original article: 2014 aba paper
The Fire at Cocoanut Grove Camille L. Stewart, MD
On November 28, 1942, a fire broke out at The Cocoanut Grove Nightclub, in Boston, Massachusetts. The fire claimed the lives of hundreds, and injured 170 patients who were treated at either Boston City Hospital or the Massachusetts General Hospital. With extraordinary leadership and scientific focus, this tragedy led to many important advances in burn management, including improvements in burn wound care, the first descriptions of inhalation injury, formulas to guide fluid resuscitation, and the initial studies of antimicrobial therapy with burns. This overview describes the treatment of the Cocoanut Gove victims, and how it transformed the management of burns forever. (J Burn Care Res 2015;36:232–235)
On November 28, 1942, a fire broke out at The Cocoanut Grove Nightclub, in Boston, Massachusetts. The fire claimed the lives of 498 individuals and resulted in the simultaneous treatment of 170 burn-injured patients at two Boston hospitals.1,2 This tragedy directly resulted in the publication of more than 30 reports related to the management of burns. Knowledge gained while treating these patients included comparisons of multiple types of burn dressings, the first descriptions of inhalation injury, improved formulas to guide fluid resuscitation, and the initial studies of antimicrobial therapy with burns, stimulating significant additional research, and ultimately resulting in many important changes for the care of burned patients. At the time, Cocoanut Gove was a popular restaurant and lounge located in the heart of Boston, just south of the Boston garden. The fire occurred on the Saturday night after Thanksgiving. Despite the fire code limiting occupancy to 600, on that particular evening the nightclub had an estimated 1000 individuals inside.1,3 A number of theories exist concerning the cause of the fire; however, after extensive investigation by the Boston fire department, the official cause was left “unknown.” It was the height From the Department of Surgery, University of Colorado School of Medicine, Aurora. This article was the winning submission for the 2014 ABA Archives History Manuscript Award. Address correspondence to Camille L. Stewart, MD, University of Colorado School of Medicine, 12631 E. 17th Ave, C302, Aurora, Colorado 80045. Copyright © 2014 by the American Burn Association 1559-047X/2015 DOI: 10.1097/BCR.0000000000000111
232
of World War II, and postulations related to arson were initially investigated, but quickly refuted. A bus boy confessed to striking a match adjacent to a faux palm tree that was seen aflame early in the fire. Other theories included faulty wiring installed by a pipe fitter, as well as leaked combustible methyl chlorine gas used as a refrigerant.3,4 Survivors of the fire report that it spread rapidly, and panic quickly ensued.5 Patrons found that all but one exit, a revolving door, was either blocked by furnishings or locked, trapping hundreds inside.6 The Regional Office of Civilian Defense had held a mass-casualty training event in Boston 1 week earlier, allowing thousands of volunteers and medical professionals to be assembled within hours of the fire outbreak.3 All but 11 burn victims were taken to either Boston City Hospital (BCH; 131 living, 180 dead on arrival) or the Massachusetts General Hospital (MGH; 39 living, 75 dead on arrival).1,7,8 The teams of providers were led by Dr. Maxwell Finland at BCH, and by Dr. Oliver Cope at MGH, both of whom later published extensively on their experiences treating these patients.
