if massive transfusion)

Anticoagulation:

  • Controversial. Limited high-quality evidence; practice varies by institution. [55,60]
  • Meta-analysis findings: Anticoagulation after vascular trauma associated with reduced graft thrombosis (OR 0.42) but increased bleeding complications (OR 2.1); net benefit remains unclear. [61]
  • Common practice:
    • "Heparin infusion (500-1000 units/h) for 24-48h post-repair: Reduces thrombosis risk"
    • Then transition to aspirin 75-100 mg daily
    • "Timing in brain injury: Delay 72h minimum; individualize based on hemorrhage risk. [62]"
    • "Contraindication: Active bleeding, coagulopathy, polytrauma with head injury"
  • Alternative: Aspirin alone (if bleeding risk)

Compartment Syndrome: The Most Common Complication [13,14]

Incidence: 10-25% after revascularization of ischemic limb [13,14]

Pathophysiology:

  • Ischemia → cell death → edema
  • Reperfusion → ischemia-reperfusion injury → MORE edema
  • Edema in closed fascial compartment → ↑ pressure
  • When pressure > capillary perfusion pressure (~30 mmHg) → ischemia
  • Vicious cycle: ischemia → edema → pressure → ischemia

Clinical Diagnosis (5 Ps):

  1. Pain: Out of proportion, worsens with passive stretch of muscles in compartment (MOST SENSITIVE SIGN)
  2. Pressure: Tense, firm compartment on palpation
  3. Paresthesias: Indicates nerve ischemia (late sign)
  4. Paralysis: Indicates muscle ischemia (late sign; irreversible injury likely)
  5. Pulselessness: Very late sign (usually still have pulses in compartment syndrome)
  6. Pallor: Late

Key Point: Pain out of proportion + pain with passive stretch = compartment syndrome until proven otherwise. Do NOT wait for 5 Ps. [42]

Diagnosis:

  • Clinical diagnosis (most important)
  • Compartment pressure measurement (adjunct, NOT required):
    • "Absolute pressure > 30 mmHg: concerning"
    • "Delta pressure (diastolic BP - compartment pressure) less than 30 mmHg: more specific [42]"
    • "Caveat: Unreliable in hypotensive patient"

Treatment: EMERGENCY FASCIOTOMY [13,14,63]

Indications:

  • Clinical diagnosis of compartment syndrome
  • Prophylactic:
    • Ischemia time \u003e 6 hours before revascularization (amputation reduced from 35% to 15% with early fasciotomy) [63]
    • Combined arterial + venous injury
    • High-energy mechanism with significant soft tissue injury
    • Delayed presentation (\u003e 12 hours)
    • Massive swelling post-revascularization

Lower Limb Fasciotomy Technique (4-Compartment):

Two-Incision Approach:

  1. Lateral incision (fibula):

    • 2 cm anterior to fibula, entire length
    • Release anterior compartment (tibialis anterior, EHL, EDL)
    • Release lateral compartment (peroneus longus/brevis)
  2. Medial incision (tibia):

    • 2 cm posterior to medial tibia edge
    • Release superficial posterior compartment (gastrocnemius, soleus)
    • Detach soleus origin to access deep posterior compartment (tibialis posterior, FHL, FDL)

Upper Limb Fasciotomy Technique:

Volar and Dorsal Incisions:

  1. Volar: Release flexor compartment (volar forearm)
  2. Dorsal: Release extensor compartment (dorsal forearm)
  3. Thenar/Hypothenar: If hand involved

Wound Management Post-Fasciotomy:

  • Leave open initially (closed fasciotomy DOES NOT work)
  • Delayed closure at 3-7 days (when edema resolves)
  • May require skin graft if cannot close primarily (~50% cases)

Complications of Missed Compartment Syndrome:

  • Volkmann's contracture (forearm): claw hand, permanent disability
  • Foot drop (leg): anterior compartment fibrosis
  • Muscle necrosis → rhabdomyolysis → renal failure → death
  • Permanent disability, often requiring amputation

Rhabdomyolysis and Myoglobinuric Renal Failure [44]

Risk Factors:

  • Ischemia time > 6 hours
  • Large muscle mass affected
  • Delay to fasciotomy if compartment syndrome

Diagnosis:

