Frostbite - Northwestern Universitysites.surgery.northwestern.edu/reading/Documents/curriculum/Box 0… · _ ~..frostbite, but recent advances in our understand." jng of the pathophysiology

Frostbite

Frederick M. Schiavone, MD.."Harold H.~ OsbOrn, MD

Series Editor:’. Harold H. Osbom, MD-.~,~ ~!U : ~ , - .

~Controversy has existed over the treatment of.. _ ~..frostbite, but recent advances in our understand." jng of the pathophysiology of frostbite have led to

~..~treatment protocols that may limit tissue damage.

.A 49-ye~-old man was brought to the h0spit~ emergen-

~ dep~m~nt on a cold day in J~u~ with a sensation; ~ of ’,’both hands frozen solid’.’ He had been found lying~ Jn a snow drift by an Emergen~ Medic~ Se~ice ~MS),_u~t~ On admission he was leth~gic but arousabl~ with

alcohol on his breath. He s~d he had been drinking:~.,::~hea~ly after,~ork at aloc~ b~.before.hea~ng for home.:,;: and did not remember¯ f~ling nor an~hing of the ~ght~~~.~haf~.had bdssed before ~h~ arrival of the EMS U~t.

~ physical ¯Examination~:The padcnt.;was a heavy smoker and intravenous drug~ abuser with,a histo~ of.upper extremity phlebitis. His

¯ i¯. i,~i~al~igns inChided a rectal temperature of 92 °F; bloodmm Hg; pulse rate, 72 beats per minute .separated with cotton. ~::~i~.: ~"~.- ~:-~:~- ~ ~..~ :::-~,-, ~.

per minute. His.head, ,.6~:~,~he p~tienLwas admitted to the surgical service and~ of his nose was a reddish blue. treated aggressively in the physiotherapy department

..,,~he lungs w~re blear, and heart sounds were regular with-/~ff~Ui~ or g’ali0piTh~ abdomen¯was Soft and no abnor-

~ii~i~ 6~ masses were n~ted. Examination of theiex~emities revealed that both hands were swollen, with.a bluish discoloration extending from the fingertips tothe midmetacarpal area, involving all digits. The range

of motion was diminished. The skin of both hands was......... ,. hard to the touch and sensation

. ~as markedly diminished overthe ventral and dorsal surfaces

?; Dr Schlavone is Chief Resident of!i: Ern~rgency Medicine, LinColn Medi-:i:iCaJ_,and ~ien~al Health Center;, and~ ~. Dr Osborn Is Director of the Depart-~ me~t of EmergencY Medicine, Our

Lady of Mercy Hospital, Bronx, NewYork. - " ~

Dr Osborn

bilaterally. The third through fifth toes of the right fool:were discolored a reddish purple but sensation was pre-.served. Pulses in all extremities were present and equalbut there was poor capillary refill in both hands.

The patient’s ECG and chest x-ray film were withinnormal limits. A complete blood count and chemistryprofile were also normal, except for blood alcohol level,which was elevated at 347 mg/dL. ¯ ¯. -

: The patient was treated initially by passive rewarmingwith blankets. Intravenous naloxone (2 mg), 50% dex-trose (50 mL), and intramuscular thiamine (100 mg) administered. His extremities were immersed in warmwater baths at 106 °to 108 °F. As rewarming proceeded,blisters filled with hemorrhagic fluid were noted on thedorsal~surface of both hands, the skin color becameredder, and blood began to ooze from multiple abrasions.(Figl). ¯ : ......... . ,... -

The patient was then given tetanus toxoid. After re-warming, the extremities .were:dried and the digits

with poyidone whirlpool baths...At nine.days the toeswere dis~olgr~d but looked Viable (Fig.2)..Th~ hands,however, were more severely affected; dry gangrene haddeveloped in several digits (Fig 3). By. one month, thismummification process involved all digits ¯(Fig 4).

At three months, the toes were almost totally healed,but the hands were not, and the patient underwent am-putation and flap reconstruction (Figs 5 and 6).

