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Recent advances in the management of burns
RECENT ADVANCES CHARLES
W.
IN THE MANAGEMENT
MCLAUGHLIN,
JR.,
M.D.
AND DELBERT
K.
OF BURNS* NEIS,
M.D.
Omaha, Nebraska
S
UCCESS or faiIure in the management of the severely burned depends upon many factors, but not the least of these is the ski11 and knowIedge of the attendant medica personne1. We have come a long way in the care of burns in the past decade due to the impetus and experience of the Iast war and the voIuminous research carried out during this period. The purpose of this articIe is to review briefly the pertinent investigative work accompIished since the war years and make some deductions as to its usefulness in the actua1 care of these patients. CrassweIIer and associateslO in reviewing Farmer’s anaIysis of 1,797 burned patients divided the mortaIity of burns into four phases, nameIy, shock, toxic, sepsis and convaIescent. This anaIysis showed a definite improvement in the mortahty rate since 1913 in the shock and septic phases but an increased mortaIity in the toxic phase. They point out that there is no specific treatment for this phase of the injury and that spontaneous recovery or death between the third and the tenth days occurs despite symptomatic measures. It is in this phase that progress wiI1 have to be made in order to improve our resuIts in the burned patient. THE
SHOCK
PHASE
The initia1 phase in the course of a severe burn is characterized by shock and Iasts for from forty-eight to seventy-two hours after the of this injury occurs. The first requirement period is the relief of pain with intravenous morphine which is superior to subcutaneous morphine. In severely burned patients who are in shock, subcutaneous morphine wiI1 be absorbed sIowly and the patient wiII not receive immediate benefit. Care must be taken not to produce over sedation and respiratory depression. It has aIso been found that morphine alone does not reIieve the pain in severe burns; but when pressure dressings are appIied, the * From the Department
of Surgery,
University
pain is often compIeteIy relieved and very little sedation is needed. l6 The cause of shock foIlowing burns has been a controversial subject among surgeons as we11 as research workers. It is certain that pain aIone is not a sufficient expIanation. Brooks and associate@ found that a sludging of the bIood occurred with 30 per cent burns of the body surface in dogs and rabbits, which is comparabIe to a second degree burn in man. This sIudging was found not only in the burned vesseIs but aIso in nearIy a11 vesseIs of the body. This phenomenon was noted aImost immediately, and as earIy as one or two minutes after a burn cIumps of red cells were visibIe in the arterioles, capiharies and postcapiIIary venuIes. They found that usuaIIy within haIf an hour, and not more than an hour, the greater part of the whoIe circuIating blood was changed to a homogeneous sIudge. Concurrently with the clumping of the red ceIIs it was noted that the white bIood ceIIs became adherent to the inner surface of the waIIs of the smaI1 venuIes, either temporariIy or for as Iong as an hour. This caused a reduction in the effective diameter of the vesseIs with reduced rate of blood IIow through the smaI1 vesseIs. At the same time the viscosity of the ffuid materia1 between the mass of red ceIIs increased. As the rate of bIood fIow decreased, masses of agglutinated red blood ceIIs couId be seen forming and breaking up in passing venuIe bIood. With slowing of the bIood the folIowing points were observed: (I) SIowing of the bIood stream to a fuI1 stop without apparent leakage of bIood fluid from the vesseIs. (2) Weakening, relaxation, buIging and saccuIation of the waIIs of smaI1 veins but no aneurysms of the smaII arteries were noted. (3) Progressive sIowing of the bIood stream whiIe the waIIs of the smaI1 venuIes Ieaked the ffuid part of the passing bIood. (4) Appearance ,of basic masses of aggIutinated red ceIIs outside the vesseIs, probabIy but not directIy observed, by diapedesis through the vessel waI1. (5) Ocof Nebraska
746
CoIIege of Medicine, Omaha, Neb.
American
Journal
of Surgery
McLaughlin,
Neis-Advances
currence of small hemorrhages which permitted varying amounts of blood with its agglutinated cells to pass through the vessel walls into the surrounding tissue. (6) Stasis and thrombosis of small vesseIs. (7) The plugging of arterioIe tips by Iarge-sized basic masses of red bIood ceIIs which also acted toward stopping bIood flow as previousIy noted. Sometimes portions of smaI1 thrombi were seen to break loose and be carried into the general circuIation. They beIieve that it may be possibIe or probabIe that muItipIe smaI1 emboIi of sIudging masses of ceIIs contribute to necrosis of the liver, Iung or other organs by occluding smaI1 vessels within their substance. In severe burns after five or six hours basic masses of red celIs were seen in increasing numbers outside the vesse1 waIIs, but actua1 rupture of the vessels was not seen. Thus with the red ceIIs outside the vessels they cease transporting oxygen and contribute to the post burn anemia and to a reduction in the circuIating bIood volume. Brooks and his co-worker@ point out that there are at least two kinds of shock folIowing burns; one in which there is not sufficient Ioss of fluid to account for the resulting state of shock but for which the mechanism is not yet known, and one in which the known part of the mechanism appears to be the loss of Auid IocaIIy into the burn site. If intravascuIar agglutination of red ceIIs occurs suffrcientIy suddenly throughout a large portion of the tota circulating bed, the rate of blood fIow wiI1 be reduced promptty enough to cause sudden shock through peripheral faiIure without excessive Auid 10s~. These authors believe that it is entirely possible that some substance or substances reIeased from burn tissue couId cause the aggIutination of red ceils in the sludging process and this substance might properIy be caIIed a sIudge-initiating toxin. HemoIysis of blood which accompanies burns may aIso contribute to the decreased blood volume. James et a1. l2 have shown experimentaIIy that hemoIysis is very great in third degree burns of more than 20 per cent of the body surface, and there is usually a constant increase in the urinary urobiIinogen noted on the third day after injury. This probabIy denotes early hepatic dysfunction and inability to catabolize properIy an increasing amount of urobilinogen. These same authorsI found an early impairment of the liver function in minor .June,
1952
in Management
of Burns
747
to extensive third degree burns, as judged by changes in the liver function tests employed in their study. The more severe the burn the greater the amount of change in liver function. AIong with hemolysis it has been shown experimentally by McLean, Moritz and Ross21 that in severeIy burned animaIs a rapid rise in pIasma potassium Ievels ordinarily considered incompatible with life may result. In a study of potassium IeveIs in burned patients Ross and associateP have shown two principa1 mechanisms which couId cause circulatory failure and death. In one periphera1 vascuIar coIlapse is brought about by conducting heat to the interior of the body causing systemic hyperthermia via the blood stream, Ieading to a rapid faI1 in blood pressure and faiture of the circulation. In the other type circuIatory faiIure is principally central due to a high concentration of reIeased erythrocytic potassium in the plasma. Either of these two types may be complicated by the effects of the other. It has been determined by McLean and associates17 that in a state of shock, sensitivity to potassium is often six to nine times above that normally found. However, it has aIso been demonstrated that excessive potassium is rapidIy removed; and if a burn patient survives one hour, the pIasma potassium IeveI is greatIy reduced. From the foregoing comments it is apparent that in treating a patient for burn shock it is not mereIy a problem of replacing pIasma loss, but rather a repIacement of the circuIating voIume including red ceIIs, eIectroIytes and water. AI1 burned patients are considered emergency cases and shouId be treated as such. If the patient is to be transported a distance from the site of the injury, the emergency treatment before transportation shouId be that of draping the patient in a clean or sterile sheet and administering an initia1 narcotic for the reIief of pain. If the patient has associated injuries such as a fracture, these shouId be treated by first aid measures before transportation is undertaken. We beIieve that a11 burned areas should be considered as open wounds, and these are best dressed in an operating room where the optimum possibIe sterile technic can be carried out. When the patient arrives at the hospita1, a definite pIan of therapy shouId be followed. Until blood and pIasma are avaiIabIe the treatment can be started by using 5 per cent
748
McLaughlin,
Neis-Advances
glucose in sodium chloride. The improvement in shock foIIowing intravenous glucose in sodium chloride will only be temporary, and pIasma which is the Aurd of choice should be started as soon as possible. There are many rules for the amount of pIasma to be administered, but probably the best is the clinica response of the patient correlated with the hematocrit determinations and urinary output. It is usuaIIy a deficient rather than an excessive amount of pIasma that causes fatalities. Brown and Dziob? have commented that untoward effects of plasma or whoIe blood in average doses are unusua1 in the absence of puImonary burns. Whole bIood should be administered as soon as possible or when avaiIabIe. We do not hesitate to give it even in the presence of hemoconcentration. This replaces the ceI1 mass Iost and prevents the post-burn anemia seen in the convalescent stage. The amount depends on the severity of the burn and the clinical status of the patient. Our working ruIe is to give 500 cc. of whole bIood each day for three days and then as indicated by the bIood picture. EIectroIyte soIutions by mouth are vaIuabIe in the treatment of the shock seen in burn patients. RosenthaI and associateF found that the body because of its need for the sodium ion folIowing burns retains large amounts of isotonic sodium chloride solution. This sodium retention which may persist for ten to twenty days as determined by urinary secretion of sodium resuIts from a sodium potassium imbalance which develops during the acute shock phase. Brown and Dziob,? and RosenthaI demonstrated experimentaily that saIt soIution reduced the mortality in burn shock in animals and that it is more efficacious if given oraIIy. Moyer and associatesIs recommend an oral solution of norma saIine and sodium bicarbonate, composed of sodium chIoride, r2g mm., and sodium bicarbonate, 25 mm., Ringer’s lactate, 137 mm. base and sodium Iactate, 27 mm. Such a soIution if taken cool is often palatabIe in amounts up to 6 to 8 L. per day. Wide clinica experience has demonstrated that the giving of saline-bicarbonate or saIinecitrate soIutions by mouth or by intragastric tube is effective in improving burn shock. These should be offered early or as soon as nausea and vomiting permit. The amount to be administered is determined by the clinical response of the patient as well as Iaboratory
