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Toxic megacolon
Toxic Megacolon A Surgical
Disease RICHARD
Acute dilatation of the colon as a complication of ulcerative colitis carries a high mortality and morbidity rate. Unfortunately, therapy for this condition has long been an enigma. Despite vigorous supportive and replacement management, valuable time is often lost in the hope that the acute phase of the illness will be reversed. Subsequent surgical intervention often becomes necessary, the timing of which is all important. Our study confirmed our impression that toxic megacolon is best treated surgically. With adequate and timely surgical intervention, good results can be obtained. We wish to demonstrate that we have had a constant response to treatment that has allowed us to formulate a method of handling these cases, and most importantly has enabled us to determine the best time to operate upon these patients. Toxic megacolon has been called the most dreaded complication of ulcerative colitis [I-A’]. The patient presents as an extremely ill person with high fever, tachycardia, abdominal cramps, bloody diarrhea, and a general appearance of severe toxicity. Objective abdominal distention may or may not be present; however, plain films of the abdomen will generally show marked colonic distention, especially of the transverse colon. Nausea and vomiting may occur, leukocytosis is present, bowel sounds are hypoactive or absent, and the abdomen is usually diffusely tender. Past history, physical examination, proctosigmoidoscopy, and abdominal roentgenograms are the essential elements in the establishment of this diagnosis. Acute dilatation of the colon may occur in any stage of ulcerative colitis. It may be the harbinger of the onset of ulcerative colitis or may occur many years later at a time when the disease is quiescent
* Formerly Michigan. 7 Formerly gan.
of
the
surgical
surgical resident,
Volume 121, March 1971
staff, Henry
Henry Ford
Ford Hospital,
Hospital, Detroit,
Detroit, Michi.
L. COLLIER,
JOHN
H. WYLIE,
JORGE
GOMEZ,
MD,*
Jr, MD,* MD,?
Lansing, Lansing,
Barnwell,
Michigan Michigan
South
Carolina
or mildly active. Considerable emphasis has been placed on the diameter of the dilated colon to substantiate the diagnosis [ 4,5]. In our series, the colon was dilated in all cases ; and the colonic distention was termed moderate to severe in more than one-third of the cases. The radiographic diameter of the transverse colon in these cases varied from 8 to 13 cm, as compared with a normal diameter of 5 to 6 cm [ 6,7]. The incidence of toxic megacolon is reported ranging from 1.6 per cent [8] to 2.5 per cent [9]. In our series, we had thirty-five such cases in 605 patients admitted to the hospital with a diagnosis of ulcerative colitis from 1953 to 1964 for an incidence of 5.5 per cent. The etiology of the process is unknown. Pathologically, it has been pointed out that extreme destruction of the bowel wall by inflammation causes severe muscle damage [2,5,9-111. It has been suggested that the myenteric plexus of the bowel wall may become involved and its function impaired [lO,ll].
