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Frostbite: review and current concepts.

BACKGROUND: A literature review was conducted to analyze developments in the epidemiology, pathogenesis, treatment, and prevention of frostbite injury. Increased participation in outdoor activities, as well as the epidemic of homelessness, makes knowledge of the treatment of frostbite crucial for physicians in both rural and urban areas. METHODS: A literature search, using the key words "frostbite" and "cold," was done using MEDLINE and Index Medicus. This search focused on the epidemiology, pathogenesis, treatment, and prevention of frostbite. RESULTS: Research done during the past 15 years has clarified the pathogenesis of frostbite injury and led to a better understanding of how to limit tissue loss. The etiology of frostbite is commonly related to alcohol use, psychiatric illness, or motor vehicle problems. The pathogenesis is linked to tissue freezing, hypoxia, and the release of inflammatory mediators. The initial clinical manifestations of frostbite injury are similar for superficial and deep tissue damage, so early treatment is identical for all injuries. Optimum therapy is based on the rapid reversal of tissue freezing by rewarming in 104-108 degrees F water and the institution of oral and topical antiprostaglandin therapy to limit the release of inflammatory mediators. CONCLUSION: Rapid triage and treatment of frostbite can lead to dramatic improvements in outcome and prognosis. Increased awareness of antiprostaglandin therapy and preventive measures is crucial for physicians in diverse practice environments.

Cold Temperature↗

[Effect of frostbite under hypoxia on microcirculatory perfusion in rats].

Changes of microcirculatory perfusion in rats following cold injury of right hind leg under hypoxia were investigated. Male Wistar rats weighing 200 +/- 20 g were randomly divided into three groups: frostbite at normoxia (FN) group; frostbite during acute hypoxia (4 h at 6000 m simulated altitude, FAH) group and frostbite during hypoxia after acclimation (exposure to hypoxia at 6000 m, 4 h daily for 4 weeks, FHAC) group. The results showed that the microcirculatory perfusion of both hind legs decreased markedly in FN after cold injury. It suggests that the frostbite damage can affect microcirculatory perfusion of another leg besides the region of frostbite. The fall of microcirculatory perfusion before freezing in FAH group indicated that there was a compensatory blood redistribution during acute hypoxia. The changes of microcirculatory perfusion in FAH group post-freezing indicated that acute hypoxia can aggravate the frostbite damage. The microcirculatory perfusion of FHAC group pre-freezing was significantly lower than that of FN and FAH group, and after freezing the perfusion of frostbitten leg in FHAC group was significantly lower than that in FN group, suggesting that hypoxia acclimation may cause disturbance of microcirculation and worsen the frostbite damage at high altitude.

Acclimatization↗

Frostbite: occurrence, risk factors and consequences.

Frostbites affect the civilian northern population more commonly than thought earlier. Cumulative lifetime incidences may be as high as 44-68% for all types of frostbite. Incidences of frostbite have mainly been reported in association with military activities but occur also during occupational duties and in recreational situations. Frostbites often affect the extremities and especially the head region. Several different predisposing factors have been reported in relation to frostbites. These can be divided mainly into environmental, individual, behavioural and occasion-linked factors. Actual risk analyses have been conducted for a limited amount of these predisposing factors. Frostbites very often result in different functional disadvantages, some of which can lead to a temporary or permanent disability to work or carry out military duties, while others may impact negatively on occupational activities, or cause hospitalization and invalidity to varying degrees. Further, frostbites often cause sequelae lasting from a few weeks to a lifetime.

Absenteeism↗

Predisposing factors and prevention of frostbite.

This review focuses on the physiological, behavioural and environmental factors which predispose to frostbite. Also prevention of frostbite is summarised. Predisposing factors may increase heat loss, decrease heat production, decrease the insulation of the clothing, make people especially susceptible to cold or make them to behave inadequately. Marked increase in convective or conductive heat loss is often the immediate reason for frostbite. Wind (as described by wind chill index) increases convective heat loss and touching of metal objects increases conductive cooling. Poor insulation of the clothing is also a common reason of frostbite. The insulation can be insufficient when clothing is wet, tight, permeable to wind or does not cover the cold sensitive body parts. Individual factors predisposing to frostbite are inadequate behaviour, low physical fitness, fatigue, dehydration, earlier cold injuries, sickness or poor circulation in peripheral parts of the body. Frostbite is often associated with the use of alcohol. To prevent frostbite, it is necessary to recognise cold risks, practise tasks in the cold, eat and drink well, have physical exercise, have sufficient clothing (also spare clothing), change into dry clothing if necessary and take care of companions. In the cold it is not advisable to get fatigued until exhaustion, sweat excessively, use tight and/or wet clothing, drink alcohol, smoke and expose oneself unnecessarily to wind, metals or fluids.

