Frostbite

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Hand Surgery 1st Edition

2004 Lippi ncott W il l iams & Wi lki ns

62 Frostbite
Lewis H . Oster Jr. F rostbite injur y occur s when the body is exposed to cold and l ocali z ed ti ssue fr eez es (1). Ti ssue fr eez es at 28F or 2C ( 2). F r ostbi te injur y can r esul t fr om any envir onmental factor that facil i tates the tr ansfer of heat away fr om the tissues. The mor e r apidl y h eat is tr ansferr ed, the less ti me is needed to cause cell ular damage and death. F actor s that enhance the development of fr ostbite i nclude wi nd chi ll ( 3), water i mmersi on (4), hi gh al titude (5), consumpti on of alcohol or dr ugs (6,7), vascular dehydr ation (8,9), fatigue (10), inactivi ty (11), previ ous col d i njur y (12), and chemi cal agent exposure (13). Mi li tar y campaigns have pr ovided a r i ch hi stor i c per spective of col d and fr ostbite i njury that has been sustai ned by human beings. Xenophon descr i bed the sever e col d i njur i es that wer e incur r ed by Spartan sol di er s who r etr eated acr oss the Car duchian mountains after they left Al exander s ar mi es (4). Aurel ius Cor neli us Cel sus, in hi s Compendium de M edicina , pr ovi ded one of the fir st pathologi c descr iptions of frostbite (4): Col d is hurtful to an older or slender man; to his ears, hi ps, pr ivate par ts, teeth, bones, ner ves, and brai n; i t r ender s the sur face of the ski n pal e, dr y, har d, and bl ack. Ten percent of G eor ge W ashi ngtons ar my per ished duri ng the wi nter campaigns of 1778 due to exposur e to extr eme col d (14). Si mi l ar effects wer e seen in Napoleons ar my dur ing its r etr eat fr om Moscow ( 15). Trench foot was seen i n epidemi c pr opor tions thr oughout W orl d W ar I as a resul t of sol di er s who stood in r ain-fil led trenches (4,16). Amer i can soldi er s who served in W or l d W ar II and the Korean War exper i enced a new eti ology of cold injur y fr om high-al ti tude flyi ng (17). Cur rentl y, fr ostbite continues to be a common pr obl em not only in mi l itar y personnel , but al so i n the incr easing population that is invol ved i n winter outdoor recr eati onal spor ts. The i nci dence of fr ostbi te i s unknown due to a lack of documentati on i n a central regi str y.

PATHOPHYSIOLOGY Definition
There i s a spectr um of cold injur y that begi ns wi th ti ssue cool i ng or fr ostni p

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and concludes wi th tissue fr eez ing or frostbite. The mi ldest for m of cold injur y i s fr ostni p. F r ostni p i s the only rever sibl e col d i njury to ti ssue ( 2). F rostnip i s char acter iz ed by bl anching and numbness of the affected ski n. There i s no damage to the der mal or subcutaneous tissue if r ewar mi ng is ini tiated i mmediately. If r ewar mi ng is not begun pr omptl y, fr ostnip can progr ess to fr ostbi te. Chi lbl ain, or pernio , i s mor e sever e than frostni p and can occur i n nonfr eezi ng temperatur es ( 18). This condition i s a recur r ent chroni c vasculi tis that occur s on exposed extr emiti es after r epeated col d exposur e. Tr ench foot, or i mmersi on foot, r esul ts from pr ol onged exposure to wet and cold condi tions between 30 and 50F for per i ods of 4 hour s or longer (4,19). Thi s also can occur i n upper extr emi ties. Ti ssue freez i ng or fr ostbite i s the most sever e type of col d i njury ( 2). The sever ity of fr ostbite injur y i s dependent on the r ate of heat loss fr om the tissue, the ti ssue temperatur e, the i ntensi ty of the ini tial exposur e, and the length of ti me befor e adequate ci r culation can be r estor ed to the affected ar ea ( 20,21).

