CURRENT CONCEPTS
Frostbite of the Hand Richard L. Hutchison, MD CME INFORMATION AND DISCLOSURES The Review Section of JHS will contain at least 3 clinically relevant articles selected by the editor to be offered for CME in each issue. For CME credit, the participant must read the articles in print or online and correctly answer all related questions through an online examination. The questions on the test are designed to make the reader think and will occasionally require the reader to go back and scrutinize the article for details. The JHS CME Activity fee of $30.00 includes the exam questions/answers only and does not include access to the JHS articles referenced. Statement of Need: This CME activity was developed by the JHS review section editors and review article authors as a convenient education tool to help increase or affirm reader’s knowledge. The overall goal of the activity is for participants to evaluate the appropriateness of clinical data and apply it to their practice and the provision of patient care.
Technical Requirements for the Online Examination can be found at http://jhandsurg. org/cme/home. Privacy Policy can be found at http://www.assh.org/pages/ASSHPrivacyPolicy.aspx. ASSH Disclosure Policy: As a provider accredited by the ACCME, the ASSH must ensure balance, independence, objectivity, and scientific rigor in all its activities. Disclosures for this Article Editors Ghazi M. Rayan, MD, has no relevant conflicts of interest to disclose.
Accreditation: The ASSH is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.
Authors All authors of this journal-based CME activity have no relevant conflicts of interest to disclose. In the printed or PDF version of this article, author affiliations can be found at the bottom of the first page.
AMA PRA Credit Designation: The American Society for Surgery of the Hand designates this Journal-Based CME activity for a maximum of 2.00 “AMA PRA Category 1 Credits”. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Planners Ghazi M. Rayan, MD, has no relevant conflicts of interest to disclose. The editorial and education staff involved with this journal-based CME activity has no relevant conflicts of interest to disclose. Learning Objectives
ASSH Disclaimer: The material presented in this CME activity is made available by the ASSH for educational purposes only. This material is not intended to represent the only methods or the best procedures appropriate for the medical situation(s) discussed, but rather it is intended to present an approach, view, statement, or opinion of the authors that may be helpful, or of interest, to other practitioners. Examinees agree to participate in this medical education activity, sponsored by the ASSH, with full knowledge and awareness that they waive any claim they may have against the ASSH for reliance on any information presented. The approval of the US Food and Drug Administration is required for procedures and drugs that are considered experimental. Instrumentation systems discussed or reviewed during this educational activity may not yet have received FDA approval.
Deadline: Each examination purchased in 2014 must be completed by January 31, 2015, to be eligible for CME. A certificate will be issued upon completion of the activity. Estimated time to complete each month’s JHS CME activity is up to 2 hours.
Provider Information can be found at http://www.assh.org/Pages/ContactUs.aspx.
Copyright ª 2014 by the American Society for Surgery of the Hand. All rights reserved.
Provide information about the pathophysiology of tissue freezing. Discuss the risk factors for frostbite injuries of the hand. Assess the methods of evaluating and diagnosing different degrees of acute frostbite injuries. Describe the clinical manifestations of various degrees of frostbite injuries. Review both nonsurgical and surgical treatment options for acute frostbite injuries.
From the Section of Hand Surgery, Division of Orthopaedic Surgery, Children’s Mercy Hospitals and Clinics, University of MissourieKansas City, Kansas City, MO.
Corresponding author: Richard L. Hutchison, MD, 2401 Gillham Rd, Kansas City, MO 64108; e-mail: [email protected].
Received for publication December 15, 2013; accepted in revised form January 22, 2014.
0363-5023/14/3909-0035$36.00/0 http://dx.doi.org/10.1016/j.jhsa.2014.01.035
No benefits in any form have been received or will be received related directly or indirectly to the subject of this article.
2014 ASSH
r
Published by Elsevier, Inc. All rights reserved.
r
1863
Current Concepts
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. (J Hand Surg Am. 2014;39(9):1863e1868. Copyright 2014 by the American Society for Surgery of the Hand. All rights reserved.) Key words Frostbite, hand, cold injury.
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the freezing of tissue, often the hands and feet, owing to exposure to extreme cold. Hand surgeons are often consulted to care for frostbite patients. The oldest example of frostbite is in 5,300-yearold skeletal remains found in the Alps in 1991. Radiographs revealed signs of healed frostbite.1 The first written report of frostbite was by the first-century encyclopedist Celsus in De Medicina.2 Baron Dominique Larrey,3 Napoleon’s chief surgeon, recognized that frostbite had similarities to burns, that warming was beneficial but that rewarming next to an open fire may cause thermal injury, and that repeated freezethaw-freeze cycles were deleterious. Unfortunately, he introduced the harmful concept of treatment by friction massage with ice or snow. Modern treatment of frostbite dates to animal experiments published in 1950s, the first report of rapid rewarming by Hamill, and clinical reports by Mills.4,5 Frostbite has been a serious problem in military populations. The literature on frostbite among civilians is limited.6 Humans are physiologically tropical animals who must consciously protect themselves from freezing temperatures. Most publications on frostbite among civilians observed a high proportion of patients with cognitive alteration due to alcohol, drugs, or psychiatric problems. These patients are more likely to be males, have frostbite on the extremities, and in the 30- to 49-year age group.7,8 Other groups prone to frostbite include those injured in vehicular accidents or breakdowns, extreme winter sports enthusiasts, mountain climbers, and those working outside in extreme cold with metal tools without adequate hand protection.4 ROSTBITE IS DAMAGE CAUSED BY
Current Concepts
PATHOPHYSIOLOGY Frostbite begins with freezing of the skin. Human skin has evolved to respond preferentially to higher rather than lower ambient temperatures. Basal cutaneous blood flow can increase about 35-fold in response to higher skin temperature and decreases about 10-fold in response to cold. In response to temperatures below 59 F (15 C), human skin demonstrates the adaptive hunting reaction, which is vasoconstriction followed by alternating cycles of vasodilatation that recur every 5 to 10 minutes.9 This response, though, is not protective against frostbite.10 Risk factors for frostbite include environmental conditions that increase heat loss, such as wind, humidity, and temperatures below 27 F (-3 C), inappropriate clothing, overexertion, fatigue, alcohol, and impaired decision making. Other risk factors, such as vasoconstriction J Hand Surg Am.
