Military dermatology: trauma caused by cold. Practical aspect

The previous article dealt with the mechanisms and factors of cold injuries that can lead to the loss of combat troops. The materials were published in the textbook of military dermatology Textbook of Military Medicine, which were provided by Tetyana Svyatenko, Professor of the Dnipro Medical University, Doctor of Medical Sciences, member of the EAHV. (Source: Military Dermatology . Translation: Galina Prit. Photo by Pexels (Pixabay)

INDIRECT COLD INJURY

Indirect cold injury is associated with the influence of low temperatures, as well as other factors, often with pathological processes that are aggravated by cold. Identification of skin lesions after exposure to cold may lead to the identification of the underlying disease.

Pernio (Pernio)

Pernio, or chills, is characterized by the development of bluish-red spots on the arms and legs, areas of which are constantly exposed to the influence of a cold, humid climate. As a mild form of cold injury pernio was described as early as 1680. This condition is common in England and less common in very cold climates, protective clothing is worn on a regular basis.

Etiology. Vasospasm is the primary mechanism causing pernio in predisposed individuals with high peripheral vascular tone. The cold in the absence of freezing temperatures is exacerbated by high humidity. Vasospasm causes local tissue hypoxia, which leads to an initial cyanotic and erythematous skin lesion.

Histological evaluation of the pernio reveals edema of the papillary dermis and superficial or superficial as well as deep perivascular lymphocytic infiltrate. Necrotizing keratinocytes and lymphocytic vasculitis have also been reported.

Clinical manifestations. Pernio is divided into acute and chronic disease. The acute form is observed mainly in children and young people, the chronic form is more common in adults.

The acute form of pernio is manifested by bluish-red, slightly swollen spots, most often on the lower extremities. The development of lesions is preceded by prolonged exposure to damp cold with inadequate protection. Skin manifestations persist for 7-10 days or less and in many cases disappear spontaneously with residual brown-red hyperpigmentation.

Chronic pernio - edematous, cyanotic lesions with secondary ulceration and hemorrhage - is observed after repeated episodes of acute pernio. Patients may develop subcutaneous nodules accompanied by a burning sensation, itching, or both. Acute pernio is more common in winter, but with repeated episodes, lesions can become persistent and atrophy and ulcers continue throughout the year. The differential diagnosis includes nodular vasculitis, erythema indura, erythema nodosum, and livedo vasculitis with ulcers.

Treatment. Protective clothing and warmth are the foundation of pernio treatment. Emollient creams can be effective. In the presence of ulcers or secondary infection, antibiotics and topical treatment may be required. Some patients may benefit from vasodilator drugs. Nifedipine was effective at a dose of 20 mg thrice daily. Sympathectomy was used only in extreme cases, but did not prevent relapses.

Livedo reticularis (Livedo reticularis)

Livedo reticularis is a persistent, reticulated red to bluish skin pattern. Spots on the skin may be temporary, as seen in infants exposed to cold and known as cutis marmorata. If the pattern persists after rewarming, the term livedo reticularis is used. Congenital livedo reticularis (cutis marmorata telangiectatica congenita) is the result of several hereditary syndromes such as Down syndrome, Cornelia de Lange syndrome, homocystinuria, and neonatal lupus erythematosus. These disorders exhibit persistent forms of livedo that are not associated with exposure to cold. The causes of acquired reticular livedo are numerous. They may be benign, as in colds, or may be a sign of a serious underlying disorder such as vasculitis, connective tissue disease, or malignancy. Livedo comes from the Latin liveo, meaning blue, black or grey. The term was first used by Gebra in 1868.

Etiology. Similar physiological explanations for the livedo model were given by Renaud (1883), Unna (1896) and Spaltegoltz (1927). All three authors postulated that the cutaneous blood flow is arranged in "cones" 1 to 3 cm in diameter, with an apex deep in the dermis and a central ascending arteriole. They suggested that the density of the arterial bed decreases at the edges, but the superficial venous plexus is more prominent at the periphery. If this theory were correct, any process that obstructs blood flow would result in most deoxygenated hemoglobin. Then on the edges of the cones there will be a brighter color, and the mesh pattern will be catchy. This hypothesis does help explain the clinical data. However, anatomical studies using serial thick sections failed to demonstrate the proposed picture.