Classification
Several types of classifi cati on systems for fr ostbi te can be found i n the li teratur e. The tr aditi onal classificati on system descr ibes fr ostbi te i n ter ms of four differ ent degr ees (22). The z one of i njury i s descri bed as being edematous and er ythematous i n fi rst-degree injur y. Patients who i ncu r second-degr ee i njur y devel op bl i ster ing of the affected ski n and par tial thi ckness skin l oss. Thi r d-degr ee injur y patients exper ience ful l -thi ckness skin loss and skin necr osi s. F our th-degr ee col d i njur y resul ts i n necr osi s of not onl y the ski n but also the deep ti ssues, i ncludi ng bone and muscl e. The two-degree classi fi cati on i s a mor e cl i nical ly useful system that descr ibes the frostbite as super fi cial or deep ( 23). Super fi cial fr ostbi te i s i njur y to the skin and subcutaneous tissue ( 23). Ther e i s mini mal ti ssue l oss. The affected ti ssue i s suppl e when i t is depressed and pai nful after r ewar mi ng. Mi nimal to moder ate edema often devel ops after r ewar ming. Clear bli ster s and r eacti ve hyperemia cover the affected ti ssues. Patients with super fici al frostbite often experi ence a permanent hyper sensi tivi ty to col d. Deep fr ostbi te i s cold injur y that extends to the deep str uctur es of P.1086 the extremiti es (23). Injur y occur s not onl y to the ski n but al so to tendon, bone, and muscl e. The affected tissue or extr emi ty i s fi rm wh en i t i s depressed and anestheti c after rewarming. Lar ge amounts of edema often develop after r ewar mi ng the extr emi ty wi th deep fr ostbite. Hemor r hagic bli ster s cover the affected tissues, and the skin is blue-gr ay. Pati ents experi ence extensive ti ssue l oss that often r equi r es amputation of the affected extremity after an episode of deep frostbite. Patients are also at r isk for the development of gangr ene. It is often difficul t to ascertai n the extent of frostbite injur y on ini tial examination of the pati ent. S ubsequent physi cal exami nati ons ar e r equi red to deter mine the extent of i njury.

Pathogenesis
The humans ini ti al physiol ogic r esponse to cold is per ipher al vasoconstr iction (24). Thi s is a pr otecti ve neur ologi c r esponse to maintain and to pr eser ve the core temper atur e of the body. The vasoconstri cti ve r esponse i s dynamic, r ather than stati c, in natur e. The vasculature of the extr emi ties vasodi lates thr ough arter iovenous shunti ng i n an effor t to rewarm the ti ssue. This is

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known as the Hunting r esponse , and i t r epeats itself ever y 7 to 10 minutes unti l the bodys cor e temper ature begins to fall (24). W hen the cor e temperatur e fal ls, the extr emi ty vasoconstr iction becomes static. Thi s r esults in tissue cool ing, unti l freez i ng occur s at 2C. When all ti ssue is froz en, the temperatur e of the extr emity fal ls to the envi ronmental temper atur e. Tissue i njury and death are bel ieved to occur not onl y whi le the affected extr emi ty i s cool ing and fr eezi ng, but al so dur i ng r ewar mi ng ( 25). Cl ini call y, it is best advised that an extremity be l eft fr oz en r ather than r ewar med and fr oz en agai n. The fr eez e-thaw-fr eeze scenari o causes r epeated cel l injur y and is mor e detr imental to the patient. Cell death duri ng the cooli ng phase is beli eved to be a consequence of prol onged vasoconstr i cti on ( 25). The sludgi ng of bl ood that occur s dur ing vasoconstri ction in the extr emity can l ead to cel l i schemia and death. The ischemi c pr ocess tri gger s chemi call y and cell ular l y medi ated pathways that induce an i nfl ammator y response. Exampl es of chemical mediators invol ved i n the pr ocess are pr ostagl andins (26), br adykini ns (27), thr omboxane (26), and histami ne (28). Exampl es of cel l medi ators are l eukocytes ( 29) and pl atel ets (30). Cell death duri ng the freez i ng phase i s bel i eved to r esult fr om cell ul ar dehydrati on (31). Pr olonged exposur e to cold causes the extracel lul ar or inter sti tial flui d to freez e fi r st. As the water i n the inter sti tial space crystall iz es, a hyper toni c sol uti on i s cr eated i n the inter sti ti um. The i onic gradi ent that i s cr eated dr aws the water out of the cel l, thus causi ng an inter cel l ular dehydr ation to occur . This dehydrati on r esults i n cel l ular dysfunction. If exposur e to the cold conti nues, the r emai ning water wi thin the cell cr ystal li z es and fur ther i nhibi ts cell function. F inal ly, i ce cr ystal s for m wi thi n the cel l membr ane i tsel f. The r esult is loss of membr ane integr ity and cell death. Tissue death after r ewar mi ng i s bel ieved to be a consequence of a local iz ed toxi c envi r onment. Rapid r ewar mi ng of the extr emi ty causes the extr emi ty temperatur e to ri se above 2C. The resul tant endother mi c r eacti on causes the i ce cr ystal s to melt. The chemical mediator s that ar e fr oz en wi thin the i ce crystals are free to continue the i nfl ammator y response that was tri gger ed duri ng the freez i ng phase. The integr ity of the cell membr ane i s l ost dur ing fr eez ing and is dysfunctional after r ewarming. The r esultant l ocal i z ed toxic envir onment is thought to contr i bute to necr osi s of adjacent vi able tissue.

