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Acute Gastrointestinal Problems in the Intensive Care Unit
Symposium on Intensive Care Units
Acute Gastrointestinal Problems in the Intensive Care Unit Alfred M. Markowitz, MD., F.A.C.S. *
While many patients with serious injuries or disease of the gastrointestinal tract may be admitted to the intensive care unit as a consequence of those problems, this paper will limit its considerations to those problems that appear to arise in patients already admitted to the intensive care unit for any grave condition. In addition, while the victim of an automobile accident with a fractured pancreas and a ruptured spleen may be properly considered a candidate for admission to the intensive care unit after surgery, the chief problems in such a patient are those of the operating room rather than the intensive care unit. Likewise the fluid and electrolyte management of patients with such severe injuries do not differ in any substantial way from management of those patients with severe injuries in other organ systems. The most intriguing and serious problem facing these critically ill patients is the development of the acute "ulcer" of the stomach and duodenum-the stress ulcer. In a patient already fighting the problems of sepsis or respiratory insufficiency, the appearance of hematemesis brings into focus a most difficult and often lethal complication in the seriously ill patient. For convenience of study, we may group together four categories of patients who often demonstrate this complication of acute ulceration in the gastroduodenal area: (1) Curling's ulcer- the severely burned patient; (2) patients with respiratory insufficiency; (3) Cushing's ulcerpatients who have undergone surgery or trauma to the central nervous system; and (4) stress ulcer-those patients who have had major surgery or illness in any organ system.
CURLING'S ULCER-THE BURN PATIENT While primacy of description of gastroduodenal ulceration in burn patients is given by Curling4, 5 who, in 1842 and again in 1866, postulated ':'Associate Professor of Clinical Surgery, Columbia University College of Physicians and Surgeons; Associate Attending Surgeon, The Presbyterian Hospital in the City of New York
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a causal relationship between the two conditions, there were earlier reports of this syndrome by Swan32 in 1823, Cooper7 in 1839 and Long23 in 1840. The latter surgeon's cases were included in Curling's report. It is Curling's name today that is applied to the acute ulcer dtathesis seen in the burned individual. In Europe, both Dupuytren l l and Billroth' called attention to the coexistence of burns and gastrointestinal ulceration, during the nineteenth century. In a carefully documented review of some 1700 burn patients at the Burn Unit at the Brooke Army Medical Center, there were 225 patients with major burns who exhibited gastroduodenal ulceration. O'Neil et al. 29 reported in great detail the clinical and pathological manifestations of this group of patients. Half the patients exhibited multiple gastric ulcerations, while one third of the patients had large duodenal ulcers. Fifteen per cent of the patients had combined gastroduodenal ulceration, and less than one per cent had ulceration elsewhere in the gastrointestinal tract. The primary complication of these burned patients with Curling's ulcers was massive hemorrhage. Approximately 10 per cent of these ulcers required surgery for control of bleeding, with a survival rate of less than 50 per cent. Of great interest was the gross pathological description of the ulcer, as simple "punched-out" areas without the surrounding areas of induration so commonly found with chronic peptic ulcer. In a more recent report from this large burn center, Pruitt et al. 30 found Curling's ulcer in 11. 7 per cent of 2772 patients. Forty-two of the 323 patients with this complication of burns required surgery, and 27 of these patients died. The overall survival of the entire group of 323 patients with Curling's ulcer was only 23 per cent, indicating the seriousness of both the underlying disease process and this complication. In 1970 O'Neil28 reported upon some mechanisms of ulcer production in the burned patient. In this clinical study involving the burned patient there was no evidence of hypersecretion of highly acid gastric juice. In addition, in experimental dogs with Heidenhain pouches, burn injury did not produce hypersecretion. Indeed, burn injury is more often associated with a decrease in the production of gastric hydrochloric acid. There is some evidence to indicate that perhaps the burn injury causes a decrease in the rate of renewal of the gastric mucous barrier and thus lays the groundwork for ulcer production. In an interesting autopsy study in 81 burn patients, primarily children, Law et al. 22 found the incidence of erosive lesions of the esophagus, stomach, and duodenum to be 46.9 per cent. A larger number of esophageal erosions were found and attributed to the prolonged use of the nasogastric tube. In 11 of the 81 patients studied, clinically significant hemorrhage was present during life. We do not have sufficient data to know whether or not a patient with a past history of "garden variety" duodenal ulcer will have a greater tendency to hemorrhage when a burn injury is sustained. A priori we might think that this indeed would be the case, and it is, therefore, important to note in the admission history whether or not such a past condition has existed in this acutely injured patient. Reasonable treatment
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of these seriously ill patients appears to be conservative, with the use of antacids and atropine-like drugs. The high mortality rate associated with surgical intervention is undoubtedly due to the fact that these patients are badly depleted before surgery is considered. In addition, we are dealing with a group of severely burned patients who have all the metabolic deficits associated with severe burns. Since such a high percentage of burned patients have gastroduodenal ulceration, it would appear wise that all severely burned patients in the intensive care unit be put on a modified ulcer regimen in that they should be offered a bland diet with frequent feedings and supplements of milk and antacids.
