11
THE ROLE OF INFECTION IN BURNS* The Theory and Treatment With Special Reference to Gentian Violet BY ROBERT HENRY ALDRICH, M.D.\s=d\ The author wishes it to be understood that to Dr. W. M. Firor, Associate Professor of Surgery in the Johns Hopkins Hospital, be- longs the full credit for conceiving the in- fectious theory in the symptomatology of burns and the treatment of the latter with gentian violet as herein described. Due to his absence from this country, he was un- able to follow up this problem fully, and delegated the privilege of publication to the author. The first cases studied were with Firor at the Johns Hopkins Hospital and the later ones were patients on the Harvard Surgical Teaching Service of the Boston City Hospital. THIS paper deals chiefly with modern con- ceptions regarding the physiology, chemistry, pathology, and treatment of burns. There is no attempt made to present a full history of any of these aspects, as a brief review of the literature reveals a certain cyclic recurrence of ideas and treatments, and also, during the last few years, a sufficiently conclusive group of theories, experiments and panaceas. Each new trend in medical progress has had some effect on the general ideas concerning burns. These new ideas were plausible at the time, but when subjected to careful analysis and experimentation, fell into disuse or were clung to out of habit or lack of a better sub- stitute. Each of these theories carried with it a form of treatment which answered the path- ology of the condition as it was understood at the time, but the majority of these theories are now se obsolete as to have no value save in an historical sense, and therefore will not be dis- cussed here. There are, however, two theories which must be considered and evaluated, and a third which will be mentioned briefly before it is discarded. Any theory, to be of value, must be able to explain the various phenomena encountered in a burned patient, from the termination of the primary shock (which, in the opinion of the au- thor, is an entity in itself similar to any other surgical shock), through the patient's hospital course, which is characterized by fever, leuco- cytosis, blood changes, secondary infection, and the other well-known sequelae, and the gross and microscopic specimens from postmortem exami- nation. A theory which will be considered briefly sup- poses that the destruction of the functions of the skin is the causative agent of the symptoms and pathology of burns; the functions included here being that of excretion, heat regulation, and sensation. A variety of ingenious experiments have been carried out along these lines. The *From the Harvard Surgical Teaching Service of the Boston City Hospital. Read at a meeting presented by the Harvard Surgical Teach- ing Service of the Boston City Hospital in February, 1932. \s=d\Aldrich\p=m-\Assistant in Surgery, Out-Patient Department, Bos- ton City Hospital. For record and address of author see "This "Week's Issue," page 335. factor of heat regulation has been studied by keeping the burned animals at different tem- peratures; this however has always proved un- satisfactory, for it has been shown that in spite of being supplied with the optimum temperature the animals still exhibited the usual symptom complex associated with burns. Likewise rab- bits have been burned over the entire extent of both ears, with and without section of the sen- sory nerves, with no variation between the two groups16. There have been no marked changes in the eatabolic substances in the blood when the skin has been experimentally robbed of its excretory function, such as in the gilding of the entire body11. In the face of these results it is impossible to consider the destruction of skin of vital importance. The two most widely accepted theories are: 1. The theory which supposes that there is some toxin liberated from the burned area which makes its way into the blood stream and pro- duces a toxemia. 2. The theory which explains the phenomena on the various known changes in the blood stream and in the altered function and com- position of the blood. The theory of toxemia has been advocated by a large group of investigators. It is based on the assumption that there is formed in the site of the burn, or in the burn itself, a toxic sub- stance which is responsible for the general reac- tion of the patient. Many substances described by observers have been found in the blood, in the burned skin, and in the urine. The variety of substances is so great, including as it does pyridine, guanidine, peptone, primary and sec- ondary proteoses, histamine and ptomaines, that it indicates a lack of agreement as to the actual toxin; added to this is the fact that few of the investigators have been able to check the results of others. Reiss20, Lustgarten13 and Spietschka25, all suc- ceeded in finding various substances in the urine of burned patients which were toxic when in- jected into animals. There was, however, no unified opinion as to what these were, nor were they always present. Greenwald10 reported two fatal burns in chil- The New England Journal of Medicine Downloaded from nejm.org at SANTA BARBARA (UCSB) on May 3, 2016. For personal use only. No other uses without permission. From the NEJM Archive. Copyright © 2009 Massachusetts Medical Society. All rights reserved.

Burn Infection

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Page 1: Burn Infection

THE ROLE OF INFECTION IN BURNS*The Theory and Treatment With Special Reference to Gentian Violet

BY ROBERT HENRY ALDRICH, M.D.\s=d\

The author wishes it to be understood thatto Dr. W. M. Firor, Associate Professor ofSurgery in the Johns Hopkins Hospital, be-longs the full credit for conceiving the in-fectious theory in the symptomatology ofburns and the treatment of the latter withgentian violet as herein described. Due to

his absence from this country, he was un-able to follow up this problem fully, anddelegated the privilege of publication to theauthor. The first cases studied were withFiror at the Johns Hopkins Hospital andthe later ones were patients on the HarvardSurgical Teaching Service of the BostonCity Hospital.