Hypokalemia, antibiotics, aerophagia, anticholinergics, barium enema, putrefaction of colonic contents, and corticosteroids have been incriminated as possible etiologic or aggravating factors [4]. The onset of acute dilatation of the colon soon after a barium enema examination has frequently been noted. The distention of the bowel probably results from intestinal atony secondary to the effects of the diffuse inflammatory process. The aggravating factors mentioned supplement the condition either by further interference with motility or by the direct mechanical effects of pressure [12]. The question of management of these patients is important since the mortality rate is reported near 50 per cent. Therapy varies. Some believe conservative medical measures should be instituted in all cases and the patients followed very closely. The proponents of this method believe that surgical intervention is indicated only for progressive abdominal distention and/or general clinical de283
Collier, Wylie, and Gomez terioration, evidence of perforation, or suspected impending perforation, uncontrolled bleeding, or lack of response to medical treatment. On the other hand, there are those who believe that the diagnosis of toxic megacolon implies that an emergency operation is indicated as soon as possible. This group believes that these patients are often too ill not to be operated upon. They also note that these critical patients, once the diseased bowel is removed, frequently improve dramatically. Attempts to reduce the distention with enemas or by proctosigmoidoscopy are ineffectual, nor does the patient’s toxicity improve with diverting ileostomy or cecostomy. Because of the multiple methods of treatment and the varied responses obtained, no standardization of therapy has ever evolved. In particular, the appropriate or best time for operating upon patients afflicted with this condition has been difficult to determine. The question of when to subject these seriously ill patients to surgery is a difficult one, and the decision to defer surgical intervention is often made hoping that remission will occur with conservative management. How long to delay surgical therapy must be weighed against the results of treatment. Evaluation of our patients in the series demonstrates a consistent response. Since we have been able to predict accurately the patient’s clinical course, we believe we now have a method of determining the best time to operate on the patient. Treatment
The usual methods of treatment instituted were (1) dietary restriction ; (2) gastrointestinal intubation (Levin and/or Miller-Abbott tubes) ; (3) anticholinergic drugs ; (4) sedation ; (5) fluid and electrolyte replacement; (6) blood transfusions; (7) broad spectrum antibiotics ; (8) corticosteroids. Corticosteroids were used in those patients who had received them previously. Despite these measures there was little improvement in the degree of toxicity and the severity of illness. The use of corticosteroids in the patient with ulcerative colitis is an issue that has been debated for many years. We elected to institute such therapy for our patients. Spencer et al [13] note that 90 per cent of their patients with ulcerative colitis demonstrated an immediate beneficial effect from the addition of corticotropin or adrenal steroids to standard therapy of the disease. In 73 per cent the favorable course persisted after steroids were withdrawn. They have also noted, as we have, a reversal of critical life-threatening illness, allowing adequate 284
preparation of patients for definitive surgery. Many hesitate to use steroids for fear of causing unrecognized perforation. We believe that the danger of perforation in the patient with toxic megacolon is a real one, but doubt that the addition of ACTH or corticosteroids to the therapeutic regimen of these patients increases this danger. Review of our cases confirms our impression. We also believe that with careful scrutiny and examination, if a patient receiving such drugs has perforation, the physician is able to recognize it. This viewpoint is supported by others who have shown that the incidence of perforation in patients with ulcerative colitis is similar whether corticosteroids are used or not [14] ; and that if patients do have perforation and are receiving corticosteroids, their clinical status can well be recognized by the usual criteria [13]. The differences of opinion regarding these drugs are not so puzzling since most of the contributors to the literature on this subject agree that the action of corticosteroids is nonspecific in ulcerative colitis. In acute fulminating colitis or toxic megacolon, the drugs may act by alleviating adrenal insufficiency caused by a general state of stress [IL]. The fact remains that in our series the use of these medications as a supplement to the usual forms of treatment was effective. We found that when we used corticosteroids in the patient who had not previously received them, a consistent and remarkable response occurred. The condition of these patients was ameliorated to the extent that in twenty-four to thirty-six hours the temperature, white blood cell count, and pulse rate returned to normal levels. The general toxic appearance of the patient disappeared and, in most, the abdominal distention gradually lessened. Smith et al [12] noted a similar response, except in his cases the bowel distention remained. All of his patients who underwent surgery while receiving corticosteroid therapy tolerated the procedure well. Results