GASTROINTESTINAL COMPLICATIONS OF RESPIRATORY DISEASE The association of acute gastrointestinal disorders with both acute and chronic respiratory problems has been observed for many years. 21 With the segregation of patients with respiratory insufficiency into special care units such as intensive care units or respiratory care units, this association has become even more noticeable. Skillman31 reported massive gastrointestinal hemorrhage occurring in 8 of the 150 patients admitted to a respiratory intensive care unit at the Beth Israel Hospital in Boston. In this group of well-studied patients, multiple superficial gastric ulcerations were found to be confined to the fundus of the stomach and ranged from 0.2 to 4.0 cm. in size. All these patients had had tracheostomies performed and were on respiratory assistance to insure adequate ventilation. Study of these patients failed to reveal any increase of hydrochloric acid secretion. The only members of this group that were considered to have abnormal increase in hydrochloric acid production were those patients who had intracranial lesions or who had undergone intracranial surgery. Only 1 patient out of 8 survived this complication. Again it must be realized that these patients were those in which other severe pathological processes were present, and recovery was extremely doubtful even before this complication of hemorrhage from the gastrointestinal tract developed. The European literature lO • 12 notes the high incidence of peptic ulcer formation in patients with chronic respiratory disease, with figures varying from 20 to 35 per cent. This high incidence of peptic ulceration in patients with respiratory insufficiency may be related to the medication being administered for the respiratory disease, namely, the cortisone group of drugs. In the Lateran Hospital in Rome,t2 4 of 151 patients with chronic pUlmonary disease had major gastrointestinal hemorrhage; all 4 died. In the Salvatore Hospital 1o in France, among the 1500 patients with severe pulmonary insufficiency, 30 had acute abdominal problems. The most common crisis was gastrointestinal hemorrhage, and half of these patients recovered following surgical intervention. The French 10 propose the theory that emphysema and peptic ulcer
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represent a common genetic disorder of the mucous glands of both respiratory and digestive tract, accounting for the high incidence of peptic ulcer problems in erythematous patients. " Another frequently cited theory is that hypoxia and hypercarbia of the respiratory insufficient patient leads to increased gastric hydrochloric acid production; this is moderated by an anticholinesterase effect, which in turn leads to increased vagal tone, causing increased production of acetylcholine; this results in increased secretion of hydrochloric acid by the gastric mucous membrane. This ingenious theory has not been documented by critical human or animal experiments. Indeed, the careful work performed by Skillman et al. 31 documents the fact that acute ulceration of the gastroduodenal area will take place in those patients in whom hypoxia and hypercarbia are prevented by means of mechanical ventilation assistance, and as noted previously these patients also do not exhibit gastric hypersecretion. We can thus see that the patients admitted to the intensive care unit with respiratory insufficiency, either as an exacerbation of a chronic underlying pulmonary disorder or as a consequence of an acute injury, must be carefully observed for evidence of gastrointestinal hemorrhage. The treatment of the hemorrhage, once it occurs, is difficult since these patients are critically ill and, secondly, the usual types of surgery may not control the hemorrhaging area.
CUSHING'S ULCER-CENTRAL NERVOUS SYSTEM DISEASE This eponym is applied to acute gastrointestinal hemorrhages which occur in patients who have had surgery or the central nervous system lesions described by Cushing in 1932.6 Globus and Ralston 17 were also able to collect cases of "Cushing's ulcers" in many types of neurological disorders. There appears tobe some evidence that this complication is related to hypersecretion of gastric acid, although it is often difficult to document this fact. Injury to the central nervous system may increase vagal tone, which leads to hypersecretion. The possibility of severe gastrointestinal hemorrhage should always be kept in mind when dealing with a patient admitted to the intensive care llilit either as a postoperative neurological patient or a patient with any acute neurological disorder or injury. Small amounts of coffee-ground material may often times herald the fact that the patient has acute gastric dilatation secondary to filling of the stomach with blood. Evacuation of the stomach of blood, determination of the amount of blood lost, and prompt replacement of blood are essential in this condition. Continued hemorrhage will make surgical intervention mandatory.
