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[Frostbite injuries].

Frostbite injuries occur mainly in toes, fingers, ears, nose and cheek. Typically an initial vasoconstriction in the skin will protect from drop in core temperature. Ice crystal development occurs when tissue temperature drops to -2 degrees C, leading to increased osmolality of the extracellular fluid and intracellular dehydration. An additional insult occurs with thawing due to reperfusion of the tissue and thereby release of inflammatory mediators. Symptoms of frostbite injury are: White-cyanotic discoloration, pain and numbness followed by hypoaesthesia. General hypothermia should be prevented and treated before managing the local frostbite injuries. Direct contact with warm skin without rubbing should be used in superficial injuries. More severe and deeper injuries should not be thawed until definite treatment could be given in a hospital. Re-freezing and mechanical influence on the injured parts must be avoided. Thawing should preferably be done in stirred water of 40-42 degrees C with mild soap. Antibiotics may be indicated when the skin barrier is broken. Surgical debridement should be postponed until a clear demarcation occurs.

Frostbite↗

The formation of the demarcation line at experimental frostbite.

Experiments were carried out to gain a better understanding of the pathogenesis of frostbite and changes at the demarcation line after freezing and thawing and to determine the forming demarcation line as early as possible. These changes were investigated by histochemical techniques, by histofluorescence, by determining noradrenaline content in the tissue and nerve, by scintigraphy and thermography. The experimental animal was New Zealand white rabbit. The frostbite was produced using a small laboratory bottle filled with liquid nitrogen pressing against the shaved skin in the middle of the proximal part of the ear. Enzyme histochemistry was good in demonstrating the demarcation line between irreversibly damaged and healing frostbitten tissue. Especially the reaction to esterase was the clearest, the demarcation line was visible already after one week. The glyoxylic acid-induced fluorescence method was available for showing adrenergic nerves around the vessels and the accumulation of catecholamines in these nerves in the demarcation line. The result of quantitative measurement of catecholamines in the nerve and tissue was similar and the reaction was the most powerful during the first three days. Scintigraphy was better than thermography and necrotic areas in the middle of the frostbitten area became clearly visible after three weeks. It seems that many changes caused by frostbite happen both in tissue and cells. The role of catecholamines in vascular circumstances is important and that's why chemical or surgical sympathectomy could be useful.

Animals↗

Some aspects on death in the cold and concomitant frostbites.

The most important risk factors and findings of acute accidental hypothermia and concomitant local frostbites are reviewed. Both external and internal risk factors are usually present when exposure to cold is leading to death. The external factors are alcohol and psychic drugs, too light a clothing for the circumstances and wetness. Important internal factors are leanness, physical exhaustion and traumas in young persons and illnesses and degeneration of physiological heat conserving and production responses at old age. The signs caused by cold on the body are variable. In immersion hypothermia cases there are almost no changes, since the death occurs rapidly, most frequently from drowning. On the victims of dry frost first degree congelations, showing up as purple oedematic skin areas or spots, can be observed on the face and extremities. Stress ulcerations or haemorrhages in the stomach mucosa develop in ca. 70% of dry hypothermia cases. In long lasting exposures to cool temperature haemorrhagic pancreatitis, lung oedema and myxomatous skin oedema have been the characteristic signs. Frostbites developing concomitantly with fatal hypothermia show only oedema and hyperaemia, but no blisters or inflammation in the skin, which are the most conspicious vital reactions of frostbites after thawing.

Autopsy↗

Pentoxifylline. Adjunctive therapy in the treatment of pedal frostbite.

Frostbite injury to the extremities has the potential for disastrous effects. Prompt recognition and treatment are paramount. The use of Pentoxifylline to minimize tissue damage in the treatment of frostbite is a viable addition to the traditional therapy of rewarming soaks, pain management, and vesicle débridement. The most well known action of Pentoxifylline is its ability to increase RBC flexibility, allowing easier vascularization. This explains its indication for PVD, arterial disease, and intermittent claudication. As is explained previously, however, Pentoxifylline has multiple actions that will enhance tissue survival. The dosage of Pentoxifylline in controlled release tablet form is one 400 mg tablet three times a day with meals. The duration of treatment should be from two to six weeks. As this drug has many actions and therefore possibilities, more research is warranted with regards to its use not only with frostbite, but with other pathological processes.