THIS paper deals chiefly with modern con-

ceptions regarding the physiology, chemistry,pathology, and treatment of burns. There isno attempt made to present a full history ofany of these aspects, as a brief review of theliterature reveals a certain cyclic recurrence ofideas and treatments, and also, during the lastfew years, a sufficiently conclusive group oftheories, experiments and panaceas.Each new trend in medical progress has had

some effect on the general ideas concerningburns. These new ideas were plausible at thetime, but when subjected to careful analysisand experimentation, fell into disuse or wereclung to out of habit or lack of a better sub-stitute. Each of these theories carried with ita form of treatment which answered the path-ology of the condition as it was understood atthe time, but the majority of these theories arenow se obsolete as to have no value save in an

historical sense, and therefore will not be dis-cussed here. There are, however, two theorieswhich must be considered and evaluated, and athird which will be mentioned briefly before itis discarded.Any theory, to be of value, must be able to

explain the various phenomena encountered ina burned patient, from the termination of theprimary shock (which, in the opinion of the au-thor, is an entity in itself similar to any othersurgical shock), through the patient's hospitalcourse, which is characterized by fever, leuco-cytosis, blood changes, secondary infection, andthe other well-known sequelae, and the gross andmicroscopic specimens from postmortem exami-nation.A theory which will be considered briefly sup-

poses that the destruction of the functions of theskin is the causative agent of the symptoms andpathology of burns; the functions included herebeing that of excretion, heat regulation, andsensation. A variety of ingenious experimentshave been carried out along these lines. The

*From the Harvard Surgical Teaching Service of the BostonCity Hospital.Read at a meeting presented by the Harvard Surgical Teach-

ing Service of the Boston City Hospital in February, 1932.\s=d\Aldrich\p=m-\Assistant in Surgery, Out-Patient Department, Bos-

ton City Hospital. For record and address of author see "This"Week's Issue," page 335.

factor of heat regulation has been studied bykeeping the burned animals at different tem-peratures; this however has always proved un-satisfactory, for it has been shown that in spiteof being supplied with the optimum temperaturethe animals still exhibited the usual symptomcomplex associated with burns. Likewise rab-bits have been burned over the entire extent ofboth ears, with and without section of the sen-sory nerves, with no variation between the twogroups16. There have been no marked changesin the eatabolic substances in the blood whenthe skin has been experimentally robbed of itsexcretory function, such as in the gilding of theentire body11. In the face of these results it isimpossible to consider the destruction of skinof vital importance.The two most widely accepted theories are:1. The theory which supposes that there is

some toxin liberated from the burned area whichmakes its way into the blood stream and pro-duces a toxemia.2. The theory which explains the phenomena

on the various known changes in the bloodstream and in the altered function and com-

position of the blood.The theory of toxemia has been advocated by

a large group of investigators. It is based onthe assumption that there is formed in the siteof the burn, or in the burn itself, a toxic sub-stance which is responsible for the general reac-tion of the patient. Many substances describedby observers have been found in the blood, inthe burned skin, and in the urine. The varietyof substances is so great, including as it doespyridine, guanidine, peptone, primary and sec-ondary proteoses, histamine and ptomaines, thatit indicates a lack of agreement as to the actualtoxin; added to this is the fact that few of theinvestigators have been able to check the resultsof others.Reiss20, Lustgarten13 and Spietschka25, all suc-

ceeded in finding various substances in the urineof burned patients which were toxic when in-jected into animals. There was, however, nounified opinion as to what these were, nor werethey always present.Greenwald10 reported two fatal burns in chil-

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Page 2: Burn Infection

dren, in which death occurred with hypogly-cemia, there being no description of the burnsthemselves. He then carried out some experi-ments on rabbits in which he found that all ofhis animals died with hyperglycemia. He de-scribed the cause of death as being due to twofactors, the first pure shock ensuing soon afterthe burn, the second, coming on later, supposed-ly caused by a degeneration of the adrenals.Again he did not describe the burns at all, ex-cept to give their depth and extent.Olbrycht17 confirms the reports emphasizing

the degenerative changes in the adrenals, hisanimals also dying in hyperglycemia. He be-lieved these changes due to the burned tissues,and advised débridement of the burn and in-jection of adrenalin. Again there is no descrip-tion of the burns.Bardeen1, in a study of five fatal burns in

children, dying from four to nine hours afterbeing burned, observed degenerative changes inthe liver, spleen, kidney, and bone-marrow, withgeneral edema of all the lymphoid tissue, theedema being most marked in the germinal cen-ters. He describes this picture of the lymphglands as being practically identical with thatseen in patients dying with an acute infection.He concludes that he has found enough path-ology to eliminate any theory other than theone of toxemia. His paper, however, was pub-lished long before Underbill29 had shown thatburns over the abdomen and chest cause anelevation of intra-abdominal temperature to as

high as 110 degrees and one wonders whetherthis factor might not have played an importantrôle in the tremendous shock and sudden deathhe observed in his patients.Pfeiffer18 was able to isolate split proteins

from the burned skin, and found these to beneurotoxic and necrotoxic. He worked out theirchemistry, and described them as being solublein water, alcohol and glycerole, and insolublein chloroform and ether.Robertson and Boyd21,22 claim that there is