This case reveals the serious and often tragic conse-quences of cold injuries. It also raises questions about.the pathophysiology of cold injuries, their treatment,and their prevention.. ,.- -¯~. ~ -.,

Cold Injuries .....Frostbite is part of a continuum of damage to local tis-sue that occurs as a result of exposure to cold. Localizedcold injury is divided into the clinical syndromes of

continued on page 25

16 HOSPITAL PHYSICIAN JANUARY 1988

Frostbite

Fi~:~i~ App~aran~e"on present~-tiom discoloration:of hands withhbmmorhagic bu!lae a nd edema.

Fig 2. Eschar form~;~i~)n~on viable Fig 3. Dry gangrene~nd mu~mmif!.toes. - ..... cation of all digits,

Fig 4. Advanced mummification. -:~.;=:~-:~ ~.;;. ~.~ ~.-;-;..!..~.:’y;" (....",~’~ :" ’ ¯ ::C*

continued from page 16 : .... ... ~ ;,,’’~. -

frgs~.nlp,.c~i!blal.n, t.ren.ch f°ot, and fros.tbite~(Table 1)._, Frostnip is the mildest form of cold injury. It mustbe distinguished from"frostbite because it is the only

Fig 5.Complete healing of toes .... -.. Fig 6. :Amputation and flap recon-_ . : ....... struction of both hands..,.’....~ ~ -

":. " : : . ~~: . . .-- "!, ?~ -’~’; ’.-:- i

swollen, blue e~i~emi.ties, accohil~ini~.b~ decreased~pul~es and loss_:9[ sqnsati0~n. With. further_., cold, andtherefore further vasoconstriction, tissue anoxiaoccurs,

immediately reversible injury. Frostnip is a simple blanch- with damage to the small vessels, nerves, and endothelialing and numbness Of the skin and involves nofurther ~:ei~.lls,resulting iffincreilsed vascular permeability and.d ~ .arnage t0.~c~tan.e,pus.P~,~{li0cutaneo.hs tiss.ue provided -edema.. .... .i ..,i~i :.. ~-"~/-!~ ,. .....:..., .~-;’~ii-!:i; - !i~!.i:i:ii~il’~

that,~ew_a~ing is effected. This mild inj " i"~:’Th~ is~hem~~i~~~ :that~fdll~wsre~i~i:ilig involves

~h~ ~0re serious" " ~¢hich the"~e~omes

injury seen in ~ com-

~s a recurrentceou~ ~iisedles~onslesions occur after ~epeate~l. 6xposure to Cold, dry,.non- :~u i ......fr~.ing: Weathe~’! It :~n~monly affe~t~yoiing :iirid ~ ,ha~ beefi r~w~d~~it is diffi-m;a~l~ ~~ ~d~n~’~i~ PatientS With R~aud’s ~he2" ~ fe~t~ 0f tren~h’/~;i frbm thos~

mac’roglob~lSne2’ 0f.ffbstbi~e.--~ .:,~::-,~:: . ? .. - ~ : :::[~;i;:~::?.~.-[ : ?- : ~mia; ~Yring6myelia;:arid Possibly chronic ~yelomono- ’. :~ ;~0d~~Y, the f~ phase of trench foot; iS ch~aeter-~ie ie,:,~e~ia 2 seem ~6 be uredis~osed t0 this ~ondifion ~’3~ed b~d6ereasing edema ’and the return :bf ’~srmal

T~Ch foSt, ~lso known as emersion foot, is another palse~ Trench fo6t may have significant s~quelae. Hotserious nonfreezing cold injury. It is usually not seen - skin, depigmenmtioa, h~ersensitMtyto Cold, p~n witham6ng civilianS, but has been studied extensively by the : ffd~htb~in~; and h~er~drosis may p~rs~stfo~ ye~s.milita~. Trench foot ~esaitS from prolonged (m0re than . ’~ :uaiik~:f;o~t~p; Chilb]~n~ and trench fo&~froStbitei2 hb~Urs) exposuke ~o ~e~; c0id 6onditioh~a~ ~empera .... . is a~ injd~ t~a~ resuit~ ~ro~.exposure tdfrbezihg tem-

