Hand Ischemia in Active Patients: Detecting and Treating Hypothenar Hammer Syndrome

Linda J. Rowan, MD, MS, ATC

THE PHYSICIAN AND SPORTSMEDICINE - VOL 26 - NO. 1 - JANUARY 98

In Brief: Occlusion of the palmar arch vessels is rare, but it can occur in athletes and workers who subject their hands to repeated blunt trauma or gripping activities. A case report examines a baseball player who presented with classic symptoms of hypothenar hammer syndrome (occlusion of the ulnar artery due to repetitive blunt trauma); evaluation also identified radial artery occlusion. Occlusive symptoms include pain, cold intolerance, and numbness. The diagnosis rests on evaluating the patency of the palmar arches. Conservative treatment involves rest, tobacco avoidance, and medications. Patients who have severe arterial compromise require resection and reconstruction.

Hypothenar hammer syndrome—ulnar artery occlusion due to repetitive blunt trauma to the palm—and other forms of arterial insufficiency of the hand are relatively rare in sports. Most cases involve athletes who use their hands for catching or striking objects (volleyball, karate, judo, handball, baseball, football) or those who grip an implement across the palm of the hand with direct contact over the hook of the hamate (racket sports, golf, baseball) (figure 1: not shown).

Few authors have reported ischemic problems in the hands of baseball players (1-3). The following case report describes a collegiate baseball player who developed circulatory compromise of the hand after he changed his grip on the bat.

Case Report

History. A 23-year-old right-handed collegiate second baseman was hit by a baseball on the tip of his right index finger, splitting the fingertip on impact. During the next 4 weeks, practice and games traumatized the fingertip, and an open ulcer and infection developed. To accommodate the discomfort, the player adjusted his bat grip by holding his injured finger off the bat. This placed the handle of the bat directly over the hypothenar eminence, subjecting the area to repetitive blunt impacts with each hit. Despite treatment, his fingertip ulcer remained open and sore.

After 4 weeks, the athlete was referred to a physician because of progressive generalized palm soreness and a dull weakness of the forearm extending into his upper arm. He reported that cooler environments exacerbated his symptoms, which included cold intolerance in the hand and fingers, pain, progressive numbness, and increased blanching with any throwing or batting. The athlete had also noted strength loss in his long-distance throwing. In addition, he had developed a very tender, round, hard, 1-cm mass over the hamate.

Physical exam. Direct pressure on the mass was acutely painful and caused immediate numbness in the hand. A small area of erythema was noted over the hypothenar eminence. Subungual petechiae were also apparent on the index and little finger. The Allen test (see "Evaluating Hand Ischemia," below) was positive for ulnar artery occlusion and demonstrated slow filling from the radial artery. Capillary refill was delayed in the index and ring fingers. Radial and ulnar pulses at the wrist were not diminished. Sensation was decreased in the ulnar distribution, though two-point discrimination was normal. Grip strength was 40 lb on the right and 130 lb on the left.

Diagnostic studies. A perfusion bone scan suggested patent ulnar and radial arteries. No perfusion deficits were seen on blood pool images (figure 2). Angiography showed occlusion of the radial and ulnar arteries at the wrist with minimal irregular filling of the palmar arch. Filling of the digital arteries was not apparent (figure 3). An intraluminal clot was also noted.

Diagnosis. These findings were felt to be a result of posttraumatic or vasospastic disease. The patient's condition was diagnosed as hypothenar hammer syndrome and radial artery occlusion.

Treatment. Treatment included intravenous dextrose solution, sublingual nitroglycerin, and a sympathetic blockade, which produced overnight improvement in hand warmth. A repeat arteriogram showed increased filling to the palmar arch but continued narrowing and irregularity of the proximal portions of the deep and superficial arch. Intra-arterial nitroglycerin was introduced, and perfusion improved on repeat arteriogram. The athlete was offered arterial reconstruction using a vein graft but declined surgery. He was placed on nifedipine and aspirin on discharge from the hospital. The athlete was advised to stop playing competitive baseball and to avoid any activities that would involve direct impact to the hypothenar eminence.

Follow-up. The patient's symptoms gradually improved over the next 6 months, and the hypothenar mass gradually disappeared after 3 months. Pain and cold intolerance decreased, and no new ischemic ulcers or subungual petechiae were evident on the fingers. By 2 months, the Allen test was negative at the wrist, though the index finger remained cooler with a positive digital artery Allen test until 6 months postinjury. Nifedipine was discontinued at 6 months.