EVALUATION History
Histor y taking i s i mpor tant in assessment of the depth and degree of fr ostbi te injur y. Al l pati ents wi th fr ostbi te injur y pr esent for medi cal treatment with a histor y of exposur e to col d. The sever i ty of the fr ostbi te i njur y is propor tionate to the temper atur e and dur ation of exposure to col d. The amount of heat that is lost fr om the tissues i s a cr itical concept i n understanding why parts of the body ar e at di ffer ent level s of r i sk for fr ostbite. Extremiti es tend to be mor e at r isk for the development of frostbite. Histor y taking should i ncl ude assessment of host and envi ronmental factors to deter mi ne the pati ents degr ee of r isk of development of frostbite. Host

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medi cal ri sk factor s ar e poor gener al health, per ipher al vascular disease, diabetes, tobacco use, consumpti on of alcohol or dr ugs, al ter ation of mental status, and sensi ti vity to cold from pr evious exposur e. Envi r onmental factor s incl ude the temper atur e dur ing exposure to col d, the time of exposur e, the for ce of the wi nd or wind chil l factor , and the r elati ve humidi ty in the ai r . It is important to ascer tain whether the affected ar ea was i n contact wi th better heat conductor s than air , such as water or metal . It i s i mpor tant to ask the pati ent i f hi s or her clothing was wet dur ing exposur e to cold. Wet cl othi ng, shoes, an d other body cover ings ar e 20 times less war m than the same dr y items of clothi ng.

Physical Examination
Physi cal exami nati on of the patient with fr ostbi te i njury incl udes i nspecti on and pal pati on of the affected extr emity. Super fici al fr ostbite occur s most often on the face and r esults i n mini mal ski n and subcutaneous ti ssue l oss. The ski n may appear waxy-l ooki ng, wi th a blanchi ng or whi teni ng i n col or (32). The i njur y si te i s suppl e and painful after rewarming, with mi nimal to moder ate edema. Lar ge cl ear bl isters appear ear ly. The bl isters often extend to the ti ps of the di gi ts. In addi tion, the injur ed ti ssue exhibi ts a reactive hyperemia after thawi ng. Deep fr ostbi te occur s most commonl y i n the lower extr emi ties and causes si gnificant ti ssue loss to the deep str uctur es of bone, muscle, and tendon. It i s sli ghtly less common in the upper extr emi ti es and is r ar e P.1087 in the head and neck. The injur y si te i s fir m when it is depressed and anesthetic after r ewar mi ng, wi th pr onounced edema. The affected ski n has a blui sh-gr ay appear ance. Hemorr hagi c bl isters develop with deep fr ostbi te injur y. These bl ister s r efl ect the damage to the subder mal str uctur es that has occur r ed. It i s i mpor tant to disti ngui sh between superfi ci al and deep frostbite injur y, because the pr oper cl assi fi cati on has pr ognosti c and ther apeutic impli cati ons for tr eatment.

Imaging Studies
Var ious i magi ng techni ques have been tri ed to mor e accur atel y deter mi ne the extent and sever ity of fr ostbi te i njur y. The goal of i magi ng studies is to deter mi ne the level of demar cati on as earl y as possi bl e. Earl y identifi cati on of demar cati on facil itates pr ompt interventi on and r ecover y and avoids the pitfall of fur ther tissue l oss that i s secondary to compl i cati ons, such as infecti on and metabol ic imbal ances. Plai n r adi ographi c fil ms ar e of l ittle value i n the deter mi nati on of the sever ity of frostbite injur y. However , the val ue of pl ai n fil ms in the fr ostbi tten upper extr emi ty l ies in the abi li ty to assess concomi tant tr auma that may have occur r ed because of an anestheti c extr emi ty. R oentgenogr ams ar e also useful to determine the degr ee of i njury i n gr owth pl ates of chi ldr en after frostbite injur y. Chi ldr en with open gr owth pl ates at the ti me of fr ostbite i njury experi ence l ong-ter m gr owth di stur bances ( 33,34). Xenon 133 has been used to pr edi ct the amount of tissue l oss after frostbite injur y (35). The scan measur es the l ocal soft ti ssue bl ood flow but not bone blood fl ow. It al so has been cr iti ci z ed for i ncr easi ng i njured-tissue pr essur e. Angiogr aphy has been used to assess vascul ar changes after frostbite injur y,