T[enCh fs3t develoP; ifi t~eePfiases. The iNtiN phase and ~d~i. ~h~ ~it~fit ana ;&v~ii~y 0finja~a~edire~tlyconsists 0f ischemia wi~h vasospasm, resulting in cold, related t0 t~erate0f heat loss, tissue tempeSature, the

JANUARY 1988 HOSPITAL PHYSICIAN 25

Frostbite

intensity of the initial exposure, and the length of time edema, with discoloration from blue to dark gr~y, fol~

before adequate circulation can be restored, lowed by the formation of violaceous or hemorrhagic

The traditional classification of frostbite into first, blisters. These blisters, after turning black, slough off.

second, third, and fourth de~rees of severity has now Part Of an e~remit3/’or e~/~)i~.~nti~gfi~ger.0rlt0~imay

been replaced by a simpler and more realistic classifica- belost. The underlyingskinieft behind is extremely:thin,

¯ tion into superficial and deep injuries." red, and sensitive to cold. In the"c~se discussedabe"e,

.... the finding of hemorrhagic blisters soon after presenta-

Superficial Frostbite .... : ’ tion to the emergency department indicates a thermal

Superficial frostbite involves only the skinand the tis-- injury of some duration involving the deeper tissue.

sues immediately underneath. Although the- skin When the patient is not seen by a physician Until the

appears waxy before it has been thawed, it remains soft extremity has thawed on its own (as is common in our

and resilient below the surface when depressed gently own patient population), the above signs may not be

and firmly. After rewarming, the area becomes numb, present, and classification of the injury. . is very difficult.blue, and mottled, with marked edema. It is painful for .

some time, especially during the rewarming period. Risk Factors

Clear fluid-filled blisters may form. If left untreated they F, rostbite tends to occur in persons in poor general health

eventually dry up and become blackened and hard. As and is less likely to be experienced by a healthy person

the edema decreases, these black, hardened plaques peel who is adequately clothed. Malnourished individuals

off, revealing a red, tender, cold-sensitive skim ....... are at increased risk for severe frostbite injuries.

- .... ’~ ..... .: ii :: ".~ ,. Acclimatization and geographic origin appeal to be

Deep Frostbite " ::’i!i’.:~ :iinportant factors influencing frostbite injury. Studies

Deep frostbite is far more severe, with damage extending have shown that soldiers from the southern regions of

to the deep structures. The injury in its frozen state t]~e United States are more susceptible to frostbite than

appears hard, solid, and blanched and cannot be de- those from Colder regions, whereas natives of the Arctic

pressed with firm pressure. The patient has no sensation slhow a particularly high resistance to cold.

in the frostbitten area and may describe the affected Acclimatization has occurred inas little as six Weeks

extremity as feeling like "a block of wbod." Afterrapid .after exposure to arctic conditiOning:The proteCtiv’~~ffect

rewarming, the extremity develops severe arid pfol0~d.0.f c01d addlim~/ti~ifi0nmhy res6K frorri efih~inced ~aso-

26 HOSPITAL PHYSICIAN JANUARY 1988

control and increased ability to augment heat

i. :Studies’ from Korea repo~ted a higher incidence of

frosl on soldiers than among white sol-i’hin6iig soldiefsifi Ala~ka~ry:and vascular reslSonses

to Cold of blacks differed significantly from those ofwhites.The "hunting (capillary shunt) response" (see

¯ below) is less pronounced in blacks; this suggests a physi-ologic basis for the increased incidence of cold injury

" i;The~orean and Alaskan~ s~udies also found an in-ilc~eased incidence Of cold injury in soldiers who hadexperienced previous injury from cold. After a.cold

tures of 20 °F (- 7 °C) or lower after several hours’ expo-sure and when deeper tissue temperature reaches 50 °F(10 °C). Ambient temperatures may be adversely affectedby w!nd. Increases in wind velocity promote faster cool-

ing of tissue. An ambient temperature of 20 °F combined-with the"wind chili" from a 45 mph wind results in an"equivalent chili temperature" of - 40 °F with a 2 rnphbreeze.5 Dil-ect contact with cold metal or wetnessgreatly increases heat loss and cools tissue morerapidly.5 " .