  • CK > 5000 U/L (often > 50,000 in severe cases)
  • Myoglobin in urine (tea-colored urine)
  • ↑ Potassium (from cell lysis)
  • ↑ Phosphate, ↓ calcium
  • Metabolic acidosis
  • Acute kidney injury (↑ creatinine)

Treatment:

  • Aggressive fluid resuscitation: Target urine output 100-200 mL/h [44]
  • Urinary alkalinization: Sodium bicarbonate (if pH less than 6.5) - reduces myoglobin precipitation
  • Mannitol: Osmotic diuresis (controversial)
  • Dialysis: If refractory hyperkalemia or renal failure
  • Monitor: K⁺ (risk of cardiac arrest), CK (trend), creatinine

Prevention:

  • Early revascularization
  • Early fasciotomy
  • Aggressive hydration peri-operatively

Infection [56]

Incidence:

  • Clean vascular trauma: 5-10%
  • Contaminated (GI injury, soil, delayed presentation): 20-30%

Risk Factors:

  • Contaminated wound
  • Synthetic graft (higher than vein graft)
  • Hypotension/shock (impaired tissue perfusion)
  • Soft tissue loss

Management:

  • Prophylactic antibiotics (cefazolin; add metronidazole if contaminated)
  • Debridement of devitalized tissue
  • Delayed primary closure or leave open
  • If graft infection:
    • Remove graft
    • Debride
    • Reconstruct with autologous tissue if possible (vein)
    • OR ligate + extra-anatomic bypass if tissue bed infected

Graft Thrombosis [53]

Incidence:

  • Vein graft: 5-10% early, 10-15% at 5 years
  • Synthetic graft: 10-15% early, 30-40% at 5 years

Causes:

  • Technical error (stenotic anastomosis, twisted graft, retained intimal flap)
  • Hypercoagulable state
  • Low flow state (poor runoff)
  • Missed distal injury

Presentation:

  • Acute ischemia (return of 6 Ps)
  • Loss of pulses

Diagnosis:

  • Doppler ultrasound
  • CTA
  • Angiography (if considering thrombectomy/thrombolysis)

Management:

  • Return to OR
  • Thrombectomy (Fogarty catheter)
  • Revise repair (if technical issue)
  • On-table angiogram to assess result
  • Anticoagulation post-operatively

Amputation: The Ultimate Failure [18]

Incidence:

  • Early revascularization (less than 6h): 5-10% [18]
  • Delayed revascularization (> 6h): 20-40% [18]
  • Associated with:
    • Prolonged ischemia (> 12 h: 50-80% amputation)
    • Mangled extremity (MESS score > 7)
    • Failed revascularization
    • Severe soft tissue loss
    • Infection

Decision: Salvage vs Amputation

Mangled Extremity Severity Score (MESS): [57]

ComponentPoints
Energy Low (stab, simple fracture): 1
Medium (open/multiple fractures): 2
High (crush, blast): 3
Very high (above + contamination): 4
1-4
Ischemia Reduced pulses without ischemia: 1
Pulseless, reduced capillary refill: 2
Cool, paralyzed, insensate: 3
x2 if > 6h
Shock SBP always > 90: 0
Transiently hypotensive: 1
Persistent hypotension: 2
0-2
Age less than 30: 0
greater than 30-50: 1
50: 2
0-2

Interpretation:

  • MESS ≥7: 100% predictive of amputation [57]
  • MESS less than 7: Attempt salvage

Other Considerations:

  • Tibial nerve injury (insensate foot): Poor functional outcome even if limb salvaged
  • Massive soft tissue loss
  • Multi-level arterial injuries
  • Patient wishes, functional goals

Primary Amputation Benefits (in selected cases):

  • Shorter hospital stay
  • Fewer operations
  • Earlier prosthesis fitting
  • Better functional outcome than non-functional salvaged limb

10. Prognosis & Outcomes

Mortality [3,8,18]

Injury LocationMortalityKey Determinants
Extremity5-10%Associated injuries, shock
Neck (carotid/vertebral)10-20%Stroke, exsanguination
Thoracic aorta15-20% (with TEVAR) vs 80% (untreated)Pre-hospital death, associated injuries [6,8]
Abdominal aorta40-60%Exsanguination, associated visceral injuries [8]
Popliteal artery5-10%Ischemia complications

Survival Determinants:

