Acute arterial insufficiency

Etiology and mechanisms of development

Acute ischemic syndrome most commonly results from acute arterial obstruction. The main culprits are thrombi. Arterial emboli typically travel from the left heart chambers into the systemic circulation in myocardial infarction (mural thrombi), valvular heart disease, or atrial fibrillation.

There is also the so-called paradoxical (crossed) embolism. It occurs in patent foramen ovale: in this case, a thrombus from the deep veins of the lower leg or thigh enters the left heart and proceeds into the arterial system, bypassing the lungs.

Extremely rarely, the vascular lumen is occluded by air bubbles (in injuries of large veins or improper IV infusion technique) or adipose tissue (in severe bone fractures when bone marrow elements enter the bloodstream).

The pathogenesis of acute ischemia syndrome consists of three key factors:

1. Mechanical occlusion — a physical barrier to blood flow and acute stretching of the vessel wall above it.
2. Arterial spasm — reflex narrowing of both the affected artery itself and its branches, as well as collateral pathways below the occlusion site.
3. Secondary thrombosis — formation of a propagated thrombus distal to the obstruction due to impaired hemostasis and slowed blood flow.

Classification and stages of ischemia (according to V.S. Savelyev)

Staging is of critical importance: it determines the surgeon's tactics and the prognosis for the affected limb.

• Stage I of functional disorders (lasts several hours). Characterized by acute pain, pallor, and coldness of the skin. Pulses in peripheral arteries are absent, but tactile and pain sensitivity are preserved. Active joint movements are limited but possible. Prognosis: with prompt restoration of blood flow, the functions of the leg or arm are fully preserved.
• Stage II of organic changes (12–24 hours). The skin becomes cyanotic, and muscular contracture develops. Pain and tactile sensitivity disappear completely, while active and passive movements are sharply limited. Prognosis: with successful surgery, the limb can be saved, but there will be a complete loss or sharp limitation of its motor functions.
• Stage III necrotic stage (occurs after 24–48 hours). Gangrene develops. All types of sensitivity and movement are totally lost. Prognosis: restoring vascular patency no longer saves tissues from necrosis. Surgery is performed for vital indications (amputation), but vascular reconstruction sometimes helps lower the demarcation level.

Clinical presentation

Symptoms of thromboembolism coincide with the moment of occlusion and develop rapidly:

• Pain syndrome: sudden, unbearable pain in the distal parts, capable of triggering shock. This is the first and most constant sign. Only in one out of ten patients does the process begin subacutely — with a feeling of numbness, "pins and needles," and coldness, which is associated with incomplete occlusion by the embolus and gradual progression of secondary thrombosis.
• Neurological disorders: pain is rapidly followed by paresthesia, then total anesthesia. Simultaneously, muscle strength drops, leading to complete paralysis (plegia) of the fingers and other distal parts.
• Local status: the limb feels cold to the touch (its temperature is 2–3 degrees lower than the healthy one). Pulses in peripheral arteries are absent. The skin turns pale, then acquires a patchy appearance ("marbled skin"), and areas of cyanosis resemble livor mortis.
• General manifestations: against the background of pain and ischemia, the patient's general condition rapidly deteriorates. A picture of shock develops: tachycardia, hypotension, rapid breathing (tachypnea), and lip cyanosis.

Without emergency care, symptoms progress. The marbled-cyanotic skin dries, wrinkles, and turns black — dry gangrene develops.

First aid and treatment tactics

At the pre-hospital stage, the patient is urgently administered analgesics and cardiac drugs. The affected limb is immobilized using a transport splint and surrounded by ice packs (to induce local hypothermia). The most crucial step is the fastest possible transport to a specialized surgical department.

In the hospital, treatment is selected individually depending on the duration of the thromboembolism and the stage of ischemia:

• Conservative therapy. Indicated in early periods (up to 6 hours from onset), for embolism of small arteries of the lower leg or forearm, and as an adjunctive measure. Trial conservative treatment lasts 1.5–2 hours. It includes anticoagulants (sodium heparin) and fibrinolytics to prevent propagated thrombosis, vasodilators, and procaine blocks to relieve spasm.
• Surgical intervention. Indicated in stages I and II of acute ischemia (if conservative treatment proves ineffective — pain and sensation do not resolve). Radical operations (embolectomy, vascular plastic surgery, or bypass) are performed to directly restore blood flow. In some cases, a palliative operation (sympathectomy) is performed to stimulate the collateral bed.
• Amputation. Performed at stage III, when restoring blood flow is already pointless and it is necessary to save the patient's life from tissue breakdown products.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Chronic lower extremity ischemic syndrome
• Acute venous insufficiency and deep vein thrombosis
• Mechanisms of pulmonary embolism (PE) development
• Technique of radical surgeries: embolectomy and vascular bypass
• Lymph circulation insufficiency: causes of lymphedema and elephantiasis

Other topics of 'CHAPTER 13. VASCULAR AND LYMPHATIC INSUFFICIENCY OF THE EXTREMITIES'

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