We compared three groups of patients. Group I had received corticosteroid therapy at some time for the treatment of ulcerative colitis. Group II had received none until acute illness manifested by toxic megacolon developed. Group III received no corticosteroids at any time. The morbidity, mortality, and results of therapy are shown in Table I. Some of the statistically important data are seen in Table II. There were twelve patients in group I. They had received corticosteroids at some time before admission. Toxic megacolon developed in these paThe
American
Journal
of Surgery
Toxic
TABLE I
Comparison of Clinical Status of Three Groups Duration of Ulcerative Colitis
Average Age (yr)
Group
(me)
Average Temperatrue
Average Pulse Rate
Average White
Average Hemoglobin
Average Hospital Stay (days)
Blood Cell Count
(gm %)
I
34.9
31.6
102
125
8.7
20.3
58.8
(Steroids prior to admission) II (No steroids prior to admission)
26.1
32.3
103
120
8.4
18.1
37.4
33.7
56.2
102
115
11.1
14.2
33.0
III (No
Complication Rate
tients who were then supported with corticosteroids and treated with general therapy. These patients demonstrated no response as far as their temperature, white blood cell count, pulse, and general toxic appearance was concerned. (Figure 1.) Six of the twelve patients are surviving and well. There were sixteen patients in group II, none of whom had received corticosteroids before admission to the hospital. Acute dilatation of the colon developed and the patients were toxic and showed no response to the usual forms of therapy, including antibiotics; however, all improved dramatically after the institution of corticosteroid therapy. These patients demonstrated within twenty-four hours a return to normal temperature and pulse rate, and their leukocytosis subsided. (Figure 1.) They lost their toxic perspiring appearance ; and remarkably, the abdominal distenTABLE II
PULSE
F’
160
IO6
150
05
140
104
130
103
120
I02
II0
IO1
100
00
90
99
Data on Thirty-Five Cases 27 Male
Sex
8 Female 8-73 yr Mean: 29.5 yr
Age
Recent
of ulcerative
O-l l-5 5-10 10
(yr)
exacerbation
Anticholinergic’s Recent barium admission Average
highest
enema
within
17 patients
3 mo of
temperature
hemoglobin
Average
white
diagnosis
= 16 patients = 13 patients = 6 patients = 1 patients
35 patients prior to admission
Average
X-ray
colitis
blood
of toxic
1971
(seen
97
60
-
-
160
106
150
105
140
104
130
103
120
102
II0
13 patients
90
99
102.6
60
96
70
97
60
96
on 30 of 32 patients
Surgery: 7 alive and well, 1 dead No surgery: 4 alive and well, 2 alive with symptoms: 2 dead Surgery: 3 alive and well No surgery: 3 alive and well: 1 dead
1.5 Complications per case
IO1 100
18,200
6 died: 6 survived
96
I
2
3
4
5
6
7
6
9
IO
DAYS
13 patients
megacolon
Disease present in rectum proctoscopic examination) Volume 121. March
(mm”)
96
70
100
9.1 cell count
-
60
Results
2 major complications per case 1 major complication
steroids)
Duration
Megacolon
Comparison Figure 1. response to supportive corticosteroids.
in all three groups of the systemic therapy and the administration of
205
Collier,
Wylie,
and Gomez
tion and dilatation of the bowel seen on roentgenogram disappeared or diminished. (Figure 2.) Half of these patients responded so dramatically and looked so well that we were convinced that perhaps they did not require surgery. Six of these eight patients are surviving. However, two did die: one of a perforation at fourteen days and the other of a pulmonary embolus. Three patients have residual symptoms requiring treatment. We believe that early surgical intervention can definitely improve these statistics. We also believe that some of the asymptomatic patients will require surgery for their ulcerative colitis at a later date. Seven of the eight patients that were operated upon are alive and doing well. (Table I.) There were seven patients in group III. They had received no corticosteroids at any time, either before or after admission. We collected the data on this group from the hospital archives, and the duration of ulcerative colitis was almost twice
as long as that of the patients in the other two groups; however, they were not quite as seriously ill. They also had less anemia and leukocytosis. This group may represent the more chronic, burned-out type of disease, and yet they too had dilatation of the coIon. We believe that these patients in group III would have shown the same response as those in groups I and II if we had used the same treatment. Prior to this time, therapy of toxic megacolon has followed two main pathways: medical management, until it was too late to reverse the progress of the disease, and emergency surgical intervention, without taking advantage of appropriate medical treatment. Comments The few simple criteria we now use in the treatment of toxic megacolon are well supported by the material reviewed. The response has been very
Figure 2A. Group 1. Typical example of patient who demonstrated no clinical or radiographic response to a!\ usual forms of therapy including supportive corticosteroids.