Clinical manifestations. The congenital form of livedo reticularis may be limited or widespread and associated with superficial ulcers. The remaining anomalies reveal up to 50% of these cases. The acquired form can be seen in many conditions. These states are aggravated by exposure to cold, but warming does not resolve the livedo picture. The red-blue mesh pattern is usually asymptomatic unless an ulcer has developed and is most commonly seen on the shins. The pattern can also be seen on other areas of the body, including the upper legs, buttocks, lower body, and arms.

It is important to identify the underlying cause of livedo, the effects of cold can make the disease more obvious and lead to a definitive diagnosis and treatment.

Treatment. There is no specific therapy for livedo reticularis. It is necessary to eliminate the main causes that can be treated.

acrocyanosis

Acrocyanosis is characterized by a symmetrical bluish discoloration and cold extremities and is often associated with hyperhidrosis of the palms and soles. The disorder is commonly seen in cold climates.

Etiology. The exact cause of acrocyanosis is unknown, but there are several theories. Biomicroscopy of the nail fold reveals decreased blood velocity and dilated capillaries and venules in patients with acrocyanosis. Various researchers have pointed to the localization of the initial events in arterioles, capillaries and the venous system. It has also been suggested that the initial change is a change in blood viscosity, which increases with cooling and leads to damage to the capillaries in the papillary dermis. There have been various reports of acrocyanosis associated with conditions such as mental retardation, but these have not been independently confirmed. A familial tendency has been noted.

Clinical manifestations. Persistent symmetrical cyanosis and coolness of the hands and feet are the most common signs of acrocyanosis, sometimes affecting the chin, lips, and nose. Hyperhidrosis and swelling of the palms and soles are also common. Cyanosis increases with a decrease in temperature and changes to erythema with the rise of the affected part. The peripheral pulse is usually unchanged and symptoms may persist for many years after the onset of the underlying disease, more commonly in the second or third decade of the patient's life. Vascular disease and ulcers are absent, which distinguishes acrocyanosis from other diseases such as Raynaud's disease.

Treatment. The basis of therapy for acrocyanosis is protection from the cold. Other forms of treatment have included alpha blockers, which may provide temporary relief.

erythrocyanosis

Erythrocyanosis consists of cyanotic coloration occurring in areas of thick subcutaneous fat, such as the thighs, and is most commonly seen in winter. Lesions may be nodular and pernio-like. Discussions of this disorder are commonly found in old British literature. Erythrocyanosis is now rare.

Etiology. Erythrocyanosis may be a form of cold spelling, but the exact etiology is unknown.

Clinical manifestations. Erythrocyanosis is commonly seen in women on the lower legs and thighs, and is common in riders. The skin is sometimes sensitive.

Treatment. The only effective treatment for erythrocyanosis is warm clothing and a reduction in the insulating fat layer.

Cold paniculitis

Cold paniculitis is manifested by tender subcutaneous nodes that occur when exposed to cold on open areas of the skin. The cheeks and legs are the most common locations.

Etiology. Because cold-paniculitis nodules are commonly seen in children, it has been hypothesized that the more saturated fat seen in newborns solidifies at a higher temperature than the less saturated fat in adults. Excessive fibrinolytic activity and cryofibrinogens have been detected in serum. It is also believed to be a hypersensitivity reaction.

Clinical manifestations. Tender nodules appear a few hours after exposure to cold on unprotected areas. Legs and cheeks are common locations, as mentioned earlier. Nodules may enlarge and turn into plaques, which then spontaneously resolve within 2-3 weeks.

Treatment. There is no specific therapy for cold paniculitis. Proper clothing and avoidance of the cold is a safeguard in most cases.

Raynaud's disease and phenomenon.

Raynaud's disease is a paroxysmal narrowing of the small arteries and arterioles of the extremities, usually provoked by cold. However, it can be caused by other stimuli, including emotions. The etiology of Raynaud's disease is unknown. By definition, Raynaud's phenomenon (syndrome) occurs as a result of an underlying systemic disease or occupational injury.