  • Time to hemorrhage control
  • Shock severity (lactate, base deficit)
  • Associated injuries
  • Age (> 65 years: 2-3x mortality)

Limb Salvage [5,18]

FactorSalvage Rate
Overall extremity vascular injury85-90%
Ischemia less than 6 hours90-95%
Ischemia 6-12 hours70-80%
Ischemia > 12 hours50-60%
Popliteal injury (high energy)70-80%
MESS less than 790%
MESS ≥70% (definition) [57]

Factors Predicting Amputation:

  • Ischemia time > 6 hours (OR 4.5) [18]
  • Severe soft tissue injury (OR 3.8)
  • Posterior tibial nerve injury (OR 3.2) [28]
  • Age > 55 years (OR 2.1)
  • Shock on presentation (OR 2.5)

Functional Outcomes

Salvaged Limbs:

  • 70-80% return to pre-injury activity level
  • 20-30% have chronic pain
  • 15-20% have permanent disability (nerve injury, contracture)

Amputated Limbs:

  • 80-90% successfully fitted with prosthesis
  • 60-70% return to independent ambulation
  • 30-40% return to employment

Long-Term Complications (1-5 Years)

1. Graft-Related:

  • Late graft stenosis: 10-20% (more common with synthetic)
  • Aneurysmal degeneration: 5% (vein grafts)
  • Graft infection: 2-5%

2. Ischemia-Related:

  • Chronic pain: 20-30%
  • Cold intolerance: 30-40%
  • Exercise limitation: 15-20%

3. Post-Traumatic Stress:

  • PTSD: 20-30% (especially if amputation or near-death event)

Prognostic Scores

MESS (Mangled Extremity Severity Score): See above [57]

NISSSA (National Inpatient Sample Severity Adjusted): Predicts mortality in vascular trauma (not routinely used clinically)


11. Evidence & Guidelines

Key Guidelines

1. Eastern Association for the Surgery of Trauma (EAST) Practice Management Guidelines [1,9]

Vascular Injury Evaluation (2011):

  • Level I: Hard signs mandate exploration (no imaging)
  • Level II: CTA for soft signs (sensitivity 95-100%, specificity 87-100%)
  • Level III: Proximity alone not indication for imaging

Extremity Vascular Trauma (2012):

  • Level I: Repair preferable to ligation for major extremity vessels
  • Level II: Temporary shunting acceptable in damage control surgery
  • Level III: Completion angiography recommended

2. Society for Vascular Surgery (SVS) Trauma Guidelines (2020) [58]

Recommendations:

  • Endovascular approaches first-line for thoracic aortic, subclavian injuries (Grade 1A)
  • Open repair first-line for femoral, popliteal injuries (Grade 1A)
  • Prophylactic fasciotomy for ischemia > 6h, combined arteriovenous injury (Grade 2B)
  • Antiplatelet therapy post-repair (Grade 2C)

3. ATLS (Advanced Trauma Life Support) 10th Edition (2018) [17]

Hemorrhage Control:

  • (C)ABC approach: Catastrophic hemorrhage before airway (NEW)
  • Tourniquet acceptable for life-threatening extremity hemorrhage
  • Damage control resuscitation (permissive hypotension, 1:1:1 ratio)
  • Tranexamic acid within 3 hours

4. Western Trauma Association Critical Decisions in Trauma (2016) [59]

Vascular Injury Management:

  • Algorithm-based approach: Hard signs → OR; Soft signs → CTA → selective intervention

Landmark Trials and Evidence

1. Blunt Thoracic Aortic Injury:

  • AAST Study (2008): TEVAR reduced mortality from 20% (open) to 5% [6]
  • Cochrane Review (2013): TEVAR superior to open repair for BTAI (Level I) [6]

2. Damage Control Resuscitation:

  • PROPPR Trial (2015): 1:1:1 ratio (RBC:FFP:Platelets) reduced 24h mortality vs 2:1:1 (Level I) [41]
  • CRASH-2 Trial (2010): Tranexamic acid reduced mortality 15% in bleeding trauma (Level I) [49]

3. Popliteal Artery Injury:

  • Mullenix et al. (2006): Ischemia > 6 h: amputation 35% vs 10% if less than 6h (Level II) [22]

