acute arterial occlusion

Acute Arterial Occlusion

Sudden obstruction of an arterial lumen leading to decrease perfusion of the tissue supplied by that artery. Sudden occlusion of an artery is caused by:
Embolism
Thrombosis of an atheromatous plague
Arterial trauma.

Embolic Arterial Occlusion or Acute Arterial Embolization:

An emboli is a body that is foreign to the blood stream (although its constituents may be part of the blood) which travels in the blood stream and may become lodged in a vessel and cause obstruction.
An embolus is most commonly is a thrombus (blood clot), but it can be a foreign body (shell, bullet,...), parasitic ova, air bubble, amniotic fluid …etc. The heart is the most common source of embolization usually due to ischemic heart disease. Sources are the left atrium in cardiac arrhythmias (particularly atrial fibrillation) and mural thrombus following myocardial infarction. Less common sources are aneurysms and thrombi formed on atheromatous plaques (so called artery-to-artery embolism or arterio-arterial embolism). Emboli may lodge in any organ and cause ischemic symptoms.
Brain: middle cerebral artery mostly occluded leading to TIA or stroke
Retina: retinal artery occlusion leading to amaurosis fugax. Mostly due to arterio-arterial embolization from an atheromatous plaque in the carotid artery.
GIT: mesenteric artery occlusion leading to ischemia and possibly gangrene to corresponding loop of intestine, acute abdomen and shock.
Spleen: resulting in splenic infarction
Kidney: renal infarction leading to pain and hematuria.
Limbs: acute limb ischemia with pain, pallor, paralysis, parasthesia, pulselessness and poikilothermia.
The leg is often affected leading to the severe pain and numbness in the affected limb. The limb is cold and the toes cannot be moved. Pulse is usually absent distal to the site of obstruction and examination of the pulse may give an idea of the site of embolic occlusion. The pulse proximal to the obstruction may be forceful (stronger than the contralateral normal side). Later on the limb may become mottled (alternating areas of pallor and cyanosis which does not blanch on pressure) and gangrenous indicating non-reversible ischemia.
Once an embolus has occluded an artery, stasis in that artery lead to formation of propagating thrombus both proximally and distally.

Diagnosis:

The diagnosis is usually made clinically in a patient who has no history of chronic ischemia and has a source of emboli, who suddenly develops severe pain or numbness of the limb, which becomes cold and pale or even mottled. Once the diagnosis is made no time should be lost in waiting for investigations.
Confirming investigations include:
Doppler
Duplex ultrasound
Peripheral angiography
CT angiography or MRA


Treatment:
Once the diagnosis has been made emergency treatment is mandatory, as in the absence of effective collaterals to the limb, non reversible ischemia tend to develop within hours of the arterial occlusion.
Immediate administration of 5000 U of heparin intravenously (80-150 U/kg body weight) can reduce the extension of the propagating thrombosis and maintain patency of the surrounding vessels.
Relieve pain usually by opiates
Emergency embolectomy (using a Fogarty balloon catheter)
Embolectomy is usually performed under local anesthesia. The common femoral artery is the most common artery used for lower limb embolectomy and the brachial artery for upper limb embolectomy. The artery is exposed and a 3-5 mm arteriotomy is done through which the embolectomy catheter is inserted, inflated and carefully withdrawn to remove both the embolus and propagating thrombus. Back and forth bleeding confirms restoration of flow and the arteriotomy is closed using fine non-absorbable sutures. Restoration of distal pulse confirms successfulness of the procedure.
Postoperatively heparin is continued until long term anticoagulation with warfarin is established to reduce the chance of further embolism.

Acute arterial thrombosis

Acute arterial thrombosis refers to sudden occlusion of an already diseased or stenosed artery.

Causes:

Spontaneous arterial thrombosis: The arterial occlusion is usually due to sudden rupture of an atheromatous plague which leads to release of its highly atherogenic lipid core resulting in platelet adhesion and thrombus formation.
Aneurysmal thrombosis: stasis within the aneurysmal sac predispose to thrombosis. This thrombosis may extend to completely occlude the artery. E.g.; popliteal artery aneurym thrombosis.
hypercoagulable state: such patients have higher risk of spontaneous thrombosis both arterial and venous
Repeated minor trauma
Iatragenic: e.g.; during arterial catheterization, invasive pressure monitoring, ...etc. An flap of intima may occlude the artery or the presence of a foreign material in the lumen of the artery may stimulate thrombosis.
This condition is often referred to as "acute on chronic" arterial occlusion
The presentation is similar to acute arterial occlusion but less severe as the chronic arterial disease has lead to development of collateral vessels over the years so that the acute occlusion of the main artery is less dramatic. Also these patients often give previous history of intermittent claudication or even rest pain in the same limb and clinical examination will show signs of chronic ischemia in the limb and in other limbs too.

Diagnosis

If acute on chronic ischemia is suspected a period of delay is justified to perform confirmative investigations before deciding on the treatment options. Exact localization of the site of arterial occlusion with the sufficiency of collaterals is mandatory with peripheral angiography being the diagnosis of choice for this option. Angiography accurately visualizes the site and length of obstruction, with visualization of important collaterals to be preserved during surgery and access the distal artery for disease process which may endanger the success of surgery.


Treatment
Surgical embolectomy here is usually not enough and more complex surgery may be required including endarterectomy, bypass procedure, sympathectomy, endovascular procedures and others. but still results are less satisfactory with higher likelihood of amputation.