The disease was first described by Rhine in 1862. In 1901, Hutchinson noted that Raynaud's clinical manifestations could be seen in connection with several different conditions. He suggested that when the underlying disease process could be identified, the condition should be called Raynaud's phenomenon. If the condition is idiopathic, it is called Raynaud's disease.

Raynaud's disease occurs 5 times more often in women than men, with a median age of onset of 31 years and a range of 4 to 68 years. Among men, 73% of patients were under 40 years of age. After long-term follow-up in two studies, 60 to 70% of patients with this pathology could be identified as having primary Raynaud's disease.

Etiology. The pathophysiology of vasospastic seizures in primary Raynaud's disease is unknown. In secondary Raynaud's phenomenon, vasospasm can be caused by sympathetic stimuli, external physical pressure (observed when vibrating instruments are used), and reduced blood flow due to increased blood viscosity or arterial disease. Research into Raynaud's disease and phenomenon has shown that vasospasm can be induced in the fingers even in the presence of digital nerve blockade with lidocaine, negating the common etiological role of sympathetic hyperactivity.

Histological vascular evaluation in Raynaud's patients revealed intimal thickening, thrombus formation, and recanalization in the digital arteries in patients with severe disease, especially those with secondary disease.

Clinical manifestations. In Raynaud's disease and phenomenon, the skin classically undergoes a triple reaction with initial pallor or pallor turning into cyanosis and is indicative of vasospasm. The third (recovery) stage is erythema, probably secondary to the final stage of hyperemia. Usually the problem is noted distally with a bilateral distribution on the finger and, ultimately, the entire finger is involved in the pathological process. Rarely, hands, feet, and thumbs are affected. Unilateral lesions have been reported. The lips, tip of the nose, ears, and less often even the tongue may be affected. Numbness is common and pain may be mild or absent; paresthesia may occur during the renewal phase. Longitudinal ribbing, increased fragility, onycholysis, koilonychia, and plate thinning may be observed on the nails. Ulcers and star-shaped scars appear on the tips of the fingers and toes. In severe cases, gangrene develops, and amputation of gangrenous fingertips has been necessary in rare cases (0.4% of cases).

Treatment. The goal of Raynaud's disease treatment is to vasodilate the affected vessels with minimal side effects. The first priority is the prevention of episodes. Protective warm clothing is important, especially for the arms and legs, to avoid local and general cooling. Sudden cooling of the skin should be avoided, for example by contact with cold objects. Patients with an underlying disease causing limited vasodilation are the most difficult to treat.

Vasodilators usually have too many side effects to be widely used in the treatment of Raynaud's disease. The use of such sympatholytic agents, including methyldopa, phenoxybenzamine, tolazoline, guanethidine, and oral or intra-arterial reserpine, has previously been more commonly avoided. However, prazosin hydrochloride has been shown to be effective and has acceptable levels of side effects. In one 8-week study, the drug was effective at doses of 1 to 2 mg orally three times a day. For the treatment of hypertension, doses up to 20 mg / day are used. Postural hypotension can occur suddenly, so initial doses should be administered carefully and when the soldier is lying on his back.

It turned out that surgical sympathectomy, once popular, was less useful, and conservative therapy is now generally advocated. Blockade of the sympathetic stellate ganglion may be useful in acute cases of severe digital infarction and can be performed every day by an experienced anesthesiologist.

Direct vasodilators such as the calcium channel blocker nifedipine have been effective in the treatment of Raynaud's disease. In a 7-week study, effective doses were started at 10 mg three times a day and, if well tolerated, increased to 20 mg three times a day. Again, patients with Raynaud's syndrome with fixed vascular disease report the least effect. Topical nitrates seem to improve blood flow and temperature and may be helpful when combined with other treatments. 2% glycerol trinitrate in lanolin applied for 3 minutes and left on for 20 minutes can provide a temporary improvement in finger blood flow and skin temperature.

Patients should not smoke under any circumstances.

Completion of the theme of cold lesions in the next publication.