r
FIGURE 1: First-degree frostbite.
due to smoking, dysautonomia, immobilization, previous cold injury, diabetes mellitus, vascular insufficiency, and thyroid and adrenal disease can decrease heat delivery.4 Frostbite can damage tissue by 2 mechanisms— direct cellular damage and progressive dermal ischemia. Direct damage starts with the formation of extracellular ice crystals, followed by changes in the cell membrane altering the osmotic gradient. This progression leads to intracellular dehydration, increased intracellular electrolyte concentration, intracellular ice formation, and the mechanical destruction of cells.11,12 The progressive dermal ischemia is usually more harmful than the direct cell damage, and its cause is similar to the events that lead to reperfusion injury. Inflammatory mediators, such as prostaglandins, thromboxanes, bradykinin, and histamine, lead to edema formation, endothelial injury, and arrest of dermal blood flow. Thawing causes momentary and initial vasoconstriction of arterioles and venules, followed by resumption of capillary circulation and blood flow. Flow is soon disrupted by showers of emboli in microvessels. These emboli and the preexisting endothelial damage cause further tissue loss from progressive thrombosis and hypoxia. The reperfusion injury is mediated by arachidonic acid metabolites and oxygen free radicals.13,14 Vol. 39, September 2014
FIGURE 2: Second-degree frostbite.
FIGURE 3: Deep frostbite 3 weeks after injury.
CLINICAL PICTURE Clinically, it is often difficult to initially estimate the severity of frostbite injury. There may be a wide discrepancy between the degree of damage to the skin versus that to the deeper structures. The initial clinical J Hand Surg Am.
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1865
impression is usually worse than the actual tissue damage. Initially, symptoms may include a feeling of numbness in the affected part, clumsiness, and lack of fine motor control. With rewarming, a throbbing sensation and/or pain develops that may last for days or even weeks in any frostbitten tissue. Frostbite can be classified into four degrees: first degree—reversible changes; second degree—superficial dermal damage; third degree—deep dermal damage; and fourth degree—damage to subcutaneous tissue, muscle, nerves, and/or bone.4,5 First-degree frostbite presents as a numb central whitish plaque with surrounding skin erythema (Fig. 1). Second degree has soft clear or milky fluid-filled blister formation with soft perfused skin under the blisters that is surrounded by erythema and mild to moderate edema (Fig. 2). Third degree has hemorrhagic blisters over nonperfused skin with severe edema. Fourth degree may present as hard, woody, blue-gray, mottled insensate tissue. For deep injury, edema appears within 3 hours and lasts 5 days or longer. Vesicles or bullae form 6 to 24 hours after rapid rewarming. Black, hard, and usually dry eschar appears in 9 to 15 days, and after 22 to 45 days, mummification forms an apparent line of demarcation (Fig. 3). Clinically, it is more useful to categorize frostbite as superficial (first and second degrees) or deep (third and fourth degrees).15 With standard treatment, superficial frostbite is expected to heal without tissue loss. In addition to physical examination, numerous diagnostic tests have been proposed to help delineate between superficial and deep frostbite damage. Plain radiographs are not helpful for early diagnosis, except to screen for concomitant fractures. It takes weeks to months for definitive radiographic changes such as osteoporosis and periosteitis to occur after deep frostbite. Results of arteriography and Doppler examination usually do not alter treatment, but they may confirm deep damage. Arteriography may demonstrate marked slowing of blood flow in sizeable branches, and residual occlusions are often noted with rewarming. Arteriograms obtained soon after injury do not sufficiently clarify levels of viability and do not visualize microcirculation, especially that of bone. The utility of magnetic resonance imaging, magnetic resonance angiography, and computed tomography angiography in the frostbite setting is not yet established.4 Some studies have proposed the utility of triplephase bone scans, as they allow evaluation of the microcirculation of soft tissue and bone. Three Vol. 39, September 2014
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FIGURE 4: Deep frostbite after amputations.
patterns can be seen: normal blood and bone pool images; little or no blood pool with diminished, but clearly visible bone pool images; or little or no flow in either the blood or the bone pool images. Bone scans have been shown to be useful at 2 to 3 weeks post injury to help clarify the extent of tissue loss. A number of studies have proposed early bone scan to identify patients who would benefit from early surgical treatment.16e18
Current Concepts
TREATMENT Treatment of frostbite is guided by our understanding of the pathophysiology. Most guidelines are based on levels IV and V evidence studies. Principles of treatment involve rapid rewarming to thaw ice and halt direct cellular damage, post thawing care to minimize progressive dermal ischemia, and active wound care to promote timely healing.12,19e21 Prehospital care involves protection of the involved part from mechanical trauma and avoidance of thawing until definitive rewarming can be performed. Thawing and refreezing result in worse injury than more prolonged freezing followed by definitive thawing.21 Prior to rewarming, comprehensive evaluation should be performed and associated hypothermia and hypovolemia should be corrected. Currently, rapid rewarming in a water bath with a mild antibacterial agent at 100.4 F to 104 F (38 Ce40 C) is recommended.22 Rewarming is continued until thawing is complete, usually for 15 to 30 minutes. Endpoint signs for rewarming are a red/ J Hand Surg Am.