STRESS ULCERS There remains a relatively large group of patients who have massive gastrointestinal bleeding or perforation following serious illness, severe
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trauma, or major surgery of any sort. The problem is described by a number of terms: Dieulafoy's ulcer,9 stress ulcer, acute gastritis, gastroduodenal malacia, etc. Indeed, precisely what is bleeding in the gastrointestinal tract is often times difficult to evaluate in the literature. While some authors such as Fogelman and Garvey15 describe a single ulcer in over two thirds of their patients, others 1B . 24. 25. 27 describe multiple bleeding points in the stomach and duodenum. This issue is important, as it will determine the rationale for therapy to be described later. There is much confusion in the literature as to what a "stress ulcer" is, or indeed if ulcer is the name that should be applied at all. Careful examination of numerous case reports indicate that there are several pathological processes involved. If we define an ulcer as a localized, deeply penetrating area of inflammation surrounded by tissues exhibiting chronic inflammatory changes with evidence of repair, it is quickly apparent that "stress ulcers" do not all conform to such a description. Indeed all studies of the problem of "stress ulcer" make a great effort to differentiate this type of disease from the usual peptic ulcer. Such terms as a "simple punched-out" ulcer, multiple superficial ulcers, gastric erosions, and gastromalaciaB give the impression that we are not dealing with a single pathological entity, but rather a complex of conditions involving the integrity of the gastroduodenal wall- sometimes superficially, sometimes quite deeply, sometimes in a single location, sometimes in multiple locations. At the moment all that we can do is to describe the outward manifestations of the "stress ulcer" syndrome, namely, hemorrhage and perforation. 15. lB. 24 Autopsy studies by Fletcher and Harkins,t4 Grosz and WU,19 and Mears 26 give an incidence of 0.5 to 5.0 per cent of acute gastroduodenal ulceration in large general hospital autopsy series. One gets the impression that the more carefully one searches for superficial erosions, the more one will see them. However, it is quite difficult to separate postmortem autolysis from premortem changes in many instances. When hemorrhage or perforation calls attention to the gastroduodenal area, we undoubtedly make the diagnosis of "stress ulcer" with greater certainty.
MECHANISMS OF ULCERATION It has been impossible thus far to produce a satisfactory experimental model that will explain the various aspects of the acute ulcerative process occurring in the gastrointestinal tract secondary to sepsis, shock, burn injury, central nervous system injury, and a host of other factors that may be at work in the acutely ill patient seen in the intensive care unit. Experiments in rabbits by Harjola and Sivula20 describe the development of areas of anemic infarct in the gastric mucosa when the animal was made hypotensive by hemorrhage. With restoration of the blood volume these areas in the gastric mucosa showed petechial formation with local hemorrhage. These findings, however, were inconstant and could not be demonstrated in all the animals in the study.
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Friesen 16 postulated that hemoconcentration in burn patients resulted in ischemia of the gastric mucosa, which was thought to be the underlying factor in the production of erosive gastritis. This has not been substantiated by clinical or laboratory work. Deficient mucin production in the acutely injured patient has been cited as a possible cause of these ulcerations. Detailed histological studies have failed to demonstrate mucin deficiency24 in acutely traumatized patients. Boley et al,2 did experimental studies in which there was created decreased blood flow in the superior mesenteric artery which resulted in increased gastric blood flow. This was thought to lead to increased acid production by the stomach and acute gastric ulceration. However we do not have good evidence that there is decreased blood flow in the superior mesenteric artery in human beings during acute stress situations, and we must consider this an isolated and interesting finding in one animal species rather than a theory we could relate to the human situation.
TREATMENT It is obvious that acute gastric bleeding appearing in a patient who is already in the intensive care unit because of another severe problem does not lend itself to a standard method of management. The initial efforts are, and should be, conservative ones. Specifically, treatment should be aimed at replacement of blood volume, keeping the stomach empty by means of suction, discontinuance of steroid administration if possible, and perhaps iced gastric lavage. Recently, endoscopic means have become available to diagnose the number and position of the bleedingpoints. When hemorrhage cannot be controlled by conservative means, one is forced to perform an operation of some sort to control the bleeding. Ferguson and Clarke 13 recommend vagotomy and pyloroplasty for these problems. This operation is described as inadequate by other authors,3, 25, 27 who reason that, in general, hypersecretion is not the mechanism of production of "stress ulceration," Indeed, Menguey et al. 27 state that total or near total gastrectomy will be needed to control hemorrhage. While one would hesitate to perform such radical surgery in a desperately ill patient, diffuse bleeding from the gastric wall will require it. On the other hand, should surgical exploration reveal solitary ulcers in the distal stomach or duodenum, lesser surgical procedures will suffice.