4. Compartment Syndrome:

  • McQueen & Court-Brown (1996): Delta pressure less than 30 mmHg: 91% sensitivity, 98% specificity for compartment syndrome (Level II) [42]

5. Tourniquets:

  • Military Combat Casualty Care (Kragh et al., 2009): Pre-hospital tourniquets reduced mortality from extremity hemorrhage (Level II) [40]

6. CTA for Vascular Trauma:

  • Soto et al. (1998): CTA sensitivity 95%, specificity 99% for vascular injury (Level II) [45]

7. Repair vs Ligation:

  • Rich et al. (Vietnam Vascular Registry, 1978): Ligation of popliteal: 70% amputation; Repair: 30% amputation (Level III) [16]

Level of Evidence Summary

InterventionLevelKey Evidence
Hard signs → direct to ORIMultiple prospective studies [1,9]
CTA for soft signsIMeta-analysis [45]
TEVAR for thoracic aortic injuryIRCT, Cochrane review [6]
Damage control resuscitation (1:1:1)IPROPPR trial [41]
Tranexamic acidICRASH-2 trial [49]
Repair superior to ligation (major vessels)IIMultiple cohort studies [15,16,53]
Fasciotomy for CSIIProspective studies [13,14,42]
Tourniquets for exsanguinationIIMilitary registry data [40]
Endovascular for extremityII-IIICase series [7]

12. Special Considerations

Pediatric Vascular Trauma

Differences:

  • More tolerant of ischemia (better collaterals)
  • Size-matched grafts difficult (too small)
  • Growth considerations (graft does not grow)
  • Generally better outcomes than adults

Special Techniques:

  • Use smallest suture possible (8-0, 9-0)
  • Consider panel reactive antibody (PRA) testing before allograft (future transplant consideration)

Geriatric Vascular Trauma

Challenges:

  • Pre-existing PAD (poor collaterals, poor runoff)
  • Calcified vessels (difficult to clamp, suture)
  • Comorbidities (diabetes, renal disease)
  • Anticoagulation (complex reversal)

Outcomes:

  • 2-3x mortality vs younger patients [26]
  • Higher amputation rate
  • Longer hospital stay

Blast Injury

Unique Features:

  • Zone of injury extends far beyond visible
  • High rate of compartment syndrome (60-70%)
  • Liberal use of prophylactic fasciotomy

Iatrogenic Vascular Injury

Common Scenarios:

  • Femoral artery injury during cardiac catheterization
  • Subclavian injury during central line placement
  • Vascular injury during orthopedic surgery

Management Principles:

  • Early recognition
  • Vascular surgery consultation
  • Repair almost always possible if recognized early

13. Viva/Exam Scenarios

Opening Statement for Viva

"Acute vascular injury is traumatic disruption of arterial or venous structures, occurring in 3-5% of civilian trauma. The critical distinction is between hard signs—which mandate immediate surgical exploration—and soft signs, which require further investigation, typically with CT angiography. Hard signs include pulsatile bleeding, absent distal pulses, expanding hematoma, bruit or thrill, and signs of ischemia. Management follows ATLS principles with hemorrhage control, resuscitation, and urgent revascularization. Time is critical—the traditional golden period of 6 hours reflects muscle ischemia tolerance, beyond which amputation rates increase from 10% to 40%. Modern management includes endovascular options for selected injuries, particularly thoracic aortic trauma, but open repair remains the gold standard for most extremity injuries." [1-6,17,18]

Common Viva Questions with Model Answers

Q1: What are the hard signs of vascular injury?

A: "There are six hard signs, the presence of ANY of which mandates immediate surgical exploration without imaging:

  1. Active pulsatile bleeding—indicating arterial injury with skin breach
  2. Expanding hematoma—indicating ongoing bleeding with failure of tamponade
  3. Palpable thrill—indicating turbulent flow from an arteriovenous fistula
  4. Audible bruit—from AVF or pseudoaneurysm
  5. Absent distal pulses—indicating arterial occlusion or transection
  6. Signs of acute ischemia—the 6 Ps: pain, pallor, pulselessness, paresthesias, paralysis, poikilothermia

The last two—paresthesias and paralysis—are late signs indicating advanced ischemia beyond 4-6 hours, which significantly reduces salvage rates." [1,9,11]

Q2: How would you manage a patient with a penetrating injury to the thigh with no hard signs but diminished pedal pulses?