Figure 2B. Group II. Example of a patient in group II who responded clinically and whose distention dsappeared after an initial course of corticosteroids was given. 286
The American Journal of Surgery
Toxic Megacolon
consistent and we are confident that the results of such therapy will improve the existing morbidity and mortality rates. Our approach is that if the patient is admitted to the hospital with acute toxic megacolon and has within six recently received corticosteroids, months to one year before admission, he should be placed on corticosteroids for support and an operation performed as soon as possible within twentyfour to forty-eight hours. In our cases, delay did not produce improvement in the patient’s general condition and actually, we believe, created a more hazardous situation. The mortality and morbidity is such that we believe that these patients should be operated on as soon as possible after the diagnosis is made and after correction of dehydration and anemia. If the patient with toxic megacolon has never received corticosteroids before, they are administered at once. These patients will respond, and in four or five days their general condition will be so improved that they can undergo elective surgery rather than emergency intervention. In our patients the dilatation of the bowel lessened, making the operation technically easier. In the patients in group I the large distended thin walled bowel increased t.he incidence of perforation during surgery. Oft.en, we had to perform less than a defini-
Figure 2C. Group II. Patients in this group usually had lessening of distension and general toxicity after corticosteroids were administered. These patients were then operated upon at a better time. Volume 121, March 1971
tive procedure in these patients because of their precarious condition. There was also a much higher complication rate in these cases. In all of our patients in group II we were able to perform definitive procedures, either total or subtotal colectomy and ileostomy or subtotal colectomy and ileoproctostomy. The chances of surgical perforation are much smaller in this group as compared to those in patients in group I, and the post operative complication rate is much less. We have, therefore, evolved a method of therapy for patients with toxic megacolon. We believe that all these patients should be operated upon. We also believe that the best time to operate on these patients to effect reversal of this critical life-threatening illness is as follows: 1. Patients that have received corticosteroids before admission should be operated upon early. This operation should be scheduled twenty-four to thirty-six hours after basic physiologic defects are corrected. 2. Delayed surgical intervention is beneficial in patients that receive corticosteroids for the first time after toxic megacolon develops. Close scrutiny of the patient is necessary, and in four to six days, when his condition is sufficiently improved, elective surgery is possible. Summary We have undertaken to demonstrate a standard method of treatment for toxic megacolon of ulcerative colitis. A methodology for the handling of these cases has not previously evolved, probably because of the protean nature of the disease and the varied responses of the patient to different forms of therapy. We evaluated the experience of thirty-five cases at the Henry Ford Hospital. Some of our patients responded very dramatically to the administration of corticosteroids to supplement the usual forms of treatment. We believe the results of this study support the assumption of certain guidelines for the treatment of toxic dilatation of the colon associated with ulcerative colitis. They are as follows : 1. Patients with toxic megacolon who have received corticosteroids previously should be placed on these drugs for support, and operation performed as soon as possible within twenty-four to forty-eight hours. 2. Such patients who have not received steroids should be given them. Their condition will improve dramatically. Delay in surgical intervention is beneficial in these instances and can be electively performed in four to six days. We have sixteen consecutive cases in this category with no failures. 287
Collier,
Wylie,
and Gomez
References 1. Tumen
JH:
Toxic
megacolon
in
fulminating
disease.
JAMA 191: 10,838, 1965. 2. Roth JL, Valdes-Dapena A, Stein GN, Bockus HL: Toxic megacolon in ulcerative colitis. Gastroenterology 37: 239,1959. 3. Case Records of Massachusetts General Hospital. New Eng J Med 208: 94, 1933. Lumb G, Protheroe RHB, Ramsay GS: Ulcerative colitis with dilatation of the colon. Brit J Surg 43: 182, 1955. 5. Marshak RH, Korelitz BI, Klein SH, Wolf BS, Janowitz HD: Toxic dilatation of colon in course of ulcerative colitis. Gastroenterology 38: 165, 1960. 6. Marshak RH, Lester LJ, Friedman Al: Megacolon: a complication of ulcerative colitis. Gastroenterology 16: 768, 1950. 7. Madison MS, Bargan JA: Fulminating chronic ulcerative colitis with unusual segmental dilatation of colon: report of case. Proc Mayo C/in 26: 21, 1951. 8. Edwards FC, Truelove SC: Course and prognosis of ulcerative colitis. Complications. Gut 5: 1, 1964. 4.