Burn Wound Care At the time of the Cocoanut Grove fire, the dressing of burn wounds was a subject of debate and varied significantly between hospitals. At BCH, most burn wound treatment focused on the formation of a protective eschar. The extremely painful tannic method was most often employed, in which tannic acid was applied to burned skin to form a protective barrier.9 At BCH there was a large influx of outside physicians and nurses who came to assist with the treatment of
Journal of Burn Care & Research Volume 36, Number 1
the burn patients. Many were unfamiliar with the tannic method, prompting the additional use of the triple dye method at this hospital. This involves the application of gentian violet, methyl green, and acriflavine to the burn wound, which were thought to possess anti-microbial powers and provided a “soft eschar.”9 Alternatively, MGH had embraced a “bland” technique, using petroleum gauze impregnated with boric acid to dress the burn wound, which was then wrapped with large elastic pressure bandages.3,10 This method was developed based on experiments performed at MGH by Dr. Bradford Cannon only a few months before the fire.11,12 A number of patients at BCH were also treated with this method. In the analysis that followed at BCH, Clowes et al9 made a comparison of tannic acid, triple dye, and petroleum gauze burn care, revealing faster healing in the petroleum gauze group and possible survival benefit, corroborating the earlier findings of Dr. Cannon. These results were subsequently reproduced,13 ultimately leading to the phasing out of tannic acid and triple dye methods in favor of the petroleum gauze dressings used to this day.13-15 Thirty years after the fire, the importance of these findings were echoed during the American Burn Association presidential address, wherein Dr. John Moncrief remarked on the “monumental treatise” on burn wound care that resulted from treatment of the Cocoanut Grove fire victims.15
Inhalation Injury Another important breakthrough from the Cocoanut Grove fire was the identification of inhalation injury related to burns. Several of the doors at Cocoanut Grove were either locked or blocked,2,6 forcing hundreds of individuals to breathe in smoke fumes for prolonged periods. Pulmonary symptoms had previously only been reported in relation to inhalation of noxious fumes from the burning of nitrocellulose during a fire at the Cleveland Clinic in 1929. As such, the respiratory complications that developed in these burn patients posed an unexpected “puzzling situation” for the providers at both the institutions.7,16,17 Many cyanotic patients died within minutes of arrival to the hospital, despite absence of obvious external burns, some with edema of the face, neck, and oral structures.7,10,16,18 Several speculated that the inhalation injury was due to an additional gas in the air of the nightclub.7,18 Dr. Cope at MGH wrote that he initially thought the pulmonary symptoms were secondary to an explosion but soon after “it had become clear that there was no explosion, and that only irritating fumes and heat were the cause of the pulmonary inflammation.”19 Dr. Finland at BCH
Stewart 233
came to a similar conclusion, writing “the respiratory irritant was probably part of the hot air, fumes, and particles which resulted directly from the burning of the contents of the various rooms.”7 Dr. Finland noted that many were found to have facial, nasal, and pharyngeal burns, and those with the greatest severity of pulmonary dysfunction had lost consciousness while they remained inside the burning building, resulting in the longest exposure to the smoke.7 Dr. Henry Beecher, a colleague of Dr. Cope at MGH, described the importance of distinguishing patients with inhalation injury from those who were in pain and those with “fear and hysteria,” since all the three presented with agitation and altered mental status.20 Dr. Finland also noted “restlessness” in a number of patients at BCH.7 Treatment of these patients primarily consisted of oxygen therapy, suctioning, and tracheotomy. At BCH, all patients with evidence of respiratory involvement were eventually given oxygen by nasal cannula—however, “because of the paucity of more suitable equipment the greatest reliance had to be placed on the ordinary rubber catheter of the urethral type.”7 There was also experimentation with administration of helium at both the hospitals, which was noted to cause tachycardia compared to oxygen alone.7,20 At the time, respiratory therapy and inhalational therapy were in their infancy, with the first professional association not coming into existence for another 4 years.21 At MGH, only one patient received “artificial respiration” for 5 hours, and two others were intubated but not ventilated for fear that positive pressure would cause hypotension.1,20 Similarly, at BCH, few patients were artificially ventilated. However, 12 patients were given oxygen under positive pressure, since Dr. John Evans of Buffalo, New York, then president of the International Anesthesia Research Society, presented with a “bulky apparatus” to provide this therapy.7 Dr. Finland quipped, “most if not all were not quite as favorably impressed as was Dr. Evans,” but concluded that positive pressure therapy “did not really receive a proper trial in these cases.”7 At MGH, after three admitted patients died from pulmonary edema, restriction of volume resuscitation and permissive hypovolemia were used to attenuate further extravasation of fluids into the lungs.19 Overall conclusions were that the pulmonary and upper airway edema were not always evident upon admission,7 and that the resuscitation of these patients was considered “difficult and unsatisfactory,”18 ending with a call for additional research.8,20 Nearly 20 years later, Dr. Cope published that respiratory tract injury was the primary cause of mortality in burn patients.22 Now, despite being well recognized,