found in the skin of burned animals a toxinwhich "circulates in the blood, either in or ad-sorbed by the red blood corpuscles, and whichcauses the symptoms seen in bad superficialburns, and in some eases, death". . . . "Thetoxic substance consists of two portions, one ofwhich is thermostabile, diffusable, and neuro-

toxic; the other is thermolabile, colloidal, andnecrotoxic. Chemically, the toxin consists of aprimary and secondary proteoses." They alsostate that an extract of normal skin preparedas a control is not toxic when injected into anormal animal, and further, that whole bloodfrom a burned animal when injected into aguinea pig will cause a toxic syndrome whichcorresponds exactly to that seen in a burn. Theyadmit that boiling of the extract tends to weakenits potency as a neurotoxic agent, in spite of

the fact that they specifically state that thetoxin is thermostabile.Underhill and Kapsinow were unable to con-

ceive of a toxin derived from burned areas, andrepeated the experiments of Robertson andBoyd, duplicating them in every detail. Theyconfirmed the results above described, in thatan extract of burned skin prepared accordingto the technique of Robertson and Boyd wastoxic when injected into guinea pigs. They alsoobtained the same results by preparing and in-jecting normal skin in the same manner. Stillunable to believe in a skin toxin, they analyzedthe extract, which is alcoholic, and found a suf-ficient quantity of alcohol to account for thesymptoms of the animals. As a control, thissame quantity of alcohol was injected into theguinea pigs with exactly the same toxic results.This observation leads one to believe that theprimary and secondary proteoses discovered byRobertson and Boyd was simple ethyl alcohol.They also cast doubt on the toxic content ofwhole blood from a burned patient by repeatingthe experiments, finding no toxicity resulting.In his report on the tannie acid treatment of

burns, Davidson9 concluded that he was deal-ing with some toxin, and thought that by coagu-lating the entire burn, he was preventing ab-sorption. He states, in his paper, that in thosecases in which he obtained a good eschar therewere very few untoward symptoms even insevere burns. This finding held true so long asthe eschar remained dry, but as soon as theeschar showed signs of softening, or where therewas underlying infection, there was an increasein temperature and the usual symptoms andphysical signs of toxemia were exhibited. Itwill be seen later that this statement is less anargument for the toxic theory than against it.It is thus seen that all the evidence in support

of the theory of the absorbed toxins is indefiniteor contradictory. There seems to have been noagreement as to the nature of the toxin, or themanner in which it works. Many of the experi-ments are refuted by repetition. The evidencewhich remains is only clinical observation andcan in no way be considered proved. The new-est and most convincing experiment to under-mine the theory of toxemia is that of Under-hill, Kapsinow, and Fisk29. They injected try-pan and méthylène blue into animals after theywere burned, and found that there was an in-creased capillary permeability from the bloodinto the edema fluid of the burn, also a dimin-ished rate of absorption of the dyes from theedema area back to the blood. In fact, theyfound that substances which rapidly pass fromthe blood into the injured area, were not reab-sorbed to a significant extent, if at all. To com-plete this experiment, they injected lethal dosesof strychnine both into the burn and theperiphery of the burned area, and found thatabsolutely no symptoms of poisoning were ex-

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Page 3: Burn Infection

hibited by the animals. It seems conclusive,therefore, that if such substances as trypan blueand strychnine were not absorbed from a burnedarea, no vague toxin would be picked up by theblood stream in sufficient concentration tocause the symptoms and signs accounting forthe so-called toxemia of burns.The second theory to be considered, is that

one based on the changes in the blood follow-ing burns. This problem has been very com-pletely and brilliantly worked out by Under-bill, Carrington, Kapsinow and Pack27. Theyfound that in extensive superficial burns therewas a concentration of blood, and that this con-centration has a great deal to do with the out-come of the patient. Their work in this experi-ment was carried out on twenty-one victims ofa local theatre fire. As long as these patientsstayed in the hospital, their blood pictures werefollowed. A summary of the findings showeda marked increase in hemoglobin and a distinctdecrease in the blood chlorides. With the con-centration of the blood, there was a fall in bloodpressure and a lowered temperature. It wasalso observed that by the restoration of normalblood concentration, there were marked evi-dences of improvement, and that the develop-ment of the usual sequelae of extensive burnswas checked. Somewhat later, Underhill, Kap-sinow and Fisk29 carried on further work as tothe mechanism of blood concentration. It wasshown that a superficial burn involving approx-imately one-sixth the total surface area of therabbit, induced within a period of six hours a

significant loss of fluid from the blood in pro-ducing a subcutaneous edema. The fluid lossreached its height in the first twenty-four tothirty-six hours and then diminished. It wasfurther demonstrated that under experimentalconditions a burn of one-sixth of the body area

gives a fluid loss of seventy per cent of the totalblood volume in twenty-four hours. If these fig-ures can be applied to man, it will be seen thatan adult weighing sixty-five kilos and having ablood volume of 5,000 cc. would lose 3,500 cc.