A: "This patient has a soft sign—diminished but present pulses. My approach would be:

First, ensure the patient is hemodynamically stable. If unstable, I'd proceed directly to operative exploration.

If stable, I'd calculate an ankle-brachial index. Using a handheld Doppler, I'd measure the systolic pressure in the affected ankle and divide by the brachial systolic pressure. If the ABI is less than 0.9, this has 85-90% sensitivity for arterial injury and I'd obtain a CT angiography.

If the CTA shows a significant arterial injury—laceration, pseudoaneurysm, or occlusion—I'd proceed to operative repair. If negative, I'd admit for 24 hours of observation with serial pulse exams.

Throughout, I'd follow ATLS principles: control any external bleeding, establish large-bore IV access, and prepare for surgery if the examination changes." [1,9,37,38]

Q3: What is your approach to a knee dislocation?

A: "Knee dislocation carries a 20-40% risk of popliteal artery injury due to tethering of the artery at the adductor hiatus proximally and the soleus arch distally. My approach:

First, immediate assessment of distal pulses, capillary refill, and neurological function. The presence of any hard signs—particularly absent pulses or signs of ischemia—mandates immediate vascular surgery consultation and preparation for operative exploration.

If pulses are present but reduced, I'd calculate an ABI. If less than 0.9, I'd obtain CTA. There's controversy about screening all knee dislocations even with normal pulses, as up to 10% can have intimal injuries. My practice is to obtain CTA for all knee dislocations given the high-risk mechanism, as delayed thrombosis from an intimal injury can be catastrophic.

If vascular injury is confirmed, this requires urgent operative repair—the popliteal is an end artery with poor collaterals, so ligation results in 70% amputation. I'd proceed to open exploration and repair, either primarily or with vein graft interposition depending on the defect size.

Finally, I'd reduce the dislocation urgently if not already done, as prolonged dislocation worsens vascular compromise." [22]

Q4: When would you use endovascular versus open repair?

A: "The decision depends on the injury location, patient stability, and available expertise.

Endovascular is first-line for:

  • Thoracic aortic injury—TEVAR has level I evidence showing reduced mortality from 20% to 5% compared to open repair
  • Subclavian and axillary injuries—difficult surgical exposure makes endovascular attractive
  • Hemorrhage from vessels that can be sacrificed—such as internal iliac branches in pelvic trauma

Open repair remains the gold standard for:

  • Most extremity injuries—femoral, popliteal, brachial arteries—where open repair has superior long-term patency
  • Unstable patients—no time for endovascular preparation
  • Injuries requiring exploration anyway—for orthopedic fixation or debridement

The emerging middle ground is iliac and superficial femoral injuries, where both approaches are used depending on operator preference and injury pattern. However, long-term patency data for endovascular repair of extremity injuries is limited—around 70-80% at one year compared to 90% for vein graft—and these patients require antiplatelet therapy which may be problematic in polytrauma." [6,7,53]

Q5: Which vessels can be safely ligated?

A: "This is a critical decision. Safe ligation depends on adequate collateral flow.

Vessels that CAN be ligated under specific conditions:

  • One forearm artery—radial OR ulnar—if the other is intact and Allen test is normal. This gives 95% limb salvage.
  • One tibial vessel—if the other TWO are intact—giving 90% salvage. You need two of three for adequate perfusion.
  • Internal iliac artery—tolerated if the contralateral side and external iliac are intact, though may cause claudication and sexual dysfunction.
  • Internal carotid artery—only in extremis if the circle of Willis is intact, but carries 30-40% stroke risk.

Vessels that must NEVER be ligated:

  • Brachial artery—the only vessel to the forearm
  • Popliteal artery—end artery, ligation results in 70% amputation
  • Common femoral, superficial femoral, common carotid, subclavian, aorta, SMA, renal arteries

The key principle: if in doubt, repair. Temporary shunting in damage control surgery allows you to restore perfusion while deferring definitive repair until the patient is stable." [15,16,53,54]

Q6: How do you prevent and manage compartment syndrome after vascular repair?

A: "Compartment syndrome occurs in 10-25% of patients after revascularization due to ischemia-reperfusion injury causing edema in closed fascial compartments.