in Management
of Burns
criteria. The administration of these fluids oraIIy has been recommended for general use by the Surgery Study Section to the National Securities Resource Council in individual burns and in the event of a nationa disaster. RecentIy there has been some interesting investigative work on the use of heparin in burns. AIrich2 found in experimental animals during the interva1 between tweIve and thirty hours an appreciabIe amount of plasma and protein returned to the circuIating bIood in heparnized animals as compared to a control group. Heparin was thought to act by reducing the amount of coagulation of exudate in the tissues and Iymphatics. The mortaIity in this experimenta group, however, was 29.4 per cent as compared to a zero mortality in the contro1 group, so they concIuded that heparin should not be used cIinicaIIy. McCIeery et al.‘” believe that heparin speeds the process of norma1 tissue repair by earlier neutrophilic infiltration, by vascuIar regeneration with a reduction of the length of time that sludging is present and by fibroblastic proliferation. Parsons and associates1g found in experimental animats that heparinization aIone resuIted in less tissue Ioss and gangrene did not appear in the heparinized animals until two days after it appeared in the controls. Elrod and associates” in animal experiments found that heparin increased significantIy the survival time of those receiving IethaI burns, the beneficial effects being accompanied with improved renal function as evidenced by a smaIIer rise in the non-protein nitrogen and increased urinary output. They aIso found a decrease in expected hemoconcentration, probabIy due to a better return of fluid and aIbumin to the circulation by the Iymphatics. They offer a theoretic concept suggesting a chemical alteration by heparin of a protein toxin. To date there is almost no data on the cIinica1 use of heparin in severeIy burned patients and we have not used it with these cases. WhiIe on a Iaboratory basis it may be found useful as an adjunct in the shock phase, it is stilt a very potent agent and its vaIue in burns must be considered in the investigative stage at the present time. THE
TOXIC
PHASE
At the end of forty-eight or seventy-two hours the severely burned patient who survives passes from the shock phase into the second American
Journal
of Surgery
McLaughlin,
Neis-Advances
more critica toxic phase. The voluminous work on burns in the past decade has been primarily concerned with the initia1 or shock period with a striking reduction in its mortality. The toxic phase which foIIows and usually lasts from five to seven days continues to carry a distressing mortality and is confusing since we have had so few agents to assist the patient through this period. Recently cortisone and ACTH have been added to our therapeutic regimen in burns. The results in only a few patients treated with these drugs have appeared in the literature to date, and we have had an opportunity to try cortisone thoroughly in only one major burn. Its action is probably during the period of socalled adrena exhaustion which may play a part in the mortality of this phase. CrassweIIer and associates” in comparing the striking parallelism between the physiologic changes folIowing burns and the physiologic effects of ACTH and cortisone suggest that a reIationship might exist between the defense response to burn trauma and the action of these substances. ExperimentaIIy they gave cortisone to burned mice for four days after the burn, the period when the so-called toxic effects of the burn were to take place, and found a definite decrease in mortaIity in the cortisone treated animal as compared to controls. These authors believe that clinically cortisone should be given in adequate amounts for the body to meet the emergency, thus supplementing the output from an exhausted adrena1. They point out that the administration of ACTH might not be expected to be useful if the adrenal gland is already exhausted. Therefore it wouId seem Iogica1 to assume that cortisone shouId be used as a repIacement therapy unti1 the adrena gIand regains its normal function after the emergency period or toxic phase of three to ten days. The question arises as to the continued use of cortisone or ACTH in a burned patient past the tenth day or bevond the toxic phase, since clinica and expeiimental work indicates that these drugs delay the formation of granuIation tissue and hence wound heaIing. Ragan and associateszO showed a deIay in granulation tissue production in rabbits treated with cortisone at both five and eight days foIIowing operation, whiIe the controIs showed good granuIation tissue growth. They suggest that the action of cortisone and ACTH on mesenchyma1 tissue is due, at Ieast in part, to inhibition of reactivity June,
1952
in Management
of Burns
749
of the connective tissue. Baker and associates3 found that when rats were given ACTH there was thinning of the skin which was due largeI) to a reduction in thickness of the subcutaneous layer of Ioose fibro-elastic connective tissue and fat. This was found to be most marked with the Iarger doses of ACTH. They aIso found evicIence of retarded deveIopment of hair foIIicIes. Baxter and associates4 observed in a study of wound healing in man under contro1 conditions and therapy with ACTH that wounds of skin and subcutaneous tissue showed a variabIe and apparently unpredictabIe response in different individuals. They beIieve that because some patients showed deIay in wound healing and others did not may be due to either a variation in adrena response or in reaction of tissues to the same amount of adrenal hormone. Dermatome donor areas were studied in two patients by these authors. Both showed cIinitally healed donor areas on the eighth and ninth days postoperatively, but microscopically one patient showed more mature healing in the control area than in the treated area. ACTH failed to prolong the surviva1 time of the epithelium of a homograft in one case. Crassweller and associates10 report two children and one aduIt with severe burns recently treated with cortisone in addition to other usual therapeutic measures. The two children with second and third degree burns of 55 per cent and 30 per cent body surface succumbed on the fifth and twenty-fourth days, whiIe the aduIt with the 70 per cent burn recovered. The autopsy in the first child was negative except for the burns, the adrenals containing adequate sudanophilic material. In the second child the postmortem sections of the adrenaIs showed a marked reduction of sudanophilic material in the fasciculi and the reticuIaris, interpreted as being indicative of adrena exhaustion. The aduIt aged twenty-one recovered in spite of a mortaIity table probability of Iess than a 5 per cent chance with modern therapy. He experienced a remarkable state of well-being amounting aImost to euphoria under cortisone therapy and was abIe to take and assimilate from 4,000 to 7,000 caIories per day under treatment. Adams and associates’ report the use of ACTH in three severely burned children. These patients, age seven, four and eleven, were given from IO to 20 mg. of ACTH every six to eight hours for variabIe periods of from two to fort?
730
McLaughlin,
Neis----Advances
days. In each instance they observed prompt improvement as evidenced by a cooperative patient, a striking increase in appetite with a dramatic rise in caloric intake. In no case \vas any adverse effect noted on heahng with subsequent grafting. In determining the vaIue of ACTH or cortisone many problems must be evaIuated. Certainly the extent of the burn must be determined in a11 three dimensions. As pointed out by Tamerinz6 one of WhitIaw’s patients excreted 900 cc. of urine in the first twenty-four hours with no noted intravascuIar hemolysis and no hemogIobinuria. Its absence would indicate that the voIume of burn destruction was not great as intravascuIar hemoIysis and hemoglobinuria are signs of severe thermal destruction. This same author states he is not ready to question the effects of ACTH on spontaneous epithehzation of the burn wound, but he cautions against postponement of skin grafting in areas that require an elastic skin enveIope to function properIy. Tamerin reports one persona1 case in which ACTH was not fife saving, and he encountered proI& granuIation tissue on which homografts did not successfuIIy grow. WhiIe some of this evidence is co&I icting and perhaps enthusiastic, it seems evident that we have in ACTH and cortisone agents which may offer real assistance in the toxic phase. We have had an opportunity to try cortisone in onIy one severeIy burned patient to date; a girl of Fifteen years admitted with second and third degree burns invoIving over 40 per cent of the body surface. CASE
REPORT
Y. M., a fifteen year oId white femaIe, was admitted to the University HospitaI on January 19, 195 I, with the history of being burned approximateIy four hours before admission when a stove expIoded and her cIothes caught fire. On admission she was treated for shock with intravenous fluids, pIasma and bIood. During the first thirty-four hours she received 1,710 cc. of pIasma and 500 cc. of bIood. She made a good cIinica1 response but her urinary output was depressed the first the next twenty-four tweIve hours. During hours there was an improvement, excreting 780 cc. Her urine was cIear unti1 the fifth day when it was definiteIy amber coIored, which cleared rapidIy in the next twenty-four hours and re-
in Management
of Burns
mained so with an adequate output. During the first twenty-four hours she had some nausea and vomited 600 cc. FoIIo\ving this she was able to take food and Auid by mouth in adequate amounts. On the fifth day cortisone was started giving 150 mg. intramuscularly daily until the TABLE PATIENT 140%
Y. THIRD
M.,
FLAME
DEGREE
I
BUKYS, BURNS,
60’,‘; ZO’l/,
OF BODY FIRST
AN”
SURFACE SECOND)
Eosinophik
14
13.6 15.4 14.6
25 27 2x ZY 32 33 34 35 39 42 46 4Y 50 53 56 60
50 38 25 13
15.7
I8 21
14.4 v.7
$5 40
5.x0 j.74
.
j.01) 5.83
555
38
*
455
466 $3 5”
505 400 461 466
35 35 39
466 466 455
55 -9 84 52
chloride
NOW2
38 38
5.01
4.91
4.38 5.84
. 54
5.Ij 5.81 5.04 5.32
.