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purple appearance and pliable texture of the involved part. Rewarming is accompanied by pain, sometimes intense, and adequate analgesia needs to be provided. Gentle active motion may be helpful. Hand surgeons are usually consulted on these patients after the affected parts have been thawed. For superficial injury, local wound care should be instituted. Ruptured blisters should be gently debrided. Treatment of intact blisters varies between authors and protocols. Intact blisters prevent the underlying wound from desiccating and protect it from bacterial colonization, but the blisters may impede motion. Blister fluid has been shown to contain high levels of prostaglandin F2-alpha and thromboxane A2, and removal of the blister fluid may theoretically be useful.23 Some authors, based on these theoretical grounds, suggest debriding the blisters and applying ointments containing agents that disrupt pathways to thromboxanes, such as aloe vera.5,24 Debridement should be considered if excellent wound care, including mechanical protection, gentle daily cleansing, and protection from desiccation with topical ointments and application of dressings, can be provided. Most guidelines include elevation of the extremity, orthosis fabrication and protective dressing, a nonsteroidal anti-inflammatory agent such as ibuprofen, adequate analgesia, and tetanus prophylaxis.4 No studies have shown benefit to prophylactic antibiotics. Multiple adjuvant therapies have been proposed. Low-molecular weight Dextran and anticoagulation have been of value in animal experiments but have not been shown to be of clinical value. Vasodilators Vol. 39, September 2014
FROSTBITE
COMPLICATIONS Long-term sequelae include cold sensitivity, sensory loss, hyperhidrosis, growth plate disturbances, osteoarthritis, chronic pain, and heterotopic calcification. Long-term residual paresthesias may develop, with occasional electric shock-type sensations.5 J Hand Surg Am.
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Although treatment with tPA shows promising preliminary results, higher level of evidence studies are needed to establish its efficacy. Future studies may establish a role for early negative-pressure wound therapy, corroborate the utility of prostacyclins, and identify the benefits of other pharmacological agents such as botulinum toxin type A. In conclusion, although frostbite remains a common problem that is evaluated and treated by hand surgeons, the therapeutic approach has not substantially advanced during the last half century. Goals remain to be limiting direct damage, mitigating progressive ischemia, and optimizing local wound care. Perhaps further evaluation of the use of thrombolytic and other pharmacological therapies will lead to improved care. REFERENCES 1. Murphy WA, Nedden Dz D, Gostner P, Knapp R, Recheis W, Seidler H. The iceman: discovery and imaging. Radiology. 2003;226(3):614e629. 2. Vogel JE, Dellon AL. Frostbite injuries of the hand. Clin Plast Surg. 1989;16(3):565e576. 3. Larrey D. Memoirs of Military Surgery, and Campaigns of the French Armies, on the Rhine, in Corsica, Catalonia, Egypt, and Syria; at Boulogne, Ulm, and Austerlitz; in Saxony, Prussia, Poland, Spain, and Austria. Baltimore: University Press of Sergeant Hall; 1814. 4. Mohr WJ, Jenabzadeh K, Ahrenholz DH. Cold injury. Hand Clin. 2009;25(4):481e496. 5. McCauley R, Killyon G, Smith D, Robson M, Heggers J. Wilderness Medicine. Philadelphia: Mosby; 2007. 6. Murphy JV, Banwell PE, Roberts AH, McGrouther DA. Frostbite: pathogenesis and treatment. J Trauma. 2000;48(1):171e178. 7. Valnicek SM, Chasmar LR, Clapson JB. Frostbite in the prairies: a 12-year review. Plast Reconstr Surg. 1993;92(4):633e641. 8. Pinzur MS, Weaver FM. Is urban frostbite a psychiatric disorder? Orthopedics. 1997;20(1):43e45. 9. Dana AS, Rex IH, Samitz MH. The hunting reaction. Arch Dermatol. 1969;99(4):441e450. 10. Su CW, Lohman R, Gottlieb LJ. Frostbite of the upper extremity. Hand Clin. 2000;16(2):235e247. 11. Heggers JP, Robson MC, Manavalen K, et al. Experimental and clinical observations on frostbite. Ann Emerg Med. 1987;16(9):1056e1062. 12. Hallam MJ, Cubison T, Dheansa B, Imray C. Managing frostbite. BMJ. 2010;341:c5864. 13. Zacarian SA, Stone D, Clater M. Effects of cryogenic temperatures on microcirculation in the golden hamster cheek pouch. Cryobiology. 1970;7(1):27e39. 14. Bulkley GB. The role of oxygen free radicals in human disease processes. Surgery. 1983;94(3):407e411. 15. Mills WJ. Summary of treatment of the cold injured patient: frostbite. 1983. Alaska Med. 1993;35(1):61e66. 16. Mehta RC, Wilson MA. Frostbite injury: prediction of tissue viability with triple-phase bone scanning. Radiology. 1989;170(2): 511e514. 17. Cauchy E, Marsigny B, Allamel G, Verhellen R, Chetaille E. The value of technetium 99 scintigraphy in the prognosis of amputation in severe frostbite injuries of the extremities: a retrospective study of 92 severe frostbite injuries. J Hand Surg Am. 2000;25(5):969e978. 18. Greenwald D, Cooper B, Gottlieb L. An algorithm for early aggressive treatment of frostbite with limb salvage directed by triplephase scanning. Plast Reconstr Surg. 1998;102(4):1069e1074.
