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Perforating curling's ulcer—a rare but lethal complication
Burns, 7,203-207
Printedin GreatBritain
203
Perforating Curling’s ulcer-a complication C. M. McConnell
rare but lethal
and R. P. Hummel
Department of Surgery, University of Cincinnati Medical Center and the Shriners Burns Institute, Cincinnati, Ohio Summary
During the last 14 years 8 of 2700 burn patients (0.3 per cent) at the University of Cincinnati Medical Center developed perforated Curling’s ulcer. Seven of the 8 patients expired, representing 2.1 per cent of the 328 deaths during that period. All patients were septic. Five of the 8 were operated upon and one of these survived. The incidence of all complications from Curling’s ulcer has been markedly decreased by widespread use of prophylactic antacid therapy and hyperalimentation by tube feeding. Only 1 of the 8 patients was receiving antacid therapy at the time of perforation. INTRODUCTION THE association of thermal
injuries and gastrointestinal ulcerations was first reported more than 140 years ago (Swan, 1823; Curling, 1842). The incidence of Curling’s ulcer ranges from I.2 to 25 per cent (Hummel et al., 1957; Bruck and Pruitt, 1972; McAlhany et al., 1976; Watson and Abston, 1976). Although more than 30 different theories have been advanced, the aetiology of this problem remains obscure, and indeed, it seems unlikely that a single cause can be indicted. Advances have been made in the management of Curling’s ulcer in the past 25 years. In the modern surgical era, those caring for burn victims have concentrated on the prevention of Curling’s ulcer as part of optimal management. Clinically significant complications of Curling’s ulcer are now less common in the burn population. This finding may be due to the increased awareness of the importance of prevention, or to the increase in high caloric oral intake (including tube feeding) as vigorous nutritional sup-
port has gained widespread acceptance. The combination of continuous oral feeding and frequent antacid administration causes an intragastric pH of 4-6 which is not conducive to pepsin activity or ulcer formation. Nevertheless, an occasional patient will manifest either massive gastrointestinal haemorrhage or perforation. The latter has been much less common in most reported series (Kirksey et al., 1968; Pruitt et al., 1970; Law et al., 1971; Bruck and Pruitt, 1972; Stone, 1972; Watson and Abston; 1976). The morbidity and mortality of perforating gastric or duodenal ulcers are significant in the patient who is not burned (Donaldson and Jarrett, 1970; Jordan et al., 1974; Sawyers et al., 1975). Recent clinical reviews report the mortality to range between 2.2 and 8 per cent. Some argument still exists as to the optimal surgical management of perforated peptic ulcers (Griffm and Organ, 1976; Jordan and Korompai, 1976). Under ordinary circumstances, the diagnosis of upper gastrointestinal perforation is usually not difficult to establish, but the undiagnosed perforation carries a significant mortality as reviewed by Felix and Stahlgren (1973). The burn patient represents special problems in the early diagnosis of perforation. Intermittent confusion, fever and ileus are symptoms seen frequently on the burn ward. To a patient with anterior trunk burns or multiple donor sites, abdominal pain may not be as obvious. Anorexia in the burn patient is not a reliable symptom of perforation. Thus the burn patient may develop unrecognized signs and symptoms of gastrointestinal perforation a significant time before the diagnosis is established.
Burns Vol. ~/NO. 3
204
Table!. Perforating Curling’s ulcer
Patient no.
Age fyrl/ sex
8/F
55/M 17/M
4
5
54/F
25/M
8/M
7/M
12/M
Burn total 3”/2”
70/50
45/40
Antacid
Day of onset
Symptoms
?
Vomiting, shock
?
Haematemesis, ileus
Treatment
Day of death
Cause of death
45
Symptomatic
45
Shock, sepsis
54
Drainage of subphrenic abscess (day 6 1)
66
Sepsis
5
Closure of perforation
9
Sepsis, G I bleeding
50/40
No
Acute abdomen
30/20
Yes, until day 50
Confusion Shock
51
Symptomatic
45
Peritonitis, sepsis
60/58
Cimetidine until day 45
Acute abdomen
47
Closure of perforation
53
Sepsis DIC
12
Vagotomypyloroplasty Way 12). antrectomy (day241
-
43138
58/50
91/90
No
Acute abdomen, Hgb drop
Yes
Abdominal distension, sepsis
No
Abdominal distensions, sepsis
7
Closure of perforation
11
13
Closure of perforation
27
Sepsis, renal failure Sepsis, pneumonia
DIC, Disseminated intravascular coagulation.