572
* 20 gm. ammonium
..
j.72
644
z,?
intravenousIy t Cortisone
42-
433 366
16.4 16.3 15.2 14.8 14.-l
63
44~) .t**
13
and 1.5 gm. potassium
chIoridc
75 mg. three times a day started
forty-second day. During this time she had an exceIIent appetite and exhibited some euphora. On the twenty-eighth dav the patient had some nausea and vomiting hvhich was foIIowed with acute gastric distention. She was treated with gastric suction, intravenous fIuids, blood and pIasma. On the thirty-third dav intravenous potassium, I.5 gm., and ammonium chIoride, 20 gm., were given with marked improvement of the aIkaIosis. On the thirty-eighth day food and fluids were again started oraIIy and subsequently she had no difficuIty and continued to have a good appetite. After the seventieth day she took a diet containing an average of 3,500 caIories. (TabIe I.) We believe that the change in her condition occurring on the twenty-eighth day was due to a state of sodium retention and hypopotassemia, probabIy caused I>yrthe cortisone. It was during this period that her eosinophi1 count was so low, indicating an excessive dose of cortisone. The cortisone was stopped on the
American
Journal
of Surgery
McLaughlin,
Neis-Advances
in Management
forty-second day and started again on the fifty-sixth day, in dosage of 25 mg. three times a day. Following this the patient continued to have a good caIoric intake but continued to Iose weight. We beIieve that this was due to a continued protein cataboIism, which is often caused I’. M., FLAME
-
Days
I
2
I-
3
II BURNS,
-
OBSEKVATIONS
4*
18.1 16.9 Hemoglobin. ................. 15.7 Pack celI volume. ...... ,59-56% 64 17-48 %15 I-50% 5:3-57% CO?. ........................ 40 4 50 Chloride. .............. .... 383 383 Protein ................. ..... 6.59 Non-protein nitrogen. ... .I ..... 52 35 None Eosinophils. ................. Plasma. ................ 1,250 500 5oo I,“00 5% dextrose in water ......... 1,000 1,000 Lactate ringers 1,000 . 5 % dextrose in NaCl ..... I ,ooo 1,000 1,000 Blood. ................. $00 500 1,000 Amigen ..................... OraI. .................. ‘Bdi 495 340 9oo Urinary output ............... 2,500 780 525 -
75’
(2) The most dramatic effect is in the striking euphoria evidenced by a state of we11 being, an amazing appetite and an aImost phenomena1 caloric intake. (3) After the tenth to fifteenth day reIativeIy little benefit was observed. There is some evidence that prolonged
TABLE PATIENT
of Burns
13.2 15.2 87-46 %b 48% 56 359 459 6.82 . 24 None
‘3
14.8 48 %..
14 8
~ jO'/;
6,‘I(, 6.
i.~~.
449 6.83
‘2’;
88
‘75 I
$00
9’
75 _.... :::::/:
1,000 1,000
.._
..,.. $00
~ 760 3,100
1,140 2,900
-
2,230 2,300
1,600 1,500
-
1,860 1,275
2,210
2,400
2,375
I,250
I
* Liquid diet t Soft diet; cortisone 50 mg. 1 Cortisone 150 mg. daily until forty-third 0 High protein, high carbohydrate diet
day
by proIonged administration of cortisone. (TabIe II.) The cortisone was discontinued on the eightythird day.and the patient continued to have an exceIIent appetite and gained weight slowly. She received a tota of 7,300 mg. of cortisone. After the cortisone was discontinued a11 grafts that had previously been appIied continued to grow. FoIIowing the termination of cortisone therapy the eosinophi1 count returned to norma1. The serum protein remained within normal Iimits. Eight major grafting procedures were required to cover the burned areas, with IOO per cent take on six occasions and 85 per cent and 40 per cent take on two occasions. (Table III.) Our impressions from this Iimited experience suppIemented by a review of the other recorded cases may be summarized as foIIows: (I) ACTH or cortisone is worthy of additiona cIinica1 trial in the toxic phase of burns, or from the third to the tenth day. On theoretic grounds cortisone should be the drug of choice. June,
rgp
administration may be contraindicated. (4) Both ACTH and cortisone deIay fibrapIasia but have Iittle effect on epitheIization. (3) In average doses and if not continued for too Iong a period, one may expect grafts to take as in a norma burn if other essentia1 factors are adequateIy controIIed. LOCAL CARE OF THE BURN
At the present time there are two accepted methods of caring for the burned area, employing either pressure dressings or the exposure method. As soon as initia1 shock is overcome with the administration of indicated fIuids, care should be directed toward the management of the open burn. We prefer pressure dressings but recent reports make us cognizant of the vaIue of the exposure method. In dressing the burn after removing the original tentative dressing, a rough estimate is made of the area and depth of the body surface invoIved. We prefer the Jassification of Lund and Browder.14 If gross contamination is present, the wound is gentIy irrigated with ade-
McLaughlin,
732
Neis-Advances
quate amounts of saIine; otherwise we do not recommend any type of wound cIeansing. AII loose skin tabs are removed by dkbridement but care is taken not to rupture blisters if present. We advise against proIonged dkbridement as it may increase Buid Ioss, blood Ioss, increase PATIENT,
TABLE III Y. M., FLAME BURNS, TREATMENT Caloric
-.,-.__
Intake Diet
Days ____--.
Average
~--
FIuids High protein Intravenous feedings Protein diet
1st to 5th.
6th to 28th.. 29th to 37th. 38th to 70th.
I
,_Cortisone
Appetite
Dose
__
25 mg. three times a day
graftings..
___.. Good
_’ Ijo mg. daily
Grafts Eight‘major
____
Medication
Days
5th to 4.znd. 56th to 70th.
900 3,500 4.00 I.400
Improving
_~__ Six, 100% take One, 85% take One, 40% take
pain and thus increase the degree of shock. For the dressing we empIoy 44 mesh gauze impregnated with Iiquid petroIatum. These strips of gauze are appIied smoothIy over the burned areas after which ceIIuIose-cotton gauze or sterile white mechanics paste is evenIy appIied over these areas, and the dressing heId in pIace by wrapping firmIy with stockinette cut on the bias. In appIying these dressings care must be taken to distribute the pressure evenIy so as not to interfere with bIood suppIy or necrosis may result over bony prominences. This dressing is usuaIIy Ieft on for from ten to tweIve days after which time the burned areas are reinspected. If granuIation tissue is cIean and the patient’s condition warrants, grafting is carried out immediateIy at the time of the first dressing in suitabIe areas. At this dressing we do not hesitate to remove sIoughs; and if the bleeding is not too extensive or can be controIIed by hot packs, these areas are immediately grafted. Otherwise we apply a pres-
in Management
of’ Burns
sure dressing incorporating many urethral catheters for saline irrigation. We find that this latter type of dressing will aid in cIeaning up infection and aIso speeds the separation of slough, so that earIy grafting is possible. PeniciIIin is routineIy empIoyed in the earIy phases of burn therapy and aIso during the stage of grafting, but we are convinced that peniciIIin has no effect on established infection in a granuIating burn wound. AI1 patients with burns are given tetanus toxoid or antitoxin early as the chance of contamination with the tetanus baciIIus is great. As soon as the patient is abIe to take nutritive Auids by mouth he is started on a high protein, high carbohydrate diet with Iarge doses of vitamins, particuIarIy vitamin C. We emphasize the importance of constant attention to the patient’s nutrition as this aids in the earIy grafting and the success of graft takes. In the exposure method of treatment the objective is to keep the wound steriIe and dry. CopeIand* in 1887 first described this method, and in 1905 Snevez5 presented its practical advantages. WaIIaceZ7 points out the foIIowing objectives in any form of IocaI treatment: (I) produce a condition of the burned surface unfavorabIe to the growth and muItipIication of bacteria by the production and maintenance of a dry surface if possibIe, the exposure of the surface to Iight if possibIe, and reduction of the temperature of the surface to that of its environment; (2) appIy an antiseptic which is bIand to tissue cells; (3) provide rest of the affected part by immobiIization; (4) Iimit edema by elevation; and (5) render nursing care simpIe. In treating the burned area Wallace cIeans the open portions with a I per cent cetavlon, the bIisters are opened and the raised skin is removed. FoIIowing this the burned surface is dried and insufllated with peniciIIin, using the caIcium salt of peniciIIin diIuted with Iactose, 10,000 units per cc. AI1 sorts of organisms may faI1 on the burned surfaces; but if they are dry, no harm is said to resuIt. BIocker5 does not appIy any type of IocaI preparation; but when the dried areas crack, he recommends pIacing gauze moistened in saIine over the cracks to cover these areas. He recommends removing the sIough as soon as possibIe and grafting before infection takes place. He reports the use of this method on seventy patients with second and third degree burns involving 40 to 50 per American
Journal
oj Surgeq-
McLaughlin,
Neis-Advances
cent of the body surface with good results. He beIieves that in this series the hospital stay was shortened and considers it the method of choice for both superficial and deep burns. Wallace*8 believes that the outstanding features of the exposure method have been as folIOU-S: a more effective controI of infection; transfusions have never been required in the second week or Iater; and no loss of appetite was observed by him. While we have had no experience with the exposure method, many of us remember the probIems encountered during the tannic acid and the tannic acid silver nitrate era in which great difficulty was encountered in keeping exposed areas dry. Certainly such a method would seem to require a great deal more nursing care which in itself offers a rea1 probIem in our modern hospitals. That this method could materially reduce the necessary administration of transfusions in severe burns if grafting is to be successfuIIy undertaken is certainly open to question. THE CONVALESCENT
1952
of Burns
753
ing at the next redressment, this phase of these very debilitating and costIy injuries can be brought to an earlier and more satisfactory termination. REFERENCES
I. A~,aws, F. II., BERGLUND, E., BALKIN, S. G. and
2.
