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This is a paroxysmal pallor of the digits provoked by cold or, rarely, emotional stress. At first the top of one or more fingers becomes white. On rewarming, a painful cyanosis appears and the area turns red before the hands return to their normal colour.
In severe disease the fingers lose pulp substance, ulcerate or become gangrenous (Fig. 11.4). Some causes are listed in Table 11.5. Raynaud’s disease, often familial, is the name given when no cause can be found. However, some patients with what seems to be Raynaud’s disease will later develop a connective tissue disease, usually scleroderma.
The main treatment is to protect the vulnerable digits from cold. Warm clothing reduces the need for peripheral vasoconstriction to conserve heat. Smoking should be abandoned. Calcium channel blockers (e.g. nifedipine 10–30 mg three times daily) are the most effective agents although they work best in patients with primary Raynaud’s disease. Patients should be warned about dizziness caused by postural hypoten-sion. Initially it is worth giving nifedipine as a 5-mg test dose with monitoring of the blood pressure in the clinic. If this is tolerated satisfactorily the starting dosage should be 5 mg daily, increasing by 5 mg every days until a therapeutic dose is achieved (e.g. 5–20 mg three times daily) or until intolerable side-effects occur.
The blood pressure should be monitored before each incremental increase in the dosage. Diltiazem (30–60 mg three times daily) is less effective than nifedipine but has fewer side-effects. Systemic vasodil-ators such as naftidrofuryl oxalate, nicotinic acid and thymoxamine (moxisylyte) are also worth trying. Glycerol trinitrate ointment, applied once daily may reduce the severity and frequency of attacks and may allow reduction in the dosage of calcium channel blockers and vasodilators. Infusions with reserpine or prostacyclin help some severe cases although occasionally sympathectomy is needed.
This is discussed in already.
Here the brunt is borne by the larger vessels of the head and neck. The condition affects elderly people and may be associated with polymyalgia rheum-atica. The classical site is the temporal arteries, which become tender and pulseless, in association with severe headaches. Rarely, necrotic ulcers appear on the scalp. Blindness may follow if the ophthalmic arteries are involved, and to reduce this risk systemic steroids should be given as soon as the diagnosis has been made. In active phases the erythrocyte sedimentation rate (ESR) is high and its level can be used to guide treatment, which is often prolonged.
This occlusive disease, most common in developed countries, will not be discussed in detail here, but involvement of the large arteries of the legs is of concern to dermatologists. It may cause intermittent claudication, nocturnal cramp, ulcers or gangrene. These may develop slowly over the years, or within minutes if a thrombus forms on an atheromatous plaque. The feet are cold and pale, the skin is often atrophic, with little hair, and peripheral pulses are diminished or absent.
Investigations should include urine testing to exclude diabetes mellitus. Fasting plasma lipids (cholesterol, triglycerides and lipoproteins) should be checked in the young, especially if there is a family history of vascular disease. Doppler ultrasound measurements help to distinguish atherosclerotic from venous leg ulcers in the elderly. Complete assessment is best carried out by a specialist in peripheral vascular disease or a vascular surgeon.
Emboli may lodge in arteries supplying the skin and cause gangrene, ulcers or necrotic papules, depending on the size of the vessel obstructed. Causes include dislodged thrombi (usually from areas of atheroscle-rosis), fat emboli (after major trauma), infected emboli (e.g. gonococcal septicaemia or subacute bacterial endocarditis) and tumour emboli.
Sustained or repeated pressure on skin over bony prominences can cause ischaemia and pressure sores. These are common in patients over 70 years old who are confined to hospital, especially those with a frac-tured neck of femur. The morbidity and mortality of those with deep ulcers is high.
The main factors responsible for pressure sores are as follows.
1 Prolonged immobility and recumbency (e.g. caused by paraplegia, arthritis or senility).
2 Vascular disease (e.g. atherosclerosis).
3 Neurological disease causing diminished sensation(e.g. in paraplegia).
4 Malnutrition, severe systemic disease and generaldebility.
The sore begins as an area of erythema which pro-gresses to a superficial blister or erosion. If pressure continues, deeper damage occurs with the develop-ment of a black eschar which, when removed or shed, reveals a deep ulcer, often colonized by Pseudomonasaeruginosa. The skin overlying the sacrum, greatertrochanter, ischial tuberosity, the heel and the lateral malleolus is especially at risk.
The following are important.
Prevention: by turning recumbent patients regu-larly and using antipressure mattresses for susceptible patients.
2 Treatment of malnutrition and the general condition.
3 Debridement. Regular cleansing with normal salineor 0.5% aqueous silver nitrate. Antibacterial prepara-tions locally. Absorbent dress-ings. Semipermeable dressings such as Opsite, if there is no infection. Appropriate systemic antibiotic if an infection is spreading.
4 Plastic surgical reconstruction may be indicated inthe young when the ulcer is clean.
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