Vol. 39, September 2014
Current Concepts
such as reserpine are useful experimentally with slow, but not with rapid, rewarming. Sympathectomy and hyperbaric oxygen therapy both have contradictory experimental evidence, limited anecdotal evidence, and no proven clinical value.4,5,25 Administration of a prostacyclin has been reported to be efficacious.26 During the last 10 years, there has been considerable enthusiasm about the use of thrombolytic agents, such as tissue plasminogen activator (tPA).27 Twomey et al28 reported a retrospective series of 19 patients treated with tPA and anticoagulation and concluded that tPA was safe and improved their predicted outcomes. Bruen et al29 retrospectively studied 7 frostbite patients with abnormal arteriograms treated with intra-arterial tPA. They concluded the patients with deep frostbite had lower amputation rates compared with historical controls.29 Other case series and reports have also been reported.30e32 If tPA is used, most protocols suggest its administration in an intensive care unit within 24 hours of thawing. Early administration offers the potential of improved results. Contraindications for tPA use include concurrent trauma, neurological impairment, recent surgery, or hemorrhage.27 The role and efficacy of tPA remain uncertain. Superficial frostbite should heal without need for surgery. Deep frostbite may need an operative procedure, but the major question relates to timing. Immediate or early surgical care is rarely needed, except in the event of compartment syndrome or infection. Traditional guidelines emphasize allowing noninfected, dry necrotic tissue to fully mummify before debridement and closure. It may take 1 to 3 months for a clear delineation of viable tissue to become evident. This is in contradistinction to burn therapy guidelines, which advocate early debridement of deep injury. Choice of debridement or amputation level and coverage follow the normal precepts for surgical care4 (Fig. 4). One proposal for earlier treatment involves the use of triplephase bone scans to identify salvageable tissue at 1 to 2 weeks post injury.18 Patients with perfusion scans that show little or no blood pool but perfusion in bone images are treated with debridement and flap coverage of the bone and tendons, potentially limiting the extent of amputation. This protocol needs further study.
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19. McCauley RL, Hing DN, Robson MC, Heggers JP. Frostbite injuries: a rational approach based on the pathophysiology. J Trauma. 1983;23(2):143e147. 20. Grieve AW, Davis P, Dhillon S, Richards P, Hillebrandt D, Imray CH. A clinical review of the management of frostbite. J R Army Med Corps. 2011;157(1):73e78. 21. McIntosh SE, Hamonko M, Freer L, et al. Wilderness Medical Society practice guidelines for the prevention and treatment of frostbite. Wilderness Environ Med. 2011;22(2):156e166. 22. Copass M, Nemiroff M. State of Alaska Cold Injuries Guidelines. Juneau: Department of Health and Social Services, Division of Public Health; 2005. 23. Robson MC, Heggers JP. Evaluation of hand frostbite blister fluid as a clue to pathogenesis. J Hand Surg Am. 1981;6(1):43e47. 24. McCauley RL, Heggers JP, Robson MC. Frostbite. Methods to minimize tissue loss. Postgrad Med. 1990;88(8):67e68, 73e67. 25. Gross EA, Moore JC. Using thrombolytics in frostbite injury. J Emerg Trauma Shock. 2012;5(3):267e271. 26. Cauchy E, Cheguillaume B, Chetaille E. A controlled trial of a prostacyclin and rt-PA in the treatment of severe frostbite. N Engl J Med. 2011;364(2):189e190.
27. Bruen KJ, Gowski WF. Treatment of digital frostbite: current concepts. J Hand Surg Am. 2009;34(3):553e554. 28. Twomey JA, Peltier GL, Zera RT. An open-label study to evaluate the safety and efficacy of tissue plasminogen activator in treatment of severe frostbite. J Trauma. 2005;59(6):1350e1354; discussion 1354e1355. 29. Bruen KJ, Ballard JR, Morris SE, Cochran A, Edelman LS, Saffle JR. Reduction of the incidence of amputation in frostbite injury with thrombolytic therapy. Arch Surg. 2007;142(6):546e551; discussion 551e553. 30. Johnson AR, Jensen HL, Peltier G, DelaCruz E. Efficacy of intravenous tissue plasminogen activator in frostbite patients and presentation of a treatment protocol for frostbite patients. Foot Ankle Spec. 2011;4(6):344e348. 31. Saemi AM, Johnson JM, Morris CS. Treatment of bilateral hand frostbite using transcatheter arterial thrombolysis after papaverine infusion. Cardiovasc Intervent Radiol. 2009;32(6):1280e1283. 32. Sheridan RL, Goldstein MA, Stoddard FJ, Walker TG. Case records of the Massachusetts General Hospital. Case 41-2009. A 16-year-old boy with hypothermia and frostbite. N Engl J Med. 2009;361(27): 2654e2662.
JOURNAL CME QUESTIONS Frostbite of the Hand Which of the following is a clinical finding of third degree frostbite to the hand? a. Central whitish plaque with surrounding skin erythema. b. Whitish plaque with surrounding skin erythema and severe edema. c. Milky fluid-filled blister formation with underlying soft perfused skin. d. Hemorrhagic blisters over nonperfused skin with severe edema. e. Hard, woody, blue-gray, mottled insensate tissue.
Which of the following is the appropriate treatment for acute-hand frostbite injury? a. Immediate thawing on site prior to arrival to the hospital. b. Addressing hypothermia and hypovolemia followed by gradual, slow rewarming. c. Continued rewarming until a red or purple appearance and pliable skin texture is achieved. d. Rewarming in bath water and an antimicrobial agent for 5 minutes. e. Rapid rewarming with water bath of 80 to 84 F.
To take the online test and receive CME credit, go to http://www.jhandsurg.org/CME/home.