3.
4.
5.
6.
7.
PHASE
This is the final period covering weeks or months after the patient has survived the shock and toxic phases and is Ieft with large open areas devoid of skin. It is this phase which is often referred to as the septic phase for in this period extensive sepsis often is present, ultimateIy Ieading to death of the patient. The objective of this convalescent period is the complete coverage of a11 open areas by new skin in the Ieast possible time. Grafting is invariabIy necessary in third degree burns of any extent and in many areas of second degree J>urns in which infection has produced further damage. Grafting shouJd be started as soon as feasibJe, preferably by the time of the second burn dressing with particuIar efforts directed toward covering the neck, axilla and al1 joint areas at the earliest possible time. Experience has shown that areas which stil1 show Iimited infection may be covered by ne\\ skin, providing the red bIood cell count, the hemoglobin and the serum-protein IeveIs are maintained at high norma readings. In addition it is our practice to maintain a vitamin C intake of at Ieast 500 mg. per day during this period. A definite scheduIe of redressment is established at intervaIs of one week with grafting on each occasion. If in this scheduIe there is pIanned preparation of a new area for coverJune,
in Management
CHISHOL.~I, T. Pituitary adrenocorticotropic hormone in severely burned children. J. A. M. A., 146: 31-33, 1951. ALHICH, ht. E. The effect of heparin on the circulating blood plasma and proteins in experimenta burns. Surgery, 25 : 676680, I 949. BAKER, B. I~., INGLE, D. W., LI, C. H. and EVANS, Il. >l. Growth inhibition in the skin-induced by parentera administration of adrenocorticotropin. Amt. Rec., 102: 313-325, 1948. BAXTER, H., SCHILLER, C. and WHITESIDE, J. II. The influence of ACTH on wound heaIing in man, Plast. CT Reconstruct. Surg., 7: 85-99, I 95 I. BLOCKER, T. G. LocaI and general treatment of acute extensive burns, the open-air regime. Lancet, I: 498-501, 1951. BROOKS, F., DRAGSTEDT, L.. R., W'AHFEK, L. and KNISELY, 31. H. SIudged bIood folIowing severe therma burns. Arch. Surg., 61: 387-418, 1950. BROWN, R. K. and DZIOB, I. hl. Primary treatment of extensive burns. Am. .I. Surg., 79: 288-294,
‘950. 8. COPELAND, W. P. The Treatment of Burns. Med. Rec., 31: 518, 1887. 9. CRASSWELLER, P. O., FARMER, A. W. and FHA~KS, \\‘. R. Experimental burn studies, including treatment with cortisone-active materia1 extractcd from UrinC. &it. M. J., 2: 242-245, 1950. IO. CRASSWELLER, P. O., FARMER, A. W., FRANKS, W. R. and MCLACHLIN, A. D. Three cases of severe burn treated with cortisone. &it. M. J.. 2: 977981, 1950. P. D., MCCLEEKY, R. S. and BALL, CON D. T. An experimenta study of the effect of heuarin on surviva1 time follow&g Iethal burns. Surg., Gynec. t!Y Obst., 92: 35-42, 1951. 12. JAMES, G. W., III, PURNELL, 0. J. and EVANS, E. I. The anemia of therma injury. I. Studies of pigment excretion. J. Clin. Investigation, 30: 181~ I I.
ELROD,
I
19% 1951. 13. JAMES, G. W., III, PUHNELL,L. J. and EVANS, E. I. The anemia of thermal injury. II. Studies of liver function. J. Clin. Investigation. _ lo: IoI-100., 195 T. 14. LUND, C. C. and BKOWDEK, N. C. &timation ot areas of burns. Surg., Gvnec. @,v Obst., 79: 352,I
358, ‘944. I 5. MCCLEERY, R. S., SCHAFFAHZICK,W. R. and LIGHT, R. A. An experimental study of the effect of heparin on the IocaI pathoIogy of burns. Surgery, 26: 548-566, 1949. 16. MCLAUGHLIN, C. LV., JR. Treatment of major burns in naval warfare. Nebraska M. J., 31: 11-19, 1946. 17. MCLEAN, R., MORITZ, A. R. and Ross, A. Studies of thermaI injury. VI. Hyperpotassemia caused by cutaneous exposure to excessive heat. J. Clin. Investigation, 26: 497-504, 1947.
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18. MOYEH, C. A., COLLER, F.A.. 106, C. and VAUGHAN, H. H. A study of the interrelationship of salt solutions, serum and defibrinated bIood in the treatment of severely scaIded, anesthetized dogs. Ann. SUrg., 120: 367-376, 1944. 19. PARSONS, R., JK., ALRICH, E. RI. and LEHUAN, E. P. Studies on burns. v. Experimental study oft he effect of heparnization and gravity on tissue loss resuIting from third degree burns. Surg., Gynec. (:+ Obst., 90: 722-724, 1950. 20. RAGAN, C. R., HO\I’ES, E. L., PLOTZ, C. r\l., hIEvEn, K. and BLUYT, J. W. Effect of cortisone on production of granulation tissue in the rabbit. Proc. Sot. Exper. Biol. c? Med., 72: 718-725, r94q. 21. Ross, R., WEISIGEH, J. R. and IMORITZ, A. R. Studies of thermat injury. VII. PhysioIogicaI mechanisms for death durmg cutaneous exposure to excessive heat. J. Clin. Inwstigution, 26: 5”$-5 19, 1947. 22. Rcscarch on burns. Lancet, 2: 635641,
1950.
in Management
of Burns
23. ROSEUTHAL, S. AI. and TABOR, H. T. EiectroIyte changes and chemotherapy in experimental burn and traumatic shock and hemorrhage. Arch. .%Ug., f 1: 244-252, 1945. 24. ROSENTHAI., S. hI. Experimental chemotherapy of burns and shock. Pub. Health Rep., 58: 513522, 1948. 25. SNEVE, H. The treatment of burns and skin grafting. J. A. M. A., 45 : r-8, I 905. 26. TAMEKIN, J. A. ACTH and burns. J. A. M. A., 145: 925, 1951. 27. \\‘ALLACF.,A. B. Treatment of burns. Med. Press, 225: 191-194, 1951. 28. \fr~~r.~c~, A. B. The exposure treatment of burns. Lancet, 1: $0r-504, 195 I. 29. WNTELAW, X1. J. and WOODMAN,T. W. The trcatment of severe burns with ACTI I. J. C/in. Endocrinol., 10: I 171, r95o; and WHITELAW, \/I. J. Physiological reaction to pituitary adrcnocorticotropic hormone CACTI I) in severe burns. J. A .111. A., 145: 85-88, 1951.
ACTINOMYCOSIS of the breast may be secondary from the lung by direct extension through the chest waI1, or primary. Early cases resemble an acute mammary abscess. Incision and drainage pIus antibiotics usuaIIy effect a cure, Advanced cases with multiple chronic abscesses and numerous fistuIous openings occasionalIy require simple mastectomy in addition to preoperative and postoperative therapy with the suifa drugs, antibiotics (especiaIIy penicillin) and genera1 supportive treatment. Some of these patients have had repeated breast abscesses with discharge of yelIow pus through the nipple-a characteristic history that shouId make the surgeon suspect the presence of the actinomyces bovis. (Richard A. Leonardo, M.D.)