288
9. Mclnerney GT, Sauer WG, Baggenstoss AH, Hodgson JR: Fulminating ulcerative colitis with marked colonic dilatation: a clinicopathologic study. Gastroenterofogy 42: 244, 1962. 10. Silverberg D, Robers AG: Toxic megacolon in ulcerative colitis. Canada Med J 90: 5, 357, 1964. 11. Bockus HL, Roth JL, Buchman E, Kalser M: Modern trends in gastroenterology, second series, p 296 (Jones, FA, ed.), New York, 1958. 12. Smith FW, Law DH, Nickel WF, Sleisenger MH: Fulminant ulcerative colitis and toxic dilatation of colon. Medical and surgical management of eleven cases with observations regarding etiology. Gastroenterology 42: 233,1962. 13. Spencer JA, Kirsner SB, Mlynatyk P, Reed PI, Palmer WL: Immediate and prolonged therapeutic effects of corticotropin and adrenal steroids in ulcerative colitis. Gastroenterology 42: 113, 1962. 14. Goldgraber M, Kirsner JB, Palmer WL: Ulcerative colitis: the risk of perforation during adrenal steroid therapy. Arch Int Med 100: 180, 1957.
The American Journal of Surgery
Disease RICHARD
Acute dilatation of the colon as a complication of ulcerative colitis carries a high mortality and morbidity rate. Unfortunately, therapy for this condition has long been an enigma. Despite vigorous supportive and replacement management, valuable time is often lost in the hope that the acute phase of the illness will be reversed. Subsequent surgical intervention often becomes necessary, the timing of which is all important. Our study confirmed our impression that toxic megacolon is best treated surgically. With adequate and timely surgical intervention, good results can be obtained. We wish to demonstrate that we have had a constant response to treatment that has allowed us to formulate a method of handling these cases, and most importantly has enabled us to determine the best time to operate upon these patients. Toxic megacolon has been called the most dreaded complication of ulcerative colitis [I-A’]. The patient presents as an extremely ill person with high fever, tachycardia, abdominal cramps, bloody diarrhea, and a general appearance of severe toxicity. Objective abdominal distention may or may not be present; however, plain films of the abdomen will generally show marked colonic distention, especially of the transverse colon. Nausea and vomiting may occur, leukocytosis is present, bowel sounds are hypoactive or absent, and the abdomen is usually diffusely tender. Past history, physical examination, proctosigmoidoscopy, and abdominal roentgenograms are the essential elements in the establishment of this diagnosis. Acute dilatation of the colon may occur in any stage of ulcerative colitis. It may be the harbinger of the onset of ulcerative colitis or may occur many years later at a time when the disease is quiescent
* Formerly Michigan. 7 Formerly gan.
of
the
surgical
surgical resident,
Volume 121, March 1971
staff, Henry
Henry Ford
Ford Hospital,
Hospital, Detroit,
Detroit, Michi.
L. COLLIER,
JOHN
H. WYLIE,
JORGE
GOMEZ,
MD,*
Jr, MD,* MD,?
Lansing, Lansing,
Barnwell,
Michigan Michigan
South
Carolina
or mildly active. Considerable emphasis has been placed on the diameter of the dilated colon to substantiate the diagnosis [ 4,5]. In our series, the colon was dilated in all cases ; and the colonic distention was termed moderate to severe in more than one-third of the cases. The radiographic diameter of the transverse colon in these cases varied from 8 to 13 cm, as compared with a normal diameter of 5 to 6 cm [ 6,7]. The incidence of toxic megacolon is reported ranging from 1.6 per cent [8] to 2.5 per cent [9]. In our series, we had thirty-five such cases in 605 patients admitted to the hospital with a diagnosis of ulcerative colitis from 1953 to 1964 for an incidence of 5.5 per cent. The etiology of the process is unknown. Pathologically, it has been pointed out that extreme destruction of the bowel wall by inflammation causes severe muscle damage [2,5,9-111. It has been suggested that the myenteric plexus of the bowel wall may become involved and its function impaired [lO,ll].