Once vasoconstriction occurs, the limb temperaturefails sharpl3: When the freezing point of deep tissue-28 °F (~-2 °C)~is reached, ice crystals form in the limbin an exothermic process. The temperature plateaus untilinjury the affected area often has an exquisite sensitivity crystallization is complete; the limb temperature then

to C01d that/naypersist indefinitely. This condition may fails, again~

.......... be’alteredb3~°~her~urgical ormedical sympathectomy. ".:" Ice crystallization in frostbite occurs extracellularlyv.The statusbfperipheral circulation plays an impor-, -in the interstitium, creating a hypertonic state within th~

:. ta~t reiein determining the ~everity of frostbite injury¯interst~itium. Water is drawn oat of the cells; producing":~ : In ihe p~esence of preexisting arterial disease and localintracellular dehydration. Increased electrolyte concen--.’tissue hypoxia, frostbite Will occur at higher, tempera-,trati0n leads to ~ell death.~ Free Water causes the ices and may be unusually:~tensive; Hypoxia Sec-crystals t~ grow. The crystals, in turn, cause further cellondary to expesure to high altitudes can be a major

. :destrdction by extrinsic pressure on blood vessels, espe-.... c6ntributingfac~or, as Was Se~nin the severe casals :of~cially capillaries, .’creating severe tissue hypoxia andfrostbite among World War lI aerial combatants andedema. With rewarming, this process may be wholly orin mountain climbers., Cigarette smoking, anemia,~and

--Partially reVer~ed. As the ice crystals melt (an ~n"d0-hemoi’rhage ,alseincrease frostbk~ severity.i.~:~%~:i~!i~ , ~

;’:thetmid pr6C~S~);~the limb temperature again plateaus"~Other faCto~:g(~dritribfitin:’gto th~iiiddence and ~6~,~ri::neal freeZing i30int Until the crystals have disappeared,t3/~of coldinjtirY:.arethe patient’Smemal status, body’:afterwhich"the limb temperatUre steadily rises.type, bmofiofial-state, and personal hygiene.: Many of

Rapid rewarming limits the time the limb remains at’the~e facto~s~ir~difficult to evdiuate and control.~Acuteor below the freezing point. Until limb hypothermia isand chronic alcoh01ism,- ~pil~p~yi:~0ma, unconsci0us~revbrsed, vasbSpasm and is~hemia are maintained.Afte~nesg:.from ~lut0in0bile a

~psychosis(:excessive rewarmlng, becorri~ hypererrii~.Rewarmed

;jncre~ised .. .........~ay occur secondary

intravenoUs -cold ~ produces vasoconstriction and vaso-

"quick~freeze" zone~ wherethe blo6d beComes"vlscous and slows the capillary circula-

~-.~.~ ,~.~ ~" tion.~:Once the blood in the capillaries is Chilled to the~’: :::: :"~’ point of inactivity, arterial blood bypasses these Capil-

Patho~hy$iology..,~,:,,~::ii:iiiil,.. ..,t.,:,~:,,~ .......laries Via arteriole-venule shunts. This mechanism,Until reCently,~he me~/~anism of CeIliJlar injury in frost2known as the "hunting response" or capillary shunt, isbite was both Controversiai and l~oerly unde~sto0d.~Inan effort by/he bedy to warm the local tissue area butthe PaSt, frostbite:injUr~C~W~ ~believed-to :h.h~/e beerlnourishment and oxygen are lacking. These shunts arecaused by one6f t~6 meehanisin~ either direct freezingn6t ~bhtinuously Closed bu "and crystal!~zat,.i0n.of tissue or inadeqtiatetissUe perfu-Can~ino~th" .:..:,_.= . ,

.t start and stop ~ cycles,¯ ’ i i. ! i !i.i~ -:- .... *, ~--; ~"u~tagerea area to warm and chill in surges.s~on secondary to va~cul~r’~pasm;:increased blood Vis= If thiS"0ycl,~:c0ntinues be o " ,cositY, and microthro~b ~ F~Stbiteiniii~; ~;,,~,; i~~-±~: ..... :~,~: ;. ~, ,~ ; !y ~d the body s capabilit to¯ ~ ..... :..~ ~y~,: ~."y~, ~a~..malntaana normal~ore tern " .... Yto involve an lmmedlat ~. h , ....... :" ,: ? :-;:~ ’ ,~, :~-~ ,~ perature, these Shunts c...... p ase caused ~ce c ...................... . ¯ , lose.... ,, , ............ -~,, ,.,: ........... ..........., ...........bY ~ ..... ryst,d and ahowt,he extrem~t . ..........formatiOnatthetl~e0f heifiiur~,ch~idado~o,;.~.l.~.,~ -: ;"’ ; .... ~ Yt°freeze~therebysacnficm an