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to choose pr oper therapy, and to deter mi ne the extent of amputati on that i s r equi r ed (36). However , ar teri ogr ams that ar e obtai ned soon after i njur y do not suffi ciently clar i fy level s of vi abil i ty ( 21). The addi ti on of vasodi lator pharmacol ogi c agents dur ing ear ly arter iogr aphy has been useful i n pr edicting demar cati on (36,37). Angiogr aphy is invasive and expensi ve and does not all ow for imagi ng of vessel s at the ar ter i ol ar or capi l lar y l evels. Doppl er ultr asoun d and digi tal pl ethysmography may be used to assess local bl ood fl ow after fr ostbi te (38). Neither of these techni ques i s abl e to assess mi croci rcul ati on or capil lar y function. The standard i maging study that i s used within a few days of injur y i s the technetium 99m pyr ophosphate scintigr aphy, whi ch al l ows for the eval uation of the micr ocir culation of the soft ti ssue and the bone ( 39). Many cli nici ans have used thi s i magi ng technique to determine the l evel of amputation ( 1). Bone scans at 48 hour s after admi ssion have been advocated ( 40). Nonoperati ve tr eatment is r ecommended in pati ents wi th nor mal scans. Ear ly ablation i s advocated in patients wi th absent, delayed images ( 40). The techniques of magnetic r esonance imaging and magneti c r esonance angiogr aphy (MRA ) compar e wel l to bone scan i n thei r abil i ty to di rectly image vascular i ty of cold-i njur ed ti ssue ( 41). Both i magi ng methodol ogies defi ne the extent of ti ssue i schemia wel l befor e cli nical si gns of necr osis occur . T2-wei ghted i mages i n M RA show i ncr eased si gnal i ntensi ty in cold-injur ed muscl e ti ssue ( 41). This is beli eved to repr esent disr uption of cell ular membr anes and incr eased extr acel lul ar water . It i s consider ed to be an i ndication of cel lul ar death. MRA scanning may be of l ittle use i n evaluation of di gital i njur i es because of the lack of str i ated muscle. As of 200 3, ther e is no pr ognosti c i magi ng techni que that pr edicts death at the cell ul ar level i n the i mmedi ate posti njury per iod. A delay of two or three weeks i s stil l necessar y to exceed the per i od of tr ansitor y vascular instabil ity befor e an y r adiol ogic techni que can rel i abl y distingui sh the li ne of demar cati on and the r equir ed level of dbr i dement or amputati on ( 21).

MANAGEMENT OF FROSTBITE Field Management

Ini tial tr eatment i n the fi eld focuses on the pr otecti on of the affected extr emi ty fr om mechanical tr auma and avoi dance of r ewar mi ng, until defi niti ve r ewar mi ng can be per formed ( 21). Cycli c thawi ng and cooli ng or inadequate r ewar mi ng can wor sen a fr ostbite i njury ( 25). The extr emi ty is placed in a wel l -padded spl i nt i n a functional posi tion for protecti on. The pati ents over al l condition should be assessed, and a compl ete histor y and physi cal should be per formed.

Hospital Care
Nonoperative Intervention
The measur ement of core body temper atur e on pati ent ar r ival to the hospital is imperati ve (42). Tr eatment of r ewar mi ng of the affected extremity shoul d not commence until the cor e body temper ature r ises above 35C. At thi s temperatur e, per ipher al vascular vessel beds r eopen. The r esul t i s an infl ux