Journal of Burn Care & Research January/February 2015
234 Stewart
inhalation injury remains difficult to treat and the subject of significant ongoing study.23
Fluid Resuscitation During the first day of treatment, 147 units of plasma were administered at MGH, and a remarkable 1065 units of plasma were administered at BCH.8,20 At the time of the Cocoanut Grove fire, a limited number of fluid resuscitation formulas existed which were calculated using laboratory values.19 At BCH patients were given plasma, albumin, and saline, and no specific formula was used.24 Dr. Finland wrote, “The amount of plasma given was, generally speaking, based on the rate and quality of the pulse, on the blood pressure, and later in the day, on hemoglobin and hematocrit.”24 However, given the large numbers of patients and little time to obtain initial lab values, a new formula was developed at MGH. This formula consisted of 500 mL fresh frozen plasma mixed with 500 mL of saline given for every 10% TBSA burned.19 Dr. Cope acknowledged that this volume was inadequate for some patients, but that the formula had “much to recommend it” because of its simplicity.19 Dr. Cope explained that “different degrees of burn may result in different amounts of edema, but it is still true, roughly that the amount of plasma lost from the circulation into the tissue spaces is proportional to the area of the burn.”19 He also noted that a key limitation to current formulas was that they only addressed the current volume deficit without anticipating future volume loss. These insights prompted Dr. Cope to further study fluid resuscitation in burn patients with therapy planned for the first 24 to 48 hours based on %TBSA.25 Higher volumes were prescribed initially and tapered off after 24 hours.25 He noted that hemoconcentration was a late maker of volume loss, and suggested that “the simplest index of the state of balance…was an hour to hour vigil over renal output….adequate hourly outputs in the normal to high range bespeak the adequacy of therapy…a falling or low hourly output calls for immediate increase in therapy.”25 These now-familiar concepts generated further development of formulas to guide fluid resuscitation in burn patients. Today, all such formulas include %TBSA as a critical element in their calculation and are adjusted based on the urine output.26,27
Antibiotic Prophylaxis Systemic antibiotics were given to burn patients at both the hospitals after the Cocoanut Gove fire. Sulfa drugs became available in the late 1930s,28 and
penicillin was given to the first human subject only 2 years earlier.29,30 Then referred to as chemotherapy, the word “antibiotic” would not be introduced for another 3 years.30 As such, experience with their use was extremely limited, “and opinions concerning the efficacy of various forms of sulfonamide therapy in wounds and burns were still divided.”31 At BCH, sulfa antibiotics were given to 76 patients.31 After final analysis, Dr. Finland concluded—“it is fair to assume that most of the surface infections developed under the sulfonamide treatment and were not affected by it.”31 This was the first of the many studies on antibiotic prophylaxis for burns. A Cochrane Database Review conducted in 2013 had conclusions similar to that of Dr. Finland’s.32 At MGH, sulfadiazine was given to all the victims. On the sixth day, patients with temperatures >101°F also received intramuscular penicillin. It was noted that nearly all patients that received penicillin had suffered third-degree burns.8 High infection rates were observed in many thirddegree burns at both the hospitals, motivating further study by Dr. Cope on early excision and grafting of these patients.7,33 The results of these experiments showed decreased infectious rates, improved graft healing, and decreased lengths of hospitalization.33 Further examination demonstrated that early excision and grafting led to improved survival,34 making this practice now the standard of care.35
Conclusions With extraordinary leadership and scientific focus, the management of the Cocoanut Gove fire victims at BCH and MGH led to many important changes in the treatment of burn patients. It is difficult to judge how long these advancements would have taken without the sheer numbers that were provided by this fire for study in such a short period. More than 70 years later, the Cocoanut Grove fire continues to be referenced as a pivotal point in the history of burn treatment.35,36 This also serves as an important reminder that observation and documentation are the principle tenants of advancement in medical science, where overwhelming tragedy can be turned into a historic opportunity for research and improvement that benefits all. References 1. Faxon NW. The problems of the hospital administration: I-the Cocoanut Grove disaster. Ann Surg 1943;117:803–8. 2. Faxon NW, Churchill ED. The Cocoanut Grove disaster in Boston: a preliminary account. JAMA 1942;120:1385–8. 3. Moulton RS. The Cocoanut Grove night club fire Boston, November 28, 1942. Boston: National Fire Protection Association; 1943.