Current Concepts J Hand Surg Am.
r
Vol. 39, September 2014
Frostbite of the Hand Richard L. Hutchison, MD CME INFORMATION AND DISCLOSURES The Review Section of JHS will contain at least 3 clinically relevant articles selected by the editor to be offered for CME in each issue. For CME credit, the participant must read the articles in print or online and correctly answer all related questions through an online examination. The questions on the test are designed to make the reader think and will occasionally require the reader to go back and scrutinize the article for details. The JHS CME Activity fee of $30.00 includes the exam questions/answers only and does not include access to the JHS articles referenced. Statement of Need: This CME activity was developed by the JHS review section editors and review article authors as a convenient education tool to help increase or affirm reader’s knowledge. The overall goal of the activity is for participants to evaluate the appropriateness of clinical data and apply it to their practice and the provision of patient care.
Technical Requirements for the Online Examination can be found at http://jhandsurg. org/cme/home. Privacy Policy can be found at http://www.assh.org/pages/ASSHPrivacyPolicy.aspx. ASSH Disclosure Policy: As a provider accredited by the ACCME, the ASSH must ensure balance, independence, objectivity, and scientific rigor in all its activities. Disclosures for this Article Editors Ghazi M. Rayan, MD, has no relevant conflicts of interest to disclose.
Accreditation: The ASSH is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.
Authors All authors of this journal-based CME activity have no relevant conflicts of interest to disclose. In the printed or PDF version of this article, author affiliations can be found at the bottom of the first page.
AMA PRA Credit Designation: The American Society for Surgery of the Hand designates this Journal-Based CME activity for a maximum of 2.00 “AMA PRA Category 1 Credits”. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Planners Ghazi M. Rayan, MD, has no relevant conflicts of interest to disclose. The editorial and education staff involved with this journal-based CME activity has no relevant conflicts of interest to disclose. Learning Objectives
ASSH Disclaimer: The material presented in this CME activity is made available by the ASSH for educational purposes only. This material is not intended to represent the only methods or the best procedures appropriate for the medical situation(s) discussed, but rather it is intended to present an approach, view, statement, or opinion of the authors that may be helpful, or of interest, to other practitioners. Examinees agree to participate in this medical education activity, sponsored by the ASSH, with full knowledge and awareness that they waive any claim they may have against the ASSH for reliance on any information presented. The approval of the US Food and Drug Administration is required for procedures and drugs that are considered experimental. Instrumentation systems discussed or reviewed during this educational activity may not yet have received FDA approval.
Deadline: Each examination purchased in 2014 must be completed by January 31, 2015, to be eligible for CME. A certificate will be issued upon completion of the activity. Estimated time to complete each month’s JHS CME activity is up to 2 hours.
Provider Information can be found at http://www.assh.org/Pages/ContactUs.aspx.
Copyright ª 2014 by the American Society for Surgery of the Hand. All rights reserved.
Provide information about the pathophysiology of tissue freezing. Discuss the risk factors for frostbite injuries of the hand. Assess the methods of evaluating and diagnosing different degrees of acute frostbite injuries. Describe the clinical manifestations of various degrees of frostbite injuries. Review both nonsurgical and surgical treatment options for acute frostbite injuries.
From the Section of Hand Surgery, Division of Orthopaedic Surgery, Children’s Mercy Hospitals and Clinics, University of MissourieKansas City, Kansas City, MO.
Corresponding author: Richard L. Hutchison, MD, 2401 Gillham Rd, Kansas City, MO 64108; e-mail: [email protected].
Received for publication December 15, 2013; accepted in revised form January 22, 2014.
0363-5023/14/3909-0035$36.00/0 http://dx.doi.org/10.1016/j.jhsa.2014.01.035
No benefits in any form have been received or will be received related directly or indirectly to the subject of this article.
2014 ASSH
r
Published by Elsevier, Inc. All rights reserved.
r
1863
Current Concepts
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. (J Hand Surg Am. 2014;39(9):1863e1868. Copyright 2014 by the American Society for Surgery of the Hand. All rights reserved.) Key words Frostbite, hand, cold injury.
1864
F
FROSTBITE
the freezing of tissue, often the hands and feet, owing to exposure to extreme cold. Hand surgeons are often consulted to care for frostbite patients. The oldest example of frostbite is in 5,300-yearold skeletal remains found in the Alps in 1991. Radiographs revealed signs of healed frostbite.1 The first written report of frostbite was by the first-century encyclopedist Celsus in De Medicina.2 Baron Dominique Larrey,3 Napoleon’s chief surgeon, recognized that frostbite had similarities to burns, that warming was beneficial but that rewarming next to an open fire may cause thermal injury, and that repeated freezethaw-freeze cycles were deleterious. Unfortunately, he introduced the harmful concept of treatment by friction massage with ice or snow. Modern treatment of frostbite dates to animal experiments published in 1950s, the first report of rapid rewarming by Hamill, and clinical reports by Mills.4,5 Frostbite has been a serious problem in military populations. The literature on frostbite among civilians is limited.6 Humans are physiologically tropical animals who must consciously protect themselves from freezing temperatures. Most publications on frostbite among civilians observed a high proportion of patients with cognitive alteration due to alcohol, drugs, or psychiatric problems. These patients are more likely to be males, have frostbite on the extremities, and in the 30- to 49-year age group.7,8 Other groups prone to frostbite include those injured in vehicular accidents or breakdowns, extreme winter sports enthusiasts, mountain climbers, and those working outside in extreme cold with metal tools without adequate hand protection.4 ROSTBITE IS DAMAGE CAUSED BY
Current Concepts
PATHOPHYSIOLOGY Frostbite begins with freezing of the skin. Human skin has evolved to respond preferentially to higher rather than lower ambient temperatures. Basal cutaneous blood flow can increase about 35-fold in response to higher skin temperature and decreases about 10-fold in response to cold. In response to temperatures below 59 F (15 C), human skin demonstrates the adaptive hunting reaction, which is vasoconstriction followed by alternating cycles of vasodilatation that recur every 5 to 10 minutes.9 This response, though, is not protective against frostbite.10 Risk factors for frostbite include environmental conditions that increase heat loss, such as wind, humidity, and temperatures below 27 F (-3 C), inappropriate clothing, overexertion, fatigue, alcohol, and impaired decision making. Other risk factors, such as vasoconstriction J Hand Surg Am.