of fluid in the first twenty-four hours. Withsuch a terrific loss of fluid, there is no need tolook farther for the cause of blood concentra-tion in superficial burns. This theory, then,which has been well worked out with controlledexperiments, offers a conclusive and reasonablebasis for at least some of the symptoms ofburned patients. However, it has also beenshown by the same experimenters, that by a

proper forcing of fluids in the treatment ofburns, it is possible to aid the body in com-

pensating for the fluid loss, and that the bloodcontent can be kept within normal limits. Evenunder these circumstances, there is still a dis-tinct mortality in burns. This observation hasbeen made by every one who has had any ex-

perience with burns, if the experimenter hasbeen careful in the forcing of fluids and has

kept a close study of the blood picture. Itwould seem, therefore, that another factor mustenter into the mortality of burns. It is withthis factor, and a treatment to control it, thatwe shall deal from now on.There are a number of obvious features which

are presented by all patients suffering fromlarge superficial burns. Careful study of thesewill reveal several important points.The first feature to be considered is the pri-

mary shock which occurs almost immediately.This seems to differ" in no way from any trau-matic or surgical shock and certainly occurs be-fore any fluid loss in the form of edema of theburned area is manifested. It also occurs beforeincreased A^aseularity around the burned areacan be demonstrated. Consequently, it seems

logical that it cannot depend on these factors.The answer to primary shock is still a debata-ble question and no attempt will be made tosolve it at this time. It is sufficient to say thatif it is combated early and adequately, withheat, rest, fluids and stimulants, it can be over-come in the majority of cases. It is our opin-ion that shock has little to do with the latercourse of the burn if the patient survives.Once the patient has recovered from shock,

he is usually fairly comfortable for the firstfew hours, regardless of the form of treatmentwhich has been used on the burn. Later, undermost forms of treatment, except tannie acidand the one to be described shortly, the follow-ing phenomena can be observed. The burnedarea becomes edematous, oozes fluid. At thesame time the blood of the patient begins toshow the characteristic concentration. The burnitself looks clean in the sense that there is noinfection or necrosis. The patient has littlepain and is not actively ill. The temperaturein this period is usually normal or only slightlyelevated. The pulse is usually of good qualityand not markedly rapid.Beginning about the twelfth to eighteenth

hour following the burn, the patient begins toshow signs of the so-called toxicity. He startsto grow stuporous, or perhaps restless. Thetemperature becomes elevated, the patient com-plains of pain ; nausea and vomiting set in. Ex-cept for a slight increase in hemoglobin, leuco-eytosis and a moderate increase in the bloodsugar and lactic acid, there is not much changein the normal blood picture, provided fluids arebeing forced adequately. From this time up toabout the seventy-second hour, a characteristicsyndrome occurs. The patient's general condi-tion obviously grows worse. He is nauseatedand cannot retain food or fluid by mouth. Hegrows restless and at times delirious. The faceis flushed, the pulse and respiration are in-creased, and the temperature becomes elevatedin a curve that is characterized by staircase in-creases, until at about the seventy-second hourit reaches a maximum of between 1021/o and

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Page 4: Burn Infection

105 where it is sustained for a time, plateau-like. This plateau remains constant for a num-ber of hours, when the typical picket-fence fluc-tuation begins. The appearance of the burnduring this period also follows a marked andcharacteristic change. After the first twelvehours, signs of early sepsis present themselves.The fluid over the burned areas, at first clearand odorless, becomes turbid and malodorous.The turbidity increases to the stage of frankpus and the pathognomonic odor of a burnedpatient is apparent. This effect also reaches itspeak at about the seventy-second hour. Duringthis time, the usual complications and sequelaesuch as albuminuria, extreme exhaustion, sec-ondary anemia and delirium take place. Thissequence of events during the first three daysin an extensive superficial burn is remarkablyconstant.Ignoring previous theories and regarding the

picture speculatively, one is impressed with thefact that there is enough obvious infection pres-ent on the burned area to account for all symp-toms and physical signs exhibited by the pa-tient. It was with this in mind that Firor de-cided to investigate burns from a bacteriologicalstandpoint.Previously all the more generally accepted

treatments of burns had been tried out, and com-

pared on the same patient and on different pa-tients. It may be stated, in passing, that theresults of this investigation proved the tannicacid technique superior to others.A review of the literature revealed the fact

that no work had been done on the bacteriologyof burns. Without any precedent to go on, itwas decided to begin bacteriological studies on

the patients as soon as they were admitted tothe hospital, and follow these right through.The procedure was simple. At the time of ad-mission, before treatment, cultures were takenof the burned area and of the fluid under theblebs, if there were any. Repeated cultures werelikewise obtained at short intervals. For thefirst twelve hours, these areas were practicallysterile, as was to be expected. A few contami-nants, such as staphylocoecus aureus and albusand B. eoli were frequently found, but thegrowth was slight. After the first twelve hourperiod it was found that in one hundred percent of the severely burned patients and in a

large majority of the minor burns, there couldbe grown from repeated cultures the beta-hemo-lytic or the gamma streptococcus. The con-centration of these organisms increased with theobvious signs of sepsis and the beginning ofthe toxicity of the patient, until after forty-eight to fifty-six hours pure cultures of thestreptococcus could be obtained, having out-grown all the other organisms. Coincidentally,the characteristic bad effects of the burn wereshown by the patient.It seems reasonable to suppose that when a