Acute Disease↗

[The reverse flow island flap nourished by sural nerve nutrition blood vessel for repair of severe frostbite of feet].

OBJECTIVE: The study was to verify the feasibility of an improved method using reverse flow island flap nourished by the sural nerve nutrition vessel to repair severe frostbite of feet. METHODS: At the proximal end of the principal flap, an auxiliary triangular skin flap of 6.5 - 7 cm in length was designed in order to cover the pedicle of the principal flap. This operation was performed on 13 patients (21 feet) with frostbite. RESULTS: All the flaps survived well. Postoperative follow-up for 5 - 18 months demonstrated satisfactory results in all the cases. No ulcer happened. CONCLUSIONS: The method is helpful to prevent constriction of the pedicle and ensure blood supply of the flap. It is an ideal treatment for severe frostbite of feet.

Adult↗

[Severe frostbites of the limbs. Apropos of 4 cases. A new approach of early prognosis].

The statistics of frostbites of the Chamonix Hospital surgical service include 1232 cases, 587 of them having been treated at the hospital. As regard four cases of severe frostbites having led to an amputation, the author reviews the complementary examinations that make possible an early prognosis. Among them, the bony scintigraphy must be privileged. It is nowadays a routine examination as it is technically easy and not difficult to interpret. Two spectroscopic examinations of living cells in NMR are reported, however no definitive conclusions could be reacted. A certain number of fundamental notions are assorted regarding the validity of the physiological mechanism what enables to reaffirm the three pillars of the treatment that must be often reduced to the simple limitation of the lesions. Two examinations show that in 1991, infection of frostbites can be always so redoutable.

Adult↗

[Creatine kinase test in frostbite].

The activity of blood serum creatine kinase was studied in 37 cases with various degree of frostbites and in healthy individuals. The dynamic study of blood serum creatine kinase in frostbites cases during the first week allows for the differentiation between deep and superficial frostbites.

Adult↗

Treatment of frostbite with intra-arterial prostaglandin E1.

Prostaglandin E1 (PGE1) is a vasodilator that inhibits platelet aggregation. Its use has been effective intra-arterially in treating ischemic peripheral vascular disease. Its potentially beneficial effect in treating frostbite injuries has not been studied and prompted this investigation. A standard frostbite injury was induced by immersing the hindlimbs of New Zealand white rabbits in an ethylene glycol bath maintained at -15 C. Forty animals were separated into eight equal groups (N = 5). Groups I through V were allowed to slowly rewarm at room temperature (21-22 C), while Groups VI through VIII underwent rapid rewarming in a water bath at 42 +/- 1 C. Groups I and VI received no further treatment. Groups II and VII received intra-arterial bolus injections of saline. Group III received intra-arterial bolus injections of reserpine (2.5 X 10(-3) mg/kg-1). Group IV received intra-arterial bolus injections of PGE1 (10(-1) micrograms/kg-1). Groups V and VIII received 3-hour intra-arterial infusions of PGE1 (10(-1) micrograms/kg-1 min-1). Tissue loss was graded numerically after 30 days. Group V (slow rewarming plus 3-hour PGE1 infusion) had significantly (P less than 0.5) less tissue loss than Group I (slow rewarming alone) and Group II (slow rewarming plus saline). Group V was not significantly different from Groups VI through VIII (rapid rewarming). Group III (slow rewarming plus bolus reserpine) and Group IV (slow rewarming plus bolus PGE1) were not significantly different from Group I (slow rewarming alone). The data suggest a clinical application for the use of PGE1 in frostbite patients who have not undergone rapid rewarming.

Animals↗

Frostbite arthritis of the foot.