A review of the combined clinical experience for the past 14 years at the Cincinnati General Hospital Burn Unit and the Shriners Bums Institute of Cincinnati reveals that the combination of thermal injury and perforated Curling’s ulcer was usually fatal. During this period of time (May 1964-May 1978) there were 2700 patients with acute burns admitted to the hospitals. These patients ranged in age from 19 months to 93 years. The percentage of total body surface burned ranged from 3 per cent to 98 per cent. In the period of time studied there were 328 deaths, an overall mortality rate of 12 per cent. Eight patients (Table I) from the total of 2700 exhibited a perforated Curling’s ulcer; 7 of these 8 expired. Perforation of Curling’s ulcer was documented to occur in 0.3 per cent of the total admissions, and was a major contributing cause in 2.1 per cent of the 328 deaths.
CASE
REPORTS
Case 1
An 8-year-old white girl was admitted 39 days after sustaining a 70 per cent total body surface bum injury. The patient was noted to have 50 per cent fullthickness injury at the time of her transfer. (The records do not demonstrate use of prophylactic antacid therapy). Split-thickness grafting was performed on day 42 post bum. On day 45, the patient vomited and became oliguric and hypotensive. She expired that evening. Post-mortem examination revealed an acute perforated duodenal ulcer and pneumonia in addition to the extensive bum injuries. Perforation was not suspected ante-mortem. The patient had, however, evidenced bum wound sepsis and an extremely poor nutritional status from the time of admission until death. Case 2 A 55-year-old white man was admitted after sustaining a 45 per cent total body surface bum in a gasoline
McConnell and
Hummel: Curling’s
205
Ulcer
explosion. Resuscitation of the patient was effected with a crystalloid fluid, and topical gentamicin was used on the bum surfaces. Split-thickness skin grafts were performed on days 26,40,43 and 47 post bum. (Records are unavailable to indicate whether or not prophylactic antacid therapy was utilized). On day 48 post bum, the patient exhibited haematemesis, and on day 54 ileus, confusion and other signs of sepsis had developed. An upright chest radiograph taken on day 54 demonstrated free air. The patient was treated with nasogastric suction, i.v. fluids and antibiotics. A right subdiaphragmatic abscess developed and was drained on day 61. On day 68 post bum, the patient expired. Autopsy findings showed that a perforated duodenal ulcer and intra-abdominal infection contributed to his death. Case 3
A l7-year-old black man sustained a 50 per cent total body surface bum and severe cerebral contusion as a result of an automobile accident. The patient was admitted to the Bum Unit where he was resuscitated with a crystalloid solution and treated with topical gentamicin. Prophylactic antacids were not administered. On day 5 post bum, the patient developed signs and symptoms ofan acute abdomen and underwent an exploratory laparotomy. Laparotomy revealed an anterior duodenal ulcer perforation. Closure was effected by oversewing and an omental patch. On day 9, the patient developed signs of gastrointestinal bleeding. Overwhelming infection and evidence of bum wound sepsis were also present. The patient expired on day 9 post bum. Autopsy revealed an acute duodenal ulcer posteriorly penetrating into the pancreas, as well as an anterior perforation surgically closed. Cerebral haemorrhage and extensive full-thickness burns were also noted at post-mortem examination. Case 4
A 54-year-old white mentally retarded woman was admitted from a mental institution after sustaining a 30 per cent total body surface burn from a hot water injury. She underwent a crystalloid resuscitation and was treated with topical silver sulphadiazine. A splitthickness skin graft to the posterior lower extremities was performed on day 32 post burn. The bum wounds were debrided on day 43. On day 50, the patient returned to the operating room for a split-thickness skin graft. Antacids had been administered throughout her hospitalization, but were not reinstated postoperatively. On day 51. the patient became confused and developed oliguria and hypotension. She went into cardiac arrest and expired. Pre-mortem. the diagnosis of perforated viscus was entertained, but the patient’s condition was rapidly deteriorating and operative therapy could not be undertaken. An autopsy confirmed a perforated gastric ulcer with early peritonitis. Case 5 A 25.year-old white man was admitted after being burned in a railroad car explosion. The patient was