Journal of Burn Care & Research Volume 36, Number 1
4. Holden, J. Cocoanut Grove nightclub fire collection, 1939–2002. Boston Public Library Archival and Manuscript Finding Aid Database. 2012. 5. Cocoanut Grove Survivors tell their stories. [YouTube video (11:46 min.)]. Quincy: National Fire Protection Association; 2012. 6. Blackington AH. Trial proves criminal negligence at Cocoanut Grove fire: owner sentenced on manslaughter charge; many safety regulations violated. Fire Engineering 1943;96:242–62. 7. Finland M, Davidson CS, Levenson SM. Clinical and therapeutic aspects of the conflagration injuries to the respiratory tract sustained by victims of the Cocoanut Grove disaster. Medicine 1946;25:215–83. 8. Koch S. Minutes of fifth meeting, Boston National Research Council, Division of Medical Sciences, Subcommittee on Burns. 1942. 9. Clowes GH, Lund CC, Levenson SM. The surface treatment of burns: a comparison of results of tannic acid, silver nitrate, triple dye, and vaseline or boric ointment as surface treatments in 150 cases. Ann Surg 1943;118:761–79. 10. Cannon B. Procedures in rehabilitation of the severely burned. Ann Surg 1943;117:903–10. 11. Cannon B, Cope O. Rate of epithelial regeneration: a clinical method of measurement, and the effect of various agents recommended in the treatment of burns. Ann Surg 1943;117:761–79. 12. Cannon B. Plastic and reconstructive surgery at the MGH. MGH Surgical Society Newsletter 2003;4:16–7. 13. Ham AW. Experimental study of the tannic acid treatment of burns: with particular reference to its effect on local fluid loss and healing. Ann Surg 1944;120:698–706. 14. Cope O. The end of the tannic acid era. Harvard Medical Alumni Bulletin 1983:57:17–9. 15. Moncrief JA. The development of topical therapy. J Trauma 1971;11:906–10. 16. Davidson CS. The Cocoanut Grove disaster. J Infectious Dis 1972;125:S58–9. 17. Cope O. Management of the Cocoanut Grove burns at the Massachusetts General Hospital. Ann Surg 1943:117:801–2. 18. Aub JC, Pittman H, Brues AM. The pulmonary complications: a clinical description. Ann Surg 1943;117:834–40. 19. Cope O, Rhinelander FW. The problem of burn shock complicated by pulmonary damage. Ann Surg 1943;117:915–28.
Stewart 235
20. Beecher HK. Resuscitation and sedation of patients with burns which include the airway: some problems of immediate therapy. Ann Surg 1943;117:825–33. 21. Weilacher RR. AARC-50 years of service. Available from https://www.aarc.org/member_services/history.html; accessed February 16, 2014. 22. Phillips AW, Cope O. Burn therapy. II. The revelation of respiratory tract damage as a principal killer of the burned patient. Ann Surg 1962;155:1–19. 23. Wolf SE, Arnoldo BD. The year in burns 2012. Burns 2013;39:1501–13. 24. Finland M, Davidson CS, Levenson SM. Effects of plasma and fluid on pulmonary complications in burned patients. Arch Intern Med 1946;77:477–90. 25. Cope O, Moore FD. The redistribution of body wa ter and the fluid therapy of the burned patient. Ann Surg 1947;126:1010–45. 26. Carvajal HF. Fluid resuscitation of pediatric burn victims: a critical appraisal. Pediatr Nephrol 1994;8:357–66. 27. Baxter CR, Shires T. Physiological response to crystal loid resuscitation of severe burns. Ann N Y Acad Sci 1968;150:874–94. 28. Stokstad EL, Jukes TH. Sulfonamides and folic acid antagonists: a historical review. J Nutr 1987;117:1335–41. 29. Abraham EP, Chain EB, Fletcher CM, et al. Further observations on penicillin. Lancet 1941;2:177. 30. Chain E. Thirty years of penicillin therapy. J R Coll Physicians Lond 1972;6:103–31. 31. Finland M, Davidson CS, Levenson SS. Chemotherapy and control of infection among victims of the Cocoanut Grove disaster. Surg Gynecol Obstet 1946;82:151–73. 32. Barajas-Nava LA, López-Alcalde J, Roqué i Figuls M, Solà I, Bonfill Cosp X. Antibiotic prophylaxis for preventing burn wound infection. Cochrane Database Syst Rev 2013;6:CD008738. 33. Cope O, Langohr JL. Expeditious care of full-thickness burn wounds by surgical excision and grafting. Ann Surg 1947;125:1–22. 34. Ong YS, Samuel M, Song C. Meta-analysis of early excision of burns. Burns 2006;32:145–50. 35. Orgill DP. Exicision and skin grafting of thermal burns. NEJM 2009;360:893–901. 36. Saffle JR. The 1942 fire at Boston’s Cocoanut Grove nightclub. Am J Surg 1993;166:581–91.