Prevention:

  • High index of suspicion—particularly if ischemia time exceeded 6 hours, combined arteriovenous injury, or high-energy mechanism
  • Prophylactic fasciotomy—I have a low threshold and would perform this for ischemia over 6 hours, severe soft tissue injury, or significant swelling immediately post-revascularization
  • Close monitoring—hourly compartment assessment post-operatively

Diagnosis is clinical:

  • Most sensitive sign: pain out of proportion to examination
  • Pathognomonic: pain with passive stretch of muscles in the affected compartment
  • Late signs: paresthesias, paralysis, pulselessness—these indicate advanced ischemia and irreversible damage is likely

Compartment pressure measurement can be used as an adjunct: delta pressure—diastolic blood pressure minus compartment pressure—less than 30 mmHg has 91% sensitivity and 98% specificity. However, I would not wait for this if the clinical diagnosis is clear.

Treatment is emergency fasciotomy:

  • For the leg: four-compartment release via two incisions—lateral for anterior and lateral compartments, medial for superficial and deep posterior compartments
  • Leave wounds open, delayed closure at 3-7 days when edema resolves, often requiring skin grafting
  • Delay leads to permanent disability—Volkmann's contracture in the arm, foot drop in the leg—or death from rhabdomyolysis." [13,14,42]

Common Mistakes That Fail Candidates

Clinical Mistakes:

  • Obtaining CTA in a patient with hard signs → DELAYS definitive treatment, increases morbidity/mortality
  • Releasing a tourniquet in the ED → Can cause sudden cardiovascular collapse; release only in OR with vascular control ready
  • Assuming normal pulses exclude vascular injury → 15% with significant injury maintain pulses via collaterals [11]
  • Missing compartment syndrome → Waiting for 5 Ps; act on pain + passive stretch

Technical Mistakes:

  • Ligating vessels that should be repaired (femoral, popliteal, brachial)
  • Blind clamping in hematoma → Risks nerve injury
  • Using synthetic graft in contaminated field → High infection risk; use vein
  • Not obtaining proximal/distal control before entering hematoma → Uncontrolled hemorrhage

Exam Mistakes:

  • Cannot list hard signs → Fundamental knowledge gap
  • Cannot describe ATLS approach → Shows lack of trauma training
  • Cannot differentiate repair vs ligation indications → Unsafe practice
  • Vague management plans → Examiners want specific, actionable steps

14. Patient/Layperson Explanation

What is a Vascular Injury?

A vascular injury is damage to the blood vessels that carry blood around your body—either arteries (which carry oxygen-rich blood from your heart to your tissues) or veins (which return blood to your heart). Think of your blood vessels like pipes in a plumbing system. When one of these "pipes" is damaged—from a stab wound, gunshot, car accident, or broken bone—you can have two major problems:

  1. Bleeding: Blood leaks out of the damaged vessel, which can be life-threatening if not stopped
  2. Lack of blood flow: The damaged vessel can't deliver blood to the area it supplies, which means that body part doesn't get the oxygen it needs

Why is this serious?

Vascular injuries are emergencies because:

Life-threatening: If a major blood vessel is injured, you can lose a dangerous amount of blood very quickly. We have about 5 liters of blood in our bodies, and losing just 2 liters can be life-threatening.

Limb-threatening: If an artery to your arm or leg is blocked or cut, that limb may not get enough blood. Without blood flow, the muscles and tissues start to die within 4-6 hours. This is why we talk about a "golden period"—if we can restore blood flow within about 6 hours, we can usually save the limb. After that, the risk of amputation increases significantly.

How is it diagnosed?

Your doctor will look for specific signs that indicate a vascular injury. We call these "hard signs":

  • Active bleeding (especially if it's pulsing with your heartbeat)
  • No pulse in the affected limb
  • The limb is pale, cold, numb, or you can't move it
  • A growing bruise or swelling
  • A vibrating feeling or whooshing sound over the injured area

If any of these are present, you need immediate surgery—no scans or X-rays, straight to the operating room.

If the signs are less clear (like a pulse that's weaker than normal), your doctor may do a special type of CT scan called a CT angiography (CTA) that shows your blood vessels to see if there's an injury.

How is it treated?

The goal is simple: Stop the bleeding and restore blood flow as quickly as possible.