Difference between acute arterial embolism and acute arterial thrombosis

Embolism
Thrombosis

Source of embolism

Present
Absent

Predisposing factors for atherosclerosis

Usually absent
Present

History

History of arrythmia or valvular heart disease
History of intermittent claudication or rest pain

Clinical examination

Features of acute ischemia. No features of chronic ischemia. Normal other limb
Skin, nail and hair changes of chronic ischemia. Distal pulse may be absent in other
limb as well


Arteriography
Not justified. Normal arterial wall with sudden sharp obstruction and poor collaterals
Mandatory. Diseased artery with gradual narrowing and well formed collaterals

Trearment

Embolectomy
Embolectomy rarely enough. More complex surgery required.

Arterial trauma:

Vascular trauma may be caused by:
penetrating injury which is the most common e.g.; injury due to knife, bullet, shell, ...etc.
blunt injury
deceleration injury
Pattern of injury are similar whatever the cause is and include
Completely severed artery: complete disruption of the artery so the divided ends constrict and retract. A clot forms on both ends and propagate.
Results: severe bleeding stops spontaneously as a result of the vasoconstriction and plug of clot formation. Distal pulse becomes negative due to interruption of blood flow. And the degree of distal ischemia depends on the presence and size of collaterals
Partially severed artery: injury just to part of the circumference of the artery. The ends constrict and retract farther enlarging the defect (the defect gapes). The overlying muscles and skin tamponade the blood loss, particularly when the patient is hypotensive. This containment may be only a temporizing measure. The hematoma may gradually increase in size, particularly after the patient's blood volume has been restored and the blood pressure normalized. When the hematoma is carefully examined, it often has a pulsatile quality, since it communicates directly with the arterial lumen.
Results: Commonly produces serious or recurrent bleeding. & could be severe. Blood flow is maintained distally, so distal pulse are positive but may be weak. With no end organ ischemia.
Non-severed artery: here there is intimal damage without actually severing the vessel's outer circumference. Such injury may occur due to blunt force or excessive stretch is applied to the arterial wall, or passage of a high-velocity missile adjacent to the artery. The torn arterial intima acts as a flap occluding the arterial lumen or causing subintimal hematoma with stenosis or occlusion of the arterial lumen.
Results: there will be no external bleeding or hematoma with absent distal pulses and features of end organ ischemia.


Clinical examination:
Signs of arterial injury include:
Pulsatile bleeding or pulsatile hematoma or an expanding one
Bruit or thrill
End organ ischemia
Absent distal pulses
Suggestive signs include:
Unexplained shock
Trauma near a known course of a major artery
A stable hematoma
Injury to a nerve known to share a common course with a major artery
History of pulsatile bleeding from a wound
Presence of positive distal pulse does not exclude the possibility of arterial injury.
Arteriography is the gold standard test for diagnosis of arterial injury and should be performed whenever possible.

Treatment:

ABC
Control of hemorrhage: direct digital pressure is the best maneuver at the scene of trauma or in the emergency department. Tourniquets should be used only as a last resort. They can occlude collateral flow and increase tissue damage. Attempts to find the artery or control bleeding by clamps or ligatures usually dislodge clots & risk damage to adjacent neurovascular structures. Even well-applied but traumatic clamps may damage enough artery to convert a simple end-to-end repair into a replacement graft. Neither embedded foreign bodies nor hematomas should be removed until proximal control is achieved.
operative treatment: most of these patients are operated on before full data is available. Both limbs are prepared and preparation for rapid volume replacement if bleeding occurs before expected.
proximal and distal arterial control should be obtained before the injury is approached. Once the injury is identified, wide debridement of the injured vessel is performed until healthy ends are obtained. Intra-luminal thrombus removed by flushing the artery or with a Fogarty's catheter. Here systemic heparin can be given except in multisystem trauma where only the injured vessel is flushed with heparinized saline
the type of arterial repair depends on the nature and extent of injury and includes
lateral arteriorrhaphy (lateral repair)
venous patch angioplasty when direct lateral repair may compromise the lumen
end-to-end anastomosis when the injury or its debridement interrupts the continuity of the artery
graft interposition using an autologus vein graft harvested from the contralateral limb. Synthetic grafts should be avoided because of the increase risk of failure and wound infection.


Complications of vascular trauma
Anastomosis dehiscence leading to recurrence of bleeding, hypovolemia and shock
Anastomosis site thrombosis leading to ischemia and gangrene
Pseudoaneurysm formation
Traumatic arterio-venous fistula formation
Wound infection
Compartment syndrome
Reperfusion injury

Compartment syndrome: increased pressure within a closed compartment to exceed the capillary pressure resulting in failure of extravasation of oxygen and nutrients into the interstitium leading to ischemia even in the presence of positive distal pulses. Such scenario can occur post revasculization of an ischemic limb, after fractures, excessive soft tissue injury,…etc. due to muscle swelling or bleeding into the muscles. Mostly seen in the leg, less common in the thigh or upper limb. The treatment is urgent fasciotomy to release the compression.

Reperfusion injury: prolonged ischemia to a certain area of the body results in anaerobic metabolism with the production of lactic acidosis. Eventually some cells die releasing potassium and myoglobin into the interstitium. Once the circulation to that area is restablished, these toxic materials will be washed into the general circulation leading to dangerous effects including; sudden death, arrhythmias, myoglobulinurea and acute renal failure depending on the amount of these substances that reached the circulation.