American
Journal
of Surgery
W.
IN THE MANAGEMENT
MCLAUGHLIN,
JR.,
M.D.
AND DELBERT
K.
OF BURNS* NEIS,
M.D.
Omaha, Nebraska
S
UCCESS or faiIure in the management of the severely burned depends upon many factors, but not the least of these is the ski11 and knowIedge of the attendant medica personne1. We have come a long way in the care of burns in the past decade due to the impetus and experience of the Iast war and the voIuminous research carried out during this period. The purpose of this articIe is to review briefly the pertinent investigative work accompIished since the war years and make some deductions as to its usefulness in the actua1 care of these patients. CrassweIIer and associateslO in reviewing Farmer’s anaIysis of 1,797 burned patients divided the mortaIity of burns into four phases, nameIy, shock, toxic, sepsis and convaIescent. This anaIysis showed a definite improvement in the mortahty rate since 1913 in the shock and septic phases but an increased mortaIity in the toxic phase. They point out that there is no specific treatment for this phase of the injury and that spontaneous recovery or death between the third and the tenth days occurs despite symptomatic measures. It is in this phase that progress wiI1 have to be made in order to improve our resuIts in the burned patient. THE
SHOCK
PHASE
The initia1 phase in the course of a severe burn is characterized by shock and Iasts for from forty-eight to seventy-two hours after the of this injury occurs. The first requirement period is the relief of pain with intravenous morphine which is superior to subcutaneous morphine. In severely burned patients who are in shock, subcutaneous morphine wiI1 be absorbed sIowly and the patient wiII not receive immediate benefit. Care must be taken not to produce over sedation and respiratory depression. It has aIso been found that morphine alone does not reIieve the pain in severe burns; but when pressure dressings are appIied, the * From the Department
of Surgery,
University
pain is often compIeteIy relieved and very little sedation is needed. l6 The cause of shock foIlowing burns has been a controversial subject among surgeons as we11 as research workers. It is certain that pain aIone is not a sufficient expIanation. Brooks and associate@ found that a sludging of the bIood occurred with 30 per cent burns of the body surface in dogs and rabbits, which is comparabIe to a second degree burn in man. This sIudging was found not only in the burned vesseIs but aIso in nearIy a11 vesseIs of the body. This phenomenon was noted aImost immediately, and as earIy as one or two minutes after a burn cIumps of red cells were visibIe in the arterioles, capiharies and postcapiIIary venuIes. They found that usuaIIy within haIf an hour, and not more than an hour, the greater part of the whoIe circuIating blood was changed to a homogeneous sIudge. Concurrently with the clumping of the red ceIIs it was noted that the white bIood ceIIs became adherent to the inner surface of the waIIs of the smaI1 venuIes, either temporariIy or for as Iong as an hour. This caused a reduction in the effective diameter of the vesseIs with reduced rate of blood IIow through the smaI1 vesseIs. At the same time the viscosity of the ffuid materia1 between the mass of red ceIIs increased. As the rate of bIood fIow decreased, masses of agglutinated red blood ceIIs couId be seen forming and breaking up in passing venuIe bIood. With slowing of the bIood the folIowing points were observed: (I) SIowing of the bIood stream to a fuI1 stop without apparent leakage of bIood fluid from the vesseIs. (2) Weakening, relaxation, buIging and saccuIation of the waIIs of smaI1 veins but no aneurysms of the smaII arteries were noted. (3) Progressive sIowing of the bIood stream whiIe the waIIs of the smaI1 venuIes Ieaked the ffuid part of the passing bIood. (4) Appearance ,of basic masses of aggIutinated red ceIIs outside the vesseIs, probabIy but not directIy observed, by diapedesis through the vessel waI1. (5) Ocof Nebraska
746
CoIIege of Medicine, Omaha, Neb.
American
Journal
of Surgery
McLaughlin,
Neis-Advances
currence of small hemorrhages which permitted varying amounts of blood with its agglutinated cells to pass through the vessel walls into the surrounding tissue. (6) Stasis and thrombosis of small vesseIs. (7) The plugging of arterioIe tips by Iarge-sized basic masses of red bIood ceIIs which also acted toward stopping bIood flow as previousIy noted. Sometimes portions of smaI1 thrombi were seen to break loose and be carried into the general circuIation. They beIieve that it may be possibIe or probabIe that muItipIe smaI1 emboIi of sIudging masses of ceIIs contribute to necrosis of the liver, Iung or other organs by occluding smaI1 vessels within their substance. In severe burns after five or six hours basic masses of red celIs were seen in increasing numbers outside the vesse1 waIIs, but actua1 rupture of the vessels was not seen. Thus with the red ceIIs outside the vessels they cease transporting oxygen and contribute to the post burn anemia and to a reduction in the circuIating bIood volume. Brooks and his co-worker@ point out that there are at least two kinds of shock folIowing burns; one in which there is not sufficient Ioss of fluid to account for the resulting state of shock but for which the mechanism is not yet known, and one in which the known part of the mechanism appears to be the loss of Auid IocaIIy into the burn site. If intravascuIar agglutination of red ceIIs occurs suffrcientIy suddenly throughout a large portion of the tota circulating bed, the rate of blood fIow wiI1 be reduced promptty enough to cause sudden shock through peripheral faiIure without excessive Auid 10s~. These authors believe that it is entirely possible that some substance or substances reIeased from burn tissue couId cause the aggIutination of red ceils in the sludging process and this substance might properIy be caIIed a sIudge-initiating toxin. HemoIysis of blood which accompanies burns may aIso contribute to the decreased blood volume. James et a1. l2 have shown experimentaIIy that hemoIysis is very great in third degree burns of more than 20 per cent of the body surface, and there is usually a constant increase in the urinary urobiIinogen noted on the third day after injury. This probabIy denotes early hepatic dysfunction and inability to catabolize properIy an increasing amount of urobilinogen. These same authorsI found an early impairment of the liver function in minor .June,
1952
in Management
of Burns
747
to extensive third degree burns, as judged by changes in the liver function tests employed in their study. The more severe the burn the greater the amount of change in liver function. AIong with hemolysis it has been shown experimentally by McLean, Moritz and Ross21 that in severeIy burned animaIs a rapid rise in pIasma potassium Ievels ordinarily considered incompatible with life may result. In a study of potassium IeveIs in burned patients Ross and associateP have shown two principa1 mechanisms which couId cause circulatory failure and death. In one periphera1 vascuIar coIlapse is brought about by conducting heat to the interior of the body causing systemic hyperthermia via the blood stream, Ieading to a rapid faI1 in blood pressure and faiture of the circulation. In the other type circuIatory faiIure is principally central due to a high concentration of reIeased erythrocytic potassium in the plasma. Either of these two types may be complicated by the effects of the other. It has been determined by McLean and associates17 that in a state of shock, sensitivity to potassium is often six to nine times above that normally found. However, it has aIso been demonstrated that excessive potassium is rapidIy removed; and if a burn patient survives one hour, the pIasma potassium IeveI is greatIy reduced. From the foregoing comments it is apparent that in treating a patient for burn shock it is not mereIy a problem of replacing pIasma loss, but rather a repIacement of the circuIating voIume including red ceIIs, eIectroIytes and water. AI1 burned patients are considered emergency cases and shouId be treated as such. If the patient is to be transported a distance from the site of the injury, the emergency treatment before transportation shouId be that of draping the patient in a clean or sterile sheet and administering an initia1 narcotic for the reIief of pain. If the patient has associated injuries such as a fracture, these shouId be treated by first aid measures before transportation is undertaken. We beIieve that a11 burned areas should be considered as open wounds, and these are best dressed in an operating room where the optimum possibIe sterile technic can be carried out. When the patient arrives at the hospita1, a definite pIan of therapy shouId be followed. Until blood and pIasma are avaiIabIe the treatment can be started by using 5 per cent
748
McLaughlin,
Neis-Advances
glucose in sodium chloride. The improvement in shock foIIowing intravenous glucose in sodium chloride will only be temporary, and pIasma which is the Aurd of choice should be started as soon as possible. There are many rules for the amount of pIasma to be administered, but probably the best is the clinica response of the patient correlated with the hematocrit determinations and urinary output. It is usuaIIy a deficient rather than an excessive amount of pIasma that causes fatalities. Brown and Dziob? have commented that untoward effects of plasma or whoIe blood in average doses are unusua1 in the absence of puImonary burns. Whole bIood should be administered as soon as possible or when avaiIabIe. We do not hesitate to give it even in the presence of hemoconcentration. This replaces the ceI1 mass Iost and prevents the post-burn anemia seen in the convalescent stage. The amount depends on the severity of the burn and the clinical status of the patient. Our working ruIe is to give 500 cc. of whole bIood each day for three days and then as indicated by the bIood picture. EIectroIyte soIutions by mouth are vaIuabIe in the treatment of the shock seen in burn patients. RosenthaI and associateF found that the body because of its need for the sodium ion folIowing burns retains large amounts of isotonic sodium chloride solution. This sodium retention which may persist for ten to twenty days as determined by urinary secretion of sodium resuIts from a sodium potassium imbalance which develops during the acute shock phase. Brown and Dziob,? and RosenthaI demonstrated experimentaily that saIt soIution reduced the mortality in burn shock in animals and that it is more efficacious if given oraIIy. Moyer and associatesIs recommend an oral solution of norma saIine and sodium bicarbonate, composed of sodium chIoride, r2g mm., and sodium bicarbonate, 25 mm., Ringer’s lactate, 137 mm. base and sodium Iactate, 27 mm. Such a soIution if taken cool is often palatabIe in amounts up to 6 to 8 L. per day. Wide clinica experience has demonstrated that the giving of saline-bicarbonate or saIinecitrate soIutions by mouth or by intragastric tube is effective in improving burn shock. These should be offered early or as soon as nausea and vomiting permit. The amount to be administered is determined by the clinical response of the patient as well as Iaboratory