........ ~.’ ~--. Y ~: ,~; ,. 7~,~S~’.V~7~ extremity :rather than ricaused by progressive, de’,mal ~schem~a and tisSUd10~S.~org~iiigm~7 , sk the death of the whol.e

:Frostbitem0st comm0nlyoccurs tttambien.t temi~ra-, : After a severe cold injury orafter repeated freeze-

JANUARY 1988 HOSPITAL PHYSICIAN

Frostbite

thaw-freeze cycles, a progressive or delayed thromboticphase occurs. This phase results from persistent tissueischemia very Similar to the ischemia encountered fol-lowing a thermal burn.. Robson and Heggers were the

.~f’n?st to show that the mechanism of p~ogressiv.e ischemia.in burn and frostbite injuries :was due to.the same:-inflammatory mediators.S,9 Evaluating the fluid in:frostbite blisters, they discovered similar levels ofprostaglandins and prostanoids. The prostanoids theyencountered (specifically thromboxane A:) have.vaso-constrictive, platelet aggregating, and leukocyte-adhe_sive properties. These properties lead to microthrombusformation, ischemia, and edema following thermal

~ ~:._Following elucidation of the role of prostaglandinsm dermal microcirculation,gqz the next step.~ .w.as the use

~ of antiprostaglandin agents t6 preserve injured tissue.Using thromboxane inhibitors, investigators have beenable to preserve dermal microcirculation following burnand frostbite .... n ~3

.:;.~ A10e vera (Dermaide Aloe) is an effec~i-~,~ iocal inhibi-tor of thromboxane in experimental animals.~ Treatingfrostbite with a Combination of aloe vera locally and

systemic.antiprostaglandin agents has been shown tosignificantly reduce, tissue loss, amputation rate, andhospital stay in affected patients.4 The discovery that~.prostanoids, especially thromboxane A~,-mayplay animp0~tar~ ibie iri ~hbprdgressive.da~ge seen infrost-

"bite injtlr~has creat~d ~he ~asis for-a new approach to

instructed

will.

AS

choicemd thedamag-

9ite in the fleld must be

wil!pr0duce

not

costs~ -If ..Permanent..... e, r~0 ’ attempt should be m~,e to

28 HOSPITAL PHYSICIAN JANUARY 1988

warm the frozen extremity until the patient arrives atthe hospital.

Once definitive health care is available, the frozen partmust immediately be warmed in a water bath at 104 °F(40 ?C) to 108 OF (42 °C) for 15 to 30 minutes. The t.ainer should be large enough to permit complete emer-s~on of the frozen extremity and to keep it from contactwith the container’s sides. A heated whirlpool bath isideal.

After rapid rewarming, the patient must be hospital-:[zed and the injured extremities protected from any con-tact. A protective cradle should be used and theextremity should be elevated. Cotton should be placedbetween the digits or toes., Although traditionally all blisters and bullae were left

imact, recent analysis of frostbite blister fluid suggestsa new approach. It is now recommended that clear blis-ters be debrided and hemorrhagic blisters left intact,since blisters filled with clear fluid contain the injuri-oas prostaglandins, whereas hemorrhagic blisters reflectalready established structural damage to the subdermalplexus. Hemorrhagic blisters are left untouched to

.prevent further damage to this microvascular networkand minimize loss of surrounding viable tissue. Apply-ing aloe vera to hemorrhagic blisters and covering them.with loose gauze is also recommended.4

[buprofen has been used as a systemic prostaglandininhibitor because, in contrast to other agents, it is veryactive against.thromboxane without permanently inhib-itirtg all prostaglandin synthesis (Clip & Carry).~