large surface of the body has been destroyedby a burn, and becomes involved with strepto-coccus infection, certain ill effects should re-sult. Furthermore, the general condition of thepatient and the characteristic chart of the fe-ver would be one which coincided with that ofany widespread streptococcus infection. Addi-tional evidence has been obtained by takingblood cultures from patients after the temper-ature has started to swing in the picket fencecurve. These cultures were positive for the in-vading streptococcus. Another bit of evidencein favor of our theory is that in fatal cases thehemolytic streptococcus was found in the heart-blood and in the lungs in instances of terminalpneumonias.It was then decided that perhaps the best

form of treatment would be one which aimedat killing the organisms thus sterilizing theburns. We felt that if we could show that no"toxic" symptoms occurred when the burns re-mained sterile, then it would be logical to as-sume that infection was the essential factor inthe production of these "toxic" symptoms. Onemight suggest here that picric and tannic acidshave some antiseptic properties, but they are inno way specific for the streptococcus. Their bac-tericidal properties are very weak, and in thecase of tannic acid, once the eschar is formed,there can be no further penetration, and henceno action on the underlying infection. The co-

agulating properties of tannic acid which David-son interpreted as rendering the toxic substancenon-absorbable, is not so interpreted by the au-thor, who feels that the value of tannic acid liesin the formation of an eschar over a practicallysterile burn, and the sealing of the burn, whichprevents fluid loss and infection. As Davidsonpointed out, the general condition 'of the patientdepended on the condition of the eschar. Alllarge burned areas treated with tannic acideventually become infected and it is at thattime the "toxemia" develops. Three disad-vantages of the tannic acid treatment are: (1)The eschar is brittle and will crack if exposedto strain. (2) The eschar is quite dense andfluid proof, so that any underlying infectionwill not present itself until quite extensive. (3)Minute islands of unburned epithelium such asthose found in practically all third degreeburns, are not preserved but are destroyed bythe infection beneath the eschar.In 1912, Churchman, working on the bacteri-

cidal and bacteriostatie properties of the ani-line dyes proved conclusively that gentian violetwas practically a specific for the gram-positiveorganisms. These experiments have been re-

peated by us and our results confirm his find-ings. In concentrations of one to one million, intest tube and agar plate, germs were not killed,but could not grow. When he increased his con-centration to one to ten thousand the gram-pos-itive organisms were killed. Churchman not

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Page 5: Burn Infection

only used gentian violet experimentally in thelaboratory, but also on patients. In the latteruse it was not always employed superficially,but was injected in the joints and the bloodstream. This dye has been used intravenouslyin one half of one per cent solutions for thetreatment of blastomycosis and septicemias andin such quantities that the entire patient becamestained, but without untoward symptoms. Thislast statement is offered to refute any objec-tion which might be made as to its toxicity. Inall the literature, there has been no report ofgentian-violet poisoning.Gentian-violet is a coal-tar derivative, try-

phenyl-methylamine, and is slightly alkaline inits reaction. It is quite cheap, and comes eitherin crystalline or tablet form. The tablets shouldnot be used, as the cohesive substance in themis quite irritating to the burned patient. It isreadily soluble and an aqueous solution of oneper cent can be made with great ease. The so-lution is sterile at all times. From this briefdiscussion of the properties of the dye it can beseen that it has two valuable characteristicswhich answer the problems offered by a burnedpatient ; it is a specific antiseptic for the invad-ing organism and because of its Ph reaction, to-gether with the contained methyl radical, itreacts with the burned flesh to form a thin, lighteschar, tough but flexible. This eschar when sit-uated in the folds of the body will bend but notcrack. The burn is thus sterilized and pro-tected from further infection by an almost idealprotective eschar. The dye also produces prac-tically instantaneous analgesia.TECHNIQUE OP THE GENTIAN VIOLET TREATMENT

When a patient is admitted with a fresh burn,unless it is covered with oils or grease, there isno need to do any preliminary cleaning, the dyein one per cent solution being sprayed on theburned area immediately. The usual proce-dures to combat any existing shock are carriedout. The patient is then sent to the ward andplaced so that the burned area is uppermost.The burn is not covered with a dressing. Thebedclothes are supported by a cradle and inthe cradle a light bulb is placed. This light andthe heat it generates is in no way to be con-fused with the dry heat treatment of burns. Itis merely there to keep the patient warm. Thetemperature under the cradle is maintained be-tween 84°F. and 88°F., this being the temper-ature found to be most comfortable for the pa-tient. For the first few hours, gentian violet issprayed on the burned areas every two hours. A.light eschar is formed very rapidly, the wet ooz-ing areas becoming dry and tough. The burnis thereby sealed sterilely under an impermeablecover. Further infection is thus kept out andthe loss of fluids through the serous ooze elim-inated. Likewise, by the time the preliminarysedative has worn off, pain has ceased. After

the eschar has formed, the patient is sprayedevery four to six hours during the day. Anyblebs that have formed are opened and the un-stained portions then presenting are sprayed.This treatment continues until healing is com-plete. One remarkable thing that has been no-