in Management
of Burns
criteria. The administration of these fluids oraIIy has been recommended for general use by the Surgery Study Section to the National Securities Resource Council in individual burns and in the event of a nationa disaster. RecentIy there has been some interesting investigative work on the use of heparin in burns. AIrich2 found in experimental animals during the interva1 between tweIve and thirty hours an appreciabIe amount of plasma and protein returned to the circuIating bIood in heparnized animals as compared to a control group. Heparin was thought to act by reducing the amount of coagulation of exudate in the tissues and Iymphatics. The mortaIity in this experimenta group, however, was 29.4 per cent as compared to a zero mortality in the contro1 group, so they concIuded that heparin should not be used cIinicaIIy. McCIeery et al.‘” believe that heparin speeds the process of norma1 tissue repair by earlier neutrophilic infiltration, by vascuIar regeneration with a reduction of the length of time that sludging is present and by fibroblastic proliferation. Parsons and associates1g found in experimental animats that heparinization aIone resuIted in less tissue Ioss and gangrene did not appear in the heparinized animals until two days after it appeared in the controls. Elrod and associates” in animal experiments found that heparin increased significantIy the survival time of those receiving IethaI burns, the beneficial effects being accompanied with improved renal function as evidenced by a smaIIer rise in the non-protein nitrogen and increased urinary output. They aIso found a decrease in expected hemoconcentration, probabIy due to a better return of fluid and aIbumin to the circulation by the Iymphatics. They offer a theoretic concept suggesting a chemical alteration by heparin of a protein toxin. To date there is almost no data on the cIinica1 use of heparin in severeIy burned patients and we have not used it with these cases. WhiIe on a Iaboratory basis it may be found useful as an adjunct in the shock phase, it is stilt a very potent agent and its vaIue in burns must be considered in the investigative stage at the present time. THE
TOXIC
PHASE
At the end of forty-eight or seventy-two hours the severely burned patient who survives passes from the shock phase into the second American
Journal
of Surgery
McLaughlin,
Neis-Advances
more critica toxic phase. The voluminous work on burns in the past decade has been primarily concerned with the initia1 or shock period with a striking reduction in its mortality. The toxic phase which foIIows and usually lasts from five to seven days continues to carry a distressing mortality and is confusing since we have had so few agents to assist the patient through this period. Recently cortisone and ACTH have been added to our therapeutic regimen in burns. The results in only a few patients treated with these drugs have appeared in the literature to date, and we have had an opportunity to try cortisone thoroughly in only one major burn. Its action is probably during the period of socalled adrena exhaustion which may play a part in the mortality of this phase. CrassweIIer and associates” in comparing the striking parallelism between the physiologic changes folIowing burns and the physiologic effects of ACTH and cortisone suggest that a reIationship might exist between the defense response to burn trauma and the action of these substances. ExperimentaIIy they gave cortisone to burned mice for four days after the burn, the period when the so-called toxic effects of the burn were to take place, and found a definite decrease in mortaIity in the cortisone treated animal as compared to controls. These authors believe that clinically cortisone should be given in adequate amounts for the body to meet the emergency, thus supplementing the output from an exhausted adrena1. They point out that the administration of ACTH might not be expected to be useful if the adrenal gland is already exhausted. Therefore it wouId seem Iogica1 to assume that cortisone shouId be used as a repIacement therapy unti1 the adrena gIand regains its normal function after the emergency period or toxic phase of three to ten days. The question arises as to the continued use of cortisone or ACTH in a burned patient past the tenth day or bevond the toxic phase, since clinica and expeiimental work indicates that these drugs delay the formation of granuIation tissue and hence wound heaIing. Ragan and associateszO showed a deIay in granulation tissue production in rabbits treated with cortisone at both five and eight days foIIowing operation, whiIe the controIs showed good granuIation tissue growth. They suggest that the action of cortisone and ACTH on mesenchyma1 tissue is due, at Ieast in part, to inhibition of reactivity June,
1952
in Management
of Burns
749
of the connective tissue. Baker and associates3 found that when rats were given ACTH there was thinning of the skin which was due largeI) to a reduction in thickness of the subcutaneous layer of Ioose fibro-elastic connective tissue and fat. This was found to be most marked with the Iarger doses of ACTH. They aIso found evicIence of retarded deveIopment of hair foIIicIes. Baxter and associates4 observed in a study of wound healing in man under contro1 conditions and therapy with ACTH that wounds of skin and subcutaneous tissue showed a variabIe and apparently unpredictabIe response in different individuals. They beIieve that because some patients showed deIay in wound healing and others did not may be due to either a variation in adrena response or in reaction of tissues to the same amount of adrenal hormone. Dermatome donor areas were studied in two patients by these authors. Both showed cIinitally healed donor areas on the eighth and ninth days postoperatively, but microscopically one patient showed more mature healing in the control area than in the treated area. ACTH failed to prolong the surviva1 time of the epithelium of a homograft in one case. Crassweller and associates10 report two children and one aduIt with severe burns recently treated with cortisone in addition to other usual therapeutic measures. The two children with second and third degree burns of 55 per cent and 30 per cent body surface succumbed on the fifth and twenty-fourth days, whiIe the aduIt with the 70 per cent burn recovered. The autopsy in the first child was negative except for the burns, the adrenals containing adequate sudanophilic material. In the second child the postmortem sections of the adrenaIs showed a marked reduction of sudanophilic material in the fasciculi and the reticuIaris, interpreted as being indicative of adrena exhaustion. The aduIt aged twenty-one recovered in spite of a mortaIity table probability of Iess than a 5 per cent chance with modern therapy. He experienced a remarkable state of well-being amounting aImost to euphoria under cortisone therapy and was abIe to take and assimilate from 4,000 to 7,000 caIories per day under treatment. Adams and associates’ report the use of ACTH in three severely burned children. These patients, age seven, four and eleven, were given from IO to 20 mg. of ACTH every six to eight hours for variabIe periods of from two to fort?
730
McLaughlin,
Neis----Advances
days. In each instance they observed prompt improvement as evidenced by a cooperative patient, a striking increase in appetite with a dramatic rise in caloric intake. In no case \vas any adverse effect noted on heahng with subsequent grafting. In determining the vaIue of ACTH or cortisone many problems must be evaIuated. Certainly the extent of the burn must be determined in a11 three dimensions. As pointed out by Tamerinz6 one of WhitIaw’s patients excreted 900 cc. of urine in the first twenty-four hours with no noted intravascuIar hemolysis and no hemogIobinuria. Its absence would indicate that the voIume of burn destruction was not great as intravascuIar hemoIysis and hemoglobinuria are signs of severe thermal destruction. This same author states he is not ready to question the effects of ACTH on spontaneous epithehzation of the burn wound, but he cautions against postponement of skin grafting in areas that require an elastic skin enveIope to function properIy. Tamerin reports one persona1 case in which ACTH was not fife saving, and he encountered proI& granuIation tissue on which homografts did not successfuIIy grow. WhiIe some of this evidence is co&I icting and perhaps enthusiastic, it seems evident that we have in ACTH and cortisone agents which may offer real assistance in the toxic phase. We have had an opportunity to try cortisone in onIy one severeIy burned patient to date; a girl of Fifteen years admitted with second and third degree burns invoIving over 40 per cent of the body surface. CASE
REPORT
Y. M., a fifteen year oId white femaIe, was admitted to the University HospitaI on January 19, 195 I, with the history of being burned approximateIy four hours before admission when a stove expIoded and her cIothes caught fire. On admission she was treated for shock with intravenous fluids, pIasma and bIood. During the first thirty-four hours she received 1,710 cc. of pIasma and 500 cc. of bIood. She made a good cIinica1 response but her urinary output was depressed the first the next twenty-four tweIve hours. During hours there was an improvement, excreting 780 cc. Her urine was cIear unti1 the fifth day when it was definiteIy amber coIored, which cleared rapidIy in the next twenty-four hours and re-
in Management
of Burns
mained so with an adequate output. During the first twenty-four hours she had some nausea and vomited 600 cc. FoIIo\ving this she was able to take food and Auid by mouth in adequate amounts. On the fifth day cortisone was started giving 150 mg. intramuscularly daily until the TABLE PATIENT 140%
Y. THIRD
M.,
FLAME
DEGREE
I
BUKYS, BURNS,
60’,‘; ZO’l/,
OF BODY FIRST
AN”
SURFACE SECOND)
Eosinophik
14
13.6 15.4 14.6
25 27 2x ZY 32 33 34 35 39 42 46 4Y 50 53 56 60
50 38 25 13
15.7
I8 21
14.4 v.7
$5 40
5.x0 j.74
.
j.01) 5.83
555
38
*
455
466 $3 5”
505 400 461 466
35 35 39
466 466 455
55 -9 84 52
chloride
NOW2
38 38
5.01
4.91
4.38 5.84
. 54
5.Ij 5.81 5.04 5.32
.
