2c:I[856015,["/_next/static/immutable/chunks/1xzisbplk9czp.js","/_next/static/immutable/chunks/3j2i1faptc_-9.js","/_next/static/immutable/chunks/1bqb83_yclja0.js","/_next/static/immutable/chunks/1on664om2hmh1.js","/_next/static/immutable/chunks/30t4sjq-27eg7.js","/_next/static/immutable/chunks/08tq8rmv423j5.js","/_next/static/immutable/chunks/32zk736rs0hqw.js","/_next/static/immutable/chunks/0lbgs964whs_0.js","/_next/static/immutable/chunks/1a_hqhrsle_n_.js","/_next/static/immutable/chunks/0hcnvyarhzl7i.js"],"default"] 2d:T6578,

CATEGORY	DETAIL
Risk Factors	Penetrating trauma (stab wounds, gunshot wounds), blunt trauma with fractures or dislocations (supracondylar humerus fracture, posterior knee dislocation), iatrogenic causes (catheterization, arterial lines), deceleration injuries
Etiology	Direct vessel wall disruption (laceration, transection), intimal tear with secondary thrombosis, external compression from fracture fragments or compartment swelling, or shearing forces causing dissection
Patient Presentation	Pain, pallor, pulselessness, or an expanding/pulsatile hematoma at or distal to the injury site; history of trauma with limb-threatening ischemia
Classic Physical Exam	Hard signs: pulsatile bleeding, expanding hematoma, absent distal pulses, palpable thrill or audible bruit, signs of distal ischemia (the "6 Ps": pain, pallor, pulselessness, paresthesia, paralysis, poikilothermia)
Key Diagnostic Results	Ankle-Brachial Index (ABI) less than 0.9 is abnormal; CT Angiography (CTA) shows vessel occlusion, intimal flap, pseudoaneurysm, or extravasation; conventional angiography remains the gold standard when intervention is planned
Management	Hard signs with hemodynamic instability: immediate surgical exploration. Stable patient with hard signs: operative repair or endovascular intervention. Soft signs only: serial exam plus CTA. Anticoagulation with heparin when not contraindicated. Fasciotomy for compartment syndrome. Temporary shunting if damage control is needed
Keywords	"Pulsatile bleeding," "expanding hematoma," "posterior knee dislocation with absent pedal pulse," "supracondylar fracture with weak radial pulse," "cool and pale extremity after trauma," "ABI less than 0.9," "intimal flap on CTA"

1. Pathophysiology

Arterial injuries result from mechanical disruption of the vessel wall, and the clinical consequences depend on which layer of the artery is damaged and to what extent.

In penetrating trauma, a sharp or ballistic object directly lacerates or transects the artery. A complete transection paradoxically may bleed less than a partial one because the severed ends retract and vasospasm can partially limit hemorrhage. A partial laceration, by contrast, keeps the vessel held open by surrounding tissue, preventing retraction and allowing continuous hemorrhage. This is why a partially cut artery can be more dangerous than a fully divided one.

In blunt trauma, the injury mechanism involves stretching, compression, or shearing of the vessel. The intima, being the most fragile and inelastic layer, tears first. An intimal flap disrupts laminar flow and creates a nidus for platelet aggregation and thrombosis, which can progress to complete vessel occlusion. This explains why a patient with a blunt arterial injury may initially have intact pulses that then disappear hours later as the thrombus propagates. This delayed presentation is a classic exam scenario.

Pseudoaneurysms form when blood escapes through a defect in the arterial wall but is contained by the adventitia or surrounding soft tissue, creating a pulsatile, encapsulated hematoma that communicates with the arterial lumen. Unlike true aneurysms, pseudoaneurysms lack a complete wall and carry a high risk of rupture.

Arteriovenous fistulas (AVFs) develop when simultaneous arterial and venous injury creates an abnormal communication. Blood follows the path of least resistance into the low-pressure venous system, producing a continuous ("machinery") murmur and a palpable thrill. Over time, the increased venous return can cause high-output cardiac failure if left untreated.

The ischemia-reperfusion cascade is also testable. When arterial flow is interrupted, tissues become ischemic. Upon restoration of flow, the sudden reintroduction of oxygen generates reactive oxygen species, and damaged cells release potassium, myoglobin, and lactic acid into the circulation. This can lead to reperfusion injury manifesting as hyperkalemia, myoglobinuria, metabolic acidosis, and potentially acute kidney injury or cardiac arrest.