Adaptation, Physiological↗

Emollients in the prevention of frostbite.

47% of Finnish conscripts had had at least one frostbite of the head (42% on the ears, 23% on the face) at the age of 19. Non-medicated ointments are traditionally used in Finland for protection against facial frostbite without scientific evidence of their benefit. In studies on cold protecting emollients it was found that 21% of the male conscripts in Finland had used them in the cold. 84% of the users had experienced their effect as somewhat or clearly protective. However, in a controlled prospective epidemiological study of 913 cold injuries of the head, the use of cold protective ointments was associated with an increased risk of frostbite to the head (odds ratio 4.5 for ear frostbite, 5.6 for nasal frostbite and 3.3 for frostbite on other parts of the face). The thermal insulation provided by different emollients in the cold was minimal in in vitro experiments using a skin model. In in vivo studies with test subjects the skin on the applied half of the face cooled at least as quickly as the untreated half. However, when white petrolatum was applied, the subjective skin perception of a test persons was warming in the majority of the tests, in contrast to objective measurements. "Protecting" emollients seem to cause a false sensation of safety leading to an increased risk of frostbite probably mainly through neglect of efficient protective measures.

Adult↗

Frostbite: an overview with case presentations.

Much of the interest in frostbite has arisen from various military experiences including the Korean war, World War II, and Napolean's battles in Russia and Poland. Historically frostbite has been not only a military problem, but also a problem in high-altitude climbers and the more recently investigated homeless population. However, the physician should not disregard frostbite as only victimizing the poor and indigent. Anyone who is exposed to harsh winter conditions over a long period of time can suffer from frostbite. Many milder cases of frostbite presented to Cook County Hospital in Chicago were simply due to prolonged winter exposure when a motorist's care broke down. The authors present a review of the variants, pathophysiology, classifications, predisposing factors, and treatment of frostbite. Five cases of frostbite will also be presented from Cook County Hospital in Chicago, IL.

Adult↗

Cold protecting ointments and frostbite. A questionnaire study of 830 conscripts in Finland.

Application of ointments to the face is one of many measures used to avoid frostbite of the head in cold climates. A recent epidemiological study indicated, however, that the use of ointments in the cold may be a considerable risk factor in development of frostbite of the face and ears. A questionnaire on the use of protective ointments was completed by 830 young male conscripts divided into 4 groups by climatic home region on the south - north axis of Finland. Personal estimates of cold exposure, sensitivity to cold, smoking, and cumulative incidence of frostbite to the face and ears were reported. Twenty-one percent of the conscripts had used cold protective ointments, mostly at school age or earlier. In 25% of the conscripts' families some other member (mostly women and children) had used emollients in order to prevent cold injuries. Both the conscripts and their families living in southern Finland used protective ointments more often than those in northern Finland. Almost half (47%) of the conscripts had had frostbites of the head, 42% of the ears and 23% of the face. Those who had used ointments in the cold had a significantly higher cumulative incidence of frostbites on the face (p=0.0031), especially on the cheeks and chin. Their subjective experience concerning the protective effect of ointments in the cold was somewhat or clearly positive in 84% of respondents. The controversy between subjective experience and increased incidence of facial frostbite in ointment users needs further investigation.

Adolescent↗

Microcirculatory studies of frostbite injury.

