Vascular Occlusive Syndromes of the Upper Extremity Clinical Presentation

Updated: Jun 15, 2022
  • Author: Jake F Hemingway, MD; Chief Editor: Harris Gellman, MD  more...
  • Print


General symptoms following vascular compromise include dysesthesias, paresthesias, pallor, cold intolerance, ulceration, and tissue necrosis. Vascular competence can often become compromised, leading to various disease pathologies.

Patient evaluation for suspected vascular pathology should include eliciting detailed descriptions of the following:

  • Trauma mechanism (penetrating or nonpenetrating)
  • Exposure to repetitive insults
  • History of familial or blood disorders
  • Drug or tobacco use
  • Any concurrent illness

Patients with insidious vascular compromise may initially report numbness, increased pain, or cold sensitivity. As vascular insufficiency progresses, patients may report weakness or even present with frank gangrene resulting from tissue necrosis.


Physical Examination

A complete physical examination of the entire upper extremity and neck is warranted. The following must be documented:

  • Capillary refill
  • Skin turgor
  • Signs of infection
  • Tissue compromise, such as ulceration or gangrene
  • Quality of pulses
  • Presence of masses, bruits, or both

An Allen test should be performed to differentially evaluate the patency of the ulnar and radial arteries at the distal forearm. Documenting time-to-refilling is valuable for serial examinations. Additionally, several diagnostic evaluations may be completed to confirm suspected diagnoses (see Workup).



Acute trauma with ensuing vascular compromise of distal extremity tissue must be treated on an emergency basis to minimize distal tissue loss. Partial vascular compromise left untreated may result in muscular fibrosis and contractures of varying severity. Without vascular supply, the involved limb may be lost within hours.

More often, partial vascular compromise is left untreated, in which case the patient may develop an intrinsic plus hand deformity associated with intrinsic muscle contraction. Signs of intrinsic contracture include metacarpophalangeal (MCP) joint flexion and interphalangeal (IP) joint extension; passive hyperextension of the MCP joint decreases active flexion capacity of IP joints (Bunnell sign).

Noncritical arterial injury may lead to pseudoaneurysm, arteriovenous fistula (AVF) formation, or endothelial injury with mural thrombosis and seeding of emboli. Traumatic, noncritical vascular injuries involve cases in which tissue perfusion is not compromised, despite vascular injury. Such injuries may result in pseudoaneurysm formation, creation of an AVF, or acute thrombosis with distal embolization.

Raynaud disease usually occurs in persons aged 30-50 years, with an increased prevalence in women. Symptoms generally last longer than 2 years. Patients demonstrate bilateral hand involvement with pallor of digits secondary to cold exposure or psychologic stressors. Complications include intermittent complaints of dysesthesia of involved digits. In contrast, CREST syndrome represents disease processes involving symptoms of generalized calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia.

Symptoms specific to Raynaud phenomenon include digital ischemic pain, nonhealing ulcers, and the development of gangrene. Patients present with progressive joint contractures, including adduction contracture of the thumb and fixed flexion contractures of proximal IP (PIP) joints, with secondary extension contracture of MCP joints. Ulcers may develop over PIP joints, secondary to ischemia, pressure, minor trauma, or a combination of factors.