admitted to the hospital 48 h after his injury. He sustained 60 per cent total body surface bums, nearly all of which were full-thickness injury. The patient was treated with topical Silvadene and daily hydrotherapy. In the fourth post bum week, the topical therapy was changed to gentamicin and Furacin, in accordance with wound culture sensitivity studies. The patient was taken to surgery on days I6 and 29 post bum for debridement of bum wounds. On day 41, a splitthickness skin graft to the right arm was performed, and on day 45, the patient underwent skin grafting to his face. Cimetidine, which had been administered prophylactically since admission, was not reinstated postoperatively. On day 47 post bum, the patient developed abdominal distention and X-ray evidence of pneumoperitoneum. A laparotomy was performed that evening, at which time a perforated Curling’s ulcer was noted and oversewn with omental patch. Fluid management was difficult postoperatively. The patient developed progressive signs of sepsis, never stabilized, and developed disseminated intravascular coagulation (DIC). He expired on day 53 post bum. Autopsy revealed no evidence of gastrointestinal bleeding. However, intracerebral bleeding had occurred and this was felt to be related to the DIC state, secondary to overwhelming infection. Case 6
An S-year-old white boy was admitted on day 5 post bum with a 43 per cent total body surface bum sustained in a gasoline explosion. He was treated with Sulfamylon topically. On day 9 he developed temperature elevation and guaiac-positive stools. His haematocrit dropped from 35 per cent to 23 per cent on day IO and he was noted to be bleeding from the upper gastrointestinal tract. On day I2 he developed acute abdominal signs, but no free air on X-ray. he underwent exploratory laparotomy on day I2 at which time an anterior perforated peptic ulcer and large posterior bleeding duodenal ulcer were found. Truncal vagotomy and pyloroplasty were performed. On day 24 post burn the patient was reoperated on for massive upper gastrointestinal bleeding, and an antrectomy and gastroenterostomy were done. The patient underwent 6 grafting and debridement procedures and was discharged on day 75 post bum. He subsequently has been readmitted three times for reconstructive surgery and has had no sequela of his gastric surgery. Case 7 A 7-year-old white boy was admitted to the Shriners Burns Institute on day 4 post burn after sustaining a 58 per cent total body surface bum from a gasoline flame. The patient’s resuscitation had been completed prior to his transfer. The patient was treated with Betadine topical therapy and systemic antibiotics. Prophylactic antacids were utilized. On day 7 he developed signs of septicaemia and abdominal distention. Radiographs revealed free peritoneal air. and on day 8 an exploratory laparotomy was done at which time a perforated peptic ulcer was managed by oversewing and an omental patch. The patient was re-explored on day IO
206
because of suspected reperforation. He had a progressive downhill course from the time of the original laparotomy, and died of sepsis and acute renal failure on day 11 post bum. Autopsy revealed severe body bums and peritonitis with surgically closed Curling’s ulcer. Case 8 A 12-year-old white boy was admitted to the Shriners Bums Institute on day 7 post bum after sustaining a 9 I per cent total body surface bum in flame fire. The patient was treated with systemic antibiotics and topical Silvadene. Prophylactic antacids were not utilized. He had repeated positive blood cultures for E. coli, Proteus vulgaris and Bacillus species. He developed respiratory distress on day 12 post bum and a tracheostomy was done. On day 13 abdominal distension occurred, and free air was demonstrated on a flat plate of the abdomen. At laparotomy, a single perforated duodenal ulcer was oversewn. The patient developed thrombosis of the left subclavian vein and required fasciotomies of the left arm and forearm. Continuing sepsis, pulmonary problems and gangrene of the arm led to his death on day 27 post burn. Autopsy revealed 90 per cent total body surface bum, bilateral lobular pneumonia, one gastric and two duodenal ulcers, thrombosis of the left subclavian vein and infection in left upper extremity. DISCUSSION