Frostbite represents a spectrum of injury ranging from irreversible cellular destruction to reversible changes seen after rewarming. These changes include increases in tissue edema, circulatory stasis, and progressive thrombosis leading to further tissue necrosis. For this reason, it is often difficult at the time of surgical debridement to determine the extent of frostbite injury. This delayed tissue injury is similar to that seen in muscle during ischemia/reperfusion injury. Muscle that initially appears viable on reperfusion may subsequently necrose due to collapse of the microcirculation. Adherent neutrophils have been specifically cited as important components in ischemia/reperfusion injury and have also been suggested to play a role in frostbite injury. We have used an intravital microscopic muscle preparation to study microcirculatory changes carefully in frostbite injury during rewarming. The right gracilis muscle of male Wistar rats is dissected free from its primary vascular pedicle and the rat is positioned on a specially constructed microsurgical stage. Temperature changes of the muscle are recorded. The prepared axial pattern flap is transilluminated with a microscope and projected on a video screen, allowing measurement of arteriolar diameters and changes in the numbers of stuck and rolling neutrophils before frostbite, during rewarming, and for several hours later. Cold silicone oil is used to freeze the muscle to -5+/-2 degrees C in 2 to 3 minutes and to hold this temperature for 5 minutes. The muscle is rewarmed with 42 degrees C normal saline placed directly on the muscle surface. Baseline vessel diameter and leukocyte counts in 100-mm segments of the microvasculature are recorded as well as at 5, 15, and 30 minutes, and at 1, 2, and 3 hours postrewarming of frozen muscle. Observations from our initial 11 animals show that reperfusion of the muscle following freezing is varied temporally and spatially, with circulation to most vascular segments restored 5 to 10 minutes after rewarming. In 9 of 11 animals we observed the shedding of "white clots" in small arterioles and venules occurring as soon as 5 minutes after thawing. In some instances shedding continued for as long as 1 hour after rewarming. Microvascular hemorrhage was widespread 1 hour following the thaw, but there was no significant increase in neutrophil adherence observed until 3 hours following rewarming. The exact nature of the vascular injury and the composition of the "white clots" are now being determined from ultrastructural studies. Blood flow in microcirculation stops during freezing, but small-vessel perfusion returns immediately on thawing. This suggests that the vascular architecture is maintained during the freezing and thawing. Unlike ischemia/reperfusion injury, neutrophil adhesion plays a smaller role in the early response to frostbite injury. The early microcirculatory observations seen after rewarming suggest progressive and severe perturbations in platelet function and fibrin formation that are significantly different from ischemia/reperfusion injury.

Animals↗

[Effects of frostbite on some factors of blood coagulation system in rats under hypoxia].

The changes of some factors of blood coagulation system in rats following frost-bite of both hind feet under hypoxia were investigated. Male Wistar rats weighed 200 +/- 20g were divided into four groups: normal control (C); frostbite at normoxia (FN); frostbite during acute hypoxia (FAH) and frostbite during hypoxia after altitude acclimation (FHAC). Bleeding time and clotting time, rate of clot-retraction, plasma content of 6-keto-PGF1 alpha and TXB2 were determined following exposure to cold. The results showed that bleeding time and clotting time were shortened, and rate of clot-retraction was decreased, plasma content of 6-keto-PGF1 alpha and TXB2, T/P ratio were increased significantly after exposure to cold in all frostbite groups, but these changes were more prominent in FHAC than those in FN and FAH. The results demonstrated that there were changes in blood coagulation system following cold injury, blood coagulability was increased. These changes were closely related to the degree of frostbite. In addition, the degree of cold injury was aggravated by altitude acclimation and this may play an important role in the pathological process of dysfunction leading to necrosis of local frostbite tissue.

Acclimatization↗

Risk of frostbite in vibration-induced white finger cases.

The rate of frostbite was examined with questionnaires filled by 1095 reindeer herders frequently exposed to cold, in particular in driving snowmobiles in the winter. Altogether 443 frostbite injuries, most (72%) of them on the face, had occurred during the last two years, especially when driving a snowmobile. The prevalence of vibration-induced white finger (VWF) was 22%. In this VWF group (N = 243) the cumulative incidence rate in two years of frostbite injuries on the extremities was 27% and in the non-VWF group (N = 852) only 5%. There was no difference in the incidence of frostbite on the face and ear lobe. The amount of frostbitten subjects, with respect to both frostbite on the extremities and head, was significantly associated with the use of snowmobiles during the last two years. According to the results VWF cases have an increased risk of frostbite in the extremities on a cold environment.

Adult↗

Incidences of frostbite in arthroscopic knee surgery postoperative cryotherapy rehabilitation.