The Fire at Cocoanut Grove Camille L. Stewart, MD
On November 28, 1942, a fire broke out at The Cocoanut Grove Nightclub, in Boston, Massachusetts. The fire claimed the lives of hundreds, and injured 170 patients who were treated at either Boston City Hospital or the Massachusetts General Hospital. With extraordinary leadership and scientific focus, this tragedy led to many important advances in burn management, including improvements in burn wound care, the first descriptions of inhalation injury, formulas to guide fluid resuscitation, and the initial studies of antimicrobial therapy with burns. This overview describes the treatment of the Cocoanut Gove victims, and how it transformed the management of burns forever. (J Burn Care Res 2015;36:232–235)
On November 28, 1942, a fire broke out at The Cocoanut Grove Nightclub, in Boston, Massachusetts. The fire claimed the lives of 498 individuals and resulted in the simultaneous treatment of 170 burn-injured patients at two Boston hospitals.1,2 This tragedy directly resulted in the publication of more than 30 reports related to the management of burns. Knowledge gained while treating these patients included comparisons of multiple types of burn dressings, the first descriptions of inhalation injury, improved formulas to guide fluid resuscitation, and the initial studies of antimicrobial therapy with burns, stimulating significant additional research, and ultimately resulting in many important changes for the care of burned patients. At the time, Cocoanut Gove was a popular restaurant and lounge located in the heart of Boston, just south of the Boston garden. The fire occurred on the Saturday night after Thanksgiving. Despite the fire code limiting occupancy to 600, on that particular evening the nightclub had an estimated 1000 individuals inside.1,3 A number of theories exist concerning the cause of the fire; however, after extensive investigation by the Boston fire department, the official cause was left “unknown.” It was the height From the Department of Surgery, University of Colorado School of Medicine, Aurora. This article was the winning submission for the 2014 ABA Archives History Manuscript Award. Address correspondence to Camille L. Stewart, MD, University of Colorado School of Medicine, 12631 E. 17th Ave, C302, Aurora, Colorado 80045. Copyright © 2014 by the American Burn Association 1559-047X/2015 DOI: 10.1097/BCR.0000000000000111
232
of World War II, and postulations related to arson were initially investigated, but quickly refuted. A bus boy confessed to striking a match adjacent to a faux palm tree that was seen aflame early in the fire. Other theories included faulty wiring installed by a pipe fitter, as well as leaked combustible methyl chlorine gas used as a refrigerant.3,4 Survivors of the fire report that it spread rapidly, and panic quickly ensued.5 Patrons found that all but one exit, a revolving door, was either blocked by furnishings or locked, trapping hundreds inside.6 The Regional Office of Civilian Defense had held a mass-casualty training event in Boston 1 week earlier, allowing thousands of volunteers and medical professionals to be assembled within hours of the fire outbreak.3 All but 11 burn victims were taken to either Boston City Hospital (BCH; 131 living, 180 dead on arrival) or the Massachusetts General Hospital (MGH; 39 living, 75 dead on arrival).1,7,8 The teams of providers were led by Dr. Maxwell Finland at BCH, and by Dr. Oliver Cope at MGH, both of whom later published extensively on their experiences treating these patients.