In our retrospective review of 8 patients with perforated Curling’s ulcer, several findings were of interest. Six of the 8 patients (75 per cent) were male. Only one patient was receiving prophylactic antacid therapy at the time of perforation. Two other patients had their prophylactic therapy discontinued on day 45 and day 50 post burn. Perforation developed within 24 and 48 h respectively. Medication records were not available for two patients seen (Cases 1 and 2), but antacids were not routinely given prophylactically. In the current management of bums, the prophylactic use of antacid therapy (McAlhany et al., 1976) has become routine, and most burn centres have had a concurrent decrease in the incidence of complications from Curling’s ulcer. However, when complications do occur, aggressive surgical therapy is warranted. The incidence of perforation is significantly less than that of massive upper gastrointestinal bleeding, but other reports have confirmed the high mortality rate with perforation (Pruitt et al., 1970; Watson and Abston, 1976). Survivors of Curling’s ulcer perforation have been reported, more commonly in children (Leix and Greaney, 1963; Chenoweth and Dimick, 1965; Shaw et al., 1966; Pruitt et al., 1970). The double stress of a major thermal injury and perforated upper
Burns Vol. ~/NO. 3
intestinal tract produces a truly critical situation. Delay in the diagnosis will certainly have lethal consequences. At the present time, several steps can be taken to aid the prevention of complications of Curling’s ulcer. Control of infection (Day et al., 1972) vigorous nutritional support, vigorous prophylactic antacid therapy (McAlhany et al., 1976; Watson and Abston, 1976) and probably prophylactic use of H, receptor antagonist (Strauss et al., 1978) all help to control the problem of post burn gastrointestinal complications. Prophylactic antacid therapy should be continued until the patient is completely covered with autogenous skin and all signs of infection have been erased. If perforation does occur, immediate recognition and prompt surgical therapy are mandatory (Day et al., 1972). Delay in diagnosis or delay in surgical treatment will usually result in a fatality. Although oversewing of the perforation is the basic method of surgical therapy, vagotomy and pyloroplasty should be considered at the time of operation since many of these patients have associated bleeding episodes as well as perforation. The one survivor in this series not only required vagotomy and pyloroplasty but had antrectomy when massive rebleeding occurred.
REFERENCES
Bruck H. M., and Pruitt B. A. (1972) Curling’s ulcer in children. A l2-year review of 63 cases. J. Trauma 12,490. Chenoweth A. and Dimick A. R. (1965) Stress ulcer in infants and children. Ann. Surg. 161,977. Curling T. B. (1842) An acute ulceration of the duodenum in cases of bums. Medico-Chir. Trans. (London) 25,260. Day S. B., MacMillan B. G. and Altemeier W. A. (1972) Curling’s Ulcer: An Experiment of Nature. Springfield, Ill., Charles C. Thomas. Donaldson G. A. and Jarrett F. (1970) Perforated gastroduodenal ulcer disease at the Massachusetts General Hospital from 1952 to 1970. Am. .I. Surg. 120,306.
Felix W. R. and Stahlgren L. H. (1973) Death by undiagnosed perforated peptic ulcer: Analysis of 3 I cases. Ann. Surg. 177,34. Griffin G. E. and Organ C. H. (1976) The natural history of the perforated duodenal ulcer treated by suture plication. Ann. Surg. 183,382. Hummel R. P., et al. (1957) Clinical experiences and studies in Curling’s ulcer. JAMA 164, I4 I. Jordan G. L., et al. (1974) Surgical management of perforated peptic ulcer. Ann. Surg. 179,628. Jordan P. H. and Korompai F. L. (1976) Evolvement of a new treatment for perforated duodenal ulcer. Surg. Gynecol. Obstet. 142,39 I.
McConnell
and Hummel: Curling’s Ulcer
Kirksey T. D., Moncrief J. A., Pruitt B. A., et al. (1968) Gastrointestinal complications in burns. Am. 1. Surg. 116,627. Law E. J., Day S. B. and MacMillan B. G. (1971) Autopsy findings in the upper gastrointestinal tract of8 I bum patients. Arch. Surg. 102,412. Leix F. and Greaney E. M. (I 963) Surgical experience with peptic ulcer in infancy and childhood. Am. J. Surg. 106, 173.