ticed is that in practically none of the burns,unless actual charring has taken place, is all theepithelium destroyed and that there exist manysmall islands throughout the lesion which willlive and spread rapidly if not destroyed by sep-sis. This spread takes place unhindered underthe eschar which acts as a scaffolding and whichwill curl up on its periphery as the healing pro-gresses. These curls can be trimmed away toprevent the forming of any pockets for infec-tion. If the burn is so deep and so extensivethat skin grafting is going to be necessary, theeschar is allowed to remain on for about threeweeks after which time it can be softened andremoved by warm compresses of sterile salt so-lution. By that time the granulations havebuilt up enough to graft, and, being sterile, theyaccept new skin readily. This is a brief descrip-tion of the way in which a fresh burn is treated.If a patient presents himself with an old

burn already septic, the treatment can also beinstigated with no initial clean up. The neerot-ic matter and pus is likewise converted into an

eschar, but this eschar differs from that of afresh burn by being irregular, in pieces, andfloating. This eschar is usually removed everyday and the area sprayed immediately after-ward. Otherwise the treatment is the same asthat described for fresh burns.It is obvious, then, that this treatment is sim-

ple, not characterized by painful daily dress-ings, by having to remove the applications ofthe preceding day, or by manipulating and dis-turbing the patient. It can be carried out bythe nursing staff with supervision.The picture of a patient under this treatment

is quite striking, especially when compared withpatients treated with the older procedures. Oninspection, whether the burn be one day or twoweeks old, it is observed that the patient doesnot feel bad. Except for the preliminaryshock, no great prostration is found. The pa-tient is usually lying quietly in bed, in no ap-parent pain ; he is not flushed or stuporous withfever. He is willing and able to take foods andfluids by mouth, and does not have to be car-ried along by the usual supportive intravenousmethods. If the burn is not too extensive, thepatient can actually be sitting up, taking care

of himself to the extent of feeding himself andbeing able to walk to the bathroom. The gen-eral condition as evidenced by the chart is usu-ally quite satisfying. The fever, if any, is mod-erate, and not the septic type. The laboratorywork gives no indication of nephritis, or unu-sual changes in the blood. There is no evidenceof increasing anemia since there is no blood de-

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Page 6: Burn Infection

struction. The chlorides remain up and there isno increase in the non-protein nitrogen. In gen-eral, the average burned patient thus treated isnot the awful spectacle that one has grown ac-customed to expect. In addition, because theburn remains clean, the difficulty of handling amalodorous patient in the open ward does notarise.It is most important to emphasize a few points.

First, it must be stressed that there is no wayto heal a burn and adequately care for the pa-tient without constant supervision and interest.There is practically no burn which is so ideal-ly situated, as to permit constant exposure toair, and so located that it is entirely free frombody secretions and contamination. For ex-

ample, in all large burns, certain portions willhave to be undermost and these must be re-garded as potentially infected. The eschar mustbe examined daily for softening, which may becaused by three factors; first, the secretions ofthe body; secondly, the underlying fat, whichin severe burns becomes liquefied; and, finally,by invading infection. As soon as softeningis seen, and this eschar unlike that formed bytannic acid does not conceal evidences of mois-ture, the soft part must be removed. This isdone by picking it up with forceps and if man-aged carefully will not cause the patient dis-comfort. The surfaces thus exposed are sprayedin the usual manner.The general care of the patient is of prime

importance. This includes forcing of fluids, anda high vitamin and high caloric diet.In brief, then, we feel that the cause of the

so-called toxic symptoms seen in burned pa-tients is secondary infection, due to the beta-hemolytie and the gamma streptococcus. Thisinfection can be kept down to a minimum bythe use of gentian violet, and if this is done, inaddition to complete general care of the patientwith special attention to the eschar, the prog-nosis in the severely burned patient is greatlvimproved.

SUMMARY

1. A review of the literature was made, whichtended to disprove the absorption theory andthe blood concentration theory as being the eti-ological agent in the toxicity of burns.2. Bacteriological studies were done on a

series of burned patients, and the beta-hemo-lytic or gamma streptococcus was found to bethe invading organism in all extensive burns.3. When a surface of the body is burned,

there are no marked constitutional changes ifthe burns are kept free of infection.4. It has been shown that the aniline dye,

gentian-violet, is highly bactericidal against thegram-positive organisms.

5. Gentian-violet is a coagulant and an anal-gesic agent in burns ; there is no loss of fluidfrom the burned area, which is sealed under the

eschar. Invasion by contaminating organisms iskept down to a minimum. The patient is prac-tically free from pain.

6. It has been shown that even in third de-gree burns, there are many small islands ofepithelium in the hair follicles that will spreadunder the scaffolding of the eschar when infec-tion is kept down, hence diminishing the neces-sity for skin grafting.7. A few typical cases are reported. One of

these is a third degree burn of three fifths of thebody area, which lived eighty-four days andshowed at autopsy none of the changes whichare supposed to be associated with burns.A REPORT OF FOUR BURNED PATIENTSTREATED IN THE BOSTON CITY HOSPITALWITH GENTIAN VIOLET TECHNIQUECase 1. The patient was a twenty-six year old

white male in very good health. He was burnedwith scalding hot water on a boat in Boston Harbor.He was brought immediately to the Boston CityHospital. On admission he was in no shock, andimmediate treatment was begun on the burns. Theburns were of second and third degrees and covered

CASE 1, PLATE I.

the entire face, the upper portion of the chest, abouthalf the neck anteriorly, and practically all of thearm surface and hands. Within twelve hours afterthe treatment was instigated an eschar had formed.This eschar remained dry throughout his stay in thehospital. During his stay, of nineteen days, from

CASE 1, PLATE II.