Burn Wound Care At the time of the Cocoanut Grove fire, the dressing of burn wounds was a subject of debate and varied significantly between hospitals. At BCH, most burn wound treatment focused on the formation of a protective eschar. The extremely painful tannic method was most often employed, in which tannic acid was applied to burned skin to form a protective barrier.9 At BCH there was a large influx of outside physicians and nurses who came to assist with the treatment of
Journal of Burn Care & Research Volume 36, Number 1
the burn patients. Many were unfamiliar with the tannic method, prompting the additional use of the triple dye method at this hospital. This involves the application of gentian violet, methyl green, and acriflavine to the burn wound, which were thought to possess anti-microbial powers and provided a “soft eschar.”9 Alternatively, MGH had embraced a “bland” technique, using petroleum gauze impregnated with boric acid to dress the burn wound, which was then wrapped with large elastic pressure bandages.3,10 This method was developed based on experiments performed at MGH by Dr. Bradford Cannon only a few months before the fire.11,12 A number of patients at BCH were also treated with this method. In the analysis that followed at BCH, Clowes et al9 made a comparison of tannic acid, triple dye, and petroleum gauze burn care, revealing faster healing in the petroleum gauze group and possible survival benefit, corroborating the earlier findings of Dr. Cannon. These results were subsequently reproduced,13 ultimately leading to the phasing out of tannic acid and triple dye methods in favor of the petroleum gauze dressings used to this day.13-15 Thirty years after the fire, the importance of these findings were echoed during the American Burn Association presidential address, wherein Dr. John Moncrief remarked on the “monumental treatise” on burn wound care that resulted from treatment of the Cocoanut Grove fire victims.15
Inhalation Injury Another important breakthrough from the Cocoanut Grove fire was the identification of inhalation injury related to burns. Several of the doors at Cocoanut Grove were either locked or blocked,2,6 forcing hundreds of individuals to breathe in smoke fumes for prolonged periods. Pulmonary symptoms had previously only been reported in relation to inhalation of noxious fumes from the burning of nitrocellulose during a fire at the Cleveland Clinic in 1929. As such, the respiratory complications that developed in these burn patients posed an unexpected “puzzling situation” for the providers at both the institutions.7,16,17 Many cyanotic patients died within minutes of arrival to the hospital, despite absence of obvious external burns, some with edema of the face, neck, and oral structures.7,10,16,18 Several speculated that the inhalation injury was due to an additional gas in the air of the nightclub.7,18 Dr. Cope at MGH wrote that he initially thought the pulmonary symptoms were secondary to an explosion but soon after “it had become clear that there was no explosion, and that only irritating fumes and heat were the cause of the pulmonary inflammation.”19 Dr. Finland at BCH
Stewart 233
came to a similar conclusion, writing “the respiratory irritant was probably part of the hot air, fumes, and particles which resulted directly from the burning of the contents of the various rooms.”7 Dr. Finland noted that many were found to have facial, nasal, and pharyngeal burns, and those with the greatest severity of pulmonary dysfunction had lost consciousness while they remained inside the burning building, resulting in the longest exposure to the smoke.7 Dr. Henry Beecher, a colleague of Dr. Cope at MGH, described the importance of distinguishing patients with inhalation injury from those who were in pain and those with “fear and hysteria,” since all the three presented with agitation and altered mental status.20 Dr. Finland also noted “restlessness” in a number of patients at BCH.7 Treatment of these patients primarily consisted of oxygen therapy, suctioning, and tracheotomy. At BCH, all patients with evidence of respiratory involvement were eventually given oxygen by nasal cannula—however, “because of the paucity of more suitable equipment the greatest reliance had to be placed on the ordinary rubber catheter of the urethral type.”7 There was also experimentation with administration of helium at both the hospitals, which was