572
* 20 gm. ammonium
..
j.72
644
z,?
intravenousIy t Cortisone
42-
433 366
16.4 16.3 15.2 14.8 14.-l
63
44~) .t**
13
and 1.5 gm. potassium
chIoridc
75 mg. three times a day started
forty-second day. During this time she had an exceIIent appetite and exhibited some euphora. On the twenty-eighth dav the patient had some nausea and vomiting hvhich was foIIowed with acute gastric distention. She was treated with gastric suction, intravenous fIuids, blood and pIasma. On the thirty-third dav intravenous potassium, I.5 gm., and ammonium chIoride, 20 gm., were given with marked improvement of the aIkaIosis. On the thirty-eighth day food and fluids were again started oraIIy and subsequently she had no difficuIty and continued to have a good appetite. After the seventieth day she took a diet containing an average of 3,500 caIories. (TabIe I.) We believe that the change in her condition occurring on the twenty-eighth day was due to a state of sodium retention and hypopotassemia, probabIy caused I>yrthe cortisone. It was during this period that her eosinophi1 count was so low, indicating an excessive dose of cortisone. The cortisone was stopped on the
American
Journal
of Surgery
McLaughlin,
Neis-Advances
in Management
forty-second day and started again on the fifty-sixth day, in dosage of 25 mg. three times a day. Following this the patient continued to have a good caIoric intake but continued to Iose weight. We beIieve that this was due to a continued protein cataboIism, which is often caused I’. M., FLAME
-
Days
I
2
I-
3
II BURNS,
-
OBSEKVATIONS
4*
18.1 16.9 Hemoglobin. ................. 15.7 Pack celI volume. ...... ,59-56% 64 17-48 %15 I-50% 5:3-57% CO?. ........................ 40 4 50 Chloride. .............. .... 383 383 Protein ................. ..... 6.59 Non-protein nitrogen. ... .I ..... 52 35 None Eosinophils. ................. Plasma. ................ 1,250 500 5oo I,“00 5% dextrose in water ......... 1,000 1,000 Lactate ringers 1,000 . 5 % dextrose in NaCl ..... I ,ooo 1,000 1,000 Blood. ................. $00 500 1,000 Amigen ..................... OraI. .................. ‘Bdi 495 340 9oo Urinary output ............... 2,500 780 525 -
75’
(2) The most dramatic effect is in the striking euphoria evidenced by a state of we11 being, an amazing appetite and an aImost phenomena1 caloric intake. (3) After the tenth to fifteenth day reIativeIy little benefit was observed. There is some evidence that prolonged
TABLE PATIENT
of Burns
13.2 15.2 87-46 %b 48% 56 359 459 6.82 . 24 None
‘3
14.8 48 %..
14 8
~ jO'/;
6,‘I(, 6.
i.~~.
449 6.83
‘2’;
88
‘75 I
$00
9’
75 _.... :::::/:
1,000 1,000
.._
..,.. $00
~ 760 3,100
1,140 2,900
-
2,230 2,300
1,600 1,500
-
1,860 1,275
2,210
2,400
2,375
I,250
I
* Liquid diet t Soft diet; cortisone 50 mg. 1 Cortisone 150 mg. daily until forty-third 0 High protein, high carbohydrate diet
day
by proIonged administration of cortisone. (TabIe II.) The cortisone was discontinued on the eightythird day.and the patient continued to have an exceIIent appetite and gained weight slowly. She received a tota of 7,300 mg. of cortisone. After the cortisone was discontinued a11 grafts that had previously been appIied continued to grow. FoIIowing the termination of cortisone therapy the eosinophi1 count returned to norma1. The serum protein remained within normal Iimits. Eight major grafting procedures were required to cover the burned areas, with IOO per cent take on six occasions and 85 per cent and 40 per cent take on two occasions. (Table III.) Our impressions from this Iimited experience suppIemented by a review of the other recorded cases may be summarized as foIIows: (I) ACTH or cortisone is worthy of additiona cIinica1 trial in the toxic phase of burns, or from the third to the tenth day. On theoretic grounds cortisone should be the drug of choice. June,
rgp
administration may be contraindicated. (4) Both ACTH and cortisone deIay fibrapIasia but have Iittle effect on epitheIization. (3) In average doses and if not continued for too Iong a period, one may expect grafts to take as in a norma burn if other essentia1 factors are adequateIy controIIed. LOCAL CARE OF THE BURN
At the present time there are two accepted methods of caring for the burned area, employing either pressure dressings or the exposure method. As soon as initia1 shock is overcome with the administration of indicated fIuids, care should be directed toward the management of the open burn. We prefer pressure dressings but recent reports make us cognizant of the vaIue of the exposure method. In dressing the burn after removing the original tentative dressing, a rough estimate is made of the area and depth of the body surface invoIved. We prefer the Jassification of Lund and Browder.14 If gross contamination is present, the wound is gentIy irrigated with ade-
McLaughlin,
732
Neis-Advances
quate amounts of saIine; otherwise we do not recommend any type of wound cIeansing. AII loose skin tabs are removed by dkbridement but care is taken not to rupture blisters if present. We advise against proIonged dkbridement as it may increase Buid Ioss, blood Ioss, increase PATIENT,
TABLE III Y. M., FLAME BURNS, TREATMENT Caloric
-.,-.__
Intake Diet
Days ____--.
Average
~--
FIuids High protein Intravenous feedings Protein diet
1st to 5th.
6th to 28th.. 29th to 37th. 38th to 70th.
I
,_Cortisone
Appetite
Dose
__
25 mg. three times a day
graftings..
___.. Good
_’ Ijo mg. daily
Grafts Eight‘major
____
Medication
Days
5th to 4.znd. 56th to 70th.
900 3,500 4.00 I.400
Improving
_~__ Six, 100% take One, 85% take One, 40% take
pain and thus increase the degree of shock. For the dressing we empIoy 44 mesh gauze impregnated with Iiquid petroIatum. These strips of gauze are appIied smoothIy over the burned areas after which ceIIuIose-cotton gauze or sterile white mechanics paste is evenIy appIied over these areas, and the dressing heId in pIace by wrapping firmIy with stockinette cut on the bias. In appIying these dressings care must be taken to distribute the pressure evenIy so as not to interfere with bIood suppIy or necrosis may result over bony prominences. This dressing is usuaIIy Ieft on for from ten to tweIve days after which time the burned areas are reinspected. If granuIation tissue is cIean and the patient’s condition warrants, grafting is carried out immediateIy at the time of the first dressing in suitabIe areas. At this dressing we do not hesitate to remove sIoughs; and if the bleeding is not too extensive or can be controIIed by hot packs, these areas are immediately grafted. Otherwise we apply a pres-
in Management
of’ Burns
sure dressing incorporating many urethral catheters for saline irrigation. We find that this latter type of dressing will aid in cIeaning up infection and aIso speeds the separation of slough, so that earIy grafting is possible. PeniciIIin is routineIy empIoyed in the earIy phases of burn therapy and aIso during the stage of grafting, but we are convinced that peniciIIin has no effect on established infection in a granuIating burn wound. AI1 patients with burns are given tetanus toxoid or antitoxin early as the chance of contamination with the tetanus baciIIus is great. As soon as the patient is abIe to take nutritive Auids by mouth he is started on a high protein, high carbohydrate diet with Iarge doses of vitamins, particuIarIy vitamin C. We emphasize the importance of constant attention to the patient’s nutrition as this aids in the earIy grafting and the success of graft takes. In the exposure method of treatment the objective is to keep the wound steriIe and dry. CopeIand* in 1887 first described this method, and in 1905 Snevez5 presented its practical advantages. WaIIaceZ7 points out the foIIowing objectives in any form of IocaI treatment: (I) produce a condition of the burned surface unfavorabIe to the growth and muItipIication of bacteria by the production and maintenance of a dry surface if possibIe, the exposure of the surface to Iight if possibIe, and reduction of the temperature of the surface to that of its environment; (2) appIy an antiseptic which is bIand to tissue cells; (3) provide rest of the affected part by immobiIization; (4) Iimit edema by elevation; and (5) render nursing care simpIe. In treating the burned area Wallace cIeans the open portions with a I per cent cetavlon, the bIisters are opened and the raised skin is removed. FoIIowing this the burned surface is dried and insufllated with peniciIIin, using the caIcium salt of peniciIIin diIuted with Iactose, 10,000 units per cc. AI1 sorts of organisms may faI1 on the burned surfaces; but if they are dry, no harm is said to resuIt. BIocker5 does not appIy any type of IocaI preparation; but when the dried areas crack, he recommends pIacing gauze moistened in saIine over the cracks to cover these areas. He recommends removing the sIough as soon as possibIe and grafting before infection takes place. He reports the use of this method on seventy patients with second and third degree burns involving 40 to 50 per American
Journal
oj Surgeq-
McLaughlin,
Neis-Advances
cent of the body surface with good results. He beIieves that in this series the hospital stay was shortened and considers it the method of choice for both superficial and deep burns. Wallace*8 believes that the outstanding features of the exposure method have been as folIOU-S: a more effective controI of infection; transfusions have never been required in the second week or Iater; and no loss of appetite was observed by him. While we have had no experience with the exposure method, many of us remember the probIems encountered during the tannic acid and the tannic acid silver nitrate era in which great difficulty was encountered in keeping exposed areas dry. Certainly such a method would seem to require a great deal more nursing care which in itself offers a rea1 probIem in our modern hospitals. That this method could materially reduce the necessary administration of transfusions in severe burns if grafting is to be successfuIIy undertaken is certainly open to question. THE CONVALESCENT
1952
of Burns
753
ing at the next redressment, this phase of these very debilitating and costIy injuries can be brought to an earlier and more satisfactory termination. REFERENCES
I. A~,aws, F. II., BERGLUND, E., BALKIN, S. G. and
2.
