Clinical Findings and Risk Factors

The Taylor and Pelmear staging system is presented in Table 123-1.⁶ In the early stages, vibration injury may be manifested as slight tingling and numbness. Later, the tips of one or more fingers experience attacks of blanching, usually precipitated by cold. With continued progression, the affected area increases in size, and the blanching extends to the entire finger. Attacks of white finger typically last about 1 hour and terminate with reactive hyperemia (red flush) and often considerable pain. Prolonged exposure may induce bluish black cyanosis in the affected fingers. Only about 1% of cases progress to ulceration or gangrene.⁸

Vibrating handheld machines (e.g., pneumatic hammers and drills, grinders, chain saws) have been implicated in HAVS. Such injury potential is not restricted to a few types of tools but applies to a variety of situations in which workers’ hands are subjected to transmission of vibration energy.⁹ There appears to be a linear relationship between the acceleration exposure dose (amount of acceleration and years of exposure) and the onset and severity of HAVS.¹⁰

The exact mechanism of injury is unknown. The frequency and intensity of vibration affect the extent of damage to the endothelium.¹¹ Local platelet adhesion seems to be an important factor in arterial occlusion. It has been shown that sympathetic hyperactivity, in combination with local factors such as vibration-induced hyperresponsiveness of the digital vessels to cold, may be responsible for the finger-blanching attacks.¹² In those with exposure to vibration injury, appearance of symptoms has also been correlated to smoking status.¹³

Diagnosis

Key features in the history include use of vibrating tools and symptoms of Raynaud’s phenomenon. For a vasospastic condition, the most promising single objective test is cold provocation and recording of the time until digital temperature recovers (see Chapter 15). Digital artery occlusion is best detected by recording the systolic pressure of the affected fingers with transcutaneous Doppler ultrasound^14–16 or duplex scanning.¹⁷ In advanced disease, arteriography is helpful. Barker et al¹⁸ documented arterial occlusion by brachial arteriography in workers who complained of hand blanching and attacks of numbness. Other authors have reported on the use of arteriography in this injury.^19–21

Arteriographic changes in HAVS can include multiple segmental occlusions of the digits and a corkscrew configuration of vessels in the hands.²¹ The extent of digital artery occlusion appears dependent on the frequency and duration of exposure.²²

Of 80 workers (chippers) with HAVS investigated at the Blood Flow Laboratory at Northwestern University, 25 (31%) exhibited a significant reduction in systolic pressure in one or more digits.²³ In 6 of the 25 workers, arteriography showed digital artery occlusion (Fig. 123-1). Incompleteness of the palmar arch was seen not only in the symptomatic hand but also in the contralateral, asymptomatic one. Raynaud’s phenomenon was present in 73 of 80 workers (91%). Abnormal cold response was observed in 53% of these workers (Fig. 123-2).

Treatment and Prevention

With onset of neurovascular symptoms that interfere with social or work activities, the initial treatment is discontinuation of use of vibratory tools.¹⁰ In advanced cases, a calcium channel blocker such as nifedipine (30 to 80 mg daily) may be useful. Calcium antagonists inhibit the response of arterial smooth muscle to norepinephrine and have been reported to be effective.²⁴ Intravenous infusion of a prostanoid (prostaglandin E₁, prostacyclin, or iloprost) is usually reserved for patients with digital gangrene.²⁵ Surgical treatment, such as cervical sympathectomy or digital sympathectomy, is rarely needed.

Prevention is likely to be more effective than treatment. Personal protective equipment, such as gloves that limit exposure to cold and dampen transmission of vibration, should be used. Standards that limit the dose and duration of exposure to vibration have been set in place for factories and workplaces in the United States and internationally.¹⁰

Etiology and Incidence

The anatomy of the ulnar artery at the hypothenar eminence makes it vulnerable to injury with repetitive use of the palm of the hand in activities that involve pushing, pounding, or twisting. The ulnar artery and nerve travel in a tunnel known as Guyon’s canal that is bound by the pisiform and hamate bones. In this region, the ulnar artery is superficial and covered only by skin, subcutaneous tissue, and the palmaris brevis muscle (Fig. 123-3). Use of the palm as a hammer compresses the artery against the hook of the hamate bone, which acts as an anvil.

Von Rosen (1934)²⁶ and Guttani (1772)²⁷ published the original reports of the disease, but it was Conn et al²⁸ who first recognized the anatomic mechanism of injury and coined the term hypothenar hammer syndrome. Mechanics, factory workers, carpenters, masons, and any laborers who habitually use their hands as a hammer are at risk for the disease.^29–31

The incidence of this rare entity is not precisely known as it is likely underrecognized. In Little and Ferguson’s study of 79 mechanics, 14% had evidence of ulnar artery occlusion but none had symptoms severe enough to seek medical attention.²⁹ Studies focusing on cases of hypothenar hammer syndrome among referrals to tertiary centers for hand ischemia have found an incidence of 1.1% to 1.6%.^31,32

The type of arterial abnormality observed often depends on the nature of the vessel injury but includes thrombotic occlusion, aneurysm formation, or both. Vasospasm and damage to the intima can result in platelet aggregation and thrombus formation.³³ Damage to the media can lead to aneurysmal degeneration of the artery (Fig. 123-4), although this occurs less frequently. Thrombus formation can also occur within the aneurysm itself and lead to distal embolization.

Research by Ferris et al³² demonstrated that, in addition to vascular damage from repetitive trauma, underlying vessel abnormalities may also be responsible. Histologic examination of 19 resected ulnar arteries showed hyperplastic proliferation of the intima or media and disruption of the internal elastic lamina suggestive of fibromuscular dysplasia. In 13 patients for whom bilateral angiograms were available, 12 of 13 (92%) showed an abnormality in the contralateral asymptomatic ulnar artery. On the basis of this evidence, they proposed that the etiology of hypothenar hammer syndrome depends on the presence of underlying ulnar artery fibromuscular dysplasia with superimposed repetitive palmar trauma.

Clinical Findings and Diagnosis

Patients typically present with Raynaud’s phenomenon. However, several key features distinguish hypothenar hammer syndrome from similar syndromes.³³ There is a preponderance of male smokers with a concomitant history of repetitive trauma to the hand.³¹ The distribution is asymmetrical, often involving only the dominant upper extremity. The cyanosis and pallor phases can occur, but the hyperemic redness is usually lacking.³⁰ The digits affected tend to be the ulnar three fingers, with a distinct lack of involvement of the thumb.^30,32