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of cold blood to the cor e body that can cause a par adoxic decr ease i n body temperatur e. Rapi d r ewar mi ng of the extr emi ty i s super ior to slow thawi ng of the extremity, because i t decr eases ti ssue necr osis and the over all peri od of fr eez ing (43). The i deal temper atur e at whi ch the col d-i njured par t should be r ewar med is between 40 and 42C (44 ). Rewarming of the affected extr emi ty i s best accompli shed i n a hydr other apy tub (i .e., a Hubbar d tank), whi ch i s commonly found in physical ther apy or burn uni ts. It i s i mpor tant to stay wi thin this narr ow temper atur e range for two r easons. F ir st, r ewar ming at a lower temperatur e l eads to gr eater thawi ng time and i s l ess benefi cial to ti ssue survi val. Second, rewar ming at hi gher temper atur es coul d compound the ti ssue i njur y by r esulti ng i n a bur n i njury to the affected area. P.1088 Rewar mi ng shoul d be conti nued for 15 to 30 mi nutes or until thawing is complete. W arming should be completed when a red or pur ple appear ance and pli able textur e of the affected extr emity occur . Thi s means the end of vasoconstri ction in the i njur ed extr emi ty. Acti ve motion duri ng rewar ming is helpful, but massage i s not recommended. The patients i nitial tr eatment shoul d i nclude anti tetanus prophyl axis, 600 mg of penici ll i n by intr avenous admi nistr ati on ever y 6 hour s for 2 to 3 days, and 400 mg of ibupr ofen by mouth ever y 6 hour s ( 45). Pain management should be accompl ished by usi ng opi ates that are appr opr i ate to the case. F r ostbi te injur y i tsel f usual ly does not demand i ntr avenous fl uid resuscitation. Intr avenous flui d may be r equir ed to tr eat associated condi ti ons, such as dehydrati on and, occasional ly, r habdomyol ysis, whi ch resul ts in possibl e r enal fai lur e. A ll or gan systems shoul d be moni tored and tr eated i n accordance wi th the i ndivi duals gener al medi cal condi tion.

Operative Intervention
It is difficul t to determine vi abl e fr om nonviabl e ti ssue in the ear l y stages of super fici al and deep frostbite injur y. The onl y absol ute indi cati on for ear l y dbri dement i s u ncontr oll able infection (2). W hi te or cl ear bli ster s suggest super fici al frostbite injur y and requi r e dbr idi ng to pr event fur ther contact wi th the hi gh l evels of pr ostagl andi ns and thr omboxane i n the bli ster exudates (26). The bli sters are unr oofed, and topi cal aloe vera is appli ed to the affected ar ea (45). Al oe ver a has been shown to be an effecti ve thr omboxane inhi bi tor and r esults i n less ti ssue loss when i t i s added to the protocol that i s outli ned her e (46). H emor rhagi c bl ister s ar e r epr esentative of str uctural i njury to the der mal plexus (21). Ther e is contr over sy over whether to dr ain or dbr i de these bl isters ( 46). Wound car e incl udes wr appi ng the affected extr emity in ster i le dr essi ngs and spl i nti ng the extr emi ty i n a functional posi tion. F i nger s should be spl inted in th e i ntr i nsic pl us posi tion to prevent late defor mi ti es that ar e secondar y to intr insi c muscl e contractur e. Mummifi cati on and black eschar occur at approxi mately 3 to 6 weeks posti njur y (17). Amputati on i s gener al ly defer r ed for 6 to 8 weeks. At thi s ti me, the affected extremity often appear s to be autoamputating , and a cl ear li ne of demar cati on occur s. The adage fr eez e i n Januar y, amputate i n Jul y i s often used because of the ti me that it takes for cl ear demar cation ( 47). Amputati on that is perfor med at the time of mummificati on i s usuall y done i n the oper ati ng r oom, ini tial ly wi thout the use of a tourni quet. The l ack of

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tour ni quet enables the sur geon to deter mi ne the level of vi able tissue dur i ng surger y. Ti ssue i s r emoved to the extent that the tissue edges exhibi t capi l lar y bl eeding or when vi able muscle contr action is obser ved, or both. The key to success i s to r emember that amputation l evel s shoul d be conser vative, because any r emai ni ng hyper emi c tissues tend to heal qui ckl y ( 42). Ski n grafts, local fl aps, and free tissue tr ansfer s have been used for wound cover age and i n an effor t to pr eser ve extr emity function.