3.
4.
5.
6.
7.
PHASE
This is the final period covering weeks or months after the patient has survived the shock and toxic phases and is Ieft with large open areas devoid of skin. It is this phase which is often referred to as the septic phase for in this period extensive sepsis often is present, ultimateIy Ieading to death of the patient. The objective of this convalescent period is the complete coverage of a11 open areas by new skin in the Ieast possible time. Grafting is invariabIy necessary in third degree burns of any extent and in many areas of second degree J>urns in which infection has produced further damage. Grafting shouJd be started as soon as feasibJe, preferably by the time of the second burn dressing with particuIar efforts directed toward covering the neck, axilla and al1 joint areas at the earliest possible time. Experience has shown that areas which stil1 show Iimited infection may be covered by ne\\ skin, providing the red bIood cell count, the hemoglobin and the serum-protein IeveIs are maintained at high norma readings. In addition it is our practice to maintain a vitamin C intake of at Ieast 500 mg. per day during this period. A definite scheduIe of redressment is established at intervaIs of one week with grafting on each occasion. If in this scheduIe there is pIanned preparation of a new area for coverJune,
in Management
CHISHOL.~I, T. Pituitary adrenocorticotropic hormone in severely burned children. J. A. M. A., 146: 31-33, 1951. ALHICH, ht. E. The effect of heparin on the circulating blood plasma and proteins in experimenta burns. Surgery, 25 : 676680, I 949. BAKER, B. I~., INGLE, D. W., LI, C. H. and EVANS, Il. >l. Growth inhibition in the skin-induced by parentera administration of adrenocorticotropin. Amt. Rec., 102: 313-325, 1948. BAXTER, H., SCHILLER, C. and WHITESIDE, J. II. The influence of ACTH on wound heaIing in man, Plast. CT Reconstruct. Surg., 7: 85-99, I 95 I. BLOCKER, T. G. LocaI and general treatment of acute extensive burns, the open-air regime. Lancet, I: 498-501, 1951. BROOKS, F., DRAGSTEDT, L.. R., W'AHFEK, L. and KNISELY, 31. H. SIudged bIood folIowing severe therma burns. Arch. Surg., 61: 387-418, 1950. BROWN, R. K. and DZIOB, I. hl. Primary treatment of extensive burns. Am. .I. Surg., 79: 288-294,
‘950. 8. COPELAND, W. P. The Treatment of Burns. Med. Rec., 31: 518, 1887. 9. CRASSWELLER, P. O., FARMER, A. W. and FHA~KS, \\‘. R. Experimental burn studies, including treatment with cortisone-active materia1 extractcd from UrinC. &it. M. J., 2: 242-245, 1950. IO. CRASSWELLER, P. O., FARMER, A. W., FRANKS, W. R. and MCLACHLIN, A. D. Three cases of severe burn treated with cortisone. &it. M. J.. 2: 977981, 1950. P. D., MCCLEEKY, R. S. and BALL, CON D. T. An experimenta study of the effect of heuarin on surviva1 time follow&g Iethal burns. Surg., Gynec. t!Y Obst., 92: 35-42, 1951. 12. JAMES, G. W., III, PURNELL, 0. J. and EVANS, E. I. The anemia of therma injury. I. Studies of pigment excretion. J. Clin. Investigation, 30: 181~ I I.
ELROD,
I
19% 1951. 13. JAMES, G. W., III, PUHNELL,L. J. and EVANS, E. I. The anemia of thermal injury. II. Studies of liver function. J. Clin. Investigation. _ lo: IoI-100., 195 T. 14. LUND, C. C. and BKOWDEK, N. C. &timation ot areas of burns. Surg., Gvnec. @,v Obst., 79: 352,I
358, ‘944. I 5. MCCLEERY, R. S., SCHAFFAHZICK,W. R. and LIGHT, R. A. An experimental study of the effect of heparin on the IocaI pathoIogy of burns. Surgery, 26: 548-566, 1949. 16. MCLAUGHLIN, C. LV., JR. Treatment of major burns in naval warfare. Nebraska M. J., 31: 11-19, 1946. 17. MCLEAN, R., MORITZ, A. R. and Ross, A. Studies of thermaI injury. VI. Hyperpotassemia caused by cutaneous exposure to excessive heat. J. Clin. Investigation, 26: 497-504, 1947.
754
McLaughlin,
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18. MOYEH, C. A., COLLER, F.A.. 106, C. and VAUGHAN, H. H. A study of the interrelationship of salt solutions, serum and defibrinated bIood in the treatment of severely scaIded, anesthetized dogs. Ann. SUrg., 120: 367-376, 1944. 19. PARSONS, R., JK., ALRICH, E. RI. and LEHUAN, E. P. Studies on burns. v. Experimental study oft he effect of heparnization and gravity on tissue loss resuIting from third degree burns. Surg., Gynec. (:+ Obst., 90: 722-724, 1950. 20. RAGAN, C. R., HO\I’ES, E. L., PLOTZ, C. r\l., hIEvEn, K. and BLUYT, J. W. Effect of cortisone on production of granulation tissue in the rabbit. Proc. Sot. Exper. Biol. c? Med., 72: 718-725, r94q. 21. Ross, R., WEISIGEH, J. R. and IMORITZ, A. R. Studies of thermat injury. VII. PhysioIogicaI mechanisms for death durmg cutaneous exposure to excessive heat. J. Clin. Inwstigution, 26: 5”$-5 19, 1947. 22. Rcscarch on burns. Lancet, 2: 635641,
1950.
in Management
of Burns
23. ROSEUTHAL, S. AI. and TABOR, H. T. EiectroIyte changes and chemotherapy in experimental burn and traumatic shock and hemorrhage. Arch. .%Ug., f 1: 244-252, 1945. 24. ROSENTHAI., S. hI. Experimental chemotherapy of burns and shock. Pub. Health Rep., 58: 513522, 1948. 25. SNEVE, H. The treatment of burns and skin grafting. J. A. M. A., 45 : r-8, I 905. 26. TAMEKIN, J. A. ACTH and burns. J. A. M. A., 145: 925, 1951. 27. \\‘ALLACF.,A. B. Treatment of burns. Med. Press, 225: 191-194, 1951. 28. \fr~~r.~c~, A. B. The exposure treatment of burns. Lancet, 1: $0r-504, 195 I. 29. WNTELAW, X1. J. and WOODMAN,T. W. The trcatment of severe burns with ACTI I. J. C/in. Endocrinol., 10: I 171, r95o; and WHITELAW, \/I. J. Physiological reaction to pituitary adrcnocorticotropic hormone CACTI I) in severe burns. J. A .111. A., 145: 85-88, 1951.
ACTINOMYCOSIS of the breast may be secondary from the lung by direct extension through the chest waI1, or primary. Early cases resemble an acute mammary abscess. Incision and drainage pIus antibiotics usuaIIy effect a cure, Advanced cases with multiple chronic abscesses and numerous fistuIous openings occasionalIy require simple mastectomy in addition to preoperative and postoperative therapy with the suifa drugs, antibiotics (especiaIIy penicillin) and genera1 supportive treatment. Some of these patients have had repeated breast abscesses with discharge of yelIow pus through the nipple-a characteristic history that shouId make the surgeon suspect the presence of the actinomyces bovis. (Richard A. Leonardo, M.D.)
American
Journal
of Surgery