McAlhany J. C., et al. (1976) Antacid control of complications from acute gastroduodenal disease after bums. J. Trauma 16,645. Pruitt B. A.. Foley F. D. and Moncrief J. A. (1970) Curling’s ulcer: A clinical pathology study of 323 cases. Ann. Surg 172,523. Sawyers J. L.. Herrington J. L., Mulherin J. L. jun., et al. (1975) Acute perforated duodenal ulcer: an evaluation of surgical management. Arch. Surg. 110, 527.
207
Shaw A., Symonds F., Bush J. et al. (1966) Surgical management of Curling’s ulcer in children. JAMA 197,922. Stone H. H. (I 972) Stress ulcers in patients with major burns. Am. Surg. 44, 107. Strauss R. J., Stein T. A. and Wise L. (1978) Prevention of stress ulcerations using H, receptor antagonists. Am. J. Surg. 135, 120. Swan J. (I 823) Case of severe bums. Edinburgh Med. J. 19,344.
Watson L. C. and Abston S. (1976) Prevention of upper gastrointestinal hemorrhage in 582 burned children. Am. J. Surg. 132,790.
Paper accepted 20 August 1979.
Rcyue~r /iv reprinrr sho~ddhe addresred /a: Dr Robert P. Hummel. Department Center, Cincinnati,
Ohio 45267, USA.
of Surgery. University
of Cincinnati
Medical
Printedin GreatBritain
203
Perforating Curling’s ulcer-a complication C. M. McConnell
rare but lethal
and R. P. Hummel
Department of Surgery, University of Cincinnati Medical Center and the Shriners Burns Institute, Cincinnati, Ohio Summary
During the last 14 years 8 of 2700 burn patients (0.3 per cent) at the University of Cincinnati Medical Center developed perforated Curling’s ulcer. Seven of the 8 patients expired, representing 2.1 per cent of the 328 deaths during that period. All patients were septic. Five of the 8 were operated upon and one of these survived. The incidence of all complications from Curling’s ulcer has been markedly decreased by widespread use of prophylactic antacid therapy and hyperalimentation by tube feeding. Only 1 of the 8 patients was receiving antacid therapy at the time of perforation. INTRODUCTION THE association of thermal
injuries and gastrointestinal ulcerations was first reported more than 140 years ago (Swan, 1823; Curling, 1842). The incidence of Curling’s ulcer ranges from I.2 to 25 per cent (Hummel et al., 1957; Bruck and Pruitt, 1972; McAlhany et al., 1976; Watson and Abston, 1976). Although more than 30 different theories have been advanced, the aetiology of this problem remains obscure, and indeed, it seems unlikely that a single cause can be indicted. Advances have been made in the management of Curling’s ulcer in the past 25 years. In the modern surgical era, those caring for burn victims have concentrated on the prevention of Curling’s ulcer as part of optimal management. Clinically significant complications of Curling’s ulcer are now less common in the burn population. This finding may be due to the increased awareness of the importance of prevention, or to the increase in high caloric oral intake (including tube feeding) as vigorous nutritional sup-
port has gained widespread acceptance. The combination of continuous oral feeding and frequent antacid administration causes an intragastric pH of 4-6 which is not conducive to pepsin activity or ulcer formation. Nevertheless, an occasional patient will manifest either massive gastrointestinal haemorrhage or perforation. The latter has been much less common in most reported series (Kirksey et al., 1968; Pruitt et al., 1970; Law et al., 1971; Bruck and Pruitt, 1972; Stone, 1972; Watson and Abston; 1976). The morbidity and mortality of perforating gastric or duodenal ulcers are significant in the patient who is not burned (Donaldson and Jarrett, 1970; Jordan et al., 1974; Sawyers et al., 1975). Recent clinical reviews report the mortality to range between 2.2 and 8 per cent. Some argument still exists as to the optimal surgical management of perforated peptic ulcers (Griffm and Organ, 1976; Jordan and Korompai, 1976). Under ordinary circumstances, the diagnosis of upper gastrointestinal perforation is usually not difficult to establish, but the undiagnosed perforation carries a significant mortality as reviewed by Felix and Stahlgren (1973). The burn patient represents special problems in the early diagnosis of perforation. Intermittent confusion, fever and ileus are symptoms seen frequently on the burn ward. To a patient with anterior trunk burns or multiple donor sites, abdominal pain may not be as obvious. Anorexia in the burn patient is not a reliable symptom of perforation. Thus the burn patient may develop unrecognized signs and symptoms of gastrointestinal perforation a significant time before the diagnosis is established.