Hypokalemia, antibiotics, aerophagia, anticholinergics, barium enema, putrefaction of colonic contents, and corticosteroids have been incriminated as possible etiologic or aggravating factors [4]. The onset of acute dilatation of the colon soon after a barium enema examination has frequently been noted. The distention of the bowel probably results from intestinal atony secondary to the effects of the diffuse inflammatory process. The aggravating factors mentioned supplement the condition either by further interference with motility or by the direct mechanical effects of pressure [12]. The question of management of these patients is important since the mortality rate is reported near 50 per cent. Therapy varies. Some believe conservative medical measures should be instituted in all cases and the patients followed very closely. The proponents of this method believe that surgical intervention is indicated only for progressive abdominal distention and/or general clinical de283
Collier, Wylie, and Gomez terioration, evidence of perforation, or suspected impending perforation, uncontrolled bleeding, or lack of response to medical treatment. On the other hand, there are those who believe that the diagnosis of toxic megacolon implies that an emergency operation is indicated as soon as possible. This group believes that these patients are often too ill not to be operated upon. They also note that these critical patients, once the diseased bowel is removed, frequently improve dramatically. Attempts to reduce the distention with enemas or by proctosigmoidoscopy are ineffectual, nor does the patient’s toxicity improve with diverting ileostomy or cecostomy. Because of the multiple methods of treatment and the varied responses obtained, no standardization of therapy has ever evolved. In particular, the appropriate or best time for operating upon patients afflicted with this condition has been difficult to determine. The question of when to subject these seriously ill patients to surgery is a difficult one, and the decision to defer surgical intervention is often made hoping that remission will occur with conservative management. How long to delay surgical therapy must be weighed against the results of treatment. Evaluation of our patients in the series demonstrates a consistent response. Since we have been able to predict accurately the patient’s clinical course, we believe we now have a method of determining the best time to operate on the patient. Treatment
The usual methods of treatment instituted were (1) dietary restriction ; (2) gastrointestinal intubation (Levin and/or Miller-Abbott tubes) ; (3) anticholinergic drugs ; (4) sedation ; (5) fluid and electrolyte replacement; (6) blood transfusions; (7) broad spectrum antibiotics ; (8) corticosteroids. Corticosteroids were used in those patients who had received them previously. Despite these measures there was little improvement in the degree of toxicity and the severity of illness. The use of corticosteroids in the patient with ulcerative colitis is an issue that has been debated for many years. We elected to institute such therapy for our patients. Spencer et al [13] note that 90 per cent of their patients with ulcerative colitis demonstrated an immediate beneficial effect from the addition of corticotropin or adrenal steroids to standard therapy of the disease. In 73 per cent the favorable course persisted after steroids were withdrawn. They have also noted, as we have, a reversal of critical life-threatening illness, allowing adequate 284
preparation of patients for definitive surgery. Many hesitate to use steroids for fear of causing unrecognized perforation. We believe that the danger of perforation in the patient with toxic megacolon is a real one, but doubt that the addition of ACTH or corticosteroids to the therapeutic regimen of these patients increases this danger. Review of our cases confirms our impression. We also believe that with careful scrutiny and examination, if a patient receiving such drugs has perforation, the physician is able to recognize it. This viewpoint is supported by others who have shown that the incidence of perforation in patients with ulcerative colitis is similar whether corticosteroids are used or not [14] ; and that if