SUMMARY An attempt has been made to describe an important complication of the gastrointestinal tract of patients admitted to the intensive care unit of a large general hospitaL The most important syndrome, namely, the stress ulcer, has been described and discussed. It has been emphasized
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that we recognize this condition only by two of its sequelae-hemorrhage and perforation. Hemorrhage, by far, is the more frequent sign that points to the presence of a "stress ulcer." How often such "stress ulcer" exists in the intensive care unit patient without hemorrhage is an unanswerable problem. We have pointed to the four large groups of patients in whom stress ulcers appear. The lack of understanding of such ulcer production is obvious when the numerous theories relating to genesis are considered. Treatment of this problem has been quite unsatisfactory, and often, tot?J or near total gastrectomy may be necessary.
REFERENCES 1. Billroth, T.: Wien. Med. Wochschr., 17:705, 1867. 2. Boley, S. J., Cohen, M. I., Winslow, P. R., Becker, N. H., Treiker, W., McNamara, H., Veith, F. J., and Gleidman, M. L.: Mesenteric ischemia-cause of increased gastric blood flow, hyperacidity and acid gastric ulceration. Surgery, 68:222,1970. 3. Bryant, L. R., and Griffen, W. 0.: Vagotomy and pyloroplasty: An inadequate operation for stress ulcer. Arch. Surg., 93: 161, 1966. 4. Curling, T. B.: Acute ulceration of the duodenum in burn cases. Med. Chir. Tr. London, 25:260,1842. 5. Curling, T. B.: Acute perforating ulcer of the duodenum after a severe burn. Lancet, 1: 484,1866. 6. Cushing, H.: Peptic ulcer and the interbrain. Surg. Gynec. Obstet., 55: 1,1932. 7. Cooper, S.: Pathology of burns and scalds. London Med. Gaz., 23 :837,1839. 8. Dalgaard, J.: Oesophago-gastro-duodenal ulceration encountered at autopsy. Acta Path. Microbiol. Scand., 41:1,1957. 9. Dieulafoy, G.: Exulceration simplex: L'Intervention chirurgicale dans les hematemesis foudroyantes consecutives. Bull. Acad. Med., 39:49,1898. 10. Dor, J., Ohresser, P., and Autran, A.: Complications abdominales aigue dans secteur de reamination respiratoire. Lyon Chir., 65:801, 1969. 11. Dupuytren, Baron A.: Clinical Lectures on Surgery. Trans. of Lecons Orales de cliniques Chirurgecale, 1832. Washington,D.C. D. Green, 1835, Chap. 16, pp. 115-142. 12. Fava, E., Misiti, G., and Malatesta P.: Gravi emorragie gastroduodali in pazienti affetti da insufficienza respiratoria cronica scompensata in corsa di rianimazione. Chir. Gastroent., 3:304, 1969. 13. Ferguson, H. L., and Clarke, J. S.: Treatment of hemorrhage from erosive gastritis by vagotomy and pyloroplasty. Amer. J. Surg., 112:739, 1966. 14. Fletcher, D. H., and Harkins, H. N.: Acute peptic ulcer as a complication of major surgery, stress or trauma Surgery, 36:212, 1954. 15. Fogelman, M J., and Garvey, J. M.: Acute gastroduodenal ulceration incident to surgery and disease. Amer. J. Surg., 112:651, 1966. 16. Friesen, S. R.: The genesis of gastroduodenal ulcer following burns. Surgery, 28:123, 1950. 17. Globus, J. H., and Ralston, B. L.: Multiple erosions and acute perforation of the esophagus, stomach and duodenum in relation to disorders of the nervous system. J. Mt. Sinai Hosp., 17:817, 1951. 18. Goodman, A. A., and Frey, C. F.: Massive upper gastrointestinal hemorrhage following surgical operations. Ann. Surg., 167:180, 1968. 19. Grosz, C., and Wu, Kwang-Tzen: Stress ulcers: A survey of experiences in a large general hospital. Surgery, 61 :853, 1967. 20. Harjola, P. T., and Sivula, A.: Gastric ulceration following experimentally induced hypoxia and hemorrhage shock. Ann. Surg., 163:21, 1966. 21. Krocker, E. J.: Pulmonary emphysema and peptic ulcer. MED. CLIN. N. AMER., 50:479, 1966. 22. Law, E. J., Day, S. B., and McMillan, B. G.: Autopsy findings in the upper gastrointestinal tract of 81 burn patients. Arch. Surg., 102:412, 1971. 23. Long, J.: On the post mo~tem appearance found after burns. London Med. Gaz., 25:743, 1840. 24. Lucas, C. E., Sugauwa, C., Riddle, J., Rector, F., Rosenberg, B., and Watt, A. J.: Natural history and surgical dilemma of "stress" gastric bleeding. Arch. Surg., 102:266, 1971. 25. Lucas, D. J., and Dragstedt, L. R., II: Massive bleeding due to acute hemorrhagic gastritis. Arch. Surg., 101 :550,1970.