Flexion contractures in the foot as a sequela of frostbite have received little attention in the medical literature. The authors provide a brief overview of frostbite and present a surgical approach to a case of frostbite arthritis associated with disabling joint deformities.

Adult↗

[Principles of the modern treatment of frostbite].

Actual questions of the treatment of frostbites are considered on the basis of an experience of the treatment of 397 patients. The experience shows that superficial frostbites are healing well when treated by any method of local treatment. High degrees of frostbites are to be operated upon not earlier than the third week after injury, when the injury degree is established and acute inflammation has subsided. It has been established that the use of free and non-free skin plasty for closure of finger stumps and extremity segments improves functional outcomes and shortens the time of the treatment.

Amputation, Surgical↗

Assessment of tissue viability by thermography after experimentally produced frostbite of the rabbit ear.

Since it is difficult and time-consuming to monitor the formation of a demarcation line in frostbite by visual inspection only, thermography was used to study experimental freezing injuries of the rabbit ear. In 8 rabbits, anesthetized with ketamine hydrochloride and xylazine hydrochloride, frostbite was induced by pressing the bottom of a glass bottle 2 cm in diameter, filled with liquid nitrogen against the shaved ear skin. Thermography was performed on both ears after 2, 24, and 48 hours, and one and 3 weeks. At 2 to 48 hours the frost-bitten area was clearly warmer than the surroundings, after one week there were ill-defined diffuse cold spots in the injured area, and after 3 weeks a cold area had become clearly demarcated with a warm zone between the cold area and the surroundings. Thermography is an easy, noninvasive method for monitoring thermal changes after experimental frostbite, but its clinical value is as yet unresolved.

Animals↗

Localized facial telangiectasias following frostbite injury.

Two patients presented with localized facial telangiectasias a consequence of superficial frostbite injury. Trauma from frostbite resulted in the permanent formation of these telangiectasias. We review the morphology of the different degrees of frostbite and discuss the involvement of angiogenesis as a response to tissue insult.

Adolescent↗

A case of bullous frostbite following recreational snowmobiling.

Frostbite is the occurrence of localized tissue freezing and injury. It results following cold exposure of sufficient magnitude or duration to cause acute tissue damage. Although there are several conditions that predispose to frostbite, all are at risk if subject to sufficient cold exposure. We discuss a case of frostbite presenting with bullae localized to the neck resulting from extreme cold encountered while snowmobiling at night in Minnesota, an entity known by some local practitioners as "polaris vulgaris."

Anti-Infective Agents, Local↗

Radiographic changes in the hands following childhood frostbite injury.

Three young adult patients who had sustained severe frostbite of the hands as children were recently evaluated for progressive deformity and joint pain in the fingers. Characteristic radiographic abnormalities including dwarfing of the middle and distal phalanges, irregular and malapposed articular surfaces, malalignments at the proximal and distal interphalangeal joints, and evidence of degenerative arthritis in the interphalangeal joints were observed. The metacarpal phalangeal joints and wrists were spared in all patients, and fingers which had been protected from the initial cold injury were similarly not affected. Articular abnormalities and phalangeal deformity are most likely due to direct chondrocyte injury following freezing, but microvascular damage may also contribute to abnormal cartilage growth. A history of severe frostbite as a child should alert the clinician to the possibility of finger deformity and arthritis developing years after the initial injury.

Adolescent↗

The role of bone scanning in severe frostbite of the extremities: a retrospective study of 88 cases.