2. Classification and Clinical Manifestation

Injury Classification by Mechanism

TYPE OF INJURY	MECHANISM	KEY CLINICAL FEATURE
Complete transection	Vessel fully divided	Vessel retraction, potential for vasospasm limiting hemorrhage initially; absent distal pulses
Partial laceration	Incomplete wall disruption	Continuous hemorrhage because vessel cannot retract; pulsatile bleeding
Intimal flap / dissection	Blunt force tears the intima	Initially intact pulses that disappear over hours as thrombus forms; delayed ischemia
Thrombosis	Intimal injury with secondary clot formation	Progressive loss of distal perfusion without external bleeding
Pseudoaneurysm	Contained perforation, adventitia intact	Pulsatile mass that expands over days to weeks; risk of delayed rupture
Arteriovenous fistula	Simultaneous arterial and venous wall injury	Continuous machinery murmur, palpable thrill, potential high-output heart failure if chronic
Spasm	Vessel wall irritation without structural breach	Transient loss of pulse that resolves spontaneously; diagnosis of exclusion

Hard Signs vs. Soft Signs

This distinction is one of the most tested concepts in vascular trauma.

CATEGORY	FINDINGS	CLINICAL IMPLICATION
Hard signs	Pulsatile or arterial hemorrhage, expanding or pulsatile hematoma, absent distal pulses, distal ischemia (6 Ps), audible bruit or palpable thrill	Mandate immediate surgical exploration without further imaging in unstable patients
Soft signs	History of hemorrhage now controlled, diminished but present pulses, small stable hematoma, nerve deficit adjacent to a named artery, proximity of wound to a major vessel	Warrant further workup (ABI measurement, CTA, observation, serial exams) but do not require emergent surgery by themselves

High-Risk Injury-Artery Associations

INJURY / DISLOCATION	ARTERY AT RISK
Posterior knee dislocation	Popliteal artery
Supracondylar humerus fracture (pediatric)	Brachial artery
First rib fracture / clavicle fracture	Subclavian artery
Pelvic fracture	Internal iliac artery branches
Midshaft femur fracture	Superficial femoral artery
Anterior shoulder dislocation (elderly)	Axillary artery
Penetrating Zone II neck trauma	Carotid artery

3. Diagnostic Workup

Diagnostic Summary Table

TEST	ROLE	KEY FINDINGS
Physical exam (hard vs. soft signs)	Initial triage at the bedside	Determines whether the patient goes directly to surgery or to imaging
Ankle-Brachial Index (ABI) / Arterial Pressure Index (API)	Best initial screening test for extremity vascular injury	ABI less than 0.9 is abnormal and warrants imaging; ABI greater than or equal to 0.9 has a negative predictive value above 95%
CT Angiography (CTA)	Best initial imaging test for stable patients	Shows intimal flap, occlusion, pseudoaneurysm, extravasation, or AVF with high sensitivity and fast acquisition
Conventional (catheter) angiography	Gold standard / most accurate test	Provides definitive anatomic detail and allows simultaneous endovascular intervention; reserved for equivocal CTA or when intervention is planned
Duplex ultrasonography	Adjunct in stable, accessible injuries	Operator-dependent; useful for follow-up of minimal injuries or pseudoaneurysms; limited in the acute trauma setting
Plain radiograph	Adjunct for associated skeletal injury	Identifies fractures or dislocations that have known vascular injury associations

The decision pathway begins at the bedside. When a trauma patient presents, the first task is to identify hard signs versus soft signs. If hard signs of vascular injury are present and the patient is hemodynamically unstable, imaging is skipped entirely and the patient proceeds directly to the operating room for surgical exploration. No test should delay a patient who is actively exsanguinating.

If the patient is hemodynamically stable, even with hard signs, the next step is CTA. Modern multidetector CT has sensitivity and a negative predictive value that approach those of conventional angiography, and it provides additional information about surrounding structures (bones, soft tissue, venous injury). CTA has largely replaced conventional angiography as the first-line imaging study in stable trauma patients.

ABI measurement is the bedside screening tool for extremity injuries. You measure systolic blood pressure at the ankle (or wrist for upper extremity injuries) and divide by the brachial systolic pressure. A value less than 0.9 indicates a hemodynamically significant arterial injury and should prompt imaging. An ABI of 0.9 or greater in a patient with only soft signs is reassuring and can be followed with serial exams and repeat ABI measurements.

