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Frostbite injury causes direct damage to tissues following exposure to temperatures below their freezing point causing tissue death potentially leading to serious amputations. After rewarming, a variety of treatment options have been employed to avoid amputation. This case report details the use of indocyanine green fluorescence microangiography to monitor the clinical progression of perfusion following hyperbaric oxygen therapy (HBOT) for severe frostbite injury. We present a case report of a man with deep frostbite of the bilateral hands treated with thrombolytics and HBOT. After rewarming, the patient received thrombolytics shortly after arrival and then went on to be treated with HBOT on hospital day 5. Patient's healing progress was monitored using serial microangiography. Microangiography evaluation was performed on day 6 and then weekly to track treatment progress. A more uniform brightness appears in his left hand by completion of his therapies, consistent with normal perfusion. The dark ischemic areas in the right hand receded in digits 1 to 3 and appeared normalized in the fourth digit. The patient received a total of 20 HBO treatments. After completion of therapy, the patient went on to have a partial amputation of his first, second, and third fingers on his right hand. Our case report demonstrates serial microangiography to monitor a frostbite patient's progress during HBOT and provided additional information allowing us to plan duration of treatments. Our case report describes the role that microangiography may serve in monitoring patient progress following severe frostbite injury.

Frostbite may cause lesions. The severity ranges from superficial wounds to severe cases with loss of limbs and tissue. Hence, proper treatment is of utmost importance. We present a case of an 18-year-old man from Arctic Greenland who was admitted with severe frostbite lesions involving both hands. The patient had fallen asleep outside during extreme temperatures. He was treated conservatively with proper wound care, antibiotics and intensive physical therapy. The patient made a full recovery without sequelae. The current report emphasises that non-operative treatment should be attempted for frostbite lesions, as conservative treatment often results in good outcomes., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Frostbite is damage caused by the freezing of tissue owing to exposure to extreme cold. Clinically, it is often difficult to identify the severity of frostbite injury. There may be a wide discrepancy between the extent of damage to the skin versus that to the deeper structures. The initial clinical impression is usually worse than actual tissue damage. In addition to physical examination, diagnostic imaging, especially triple-phase bone scan, has been proposed to help differentiate between superficial and deep damage. Principles of treatment involve rapid rewarming to thaw the tissues and halt direct cellular damage, methods to minimize progressive dermal ischemia, and active wound care to promote timely healing. Pharmacological adjuncts, such as fibrinolytics, have been proposed to minimize tissue damage. Surgical therapy is postponed until there is clear demarcation between healthy and necrotic tissue., (Copyright © 2014 American Society for Surgery of the Hand. Published by Elsevier Inc. All rights reserved.)

The treatment of cold injuries to the periphery has advanced substantially in the last 10 years and optimal outcomes are only likely to be achieved if a multidisciplinary team uses the full range of diagnostic and treatment modalities that are now available. The internet and satellite phones with digital images allow immediate access by patients from remote geographical locations to hospital based specialists who can assess cold injuries and advise on early field care. The severity of frostbite injuries can now be assessed with triple phase bone scanning, allowing early prediction of likely subsequent tissue loss. Early hyperbaric oxygen therapy appears to improve outcome and the use of intravenous drugs such as synthetic prostaglandin analogues infusions and tissue plasminogen activator have been shown to reduce amputation rates. In non-freezing cold injuries the early administration of analgesia, the avoidance of secondary exposure, and the use of infrared thermography to assess the injuries are among newer approaches being introduced.

Unlabelled: An 11-year-old boy in good general health conditions suffered deep frostbite on six fingers while he was working without gloves as a beater during a hunt in Poland at an outdoor temperature of -32 degrees C over a 4 h-period. Three days later he was first seen by a physician who planned to amputate the affected fingers. The patient was transferred by his family to our University Hospital in Aachen, Germany. We found third degree frostbite on four fingers of the right and on two fingers of the left hand. Because of the late beginning of the therapy, the patient was treated by HBO(2) according to the Marx-schema for problem wounds (2,4 bar, total time at depth: 90 min, alternations of 100% O(2) and air breathing). HBO(2)-treatment was repeated daily for 14 days. No adverse events were recorded during the course of therapy. A total recovery of the severe frostbite was observed after 14 days of HBO(2)-treatment. Twenty-eight months after the injury the patient reports fully regained sensibility and no pain. The plain X-ray after this period showed no premature closure of the epiphyses or sclerosis of the metaphyses., Conclusions: Because of the low risk associated with HBO(2), and its potential therapeutic efficiency, HBO(2) should be recommended as adjunct therapy in the treatment of deep frostbite.

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.

The breakdown products of arachidonic acid have been implicated as mediators of progressive dermal ischemia in both cold and thermal injuries. Increased tissue survival can be demonstrated experimentally with the preservation of the dermal microcirculation by using antiprostaglandin agents and thromboxane inhibitors. Thirty-eight consecutive patients (28 males and 10 females aged 2 mo to 46 yr) with frostbite injuries were treated at the University of Chicago's Burn Center in January 1982 with a protocol designed to decrease the production of thromboxane locally and prostaglandins systemically. All patients recovered without significant tissue loss. The average hospital stay was 5.6 days for acute injuries and 6.9 days for subacute injuries.

The management of patients with cold injuries of the hands may be extremely simple or relatively complex. The extent of the injury and the systemic response to the cold are the major influencing factors. In patients with extensive cold injuries, where all or a large portion of more than one extremity is cold or frozen and there has been a significant systemic response, treatment should be both systemic and local. Treatment should be directed toward both the preservation of tissue and maintenance of function of the damaged part. Minimal daily débridement and late amputation are important guidelines for care.

The use of thymalin in the complex therapy of 19 patients with frostbites was shown by the authors to promote the stimulation of cell immunity, decrease the intensity of intravascular blood coagulation, to increase fibrinolysis, to improve the development of reparative processes in the wound and outcomes of autoplasty. It also decreased the percentage of infectious complications.