r
FIGURE 1: First-degree frostbite.
due to smoking, dysautonomia, immobilization, previous cold injury, diabetes mellitus, vascular insufficiency, and thyroid and adrenal disease can decrease heat delivery.4 Frostbite can damage tissue by 2 mechanisms— direct cellular damage and progressive dermal ischemia. Direct damage starts with the formation of extracellular ice crystals, followed by changes in the cell membrane altering the osmotic gradient. This progression leads to intracellular dehydration, increased intracellular electrolyte concentration, intracellular ice formation, and the mechanical destruction of cells.11,12 The progressive dermal ischemia is usually more harmful than the direct cell damage, and its cause is similar to the events that lead to reperfusion injury. Inflammatory mediators, such as prostaglandins, thromboxanes, bradykinin, and histamine, lead to edema formation, endothelial injury, and arrest of dermal blood flow. Thawing causes momentary and initial vasoconstriction of arterioles and venules, followed by resumption of capillary circulation and blood flow. Flow is soon disrupted by showers of emboli in microvessels. These emboli and the preexisting endothelial damage cause further tissue loss from progressive thrombosis and hypoxia. The reperfusion injury is mediated by arachidonic acid metabolites and oxygen free radicals.13,14 Vol. 39, September 2014
FIGURE 2: Second-degree frostbite.
FIGURE 3: Deep frostbite 3 weeks after injury.
CLINICAL PICTURE Clinically, it is often difficult to initially estimate the severity of frostbite injury. There may be a wide discrepancy between the degree of damage to the skin versus that to the deeper structures. The initial clinical J Hand Surg Am.
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impression is usually worse than the actual tissue damage. Initially, symptoms may include a feeling of numbness in the affected part, clumsiness, and lack of fine motor control. With rewarming, a throbbing sensation and/or pain develops that may last for days or even weeks in any frostbitten tissue. Frostbite can be classified into four degrees: first degree—reversible changes; second degree—superficial dermal damage; third degree—deep dermal damage; and fourth degree—damage to subcutaneous tissue, muscle, nerves, and/or bone.4,5 First-degree frostbite presents as a numb central whitish plaque with surrounding skin erythema (Fig. 1). Second degree has soft clear or milky fluid-filled blister formation with soft perfused skin under the blisters that is surrounded by erythema and mild to moderate edema (Fig. 2). Third degree has hemorrhagic blisters over nonperfused skin with severe edema. Fourth degree may present as hard, woody, blue-gray, mottled insensate tissue. For deep injury, edema appears within 3 hours and lasts 5 days or longer. Vesicles or bullae form 6 to 24 hours after rapid rewarming. Black, hard, and usually dry eschar appears in 9 to 15 days, and after 22 to 45 days, mummification forms an apparent line of demarcation (Fig. 3). Clinically, it is more useful to categorize frostbite as superficial (first and second degrees) or deep (third and fourth degrees).15 With standard treatment, superficial frostbite is expected to heal without tissue loss. In addition to physical examination, numerous diagnostic tests have been proposed to help delineate between superficial and deep frostbite damage. Plain radiographs are not helpful for early diagnosis, except to screen for concomitant fractures. It takes weeks to months for definitive radiographic changes such as osteoporosis and periosteitis to occur after deep frostbite. Results of arteriography and Doppler examination usually do not alter treatment, but they may confirm deep damage. Arteriography may demonstrate marked slowing of blood flow in sizeable branches, and residual occlusions are often noted with rewarming. Arteriograms obtained soon after injury do not sufficiently clarify levels of viability and do not visualize microcirculation, especially that of bone. The utility of magnetic resonance imaging, magnetic resonance angiography, and computed tomography angiography in the frostbite setting is not yet established.4 Some studies have proposed the utility of triplephase bone scans, as they allow evaluation of the microcirculation of soft tissue and bone. Three Vol. 39, September 2014
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FIGURE 4: Deep frostbite after amputations.
patterns can be seen: normal blood and bone pool images; little or no blood pool with diminished, but clearly visible bone pool images; or little or no flow in either the blood or the bone pool images. Bone scans have been shown to be useful at 2 to 3 weeks post injury to help clarify the extent of tissue loss. A number of studies have proposed early bone scan to identify patients who would benefit from early surgical treatment.16e18
Current Concepts
TREATMENT Treatment of frostbite is guided by our understanding of the pathophysiology. Most guidelines are based on levels IV and V evidence studies. Principles of treatment involve rapid rewarming to thaw ice and halt direct cellular damage, post thawing care to minimize progressive dermal ischemia, and active wound care to promote timely healing.12,19e21 Prehospital care involves protection of the involved part from mechanical trauma and avoidance of thawing until definitive rewarming can be performed. Thawing and refreezing result in worse injury than more prolonged freezing followed by definitive thawing.21 Prior to rewarming, comprehensive evaluation should be performed and associated hypothermia and hypovolemia should be corrected. Currently, rapid rewarming in a water bath with a mild antibacterial agent at 100.4 F to 104 F (38 Ce40 C) is recommended.22 Rewarming is continued until thawing is complete, usually for 15 to 30 minutes. Endpoint signs for rewarming are a red/ J Hand Surg Am.