Conventional angiography is reserved for cases where CTA is equivocal, when endovascular repair is being planned (since the catheter is already in place), or in settings where CTA is not available. It remains the most accurate test, but its invasive nature and need for specialized resources make it a second-line study in most trauma centers today.

For proximity injuries (a wound near a named vessel but no hard or soft signs), current evidence supports observation with serial exams and ABI rather than routine angiography. Mandatory exploration for proximity alone has been abandoned.

4. Management and Treatment

Management Summary Table

SCENARIO	MANAGEMENT	KEY DETAILS
Hard signs + hemodynamic instability	Immediate operative exploration	Direct pressure or tourniquet for hemorrhage control en route; do not delay for imaging
Hard signs + hemodynamically stable	CTA then operative or endovascular repair	CTA guides surgical planning; endovascular stenting for select injuries (e.g., subclavian, iliac)
Soft signs only	ABI + CTA if ABI less than 0.9	Serial exams every 6 to 8 hours for 24 to 48 hours; repeat ABI
Minimal intimal injury (less than 5 mm, non-flow-limiting)	Observation + antiplatelet therapy	Many resolve spontaneously; follow-up duplex ultrasound at 1 to 2 weeks
Compartment syndrome suspected	Four-compartment fasciotomy	Clinical diagnosis (pain out of proportion, pain with passive stretch); do not wait for compartment pressure measurement if clinical suspicion is high
Damage control (polytrauma, hypothermia, coagulopathy)	Temporary intraluminal shunt	Restores perfusion while addressing other life-threatening injuries; definitive repair later

Acute stabilization follows standard trauma principles: airway, breathing, circulation. For external hemorrhage from an arterial source, direct pressure is applied first. If direct pressure fails, a tourniquet should be placed proximal to the injury, and the time of application must be documented. Tourniquets are safe for up to 6 hours in most clinical contexts, though ischemic tolerance varies by tissue type.

Systemic anticoagulation with unfractionated heparin (bolus of 80 units/kg followed by an infusion of 18 units/kg/hour, titrated to a PTT of 1.5 to 2.5 times normal) is administered when there is no contraindication (such as active intracranial hemorrhage or other ongoing bleeding). Heparin prevents thrombus propagation proximal and distal to the injury and improves outcomes of surgical repair.

Operative repair options depend on the type and extent of injury:

For clean lacerations, primary repair with interrupted sutures (typically 5-0 or 6-0 polypropylene) is performed if the repair does not narrow the lumen by more than 50%.

For segmental loss or transection, an interposition graft is required. The reversed saphenous vein graft is the conduit of choice for infrainguinal repairs because of superior long-term patency and resistance to infection compared to prosthetic grafts. Prosthetic grafts (PTFE or Dacron) are used when autologous vein is unavailable or for large-caliber vessels (aorta, iliac arteries).

Endovascular repair with covered stents is increasingly used for injuries to vessels that are surgically difficult to access, such as the subclavian, axillary, and iliac arteries. It is also appropriate for pseudoaneurysms and select AVFs in stable patients.

Fasciotomy must be performed liberally in the setting of prolonged ischemia (greater than 4 to 6 hours), combined arterial and venous injury, or any clinical suspicion of compartment syndrome. In the lower leg, a two-incision, four-compartment fasciotomy is the standard technique. The key teaching point is that compartment syndrome is a clinical diagnosis: waiting for compartment pressure measurements (greater than 30 mmHg, or within 20 to 30 mmHg of diastolic pressure) is acceptable only when the clinical exam is unreliable (e.g., intubated or obtunded patient).

After reperfusion, monitor for the systemic effects of the ischemia-reperfusion cascade: hyperkalemia (treat with calcium gluconate, insulin/glucose, and bicarbonate), myoglobinuria (aggressive IV fluid resuscitation to maintain urine output greater than 100 mL/hour, alkalinize urine), and metabolic acidosis.

Contraindications and caveats: Heparin is contraindicated in patients with active hemorrhage from other sites, heparin-induced thrombocytopenia, or intracranial bleeding. In these situations, mechanical thrombectomy or local thrombolysis may be considered on a case-by-case basis. Saphenous vein harvest should be avoided from an extremity with concomitant venous injury.