patients do have perforation and are receiving corticosteroids, their clinical status can well be recognized by the usual criteria [13]. The differences of opinion regarding these drugs are not so puzzling since most of the contributors to the literature on this subject agree that the action of corticosteroids is nonspecific in ulcerative colitis. In acute fulminating colitis or toxic megacolon, the drugs may act by alleviating adrenal insufficiency caused by a general state of stress [IL]. The fact remains that in our series the use of these medications as a supplement to the usual forms of treatment was effective. We found that when we used corticosteroids in the patient who had not previously received them, a consistent and remarkable response occurred. The condition of these patients was ameliorated to the extent that in twenty-four to thirty-six hours the temperature, white blood cell count, and pulse rate returned to normal levels. The general toxic appearance of the patient disappeared and, in most, the abdominal distention gradually lessened. Smith et al [12] noted a similar response, except in his cases the bowel distention remained. All of his patients who underwent surgery while receiving corticosteroid therapy tolerated the procedure well. Results
We compared three groups of patients. Group I had received corticosteroid therapy at some time for the treatment of ulcerative colitis. Group II had received none until acute illness manifested by toxic megacolon developed. Group III received no corticosteroids at any time. The morbidity, mortality, and results of therapy are shown in Table I. Some of the statistically important data are seen in Table II. There were twelve patients in group I. They had received corticosteroids at some time before admission. Toxic megacolon developed in these paThe
American
Journal
of Surgery
Toxic
TABLE I
Comparison of Clinical Status of Three Groups Duration of Ulcerative Colitis
Average Age (yr)
Group
(me)
Average Temperatrue
Average Pulse Rate
Average White
Average Hemoglobin
Average Hospital Stay (days)
Blood Cell Count
(gm %)
I
34.9
31.6
102
125
8.7
20.3
58.8
(Steroids prior to admission) II (No steroids prior to admission)
26.1
32.3
103
120
8.4
18.1
37.4
33.7
56.2
102
115
11.1
14.2
33.0
III (No
Complication Rate
tients who were then supported with corticosteroids and treated with general therapy. These patients demonstrated no response as far as their temperature, white blood cell count, pulse, and general toxic appearance was concerned. (Figure 1.) Six of the twelve patients are surviving and well. There were sixteen patients in group II, none of whom had received corticosteroids before admission to the hospital. Acute dilatation of the colon developed and the patients were toxic and showed no response to the usual forms of therapy, including antibiotics; however, all improved dramatically after the institution of corticosteroid therapy. These patients demonstrated within twenty-four hours a return to normal temperature and pulse rate, and their leukocytosis subsided. (Figure 1.) They lost their toxic perspiring appearance ; and remarkably, the abdominal distenTABLE II
PULSE
F’
160
IO6
150
05
140
104
130
103
120
I02
II0
IO1
100
00
90
99
Data on Thirty-Five Cases 27 Male
Sex
8 Female 8-73 yr Mean: 29.5 yr
Age
Recent
of ulcerative
O-l l-5 5-10 10
(yr)
exacerbation
Anticholinergic’s Recent barium admission Average
highest
enema
within
17 patients
3 mo of
temperature
hemoglobin
Average
white
diagnosis
= 16 patients = 13 patients = 6 patients = 1 patients
35 patients prior to admission
Average
X-ray
colitis
blood
of toxic
1971
(seen
97
60
-
-
160
106
150
105
140
104
130
103
120
102
II0
13 patients
90
99
102.6
60
96
70
97
60
96
on 30 of 32 patients
Surgery: 7 alive and well, 1 dead No surgery: 4 alive and well, 2 alive with symptoms: 2 dead Surgery: 3 alive and well No surgery: 3 alive and well: 1 dead
1.5 Complications per case
IO1 100
18,200
6 died: 6 survived
96
I
2
3
4
5
6
7
6
9
IO
DAYS
13 patients
megacolon
Disease present in rectum proctoscopic examination) Volume 121. March
(mm”)
96
70
100
9.1 cell count
-
60
Results
2 major complications per case 1 major complication
steroids)
Duration
Megacolon
Comparison Figure 1. response to supportive corticosteroids.