April 18, 1931 to May 6, 1931, his temperaturereached 100°F. five times. The rest of the time itwas under 99°F. An examination of the blood andurine revealed no abnormalities at any time duringhis stay. Within a week after admission the eschar

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Page 7: Burn Infection

began to peel off as healing took place under it.He was discharged as completely well nineteen daysafter admission. The scars left by the burns were

CASE 1, PLATE III.

composed of soft, new, pink epithelium. No skingrafting was necessary. Photographs showed thepatient one day after admission and on the day ofdischarge.Case 2. W. M. A forty-seven year old white

male, admitted to the Boston City Hospital, March17, 1931; discharged May 22, 1931. On the eveningof March 17, 1931, the patient's clothes caught onfire when he fell asleep smoking a cigarette. Hedid not awaken immediately, because he was intox-icated. When he finally came to, the upper portionof his clothing had almost burned off. He wasbrought into the hospital in a state of mild shock.The temperature on admission was 97°F., the pulse100, and he was in no pain. An examination re-vealed a third degree burn over the entire back, theback of the neck, left arm, left hand, left axilla,left chest, and about half of the right arm. Hewas placed immediately under a cradle lying on hisabdomen and gentian violet technique was begun.The patient remained completely afebrile and freefrom symptoms, such as pain, discomfort, or tox-icity for one week. The urine showed no casts, redcells, white cells, or albumen. At the end of thefirst week he became so uncomfortable lying onhis abdomen that he had to be turned over on hisright side. This was done only at night, as thepatient was up and about during the day. It wasconsidered more important to get the wide expanseof the back healed than to cause the patient dis-comfort and loss of sleep by forcing him to remainon his abdomen. Putting him on his right side, al-lowed the left arm to come into contact with theleft chest wall. This put two burned surfaces to-gether. However, it was deemed" advisable to sac-rifice the inner surface of the left arm and the leftchest wall in an effort to heal the back rapidly.Within two days the eschar of the arm and chestwall had become soft and septic. Every day the soft

pieces of eschar were removed, and the exposed sur-faces sprayed with gentian violet. The eschar oathe back began to curl up around the periphery and

CASE 2, PLATE I.

was trimmed off daily. At all times it remaineddry. As fast as the primary eschar was removedthe broken secondary eschar formed. The first pho-tograph shows the patient shortly after the primaryeschar of the back was removed. During this timehe ran a low-grade fever, the temperature going to

CASE 2, PLATE II.

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99°F. every day. At the end of five weeks the entireback had become covered with new, smooth, softepithelium. He was then placed on his back atnight, and the left arm was elevated and kept away

CASE 2, PLATE III.

from the chest wall by means of a Balkan frame.The second and third photographs show the patientthree days after this procedure was started. Onearea in the midline in the low thoracic region of the

CASE 2, PLATE IV.

back broke down under the patient's weight. Thisarea was treated with gentian violet. The burnedareas on the inside of the left arm and on the left

chest wall, which had been allowed to become sep-tic, did not epithelialize. Here, gentian violet wascontinued until the granulations had built up enoughfor skin grafting. Full thickness pinch grafts weretransposed from the inner aspect of the left thighto these granulations forty-two days after admis-

CASE 2, PLATE V.

sion to the hospital. From then on healing pro-gressed rapidly, and the patient was discharged May22 in the condition shown in the fourth and fifthphotographs. At no time during the patient's stayin the hospital were there any pathological changesdiscovered in the blood or the urine. He was am-bulatory throughout his stay, was able to take careof himself in that he could feed himself and had lav-atory privileges, and throughout his entire stay hadso little pain that no sedatives were required.Case 3. E. A. A thirty-six year old white mar-

ried female. Height, five feet, two. Weight, 212lbs. On the evening of January 9, 1931, the patientwas building a fire in a stove when her clothes be-came ignited. There was no one to help her extin-guish the fire, and before she could do so herself,she had suffered severe burns. She was rushed im-mediately to the Boston City Hospital and arrivedin the Accident Ward in a state of profound shock.Temperature was 97.4°F. Her pulse was very weakand thready but was only 70. She felt cold to thetouch and was wet with perspiration. On examina-tion it was found that all of her burns were thirddegree, and covered her left arm, left axilla, leftside of the thorax, entire back, both buttocks, includ-ing the anus and vulva and the posterior portion ofboth thighs to the knee and the left calf. The pa-tient was put on the dangerous list, and her rela-tives were told that she could not possibly live. Hershock was treated with heat, fluids, given both sub-cutaneously and intravenously, and stimulants inthe form of caffeine and adrenalin. Within 24 hoursthe patient was out of her shock, temperature hadreturned to normal, and the pulse had risen to 90but was of good quality. Twelve hours after heradmission, gentian violet technique was begun andan eschar formed over all the burned areas withineighteen hours. Because of the burn around the