noted to cause tachycardia compared to oxygen alone.7,20 At the time, respiratory therapy and inhalational therapy were in their infancy, with the first professional association not coming into existence for another 4 years.21 At MGH, only one patient received “artificial respiration” for 5 hours, and two others were intubated but not ventilated for fear that positive pressure would cause hypotension.1,20 Similarly, at BCH, few patients were artificially ventilated. However, 12 patients were given oxygen under positive pressure, since Dr. John Evans of Buffalo, New York, then president of the International Anesthesia Research Society, presented with a “bulky apparatus” to provide this therapy.7 Dr. Finland quipped, “most if not all were not quite as favorably impressed as was Dr. Evans,” but concluded that positive pressure therapy “did not really receive a proper trial in these cases.”7 At MGH, after three admitted patients died from pulmonary edema, restriction of volume resuscitation and permissive hypovolemia were used to attenuate further extravasation of fluids into the lungs.19 Overall conclusions were that the pulmonary and upper airway edema were not always evident upon admission,7 and that the resuscitation of these patients was considered “difficult and unsatisfactory,”18 ending with a call for additional research.8,20 Nearly 20 years later, Dr. Cope published that respiratory tract injury was the primary cause of mortality in burn patients.22 Now, despite being well recognized,
Journal of Burn Care & Research January/February 2015
234 Stewart
inhalation injury remains difficult to treat and the subject of significant ongoing study.23
Fluid Resuscitation During the first day of treatment, 147 units of plasma were administered at MGH, and a remarkable 1065 units of plasma were administered at BCH.8,20 At the time of the Cocoanut Grove fire, a limited number of fluid resuscitation formulas existed which were calculated using laboratory values.19 At BCH patients were given plasma, albumin, and saline, and no specific formula was used.24 Dr. Finland wrote, “The amount of plasma given was, generally speaking, based on the rate and quality of the pulse, on the blood pressure, and later in the day, on hemoglobin and hematocrit.”24 However, given the large numbers of patients and little time to obtain initial lab values, a new formula was developed at MGH. This formula consisted of 500 mL fresh frozen plasma mixed with 500 mL of saline given for every 10% TBSA burned.19 Dr. Cope acknowledged that this volume was inadequate for some patients, but that the formula had “much to recommend it” because of its simplicity.19 Dr. Cope explained that “different degrees of burn may result in different amounts of edema, but it is still true, roughly that the amount of plasma lost from the circulation into the tissue spaces is proportional to the area of the burn.”19 He also noted that a key limitation to current formulas was that they only addressed the current volume deficit without anticipating future volume loss. These insights prompted Dr. Cope to further study fluid resuscitation in burn patients with therapy planned for the first 24 to 48 hours based on %TBSA.25 Higher volumes were prescribed initially and tapered off after 24 hours.25 He noted that hemoconcentration was a late maker of volume loss, and suggested that “the simplest index of the state of balance…was an hour to hour vigil over renal output….adequate hourly outputs in the normal to high range bespeak the adequacy of therapy…a falling or low hourly output calls for immediate increase in therapy.”25 These now-familiar concepts generated further development of formulas to guide fluid resuscitation in burn patients. Today, all such formulas include %TBSA as a critical element in their calculation and are adjusted based on the urine output.26,27
Antibiotic Prophylaxis Systemic antibiotics were given to burn patients at both the hospitals after the Cocoanut Gove fire. Sulfa drugs became available in the late 1930s,28 and