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purple appearance and pliable texture of the involved part. Rewarming is accompanied by pain, sometimes intense, and adequate analgesia needs to be provided. Gentle active motion may be helpful. Hand surgeons are usually consulted on these patients after the affected parts have been thawed. For superficial injury, local wound care should be instituted. Ruptured blisters should be gently debrided. Treatment of intact blisters varies between authors and protocols. Intact blisters prevent the underlying wound from desiccating and protect it from bacterial colonization, but the blisters may impede motion. Blister fluid has been shown to contain high levels of prostaglandin F2-alpha and thromboxane A2, and removal of the blister fluid may theoretically be useful.23 Some authors, based on these theoretical grounds, suggest debriding the blisters and applying ointments containing agents that disrupt pathways to thromboxanes, such as aloe vera.5,24 Debridement should be considered if excellent wound care, including mechanical protection, gentle daily cleansing, and protection from desiccation with topical ointments and application of dressings, can be provided. Most guidelines include elevation of the extremity, orthosis fabrication and protective dressing, a nonsteroidal anti-inflammatory agent such as ibuprofen, adequate analgesia, and tetanus prophylaxis.4 No studies have shown benefit to prophylactic antibiotics. Multiple adjuvant therapies have been proposed. Low-molecular weight Dextran and anticoagulation have been of value in animal experiments but have not been shown to be of clinical value. Vasodilators Vol. 39, September 2014
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COMPLICATIONS Long-term sequelae include cold sensitivity, sensory loss, hyperhidrosis, growth plate disturbances, osteoarthritis, chronic pain, and heterotopic calcification. Long-term residual paresthesias may develop, with occasional electric shock-type sensations.5 J Hand Surg Am.
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Although treatment with tPA shows promising preliminary results, higher level of evidence studies are needed to establish its efficacy. Future studies may establish a role for early negative-pressure wound therapy, corroborate the utility of prostacyclins, and identify the benefits of other pharmacological agents such as botulinum toxin type A. In conclusion, although frostbite remains a common problem that is evaluated and treated by hand surgeons, the therapeutic approach has not substantially advanced during the last half century. Goals remain to be limiting direct damage, mitigating progressive ischemia, and optimizing local wound care. Perhaps further evaluation of the use of thrombolytic and other pharmacological therapies will lead to improved care. REFERENCES 1. Murphy WA, Nedden Dz D, Gostner P, Knapp R, Recheis W, Seidler H. The iceman: discovery and imaging. Radiology. 2003;226(3):614e629. 2. Vogel JE, Dellon AL. Frostbite injuries of the hand. Clin Plast Surg. 1989;16(3):565e576. 3. Larrey D. Memoirs of Military Surgery, and Campaigns of the French Armies, on the Rhine, in Corsica, Catalonia, Egypt, and Syria; at Boulogne, Ulm, and Austerlitz; in Saxony, Prussia, Poland, Spain, and Austria. Baltimore: University Press of Sergeant Hall; 1814. 4. Mohr WJ, Jenabzadeh K, Ahrenholz DH. Cold injury. Hand Clin. 2009;25(4):481e496. 5. McCauley R, Killyon G, Smith D, Robson M, Heggers J. Wilderness Medicine. Philadelphia: Mosby; 2007. 6. Murphy JV, Banwell PE, Roberts AH, McGrouther DA. Frostbite: pathogenesis and treatment. J Trauma. 2000;48(1):171e178. 7. Valnicek SM, Chasmar LR, Clapson JB. Frostbite in the prairies: a 12-year review. Plast Reconstr Surg. 1993;92(4):633e641. 8. Pinzur MS, Weaver FM. Is urban frostbite a psychiatric disorder? Orthopedics. 1997;20(1):43e45. 9. Dana AS, Rex IH, Samitz MH. The hunting reaction. Arch Dermatol. 1969;99(4):441e450. 10. Su CW, Lohman R, Gottlieb LJ. Frostbite of the upper extremity. Hand Clin. 2000;16(2):235e247. 11. Heggers JP, Robson MC, Manavalen K, et al. Experimental and clinical observations on frostbite. Ann Emerg Med. 1987;16(9):1056e1062. 12. Hallam MJ, Cubison T, Dheansa B, Imray C. Managing frostbite. BMJ. 2010;341:c5864. 13. Zacarian SA, Stone D, Clater M. Effects of cryogenic temperatures on microcirculation in the golden hamster cheek pouch. Cryobiology. 1970;7(1):27e39. 14. Bulkley GB. The role of oxygen free radicals in human disease processes. Surgery. 1983;94(3):407e411. 15. Mills WJ. Summary of treatment of the cold injured patient: frostbite. 1983. Alaska Med. 1993;35(1):61e66. 16. Mehta RC, Wilson MA. Frostbite injury: prediction of tissue viability with triple-phase bone scanning. Radiology. 1989;170(2): 511e514. 17. Cauchy E, Marsigny B, Allamel G, Verhellen R, Chetaille E. The value of technetium 99 scintigraphy in the prognosis of amputation in severe frostbite injuries of the extremities: a retrospective study of 92 severe frostbite injuries. J Hand Surg Am. 2000;25(5):969e978. 18. Greenwald D, Cooper B, Gottlieb L. An algorithm for early aggressive treatment of frostbite with limb salvage directed by triplephase scanning. Plast Reconstr Surg. 1998;102(4):1069e1074.