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Page 10: Burn Infection

anus, the bowels were kept completely closed forone week with opium. During this first week thepatient's temperature rose to 100°F. on two occasionsand 101°F. once. She was somewhat uncomfortablebecause of her position on her abdomen, but suf-fered no real pain. Aspirin and codeine were theonly sedatives required to quiet her. The escharremained dry, and no evidence of infection was no-ticed. In the second week the bowels were movedwith enemata and mild laxatives. Infection spreadimmediately under the eschar between the buttocks.During the second week the temperature rose to101°F. twice, and in the fourth week to 101°F. once.During the remainder of the time she ran a low-grade, swinging fever which ranged from 99 °F. to100°F. or slightly above. From the second day ofher admission until discharge, she was on warddiet, and took all of her fluids by mouth. Duringthe middle of the second week the eschar over mostof the burned areas began to soften due to theburned fat beneath. As fast as any softening ap-peared, that portion of the eschar was removed andthe spray continued. She was completely healedat the end of forty-nine days. At this time she wasallowed to sit up with the result that the weightof the body on the new epithelium on the buttockscaused large cracks and fissures to appear. She hadto be put back in bed and wait until these healed."She was finally- discharged on March 20, 1931, com-pletely healed. During her stay there was no changein the urine, and the only change in the blood wasa leucocytosis. The smear, however, was normal.The final healing obtained was without skin graft-ing. There were no contractions, and the scar wasthe same soft, pink epithelium as observed in theprevious cases. It is unfortunate that no photo-graphs were obtained of this patient, for she is anexample of a third-degree burn extending over one-third of the body area that was not a fatality.Case 4. R. B. A nine-year old white female, ad-

mitted to the Boston City Hospital April 4, 1931.Died June 26, 1931. The patient was playing by her-self at home with some matches when her clothingcaught fire. She ran into the street for help. No as-sistance could be obtained until all of her clothinghad burned off of her with the exception of a pairof short woolen drawers. She was admitted to thehospital in extremis. Her temperature was 96°F.Her pulse could not be obtained anywhere. At theapex the heart sounds could be heard very faintly.The rate was about 140. An examination of thepatient revealed a third-degree burn which involvedthe entire thorax, anterior, posterior, and lateral

CASE 4, PLATE I.

aspects, the entire circumference of the neck, theoccipital region of the head, both arms from theshoulder to the mid-lower arm, both axillae, the leftthigh on its lateral aspect for about one-half of its

surface and both ankles. A moderately accurate es-timation of the body surface and of the burned arearevealed that somewhat over three-fifths of the

CASE 4, PLATE III.

body had been burned. She was immediately wrappedup in a sterile sheet and then blankets. A cradlewas put over the bed. She was surrounded by hot-water bottles and put up in reverse Fowler's posi-tion. A subcutaneous infusion of normal saline wasbegun in the right thigh. In an hour's time intra-venous saline and glucose were given. About fourhours after admission the blankets and sheet wereremoved and the burned areas sprayed with gentianviolet. This spraying was repeated every half-hourin an effort to form an eschar as rapidly as possible.At no time did she complain of pain. Six hours afteradmission she was definitely improved. The pulsecould be obtained in the radial arteries and thoughrapid, the quality was not bad. One day after ad-mission she was entirely out of her shock. Hertemperature had risen from 96°F. to 102°F. Thepulse rate varied between 120 and 150. Her respira-tions, which had been 40 on admission, had settleddown to 30. From this day on until her death, eighty-four days after admission, the form of treatmentconsisted of gentian violet aided by all the suppor-tive measures that could be employed. The treat-ment in short was simply a fight against infec-tion all the way through. Because of the positionof the burns, it was impossible to expose more thanhalf of them to air. She was compelled to lie onher back and in order to keep this part sterile, shewas placed on large pads soaked in hexylresorcinol.Repeated transfusions were given; she was put ona high-caloric and high-vitamine diet. As the escharssoftened they were soaked off with sterile normalsaline. She continued to run a swinging tempera-ture of the picket-fence type which varied between100 and 103°F. The pulse remained between 110 and150. After a period of two months had elapsed theanterior and lateral aspects of the thorax and theanterior portions of both arms and the left thighhad formed sufficient granulations for skin grafting.It seemed at this point that recovery was possibleand that as soon as the anterior portion of the body

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Page 11: Burn Infection

had become covered with epithelium, the position ofthe patient could be changed and adequate treat-ment started on the back. However, on the eightiethday the child began to show marked evidence ofcardiac fatigue, in spite of the fact that she hadbeen digitalized twice to the point of vomiting in

CASE 4, PLATE IV.

an effort to slow down the pulse. From this timountil her death four days later, she went steadilydownhill and died of decompensation. Throughouther existence in the hospital there were no changesin the blood other than a leucocytosis. There was

CASE 4, PLATE V.

absolutely no evidence of concentration of theblood, of a change in the non-protein nitrogen or ofthe blood chlorides. The urine remained complete-

ly negative throughout and did not even show theso-called febrile changes. Repeated blood cultureswere also negative. An autopsy was obtained andthe pathological report was practically negative.She had chronic passive congestion of liver, kid-neys, and spleen. There was also slight cerebraledema and congestion. All of these changes canbe explained by the terminal decompensation of theheart. This case is reported as an example of howmuch can be accomplished in an obviously fatalburn.

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