penicillin was given to the first human subject only 2 years earlier.29,30 Then referred to as chemotherapy, the word “antibiotic” would not be introduced for another 3 years.30 As such, experience with their use was extremely limited, “and opinions concerning the efficacy of various forms of sulfonamide therapy in wounds and burns were still divided.”31 At BCH, sulfa antibiotics were given to 76 patients.31 After final analysis, Dr. Finland concluded—“it is fair to assume that most of the surface infections developed under the sulfonamide treatment and were not affected by it.”31 This was the first of the many studies on antibiotic prophylaxis for burns. A Cochrane Database Review conducted in 2013 had conclusions similar to that of Dr. Finland’s.32 At MGH, sulfadiazine was given to all the victims. On the sixth day, patients with temperatures >101°F also received intramuscular penicillin. It was noted that nearly all patients that received penicillin had suffered third-degree burns.8 High infection rates were observed in many thirddegree burns at both the hospitals, motivating further study by Dr. Cope on early excision and grafting of these patients.7,33 The results of these experiments showed decreased infectious rates, improved graft healing, and decreased lengths of hospitalization.33 Further examination demonstrated that early excision and grafting led to improved survival,34 making this practice now the standard of care.35
Conclusions With extraordinary leadership and scientific focus, the management of the Cocoanut Gove fire victims at BCH and MGH led to many important changes in the treatment of burn patients. It is difficult to judge how long these advancements would have taken without the sheer numbers that were provided by this fire for study in such a short period. More than 70 years later, the Cocoanut Grove fire continues to be referenced as a pivotal point in the history of burn treatment.35,36 This also serves as an important reminder that observation and documentation are the principle tenants of advancement in medical science, where overwhelming tragedy can be turned into a historic opportunity for research and improvement that benefits all. References 1. Faxon NW. The problems of the hospital administration: I-the Cocoanut Grove disaster. Ann Surg 1943;117:803–8. 2. Faxon NW, Churchill ED. The Cocoanut Grove disaster in Boston: a preliminary account. JAMA 1942;120:1385–8. 3. Moulton RS. The Cocoanut Grove night club fire Boston, November 28, 1942. Boston: National Fire Protection Association; 1943.
Journal of Burn Care & Research Volume 36, Number 1
4. Holden, J. Cocoanut Grove nightclub fire collection, 1939–2002. Boston Public Library Archival and Manuscript Finding Aid Database. 2012. 5. Cocoanut Grove Survivors tell their stories. [YouTube video (11:46 min.)]. Quincy: National Fire Protection Association; 2012. 6. Blackington AH. Trial proves criminal negligence at Cocoanut Grove fire: owner sentenced on manslaughter charge; many safety regulations violated. Fire Engineering 1943;96:242–62. 7. Finland M, Davidson CS, Levenson SM. Clinical and therapeutic aspects of the conflagration injuries to the respiratory tract sustained by victims of the Cocoanut Grove disaster. Medicine 1946;25:215–83. 8. Koch S. Minutes of fifth meeting, Boston National Research Council, Division of Medical Sciences, Subcommittee on Burns. 1942. 9. Clowes GH, Lund CC, Levenson SM. The surface treatment of burns: a comparison of results of tannic acid, silver nitrate, triple dye, and vaseline or boric ointment as surface treatments in 150 cases. Ann Surg 1943;118:761–79. 10. Cannon B. Procedures in rehabilitation of the severely burned. Ann Surg 1943;117:903–10. 11. Cannon B, Cope O. Rate of epithelial regeneration: a clinical method of measurement, and the effect of various agents recommended in the treatment of burns. Ann Surg 1943;117:761–79. 12. Cannon B. Plastic and reconstructive surgery at the MGH. MGH Surgical Society Newsletter 2003;4:16–7. 13. Ham AW. Experimental study of the tannic acid treatment of burns: with particular reference to its effect on local fluid loss and healing. Ann Surg 1944;120:698–706. 14. Cope O. The end of the tannic acid era. Harvard Medical Alumni Bulletin 1983:57:17–9. 15. Moncrief JA. The development of topical therapy. J Trauma 1971;11:906–10. 16. Davidson CS. The Cocoanut Grove disaster. J Infectious Dis 1972;125:S58–9. 17. Cope O. Management of the Cocoanut Grove burns at the Massachusetts General Hospital. Ann Surg 1943:117:801–2. 18. Aub JC, Pittman H, Brues AM. The pulmonary complications: a clinical description. Ann Surg 1943;117:834–40. 19. Cope O, Rhinelander FW. The problem of burn shock complicated by pulmonary damage. Ann Surg 1943;117:915–28.
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