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such as reserpine are useful experimentally with slow, but not with rapid, rewarming. Sympathectomy and hyperbaric oxygen therapy both have contradictory experimental evidence, limited anecdotal evidence, and no proven clinical value.4,5,25 Administration of a prostacyclin has been reported to be efficacious.26 During the last 10 years, there has been considerable enthusiasm about the use of thrombolytic agents, such as tissue plasminogen activator (tPA).27 Twomey et al28 reported a retrospective series of 19 patients treated with tPA and anticoagulation and concluded that tPA was safe and improved their predicted outcomes. Bruen et al29 retrospectively studied 7 frostbite patients with abnormal arteriograms treated with intra-arterial tPA. They concluded the patients with deep frostbite had lower amputation rates compared with historical controls.29 Other case series and reports have also been reported.30e32 If tPA is used, most protocols suggest its administration in an intensive care unit within 24 hours of thawing. Early administration offers the potential of improved results. Contraindications for tPA use include concurrent trauma, neurological impairment, recent surgery, or hemorrhage.27 The role and efficacy of tPA remain uncertain. Superficial frostbite should heal without need for surgery. Deep frostbite may need an operative procedure, but the major question relates to timing. Immediate or early surgical care is rarely needed, except in the event of compartment syndrome or infection. Traditional guidelines emphasize allowing noninfected, dry necrotic tissue to fully mummify before debridement and closure. It may take 1 to 3 months for a clear delineation of viable tissue to become evident. This is in contradistinction to burn therapy guidelines, which advocate early debridement of deep injury. Choice of debridement or amputation level and coverage follow the normal precepts for surgical care4 (Fig. 4). One proposal for earlier treatment involves the use of triplephase bone scans to identify salvageable tissue at 1 to 2 weeks post injury.18 Patients with perfusion scans that show little or no blood pool but perfusion in bone images are treated with debridement and flap coverage of the bone and tendons, potentially limiting the extent of amputation. This protocol needs further study.
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19. McCauley RL, Hing DN, Robson MC, Heggers JP. Frostbite injuries: a rational approach based on the pathophysiology. J Trauma. 1983;23(2):143e147. 20. Grieve AW, Davis P, Dhillon S, Richards P, Hillebrandt D, Imray CH. A clinical review of the management of frostbite. J R Army Med Corps. 2011;157(1):73e78. 21. McIntosh SE, Hamonko M, Freer L, et al. Wilderness Medical Society practice guidelines for the prevention and treatment of frostbite. Wilderness Environ Med. 2011;22(2):156e166. 22. Copass M, Nemiroff M. State of Alaska Cold Injuries Guidelines. Juneau: Department of Health and Social Services, Division of Public Health; 2005. 23. Robson MC, Heggers JP. Evaluation of hand frostbite blister fluid as a clue to pathogenesis. J Hand Surg Am. 1981;6(1):43e47. 24. McCauley RL, Heggers JP, Robson MC. Frostbite. Methods to minimize tissue loss. Postgrad Med. 1990;88(8):67e68, 73e67. 25. Gross EA, Moore JC. Using thrombolytics in frostbite injury. J Emerg Trauma Shock. 2012;5(3):267e271. 26. Cauchy E, Cheguillaume B, Chetaille E. A controlled trial of a prostacyclin and rt-PA in the treatment of severe frostbite. N Engl J Med. 2011;364(2):189e190.
27. Bruen KJ, Gowski WF. Treatment of digital frostbite: current concepts. J Hand Surg Am. 2009;34(3):553e554. 28. Twomey JA, Peltier GL, Zera RT. An open-label study to evaluate the safety and efficacy of tissue plasminogen activator in treatment of severe frostbite. J Trauma. 2005;59(6):1350e1354; discussion 1354e1355. 29. Bruen KJ, Ballard JR, Morris SE, Cochran A, Edelman LS, Saffle JR. Reduction of the incidence of amputation in frostbite injury with thrombolytic therapy. Arch Surg. 2007;142(6):546e551; discussion 551e553. 30. Johnson AR, Jensen HL, Peltier G, DelaCruz E. Efficacy of intravenous tissue plasminogen activator in frostbite patients and presentation of a treatment protocol for frostbite patients. Foot Ankle Spec. 2011;4(6):344e348. 31. Saemi AM, Johnson JM, Morris CS. Treatment of bilateral hand frostbite using transcatheter arterial thrombolysis after papaverine infusion. Cardiovasc Intervent Radiol. 2009;32(6):1280e1283. 32. Sheridan RL, Goldstein MA, Stoddard FJ, Walker TG. Case records of the Massachusetts General Hospital. Case 41-2009. A 16-year-old boy with hypothermia and frostbite. N Engl J Med. 2009;361(27): 2654e2662.
JOURNAL CME QUESTIONS Frostbite of the Hand Which of the following is a clinical finding of third degree frostbite to the hand? a. Central whitish plaque with surrounding skin erythema. b. Whitish plaque with surrounding skin erythema and severe edema. c. Milky fluid-filled blister formation with underlying soft perfused skin. d. Hemorrhagic blisters over nonperfused skin with severe edema. e. Hard, woody, blue-gray, mottled insensate tissue.
Which of the following is the appropriate treatment for acute-hand frostbite injury? a. Immediate thawing on site prior to arrival to the hospital. b. Addressing hypothermia and hypovolemia followed by gradual, slow rewarming. c. Continued rewarming until a red or purple appearance and pliable skin texture is achieved. d. Rewarming in bath water and an antimicrobial agent for 5 minutes. e. Rapid rewarming with water bath of 80 to 84 F.
To take the online test and receive CME credit, go to http://www.jhandsurg.org/CME/home.
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