Step 1: Control the Bleeding

  • Direct pressure: The most effective way to stop bleeding is firm, direct pressure on the wound
  • Tourniquet: For severe bleeding from an arm or leg that won't stop with pressure, we may use a tourniquet—a tight band that stops all blood flow. This is only used when absolutely necessary because it also stops blood flow to the limb

Step 2: Resuscitation

  • You'll get IV fluids and possibly blood transfusions to replace what you've lost
  • We'll give medications to help your blood clot properly
  • We'll monitor your vital signs closely

Step 3: Surgery This is where we fix the damaged vessel. There are two main approaches:

Open surgery (most common for arm and leg injuries):

  • The surgeon makes an incision to expose the damaged vessel
  • Removes any damaged portions
  • Repairs the vessel by either:
    • Sewing it back together if the gap is small
    • Using a piece of vein from another part of your body (usually your leg) as a "patch" or "bypass" if the gap is large
    • In rare cases, tying off the vessel if there's good blood flow from other vessels nearby

Endovascular repair (like keyhole surgery):

  • For some injuries, especially in the chest or neck, we can fix the vessel from the inside
  • A tube is inserted through a small puncture in your groin
  • A small metal mesh tube (stent) is guided to the injury site and expanded to seal the leak
  • This avoids a large incision but isn't suitable for all injuries

Step 4: Watching for Complications After surgery, we monitor you very closely, particularly for a complication called "compartment syndrome":

  • When blood flow is restored after being blocked, the affected area can swell significantly
  • This swelling can become so severe that it cuts off blood flow again
  • If this happens, we need to make incisions to release the pressure (fasciotomy)
  • This is why we check your pulses, color, and sensation every hour after surgery

What can you expect?

If treated quickly (within about 6 hours):

  • 85-90% chance of saving the limb
  • Most people recover well and return to normal activities
  • Hospital stay typically 5-14 days depending on severity

If treatment is delayed:

  • Risk of amputation increases significantly (up to 40-50% if over 12 hours)
  • Higher risk of complications
  • Longer recovery

Recovery:

  • You may need physical therapy to regain strength and movement
  • Full recovery can take 3-6 months
  • Some people have long-term issues like chronic pain or cold sensitivity in the affected area

When should you seek emergency care?

Call 999 (or your local emergency number) immediately if:

  • You have severe bleeding that won't stop with pressure
  • You have an injury and can't feel a pulse in the affected arm or leg
  • Your limb is pale, cold, numb, or you can't move it after an injury
  • You have a penetrating injury (stab, gunshot) near major blood vessels (neck, armpit, groin, inside of elbow or knee)

Do NOT:

  • Remove any objects stuck in the wound (they may be plugging the hole)
  • Release a tourniquet that's been applied (unless instructed by medical personnel)
  • Delay getting help—every minute counts

The bottom line

Vascular injuries are serious but treatable emergencies. The key is recognizing them quickly and getting to definitive surgical care as fast as possible. With modern surgical techniques, most people survive and keep their limbs, especially when treatment is prompt. Time is the most important factor—which is why we emphasize getting to the operating room within that "golden 6 hours."


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Last Reviewed: 2026-01-17 | MedVellum Editorial Team


Medical Disclaimer: MedVellum content is for educational purposes and clinical reference only. Clinical decisions should account for individual patient circumstances and be made in consultation with appropriate specialists. This information is not a substitute for professional medical advice, diagnosis, or treatment. All treatment recommendations should be verified against current local guidelines and protocols.

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Frequently asked questions

Quick clarifications for common clinical and exam-facing questions.

When should I seek emergency care for acute vascular injury?

Seek immediate emergency care if you experience any of the following warning signs: Active pulsatile bleeding, Hard signs: absent distal pulses, expanding hematoma, bruit/thrill, Acute limb ischemia (6 Ps), Signs of compartment syndrome, Hemodynamic instability/shock, Neurological deficit with vascular injury.

Learning map

Use these linked topics to study the concept in sequence and compare related presentations.

Prerequisites

Start here if you need the foundation before this topic.

  • Vascular Anatomy
  • ATLS Principles

Differentials

Competing diagnoses and look-alikes to compare.

  • Acute Arterial Thrombosis
  • Arterial Embolism

Consequences

Complications and downstream problems to keep in mind.

  • Acute Limb Ischemia
  • Compartment Syndrome
  • Hemorrhagic Shock