Burns Vol. ~/NO. 3
204
Table!. Perforating Curling’s ulcer
Patient no.
Age fyrl/ sex
8/F
55/M 17/M
4
5
54/F
25/M
8/M
7/M
12/M
Burn total 3”/2”
70/50
45/40
Antacid
Day of onset
Symptoms
?
Vomiting, shock
?
Haematemesis, ileus
Treatment
Day of death
Cause of death
45
Symptomatic
45
Shock, sepsis
54
Drainage of subphrenic abscess (day 6 1)
66
Sepsis
5
Closure of perforation
9
Sepsis, G I bleeding
50/40
No
Acute abdomen
30/20
Yes, until day 50
Confusion Shock
51
Symptomatic
45
Peritonitis, sepsis
60/58
Cimetidine until day 45
Acute abdomen
47
Closure of perforation
53
Sepsis DIC
12
Vagotomypyloroplasty Way 12). antrectomy (day241
-
43138
58/50
91/90
No
Acute abdomen, Hgb drop
Yes
Abdominal distension, sepsis
No
Abdominal distensions, sepsis
7
Closure of perforation
11
13
Closure of perforation
27
Sepsis, renal failure Sepsis, pneumonia
DIC, Disseminated intravascular coagulation.
A review of the combined clinical experience for the past 14 years at the Cincinnati General Hospital Burn Unit and the Shriners Bums Institute of Cincinnati reveals that the combination of thermal injury and perforated Curling’s ulcer was usually fatal. During this period of time (May 1964-May 1978) there were 2700 patients with acute burns admitted to the hospitals. These patients ranged in age from 19 months to 93 years. The percentage of total body surface burned ranged from 3 per cent to 98 per cent. In the period of time studied there were 328 deaths, an overall mortality rate of 12 per cent. Eight patients (Table I) from the total of 2700 exhibited a perforated Curling’s ulcer; 7 of these 8 expired. Perforation of Curling’s ulcer was documented to occur in 0.3 per cent of the total admissions, and was a major contributing cause in 2.1 per cent of the 328 deaths.
CASE
REPORTS
Case 1
An 8-year-old white girl was admitted 39 days after sustaining a 70 per cent total body surface bum injury. The patient was noted to have 50 per cent fullthickness injury at the time of her transfer. (The records do not demonstrate use of prophylactic antacid therapy). Split-thickness grafting was performed on day 42 post bum. On day 45, the patient vomited and became oliguric and hypotensive. She expired that evening. Post-mortem examination revealed an acute perforated duodenal ulcer and pneumonia in addition to the extensive bum injuries. Perforation was not suspected ante-mortem. The patient had, however, evidenced bum wound sepsis and an extremely poor nutritional status from the time of admission until death. Case 2 A 55-year-old white man was admitted after sustaining a 45 per cent total body surface bum in a gasoline
McConnell and
Hummel: Curling’s
205
Ulcer
explosion. Resuscitation of the patient was effected with a crystalloid fluid, and topical gentamicin was used on the bum surfaces. Split-thickness skin grafts were performed on days 26,40,43 and 47 post bum. (Records are unavailable to indicate whether or not prophylactic antacid therapy was utilized). On day 48 post bum, the patient exhibited haematemesis, and on day 54 ileus, confusion and other signs of sepsis had developed. An upright chest radiograph taken on day 54 demonstrated free air. The patient was treated with nasogastric suction, i.v. fluids and antibiotics. A right subdiaphragmatic abscess developed and was drained on day 61. On day 68 post bum, the patient expired. Autopsy findings showed that a perforated duodenal ulcer and intra-abdominal infection contributed to his death. Case 3
A l7-year-old black man sustained a 50 per cent total body surface bum and severe cerebral contusion as a result of an automobile accident. The patient was admitted to the Bum Unit where he was resuscitated with a crystalloid solution and treated with topical gentamicin. Prophylactic antacids were not administered. On day 5 post bum, the patient developed signs and symptoms ofan acute abdomen and underwent an exploratory laparotomy. Laparotomy revealed an anterior duodenal ulcer perforation. Closure was effected by oversewing and an omental patch. On day 9, the patient developed signs of gastrointestinal bleeding. Overwhelming infection and evidence of bum wound sepsis were also present. The patient expired on day 9 post bum. Autopsy revealed an acute duodenal ulcer posteriorly penetrating into the pancreas, as well as an anterior perforation surgically closed. Cerebral haemorrhage and extensive full-thickness burns were also noted at post-mortem examination. Case 4
