Acute arterial occlusion

Highlights :

Acute arterial occlusion

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Thursday, 08 October 2009 04:41

minimal atherosclerotic change in the three-vessel runoff to bilateral ankles

Causes:
I. Intrinsic causes:
1.Embolism
2. Acute Thrombosis
II. Extrinsic causes:

1.   Trauma:
2.   Neglected Tourniquet
3.   Compartment Syndrome
4.   Intra-arterial Injection
5.   Low Flow States
6.   Venous outflow blockade
7.   Drug Induced

Trauma:
[II] Neglected bandage or torniquet or tight plaster.
[III] Arterial embolism: Sources of emboli :
1- Commonest from the heart in cases of A.F.
2- Detached atheromatous patch thrombus.
3- Detached thrombus from aneurysm.
4- Paradoxical embolus: comes from venous side through patent foramen ovale.
[IV] Acute thrombosis:
 Commoner cause than embolism.
 due to the same factors of gradual thrombosis But it is not known why the onset is sudden.
Clinical picture:
5 Ps
   Pain
   Pallor
   Pulselessness
   Parasthesia
   Paralysis

1- Pain distal to the site of occlusion & tenderness over it.
   It indicates viable sensory nerves
   Its severity reflects degree of Ischemia
   It may be lost in late stages
   It may be absent in Hemiplegic insensitive limb
2- Pallor distal to the site of occlusion with cold Limb.
   It is felt in comparison with the other limb
   On palpation ischemic limb become colder
   Coldness increase with time
   Coldness may be absent in high surrounding atmospheric temperature
3- Pulselessness: No pulse can be felt from the site of occlusion and distal to it.
4- Parasthesia & burning sensation instead of pain due to ischaemic damage of sensory nerves. Numbness and tingling my be present without pain due to mild injury of sensory nerves
6- Paralysis of the affected limb in neglected cases.
   Early due to:
    neuropraxia (Rapidly revesible after reperfusion)
   Late due to:
   Nerve damage despite of viable soft muscles (Slowly reversible after reperfusion)
   Muscle cell damage (The muscles become stiff and rigid and paralysis is irreversible even after reperfusion)

Site of occlusion can be suspected according to the level of temperature change:
 Mid or upper thigh  obstruction at aortic bifurcation.
 Just above the knee  Common femoral obstruction.
 Lower part of the calf  upper popliteal obstruction.
 At the level of malleoli  lower popliteal obstruction.
In late cases manifestations of irreversible tissue damage are:
   Permanent mottling of the skin
   Stiff muscle
Clinical Categories of Acute Limb Ischemia

Category   Sensory Change   Motor Change   Doppler Signals
         Arterial   Venous
Viable   None   None   Audible   Audible
Threatened   Rest pain   Moderate   Inaudible   Audible
Irreversible   Anesthetic   Paralysis   Inaudible   Inaudible

Diagnosis of the cause:
   All extrinsic causes can be reached from history taking
   History of cardiac troubles suggest cardio-embolism
   History of intermittent claudication in old age and cardilogically free patient is in favor of acute thrombosis.

Investigations:
   Plain X ray chest: For exclusion of thoracic aortic aneurysm as a source of embolism
   Abdominal ultrasonography and duplex scanning:
1.   Exclude abdominal aortic aneurysm (AAA).
2.   Can detect the actual site of occlusion and its propagation.
3.   Assess the condition of the arteries and atherosclerosis of its wall.
   Echocardiography: For diagnosis of cardiac source of embolism e.g. left atrial thrombus or mitral valve vegetations.
   Angiography: It is indicated in:
o   Preoperative: In cases of acute thrombosis on top of atherosclerosis is suspected.
o   Intraoperative: As a completion angiography.
o   Postoperative: When early postoperative the pulsation become absent after being palpable and mild degree of ischemia starts to appear

   Laboratory Investigations:
1.   CBC for diagnosis of cases with polycythemia and thrombocytosis.
2.   Coagulation profile to obtain a baseline for anticoagulant therapy.
3.   Renal function to assess the the capability of kidney to secrete the dye of angiography and to compare with its function after reperfusion of the ischemic limb.

Treatment:
It is a case of emergency, best treated within 6hs.
1- Heparinization Once diagnosis is made heparin should be given as 10000 I.U. intravenous bollus dose followed by 1000 I.U. / hour continuos drip.
2- Operation: It depends on the underlying cause:
(A)   Cases of cardioembolism.
(B)   Acute thrombosis on top of chronic atherosclerosis.
(C)   Traumatic injury.
(A)   Cases of cardioembolism.
o   Early cases
   Heparinization
   Embolectomy
o   Late cases with no manifestations of irreversible tissue damage:
   Delayed embolectomy
   Conservative treatment
o   Late cases with irreversible tissue damage
   Early amputation

(B)   Acute thrombosis on top of chronic atherosclerosis.
•   Heparin
•   If the patient does not respond to heparin
•   For early cases with iliac stenosis
•   For early cases with distal atherosclerosis
•   For late cases with long segment femoral or popliteal stenosis.

(C) Traumatic injury.
•   Rapid evalution and arrest of bleeding
•   While preparation for operation resuscitation of the patient should be performed
•   If hard signs of arterial injury is found:
o   Pulsating arterial bleeding
o   Increasing pulsating hematoma
o   Manifestations of severe ischemia
Angiography is not needed and exposure of the suspected site of injury should not be delayed.
•   If there is Soft signs of arterial injury:
o   Dimminished pulsation with mild ischema
o   Bruit at or distal to the suspected site of injury
o   Injury of anatomically related nerves
Angiography is done for accurate preoperative diagnosis of the site and
nature of injury.

•   During operation:
The vessels are dissected and the damage ends are carefully trimmed and managed according to the type of injury.The continuity of the vessel is regained using autogenous or synthetic graft according to the situation.

SOURCE: DR AYMAN SALEM'S BOOK