in all three groups of the systemic therapy and the administration of
205
Collier,
Wylie,
and Gomez
tion and dilatation of the bowel seen on roentgenogram disappeared or diminished. (Figure 2.) Half of these patients responded so dramatically and looked so well that we were convinced that perhaps they did not require surgery. Six of these eight patients are surviving. However, two did die: one of a perforation at fourteen days and the other of a pulmonary embolus. Three patients have residual symptoms requiring treatment. We believe that early surgical intervention can definitely improve these statistics. We also believe that some of the asymptomatic patients will require surgery for their ulcerative colitis at a later date. Seven of the eight patients that were operated upon are alive and doing well. (Table I.) There were seven patients in group III. They had received no corticosteroids at any time, either before or after admission. We collected the data on this group from the hospital archives, and the duration of ulcerative colitis was almost twice
as long as that of the patients in the other two groups; however, they were not quite as seriously ill. They also had less anemia and leukocytosis. This group may represent the more chronic, burned-out type of disease, and yet they too had dilatation of the coIon. We believe that these patients in group III would have shown the same response as those in groups I and II if we had used the same treatment. Prior to this time, therapy of toxic megacolon has followed two main pathways: medical management, until it was too late to reverse the progress of the disease, and emergency surgical intervention, without taking advantage of appropriate medical treatment. Comments The few simple criteria we now use in the treatment of toxic megacolon are well supported by the material reviewed. The response has been very
Figure 2A. Group 1. Typical example of patient who demonstrated no clinical or radiographic response to a!\ usual forms of therapy including supportive corticosteroids.
Figure 2B. Group II. Example of a patient in group II who responded clinically and whose distention dsappeared after an initial course of corticosteroids was given. 286
The American Journal of Surgery
Toxic Megacolon
consistent and we are confident that the results of such therapy will improve the existing morbidity and mortality rates. Our approach is that if the patient is admitted to the hospital with acute toxic megacolon and has within six recently received corticosteroids, months to one year before admission, he should be placed on corticosteroids for support and an operation performed as soon as possible within twentyfour to forty-eight hours. In our cases, delay did not produce improvement in the patient’s general condition and actually, we believe, created a more hazardous situation. The mortality and morbidity is such that we believe that these patients should be operated on as soon as possible after the diagnosis is made and after correction of dehydration and anemia. If the patient with toxic megacolon has never received corticosteroids before, they are administered at once. These patients will respond, and in four or five days their general condition will be so improved that they can undergo elective surgery rather than emergency intervention. In our patients the dilatation of the bowel lessened, making the operation technically easier. In the patients in group I the large distended thin walled bowel increased t.he incidence of perforation during surgery. Oft.en, we had to perform less than a defini-
Figure 2C. Group II. Patients in this group usually had lessening of distension and general toxicity after corticosteroids were administered. These patients were then operated upon at a better time. Volume 121, March 1971
tive procedure in these patients because of their precarious condition. There was also a much higher complication rate in these cases. In all of our patients in group II we were able to perform definitive procedures, either total or subtotal colectomy and ileostomy or subtotal colectomy and ileoproctostomy. The chances of surgical perforation are much smaller in this group as compared to those in patients in group I, and the post operative complication rate is much less. We have, therefore, evolved a method of therapy for patients with toxic megacolon. We believe that all these patients should be operated upon. We also believe that the best time to operate on these patients to effect reversal of this critical life-threatening illness is as follows: 1. Patients that have received corticosteroids before admission should be operated upon early. This operation should be scheduled twenty-four to thirty-six hours after basic physiologic defects are corrected. 2. Delayed surgical intervention is beneficial in patients that receive corticosteroids for the first time after toxic megacolon develops. Close scrutiny of the patient is necessary, and in four to six days, when his condition is sufficiently improved, elective surgery is possible. Summary We have undertaken to demonstrate a standard method of treatment for toxic megacolon of ulcerative colitis. A methodology for the handling of these cases has not previously evolved, probably because of the protean nature of the disease and the varied responses of the patient to different forms of therapy. We evaluated the experience of thirty-five cases at the Henry Ford Hospital. Some of our patients responded very dramatically to the administration of corticosteroids to supplement the usual forms of treatment. We believe the results of this study support the assumption of certain guidelines for the treatment of toxic dilatation of the colon associated with ulcerative colitis. They are as follows : 1. Patients with toxic megacolon who have received corticosteroids previously should be placed on these drugs for support, and operation performed as soon as possible within twenty-four to forty-eight hours. 2. Such patients who have not received steroids should be given them. Their condition will improve dramatically. Delay in surgical intervention is beneficial in these instances and can be electively performed in four to six days. We have sixteen consecutive cases in this category with no failures. 287
Collier,
Wylie,
and Gomez
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