At 1 year, a repeat bone scan suggested patent arteries at the wrist and fingers, and the athlete chose to resume playing recreational baseball although he continued to have minimal discomfort and transient finger pallor when batting. Two years after the initial injury, the athlete was active in multiple sports and had no symptoms. He resumed playing baseball in a weekend league without reappearance of his symptoms. His grip strength was equal bilaterally. A Doppler exam was unremarkable except for slightly decreased flow in the radial branch to the index finger.

History Lessons

Guattani first reported arterial insufficiency in the hand in 1772. He presented a case of an ulnar artery aneurysm in a coachman who repeatedly struck the butt of his horsewhip against the palm of his hand (1,4). In 1934, Von Rosen identified blunt-trauma-related thrombosis of the ulnar artery as a separate entity (5,6). Since then, there have been numerous case reports of arterial insufficiency in the hand from occupational trauma—directly from pounding and hammering or indirectly from vibrating tools (1,2,7-10). This led Conn et al (11) in 1970 to coin the term "hypothenar hammer syndrome."

Classically, this syndrome is seen in men, involves only the dominant hand, and most often is manifested by pain, numbness, and cold intolerance. The history generally consists of blunt trauma to the hypothenar eminence; exposure to cold and continued repetitive hand activity aggravate the patient's symptoms. Smoking and emotional upset can also worsen symptoms (table 1) (5,11-15).

Table 1. Typical History in Hypothenar Hammer Syndrome

Acute or blunt trauma to the palm Hand pain or soreness (may be nonspecific) Hand and/or finger numbness Cold intolerance Hand and digit coolness—not easily alleviated Grip weakness Tenderness over the hypothenar eminence Nonhealing finger sores

As blockage progresses, patients experience increased pain, numbness, cold intolerance, cooling of fingers, and hand pallor. Development of a tender hypothenar mass is not uncommon. Patients who have had prolonged vascular deficiency may have nonhealing ulcers of the fingertips and atrophic skin changes (table 2).

Table 2. Typical Clinical Exam Findings in Patients Who Have Hypothenar Hammer Syndrome

Positive Allen test Hand pallor, coolness, mottling Paresthesias Finger stiffness, particularly of the 4th and 5th digits Delayed capillary refill Subungual petechiae Open fingertip sores Ischemic ulcers, gangrene Atrophic hand changes such as softening of the fingertip pads Thickening, tender mass, or callus over the hypothenar eminence Possible thrill on auscultation if aneurysm is present

Many etiologies should be considered in a differential diagnosis (table 3); however, such clinical findings in a healthy athletic patient strongly suggest hypothenar hammer syndrome (1-29).

Table 3. Differential Diagnosis of Hypothenar Hammer Syndrome in Active People

Localized or Mechanical Direct trauma Median or ulnar nerve compression Edema Anomalous muscle Ganglion Tumors of hand or wrist that compress the ulnar nerve Corkscrew configuration of the ulnar artery Embolic occlusion Tenosynovitis Thoracic outlet syndrome Old fracture Systemic Arteriosclerosis Ergot poisoning Thromboangiitis obliterans Collagen diseases (eg, scleroderma) Raynaud's disease Polycythemia Giant cell arteritis

Mechanism of Injury

The pathogenesis of this syndrome can be related to the anatomic course of the ulnar and radial arteries as they enter the palm. The ulnar artery, at the level of Guyon's canal, gives off a branch to help form the deep palmar arch and continues on to form the superficial palmar arch. The superficial branch crosses the surface of the hypothenar muscles for approximately 2 cm before penetrating the palmar aponeurosis (figure 4). This 2-cm section of artery is vulnerable to injury because it is minimally protected by the skin and subcutaneous tissue and a few strands of the palmaris brevis muscle. In addition, it is firmly held in place between the volar carpal ligament and the transverse carpal ligament, and it rests on the bony hook of the hamate (1,4,9,11,16-19).

Repetitive blunt trauma compresses the fixed ulnar artery against the hamate, which acts as an anvil (11,19). This process triggers distal vasospasm with diminished perfusion. Continued repetitive trauma increases arterial wall shear stress, further damaging the vessel intima and exposing subendothelial collagen. This, combined with vasospastic slowing of flow and turbulence, encourages platelet aggregation and thrombus formation. As the thrombus develops, sympathetic activity and vasospasm increase. Small emboli may dislodge from the thrombus and block digital arteries, worsening the ischemic effects. With prolonged injury, the tunica media weakens, leading to aneurysm formation, continued distal vasospasm, and embolization (11,12,17,20,21).