A retrospective study of 4 cases of frostbite was undertaken to examine causes and to identify related contributory behaviors and circumstances. These patients underwent various surgical interventions before the onset of frostbite during similar postoperative care regimens. Surgical procedures included some of the following in each patient: lateral retinacular release, vastus medialis oblique muscle advancement, partial medial meniscectomy, chondromalacia patella, trochlea, medial and lateral femoral condyle debridement, lateral retinaculum release, and excision of medial plica. The mechanism of onset, development, and sites of frostbite were uniform in all patients. In every case, the sites were located in the area on top of the patella including some adjacent regions depending on the size of each injury. Frostbite locations were correlated with the part of the cryotherapy cold cuff device located on top of the patellar region. This cuff portion was originally designed to accommodate surgical trauma induced during autogenous bone-tendon-bone graft harvest in anterior cruciate ligament reconstruction surgery. Locating cryotherapy over this region assisted in minimizing pain and effusion for patients subsequent to distal patella bone plug harvest trauma. However, the requirement for use of the pad in the patella area for patients not undergoing anterior cruciate ligament reconstruction with autograft was found to be unnecessary and was the primary cause of frostbite in the cases presented here.

Cryotherapy↗

Frostbite injuries treated in the Helsinki area from 1995 to 2002.

BACKGROUND: : Exposure to cold results in frostbite, superficial or deeper tissue damage. In severe frostbites, amputations are life-saving but diminish quality of life (QOL). METHODS: : Retrospective study was performed. RAND 36- questionnaire was administered to assess QOL. Our aim was to investigate risk factors and adjustment to everyday life of hospitalized patients. RESULTS: : 92 frostbites in 42 patients were recorded. One third of the patients were chronic alcoholics. Age and temperature were statistically significant factors for unfavorable outcome. 20% of patients required secondary reconstructive procedures. One-third reported their emotional well-being very poor. Half had limitations in social life. CONCLUSIONS: : Hospitalized cases of frostbite are rare. Anti-social behavior increases the risk in general, and patients present with complicated problems similar to those encountered in burns victims. We recommend that frostbite patients requiring hospital attendance are treated in specialized units, where sufficient expertise for acute as well as reconstructive surgery is available.

Adolescent↗

An open-label study to evaluate the safety and efficacy of tissue plasminogen activator in treatment of severe frostbite.

BACKGROUND: Severe frostbite can have devastating consequences with loss of limbs and digits. One of the mechanisms of cold injury to human tissue is vascular thrombosis. The effect of tissue plasminogen activator (tPA) and heparin in limb and digit preservation in severe frostbite patients has not been previously studied. METHODS: Intra-arterial (6 patients) or intravenous (i.v., 13 patients) tPA and IV heparin were used in patients with severe frostbite. All patients between January 1, 1989 and February 1, 2003 with severe frostbite not improved by rapid rewarming, with absent Doppler pulses in distal limb or digits, without perfusion by Technetium (Tc) 99m three-phase bone scan, and no contraindication to tPA use were eligible. Efficacy was assessed on the basis of predicted digit amputation before therapy, given the clinical and Tc-99m scan results, versus partial or complete digits removed. RESULTS: There were no complications with i.v. tPA. Two patients with intra-arterial TPA had bleeding complications. We know from historical Tc-99m scan data which digits were at risk for amputation. In this study, there were 174 digits at risk in 18 patients and only 33 were amputated. CONCLUSION: Intravenous tPA and heparin after rapid rewarming is safe and reduced predicted digit amputations considerably. Patients with no response to thrombolytic therapy were those with more than 24 hours of cold exposure, warm ischemia times greater than 6 hours, or evidence of multiple freeze-thaw cycles. Our algorithm for treatment of severe frostbite now includes use of i.v. tPA for patients without contraindications.

Adult↗

The use of pegorgotein in the treatment of frostbite.

Free oxygen radicals have been postulated to be an important mediator of injury in frostbite. A long-acting version of the endogenous scavenger enzyme, superoxide dismutase, has been created by conjugating it with polyethylene glycol (pegorgotein, formerly known as PEG-SOD). This study evaluated the efficacy of pegorgotein on frostbite tissue survival when administered prior to rewarming. In a prospective study, two groups of nine rabbits received a standardized frostbite injury using a modified Weatherley-White model. A control group received no pharmacologic therapy; the treatment group received 10,000 IU/kg pegorgotein intravenously immediately postinjury. Healing was followed until a clear line of demarcation was apparent (10 days). The percentage of viable ear surface remaining at the end of the study was measured and used to compare the effectiveness of treatment. Student's t-test was used to determine statistical significance. The study was designed to have an 80% ability to detect a 35% difference in tissue survival. No significant difference in frostbite injury (p = 0.967) was observed between the control and treatment groups. The treatment group showed a 9.3 +/- 15.5% tissue survival, whereas the control group had 9.6 +/- 14.5% tissue survival. These results indicate no significant treatment effect for pegorgotein on tissue survival in a rabbit frostbite injury model when administered immediately postinjury.