A~mcal trials of heparin, oral anticoagulants, and lowmolecular.., weight dextran (all of.which have been usedm o prevent ..... vascular sludging,.intravascular

and dermal show

not~gents is

great .deal of attention ,was paid to thesurgical sympathectomy in cold injuries. Some

evidence suggests that this technique speeds healing andpromotes earlier demarcation when .used as an acute

treatment of frostbite. However, there is no evidence thatsurgical sympathectomy preserves tissue, and it is nolonger advised in the early management of frostbiteinjuries. Many authors believe that this technique may

patient feel better but .be useful in treating/ate sequelae, and it has p?oved help-part. The use .of;~cohol out- ful in reducing Postfrostbite pain, hyperhidrosis, and.°uld, be..’strongly ....discouraged. cold sensitivity. Reversible sympathectomy has also been

eri0uslyim¯ Medical ~’s

etheb e regional in~rY~’t~" enefits of surgical Sympa!

Of two to four weeks, with lessadverse effects.~5.~ ~

Vasodilatorydrugs have given generally poo~ results.

continued

(32 ° to 37 °C) twice daily is sufficient to prevent deepinfections. It is agreed’tha~once infection becomesapparent, prompt treatment with appropriate antibiotics

:~~~e ~f ~algesi~S is recommended, since it hasbeen shown that rewarming can be quite painful, andthe pain may continue for some time afterwards.

Surgical debridement or amputation should be de-layed until either spontaneous amputation occurs orthere is absolutely no question about the viabilky of theunderlying tissue. (The adage, "always wait before youamputate," should be remembered.) The appearance ofwet gangrene signifying infection is a definite indicationfor surgical debridement or amputation. The treatmentof hypothermia when accompanied by frostbite always

,takes precedence, and another adage, "first life, thenlimb,’,, must not be forgotten.

Late sequelae of FrostbiteLate seqiielae of frostbite appear fairly frequently, al-though there are relatively few reported series document-ing Sequelae. ina series byErvasti of 812 cases of frost-bite Studied five to 18 Years after the injury, the mostcommoiilsymptoms were cold sensitivity (82%), ~olorchanges of the skin (73%), hyperhidrosis (59%)~ pain with the use of extremities. Other fairly common~signs or symp~t0haS W~re fi~perkeratosis, ulcerations,.hyi~er~th~ia;pain ht ~e~~, b0n~, Changes~ skin a~rophy,transitory edema, and nail-bed changes.

Fro-~tbi~injuries in child~eh ’ffiay cause damag~ toepiph}Seal grbwth¯plate~, with resultant bone growthabnormdlitie~.: Ini~ither Children 0~ ~tdult~s these bony~hbn~ifie~~ ii~ay 6ause arthritismbiiths or years after

other techniques that have been used with some suc-cess.2° However, their long-term benefits are uncertain.

Prevention _Frostbite prevention can be maximized by controllingany or all of the risk factors that have been mentioned.The best general insurance against frostbite is overallphysical well-being, appropriate attire for weatherconditions, avoidance of alcohol and cigarettes, and ahealthy diet. []

References1. Jacot~ JR, .Weisman MH, Rosenblatt SI, et al: Chronic pernio:A hi’storical perspective of cold induced vascular disease. ArchIntern Med 1986;146(8):1589-1592.2. Kelly JW, Dowling JP: Pernio--A possible association withchronic myelomonocytic leukemia. Arch Dermato11985;121(8):104,~-1052.3. Meehan JP Jr: Individual and racial variations in a vascularresponse to cold stimulus. Milit Meal 1955;116:330-334.4. McCauley RL, Hing DN, Martin RC, Heggers JP: Frostbiteinjuries: A rational approach based on the pathophysiology.J Trauma 1983;23:143-147. - ....5. Bangs CC, Boswick JA, Murray PH, et al: When Your patientsuffers frostbite. Patient Care 1977;February:132-157.6. Weatherly-White RC, Sjostrom JB, Paten BC: Expei’imentalstu<;lies in cold injury: The pathogenesis of frostbite. J SurgRes 1964;4:17-22: ... ~. ._..7. Washburn B: Frostbite: What it is--How to prevent it--Emer-gency treatment. N Engl J Med 1962;266 974 . ’..."i~ . .8. Robson MC, De Beccaro EJI Heggers J P: The ~:~f~’~t0f ~i’os-taglandins on the dermal microcirculation after bUrning andthe ~hibition of the effect by specific pharmacologic agents.Plas;~ Reconstr.Surg 1979;6~3:781-787................9. Robson MC, Heggers JP: Evaluation 0~l~ndfros:tbite blisterfluid as a clue to pathogenesis)J Hand,Surg 1981;6:43-47.~10. Robson MC, DelBeccaro E J, Heggers JP, et al: Increas ngdermal perfusion after burhing by decreasing tli~0mb0xane