5. Differential Diagnosis and Distractors

DIFFERENTIAL	WHY IT IS SIMILAR	KEY DISCRIMINATOR
Compartment syndrome (without arterial injury)	Both cause limb pain, pallor, and paresthesia after trauma	In compartment syndrome, pulses are often preserved until very late; the hallmark is pain out of proportion to the injury and pain with passive stretch of the compartment muscles. In arterial injury, pulses are diminished or absent early
Venous injury	Can produce significant hematoma and limb swelling after penetrating trauma	Venous bleeding is dark, non-pulsatile, and controlled with direct pressure. The limb is swollen and congested rather than pale and cool. Distal arterial pulses remain intact
Deep vein thrombosis (DVT)	Presents with a swollen, painful extremity	DVT causes edema and calf tenderness without signs of ischemia; pulses are intact. There is no history of direct vascular trauma. Duplex ultrasound confirms venous thrombus
Neurogenic shock (spinal injury)	Can present with hypotension and poor distal perfusion after trauma	Neurogenic shock produces warm, dry extremities with bradycardia (loss of sympathetic tone), unlike the cold, pale, pulseless limb of arterial occlusion
Traumatic neuropathy	Nerve injury near a vessel can cause numbness, weakness, and pain mimicking ischemia	Neuropathy affects motor and sensory function in a dermatomal or peripheral nerve distribution without changes in pulse, capillary refill, or limb temperature
Vasospasm	Transient loss of pulse after blunt trauma or catheterization	Vasospasm is self-limited, typically resolving within minutes to hours. Pulses return spontaneously, and there is no structural injury on imaging. It is a diagnosis of exclusion
Aortic injury (traumatic aortic disruption)	Involves arterial trauma from a deceleration mechanism	Aortic injury presents with widened mediastinum on chest X-ray and involves the thoracic aorta at the isthmus, not a peripheral vessel. The clinical concern is central rather than limb ischemia

6. Traps and High-Yield Pearls

The single most common trap with arterial injury questions is delayed presentation after blunt trauma. Students read a vignette about a patient with a posterior knee dislocation whose initial exam shows intact pedal pulses and assume the vasculature is fine. The question then describes worsening pain and a cool, pale foot several hours later. The tested concept is that an intimal flap with progressive thrombosis can cause initially normal pulses to disappear over time. The correct answer is serial vascular exams and ABI measurement in every patient with a high-risk mechanism, regardless of initial pulse status.

Another frequent error involves confusing the indications for immediate surgery versus imaging. Students may select "obtain CTA" for a patient with pulsatile hemorrhage and hemorrhagic shock. The rule is clear: hard signs plus hemodynamic instability equals the operating room, not the CT scanner. Imaging is only appropriate when the patient is stable enough to lie on the scanner table.

Students also lose points by conflating compartment syndrome with arterial insufficiency. Both appear after extremity trauma with pain and neurovascular changes, but the vignette will include the discriminating clue: in compartment syndrome, the key finding is pain with passive stretch and tense swelling with preserved pulses, while arterial injury features absent pulses and pallor as the dominant findings.

Finally, do not forget the fasciotomy question. When a vignette describes restoration of arterial flow after prolonged ischemia (more than 4 to 6 hours) followed by a tense, painful extremity, the next best step is fasciotomy, not observation or repeat imaging. The exam tests whether you understand that reperfusion itself can trigger compartment syndrome, and that delay in fasciotomy leads to irreversible muscle necrosis and potential limb loss.

The core competency being tested across arterial injury questions is clinical decision-making under time pressure: recognizing hard signs, triaging correctly between the operating room and imaging, and anticipating complications like compartment syndrome and reperfusion injury before they become irreversible.

1d:["$","$L2c",null,{"article":{"id":"efb9603a-ee5c-4c87-a53e-18694c4a10ec","title":"Cedera Arteri","content":"$2d","category":"Muskuloskeletal","created_at":"2026-09-05T15:50:52.046924+00:00","status":"published","subcategory":null},"questionCount":0,"sections":[{"id":"section-pathophysiology","num":"01","title":"Pathophysiology"},{"id":"section-classification-and-clinical-manifestation","num":"02","title":"Classification and Clinical Manifestation"},{"id":"section-diagnostic-workup","num":"03","title":"Diagnostic Workup"},{"id":"section-management-and-treatment","num":"04","title":"Management and Treatment"},{"id":"section-differential-diagnosis-and-distractors","num":"05","title":"Differential Diagnosis and Distractors"},{"id":"section-traps-and-high-yield-pearls","num":"06","title":"Traps and High-Yield Pearls"}],"hasSummaryTable":true}]