A 54-year-old white mentally retarded woman was admitted from a mental institution after sustaining a 30 per cent total body surface burn from a hot water injury. She underwent a crystalloid resuscitation and was treated with topical silver sulphadiazine. A splitthickness skin graft to the posterior lower extremities was performed on day 32 post burn. The bum wounds were debrided on day 43. On day 50, the patient returned to the operating room for a split-thickness skin graft. Antacids had been administered throughout her hospitalization, but were not reinstated postoperatively. On day 51. the patient became confused and developed oliguria and hypotension. She went into cardiac arrest and expired. Pre-mortem. the diagnosis of perforated viscus was entertained, but the patient’s condition was rapidly deteriorating and operative therapy could not be undertaken. An autopsy confirmed a perforated gastric ulcer with early peritonitis. Case 5 A 25.year-old white man was admitted after being burned in a railroad car explosion. The patient was
admitted to the hospital 48 h after his injury. He sustained 60 per cent total body surface bums, nearly all of which were full-thickness injury. The patient was treated with topical Silvadene and daily hydrotherapy. In the fourth post bum week, the topical therapy was changed to gentamicin and Furacin, in accordance with wound culture sensitivity studies. The patient was taken to surgery on days I6 and 29 post bum for debridement of bum wounds. On day 41, a splitthickness skin graft to the right arm was performed, and on day 45, the patient underwent skin grafting to his face. Cimetidine, which had been administered prophylactically since admission, was not reinstated postoperatively. On day 47 post bum, the patient developed abdominal distention and X-ray evidence of pneumoperitoneum. A laparotomy was performed that evening, at which time a perforated Curling’s ulcer was noted and oversewn with omental patch. Fluid management was difficult postoperatively. The patient developed progressive signs of sepsis, never stabilized, and developed disseminated intravascular coagulation (DIC). He expired on day 53 post bum. Autopsy revealed no evidence of gastrointestinal bleeding. However, intracerebral bleeding had occurred and this was felt to be related to the DIC state, secondary to overwhelming infection. Case 6
An S-year-old white boy was admitted on day 5 post bum with a 43 per cent total body surface bum sustained in a gasoline explosion. He was treated with Sulfamylon topically. On day 9 he developed temperature elevation and guaiac-positive stools. His haematocrit dropped from 35 per cent to 23 per cent on day IO and he was noted to be bleeding from the upper gastrointestinal tract. On day I2 he developed acute abdominal signs, but no free air on X-ray. he underwent exploratory laparotomy on day I2 at which time an anterior perforated peptic ulcer and large posterior bleeding duodenal ulcer were found. Truncal vagotomy and pyloroplasty were performed. On day 24 post burn the patient was reoperated on for massive upper gastrointestinal bleeding, and an antrectomy and gastroenterostomy were done. The patient underwent 6 grafting and debridement procedures and was discharged on day 75 post bum. He subsequently has been readmitted three times for reconstructive surgery and has had no sequela of his gastric surgery. Case 7 A 7-year-old white boy was admitted to the Shriners Burns Institute on day 4 post burn after sustaining a 58 per cent total body surface bum from a gasoline flame. The patient’s resuscitation had been completed prior to his transfer. The patient was treated with Betadine topical therapy and systemic antibiotics. Prophylactic antacids were utilized. On day 7 he developed signs of septicaemia and abdominal distention. Radiographs revealed free peritoneal air. and on day 8 an exploratory laparotomy was done at which time a perforated peptic ulcer was managed by oversewing and an omental patch. The patient was re-explored on day IO