Animals↗

Incidence of frostbite and ambient temperature in Finland, 1986-1995. A national study based on hospital admissions.

OBJECTIVES: The association of frostbite with ambient temperature in Finland is not known. The present study determined the incidence of frostbite and its association with sex, age and ambient temperature in a nationwide sample. STUDY DESIGN: The first admissions of all patients (n=1,275) admitted to hospital in Finland during the period 1986-1995 with frostbite as a principal or secondary diagnosis were associated with ambient temperature on the day of admission. RESULTS: The incidence of frostbite was 2.5 per 100,000 inhabitants, it was higher in males than females and increased linearly with age. The annual incidence of frostbite started to rise at below -15 degrees C and was considerable at under -20 degrees C, particularly in northern Finland. However, the daily incidence increased most in the urban area of Helsinki. CONCLUSION: In the north, the main factor is the large number of cold days in the year. The daily incidence may be affected by urban lifestyle, possibly fashion, and inability to protect oneself against the cold.

Adolescent↗

Is urban frostbite a psychiatric disorder?

We reviewed the records of 20 patients admitted with a diagnosis of frostbite. In addition to their thermal injury, all had overt, or covert, psychiatric disease. This prompted us to review hospital records of patients admitted to the Department of Veterans Affairs (DVA) Hospital system with a diagnosis of frostbite. During fiscal years 1991 and 1992, 37% and 36.7% of all patients admitted to DVA hospitals had a psychiatric disorder as primary or secondary diagnosis. When we selected those patients who additionally had a primary or secondary diagnosis of frostbite, the incidence increased to 61% and 65.6%, respectively. Urban patients with frostbite sufficiently severe to necessitate hospital admission have concomitant psychiatric disease at a rate that far exceeds the expected. Urban patients admitted to the hospital with a diagnosis of frostbite should be carefully screened for the presence of psychiatric disorder.

Adolescent↗

Frostbite of the upper extremity.

Human capacity for physiologic adaptation to cold is minimal; we survive by insulating ourselves with protective clothing. In addition to the irreversible direct injury caused by ice crystallization, the authors have outlined four possible mechanisms by which indirect injury may damage tissue. Other than rapid rewarming, there is no uniformly accepted protocol for the treatment of frostbite injury. Attempting to sort out the world's literature on frostbite in an effort to present a comprehensive treatment protocol is a daunting task. In addition to the probably irreversible direct injury caused by ice crystallization, the authors have outlined at least four possible mechanisms by which indirect injury may damage tissue. The literature is full of various treatment protocols that allegedly are beneficial despite addressing different mechanisms. Mills described 10 different categories of medications, each addressing one of four possible mechanisms, used in the clinical treatment of frostbite injury over a 30-year period. Analyzing this information is even more confusing when one realizes that there is little uniformity in animal models employed to generate these data. This is further complicated by the lack of clinical correlation with the most common experimental model--liquid nitrogen rapid freezing. The risk of frostbite is highest when psychiatric disturbance, intoxication, or unplanned circumstances lead to cold exposure without adequate protective clothing. As tissue freezes, both direct and indirect factors cause injury. Most therapies have been aimed at limiting indirect injury, in an attempt to limit progressive tissue loss. Rapid rewarming is universally accepted, but the benefits of other modalities are still controversial. Traditionally, observation and delayed amputation have been employed to manage frostbite. More recently, triple-phase bone scans have been used to distinguish between tissue that is irreversibly destined for necrosis and tissue that is at-risk for necrosis, but potentially salvageable. Early operation can be used to provide at-risk tissue with a new blood supply and preserve both function and length in the upper extremity.

Amputation, Surgical↗

[Oxyproline excretion in the urine in frostbite].

Hyperoxyprolinuria associated with the processes occuring in frostbitten tissues is observed in frostbites of II--III degree. In frostbites of I--II and III--IV degree the level of urine oxyproline excretion does not differ from the normal one throughout the posttraumatic period. In frostbites of I--II degree this is due to a limited volume of tissue injury, in frostbites of III--IV degree-to the fixation of decay products in the pathological focus, resulting from blood circulation disorders in the frostbitten zone. Differences in oxyprolinuria level may serve as a useful tool for differential diagnosis of frostbites.

Adult↗