Cedera Arteri

01Pathophysiology

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.

02Classification and Clinical Manifestation

Injury Classification by Mechanism

Hard Signs vs. Soft Signs

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

High-Risk Injury-Artery Associations

03Diagnostic Workup

Diagnostic Summary Table

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.

04Management and Treatment

Management Summary Table

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.

05Differential Diagnosis and Distractors

06Traps 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.