Occlusion may also be caused by thickening and scarring of periadventitial tissues from chronic blunt insult. This further immobilizes and constricts the artery and contributes to the occlusive process (12).

The radial artery, which supplies the deep palmar arch, may also be injured as it enters the palm. Like the ulnar artery, it is firmly fixed by the adjoining muscles (the abductor pollicis brevis and opponens pollicis), lacks protection from the palmar aponeurosis for a short distance, and leans against bone. Blunt-impact injuries to this artery are less common because the contact point is not over the radial artery (8). Excessive sympathetic tone from an ulnar artery injury, however, may trigger vasospasm in the radial artery, making it appear as though it is occluded because of a direct-impact injury (12).

Evaluating Hand Ischemia

A variety of evaluation tools aid in the diagnosis of arterial blockage (6,19). The Allen test assesses capillary refill, and most patients who have hypothenar hammer syndrome will have a positive test. To perform the Allen test, the examiner occludes the patient's radial and ulnar arteries at the wrist after the patient rapidly opens and closes the hand several times. The maneuver drains blood from the hand and causes the palm to blanch. With the patient's hand partially relaxed, the examiner first releases the ulnar artery. A delay or absence of return of color suggests arterial stenosis or occlusion. The examiner similarly releases the radial artery, and flushing of the palm indicates a functional radial artery. To avoid false-positive results, the patient's hand and fingers should be partially relaxed to prevent tightness of the palmar fascia (8,12,19,20,25).

Thermography and temperature probes measure surface and digital pulp temperatures and can assess blood flow. Deficiencies are seen as absence of detectable heat of involved palmar tissues and cooler temperatures. Cold stress testing evaluates the vasculature's response to temperature changes. Digital pulse volume recordings show pulsatile flow in the digits, and strain-gauge plethysmography establishes digital pressures. Doppler mapping noninvasively assesses blood flow and identifies the level of a thrombus. A triple-phase bone scan provides dynamic images of blood flow and perfusion. Alone, these tests are not diagnostic, but they are helpful in the clinical assessment.

Arteriography continues to be the most valuable diagnostic study (4,6,14). It confirms the location of vascular blockage, reveals collateral circulation, confirms the cause of the circulatory disruption (vasospasm vs thrombus vs aneurysm), assesses embolic events in the digital arteries and excludes those that might be originating in the subclavian artery, and aids in preoperative planning.

Treatment Options

Multiple options are available for treatment, depending on the vascular integrity at presentation. If the patient has good collateral circulation or the arteriogram suggests a vasospastic cause, conservative measures may be effective. Stopping the offending activity, resting the hand, keeping the hand warm, and avoiding nicotine are simple options.

Vasodilators, corticosteroids, calcium channel blockers, anticoagulants, sympathectomy, and/or ganglion blocks may also restore hand circulation. If vascular damage is significant, collateral circulation is poor, or conservative measures fail, arterial reconstruction may be required, either by end-to-end repair or with a vein graft (6,12,14,19,29).

Acting on Subtle Clues

Though vascular occlusive injury of the hand in athletes is rare, subclinical vasospastic compromise that resolves during the off-season may be more common. One report (9) suggests that arterial damage often goes undetected and that the number of cases is higher than reported. The hand's collateral circulation is abundant, and obstruction of only one of the main blood vessels may not impair circulation enough for an individual to seek treatment (8). Symptoms may be so vague that the athlete may not recognize that a problem exists.

The case literature also suggests that problems may arise only when repetitive subacute trauma occurs over time (figure 1: not shown). Buckhout and Warner (22) studied digital perfusion in handball players and suggested that symptoms increase in a dose-dependent fashion. Athletes who played more than 2 years or who had more than 200 hours of accumulated playing time were at increased risk. Because most athletes have an off-season, vessels may normalize before symptoms develop that require medical attention. These factors suggest that athletes may have undetected vascular compromise.

The subtlety of the symptoms underscores the need to have a high index of suspicion whenever a patient or worker in a pounding, gripping, or catching activity reports pain, numbness, and cold intolerance in the hand.

References

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Dr Rowan is a research intern at the University of Hawaii Orthopedic Residency Program in Honolulu. Address correspondence to Linda J. Rowan, MD, MS, ATC, University of Hawaii, Orthopedic Residency Program, 1356 Lusitana St, Room 614, Honolulu, HI 96813-2478.

The author thanks Robert Atkinson, MD, for his suggestions during preparation of the manuscript and Gary Belcher, MEd, for his technical assistance with radiographs and figures.

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