the ~ini~i~i .... ~.11. Massiha H, Monafo WW: Dermal ischemia in thermal injury:::-~-~ :. :’ :.i-~!,~ .i~-!~.~i, : ..... The importance of venous occl us on.JTraumal974705-711............. ¯ : ~.;,:-=-, ....... :, .... - =:.12. Raine

~.Trl ~iJ :!;?~ ’~ ~-~ (~: " ~_ :~ ~: .... -: ,-:in the g~[h~a’pig fofio~ng~lding’The vas0ff~astic ~omponent o~fr~stbke cab Persis~ a~d .. ~3. D,,IBeccaroEJ, aobsfn MC, Hegge~s JR et ~l:X~~e of’~a~~~ie f~r lat~ ~~q~lae. Th~g~ ~ffec~s may . s~ecific~hrdmbo~ane in, bito~t0 presage thede?~h m cr0-be reliO~d ~Y s~gical s~p~thectomy. HoWever, the ’circul~fif~a~t~?both~ng:su~gery1980;87:1372~4~’.’’~,:~ ~:,~..:.., ¯pare~th~sias-.’th~ resuk fr0m~ the ~Our0pathy seen in ~4:C~,m LM, H~gg~rs JP, Robson MC, etal:.The the=peutie

efficacy of a(oe.vem in thermal injuries: Two case repoffs. "frostbite.ar~wOr~n~d b~’ ~pathe~tfmy. Am A.~im~ HO~AS~OC ~980;16:768S772.Additional studies supp0~ the long:t~rm benefits 0f 15.Po~r9 M, Wesohe DH, Rosche J, et al: Intraa~e~iai’sy~pa-

sympathectomy. Correction of persistent vasospasmlessens the cold ~ensitivity and chronic hyperhidrosisand protects against repeated cold stimuli.

Classic conditioning (ie, altering the sympathetic ner-vous System:using ~he conditioning tecian-lque) can en-hanc~ the"vasculilr re’sPonse ~nd pro~Ki~ aii effe6five

t,~e~!m~nt, bf Co!d, Sensitivity in Ra~niaud’s ~en0nag ~eil as in frbstbite. This p~o~edur~"~ ~n~~tte~n~ti~eto the phafma~61ogic or surgic~l i:nafidgem~nt-ofvasospasm. 19 ~ !-

Biofeedback and electrically induced vasodilation are

thetic blockage in the treatment of clinical frostbite.AmJSurg1976;132:625-630.: ,-, ........ -16. Snide(RE, Po, rte~- JMiT~:e’~ment of expPimeMa’iff6~tbwith intraar:teriaisy~patheti~ blocking drugs. Sd~b~’y 1975;

17. Dowd PM, austin MR, Lanigan S: N fediPin~’[h¯~"treat.ment of chilblain& BFMed J ~986;293(6652) 923:924:

¯ t8. ErvaSti E: Frostbites of the ~trem ties ahd 0th~~:~~i~ielab:¯A clinical study. Acta Chir Scandinav 1962;(sdppl’299’}:~69

19. Brown FE,JobeJB, Hamlet M, et al: Induce~J ~,d~dilafionin the.treath3oh~ of pOsttraurhatic dig ta cold int0feranb~

~20. Jobe J B, Sampson J B, Roberts DE, et al: Induced rasedtion as treatment for RaynaUd’s disea ¯........ ...... se. Ann Intern Med 19__;~1: (Ub--/UtJ.

~. -:

-JANUARY 1988 HOSPITAL PHYSICIAN 31