We performed a retrospective study of the results of two-phase technetium-99m hydroxymethylene diphosphonate bone scans in 88 patients with severe frostbite of the extremities. All patients were evaluated within 48 h after rewarming and all underwent a first bone scan (BS1) within 5 days after rewarming (median, day 2) (group 1). An excellent correlation was found between absence of tracer uptake in the phalanges and later amputation; this correlation was especially strong during the bone phase of the scans (specificity = 0.99, sensitivity = 0.96, positive predictive value = 0.92). Normal or high uptake in the phalanges was a reliable indicator of ultimate healing (negative predictive value = 0.99). The sensitivity of the examination was enhanced by performing a second scan (BS2) more than 5 days (median, day 8) after rewarming (group 2, n = 36). A comparative analysis of BS1 and BS2 demonstrated that some of the lesions continued to evolve between day 2 and day 8. This suggests that the lesions could still be modified during this period. On the basis of the findings it is recommended that bone scan be performed close to day 2 in all patients who present with lesions extending proximally to include the entirety of one or more phalanges. In the case of severe sepsis, the results of the first bone scan, BS1, can serve as an indication for emergency amputation. BS2 should be performed close to day 8 only if there is an area of low or absent uptake on BS1. It is concluded that scintigraphy is an excellent means of evaluating patients with severe frostbite of the extremities: as early as day 2 after the injury it can indicate whether amputation is necessary, and between days 2 and 8 it provides valuable information on the efficacy of treatment.

Adult↗

Carcinoma on old frostbites.

Two cases of carcinoma developing on old frostbite scars of the heel are presented. A short review of the subject follows, stressing the rarity of these "secondary" tumors and their general context within the skin cancers and the tragic experience of Greece with frostbite in the campaign of 1940-1941.

Aged↗

Vascular casts demonstrate microcirculatory insufficiency in acute frostbite.

The use of vascular microcorrosion casts (vascular replicas) has made it possible to demonstrate the degree of damage to the microcirculation in experimentally induced frostbite. This approach provides a direct method for demonstrating vascular patency. Four groups of animals were used in this investigation. The left hind limbs of anesthetized rats were cooled to -10 degrees C in groups one and three and to -20 degrees C in groups two and four, as measured by needle thermocouples placed under the gastrocnemius muscles. Thermocouples were also placed in the left hind footpads of groups three and four. The sheathed limbs were cooled in an alcohol bath at approximately 1.1 degree C per minute. All limbs exposed to the cold bath were rewarmed to 37 degrees C in a 40 degree C water bath. The right hind limbs served as uninjured controls. The footpad temperatures recorded in groups three and four were used in conjunction with the temperatures recorded under the gastrocnemius muscles to characterize the footpad temperatures in groups one and two. Vascular microcorrosion casts were made from the left and right hind paws of groups one and two using Batson's modified methyl methacrylate. Scanning electron microscopic examination of the casts demonstrated dramatic differences between the vascular integrity of control paws and that of frozen paws. Exposure to the cold temperatures destroyed most of the microcirculation. In addition, the weights of the casts from the control paws were significantly different from the weights of the casts from the frozen paws. It was concluded that this model for evaluating frostbite injury accurately demonstrates the extent of microvascular damage and has significant potential as a method for evaluating therapeutic drug regimens.

Animals↗

Analysis of microvascular changes in frostbite injury.

Reported here is the characterization of the hairless mouse ear as a model system for defining the microvascular effects of minimal frostbite injury by means of gross, in vivo microscopic, histologic, and electron microscopic analysis. Initial efforts, using controlled temperatures and time of freezing, defined the minimum conditions necessary to produce consistent tissue necrosis to be -4 degrees C for 3 min. In vivo observation, after rapid thaw, showed a return of blood flow to apparent normal prefreeze rates, followed by a gradual sludging of blood 15 to 20 min post-thaw and eventually in cessation of blood flow. No vascular spasm was observed. Histologic and electron microscopic examination, unexpectedly, did not reveal evidence of early platelet or fibrin thrombi. However, marked vasodilatation and circulatory congestion began 2-3 hr after thawing. Subsequently, prominent discontinuities between damaged endothelial cells and breaks in the microvascular basement membranes were found at the light and ultrastructural level. Interstitial edema and extravasated erythrocytes occurred shortly thereafter, preceding gross tissue necrosis evident at post-freeze Day 3. We conclude that in this animal system thrombus formation is not an initial event, but rather that vascular injury in the form of endothelial cell damage predominates in early frostbite injury.

Animals↗