Adjunctive Therapies
A number of adjuncti ve ther apies have been studi ed i n an attempt to r educe the amount of cell ular ischemi a that i s seen in frostbite. One focus to l imit ischemi a i s by pr eventi ng thr ombosis. Weatherl y-Whi te et al . ( 48) r eported that ti ssue l oss was reduced compared to control rabbi ts after the admi nistrati on of dextr an. Anticoagulati on wi th hepar in and dextr an has been suggested as a method to improve tissue per fusi on and sur vival ( 48,49 and 50). Investi gati ve studies that have used anti coagul ants have thus far been i nconcl usive in their infl uence on the degree of tissue loss ( 51). Injection of vasodil ator s has been used as a method to impr ove ti ssue vascul ar supply (52,53). The use of many differ ent vasodi lators in combinati on wi th anti coagul ants has fail ed to exhibi t i mpr oved tissue survi val compar ed to r api d r ewar mi ng al one. Studi es continue to demonstr ate that thr ombolysi s i s a key el ement i n the r ecogni ti on of the pr ogressi on of fr ostbi te i njur y. The use of thr ombol yti c agents, such as streptokinase, ti ssue plasminogen factor, and ur okinase, has been i nvesti gated and suggests a benefi cial r ol e i n fr ostbi te treatment ( 54,55 and 56). Sur gical sympathectomy has been used as a method to tr eat frostbite. Ther e is evidence that edema pai n r esoluti on, r etur n of sensati on, demar cati on, and heali ng of ulcer s occur s mor e rapi dly after sur gi cal sympathectomy ( 57,58 and 59). However , i t has not been shown that sympathectomy decr eases the amount of ti ssue l oss after fr ostbi te i njur y. Hyperbar i c oxygen ther apys rol e in th e tr eatment of frostbite remains unclear . It i s a theor etical ly attr acti ve modali ty because of i ts abi li ty to deli ver i ncr eased di ssolved oxygen to the pl asma and ti ssues (60,61). Hyperbar i c oxygen ther apy has been associated with accel erati on of capi ll ary for mati on (62) and i mpr oved whi te cell function ( 63). However , its cl i nical effi cacy remains in confl i ct, but no del eter i ous effect has been r epor ted in the tr eatment of fr ostbi te (21).

ALGORITHM FOR TREATMENT

The author s prefer red treatment protocol is pr esented in Table 1 .

COMPLICATIONS OF FROSTBITE
Earl y common compli cati ons of fr ostbi te i njur y ar e i nfection and gangr ene. F requent late sequel ae after fr ostbite ar e P.1089 r esi dual pain and col d intoler ance of the affected site (17). Less common

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compli cati ons i nclude hyper hidr osis, pi gment changes, and ski n atr ophy ( 64). Local iz ed osteopor osis and pr onounced subchondral bon e l oss have been r epor ted as earl y as 4 weeks posti njury and as l ate as sever al months l ater (65). Physeal i njury wi th subsequent gr owth di stur bance has been observed in chil dr en (33,34,66,67). Long-ter m compl ications that invol ve joints and soft ti ssue i njur y resul t i n a defor mi ng joi nt contr acture and, occasional ly, spontaneous fusi on. These may occur as l ate as 16 mon ths after the ini ti al insul ts.

TA BLE 1. A UTHO RS PRE FERRED TREA TMENT PRO TOCOL FOR FR OSTBITE

Rapidl y r ewar m extremity in whi rl pool bath. Temper atur e: 4042C, 104108F . Dur ati on: 1530 mi n or until thawed. Repeat whi rl pool dai ly. Initiate pain management ther apy. Bl isters. Clear : Dbr i de. Dar k: Leave i ntact. Cultur e wounds, then apply aloe ver a, ster i le dressi ng, and a spli nt in a functional posi ti on, and elevate. Tetanus pr ophyl axis. Ibupr ofen, 400 mg by mou th every 12 h. Penici ll in G , 500,000 U by i .v. admini stration q6h for 3 d. No tobacco pr oducts. If at al ti tude, dail y hyper bar ic oxygen therapy. 1 h q6h for 3 d. Dbr ide or amputate, if the necr oti c ar ea becomes infected. Otherwise, obser ve for a defi niti ve margi n of demar cati on.

Adapted from M cCaul ey RL, Hing DN, Robson MC, et al. F rostbite injur ies: a r ational appr oach based on the pathophysiol ogy. J Tr auma 1983;23:143147.

REFERENCES
1. Su CW , Lohman R, G ottli eb LJ. F r ostbi te of the upper extr emity. Hand Clin 2000;16:235247 .

2. Vogel JE, Dell on AL. F rostbite injur ies of the hand. Clin Plast S urg 1989;16;565576.

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