206
because of suspected reperforation. He had a progressive downhill course from the time of the original laparotomy, and died of sepsis and acute renal failure on day 11 post bum. Autopsy revealed severe body bums and peritonitis with surgically closed Curling’s ulcer. Case 8 A 12-year-old white boy was admitted to the Shriners Bums Institute on day 7 post bum after sustaining a 9 I per cent total body surface bum in flame fire. The patient was treated with systemic antibiotics and topical Silvadene. Prophylactic antacids were not utilized. He had repeated positive blood cultures for E. coli, Proteus vulgaris and Bacillus species. He developed respiratory distress on day 12 post bum and a tracheostomy was done. On day 13 abdominal distension occurred, and free air was demonstrated on a flat plate of the abdomen. At laparotomy, a single perforated duodenal ulcer was oversewn. The patient developed thrombosis of the left subclavian vein and required fasciotomies of the left arm and forearm. Continuing sepsis, pulmonary problems and gangrene of the arm led to his death on day 27 post burn. Autopsy revealed 90 per cent total body surface bum, bilateral lobular pneumonia, one gastric and two duodenal ulcers, thrombosis of the left subclavian vein and infection in left upper extremity. DISCUSSION
In our retrospective review of 8 patients with perforated Curling’s ulcer, several findings were of interest. Six of the 8 patients (75 per cent) were male. Only one patient was receiving prophylactic antacid therapy at the time of perforation. Two other patients had their prophylactic therapy discontinued on day 45 and day 50 post burn. Perforation developed within 24 and 48 h respectively. Medication records were not available for two patients seen (Cases 1 and 2), but antacids were not routinely given prophylactically. In the current management of bums, the prophylactic use of antacid therapy (McAlhany et al., 1976) has become routine, and most burn centres have had a concurrent decrease in the incidence of complications from Curling’s ulcer. However, when complications do occur, aggressive surgical therapy is warranted. The incidence of perforation is significantly less than that of massive upper gastrointestinal bleeding, but other reports have confirmed the high mortality rate with perforation (Pruitt et al., 1970; Watson and Abston, 1976). Survivors of Curling’s ulcer perforation have been reported, more commonly in children (Leix and Greaney, 1963; Chenoweth and Dimick, 1965; Shaw et al., 1966; Pruitt et al., 1970). The double stress of a major thermal injury and perforated upper
Burns Vol. ~/NO. 3
intestinal tract produces a truly critical situation. Delay in the diagnosis will certainly have lethal consequences. At the present time, several steps can be taken to aid the prevention of complications of Curling’s ulcer. Control of infection (Day et al., 1972) vigorous nutritional support, vigorous prophylactic antacid therapy (McAlhany et al., 1976; Watson and Abston, 1976) and probably prophylactic use of H, receptor antagonist (Strauss et al., 1978) all help to control the problem of post burn gastrointestinal complications. Prophylactic antacid therapy should be continued until the patient is completely covered with autogenous skin and all signs of infection have been erased. If perforation does occur, immediate recognition and prompt surgical therapy are mandatory (Day et al., 1972). Delay in diagnosis or delay in surgical treatment will usually result in a fatality. Although oversewing of the perforation is the basic method of surgical therapy, vagotomy and pyloroplasty should be considered at the time of operation since many of these patients have associated bleeding episodes as well as perforation. The one survivor in this series not only required vagotomy and pyloroplasty but had antrectomy when massive rebleeding occurred.
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and Hummel: Curling’s Ulcer
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Paper accepted 20 August 1979.
Rcyue~r /iv reprinrr sho~ddhe addresred /a: Dr Robert P. Hummel. Department Center, Cincinnati,
Ohio 45267, USA.
of Surgery. University
of Cincinnati
Medical