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26. Mears. F. B.: Autopsy survey of peptic ulcer associated with other diseases. Surgery. 34: 640,1953. 27. Menguey, R., Gadaez, T., and Zalctrick, R.: The surgical management of acute gastric mucosal bleeding: Stress ulcer, acute erosive gastritis and acute hemorrhagic gastritis. Arch. Surg., 99: 198, 1969. 28. O'Neil, J. A.: The influence of thermal burns on gastric secretion. Surgery, 67:207, 1970. 29. O'Neil, J. A., Pruitt, B. A., and Moncrief, J. A.: Surgical treatment of Curling's ulcer. Surg. Gynec. Obstet., 126:40, 1968. 30. Pruitt, B. A., Foley, F. D., and Moncrief, J. A.: Curling's ulcer: A clinical-pathological study of 323 cases. Ann. Surg., 172:523, 1970. 31. Skillman, J. J., Bushnell, L. S., Goldman, H., and Silen, W.: Respiratory failure, hypotension, sepsis and jaundice: A clinical syndrome associated with lethral hemorrhage from acute stress ulceration of the stomach. Amer. J Surg., 117:523, 1969. 32. Swan, J: Case of severe burn. Edinburg, M. S. J., 19:344, 1823. The Presbyterian Hospital in The City of New York 622 West 168th Street New York, New York 10032
Acute Gastrointestinal Problems in the Intensive Care Unit Alfred M. Markowitz, MD., F.A.C.S. *
While many patients with serious injuries or disease of the gastrointestinal tract may be admitted to the intensive care unit as a consequence of those problems, this paper will limit its considerations to those problems that appear to arise in patients already admitted to the intensive care unit for any grave condition. In addition, while the victim of an automobile accident with a fractured pancreas and a ruptured spleen may be properly considered a candidate for admission to the intensive care unit after surgery, the chief problems in such a patient are those of the operating room rather than the intensive care unit. Likewise the fluid and electrolyte management of patients with such severe injuries do not differ in any substantial way from management of those patients with severe injuries in other organ systems. The most intriguing and serious problem facing these critically ill patients is the development of the acute "ulcer" of the stomach and duodenum-the stress ulcer. In a patient already fighting the problems of sepsis or respiratory insufficiency, the appearance of hematemesis brings into focus a most difficult and often lethal complication in the seriously ill patient. For convenience of study, we may group together four categories of patients who often demonstrate this complication of acute ulceration in the gastroduodenal area: (1) Curling's ulcer- the severely burned patient; (2) patients with respiratory insufficiency; (3) Cushing's ulcerpatients who have undergone surgery or trauma to the central nervous system; and (4) stress ulcer-those patients who have had major surgery or illness in any organ system.
CURLING'S ULCER-THE BURN PATIENT While primacy of description of gastroduodenal ulceration in burn patients is given by Curling4, 5 who, in 1842 and again in 1866, postulated ':'Associate Professor of Clinical Surgery, Columbia University College of Physicians and Surgeons; Associate Attending Surgeon, The Presbyterian Hospital in the City of New York
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a causal relationship between the two conditions, there were earlier reports of this syndrome by Swan32 in 1823, Cooper7 in 1839 and Long23 in 1840. The latter surgeon's cases were included in Curling's report. It is Curling's name today that is applied to the acute ulcer dtathesis seen in the burned individual. In Europe, both Dupuytren l l and Billroth' called attention to the coexistence of burns and gastrointestinal ulceration, during the nineteenth century. In a carefully documented review of some 1700 burn patients at the Burn Unit at the Brooke Army Medical Center, there were 225 patients with major burns who exhibited gastroduodenal ulceration. O'Neil et al. 29 reported in great detail the clinical and pathological manifestations of this group of patients. Half the patients exhibited multiple gastric ulcerations, while one third of the patients had large duodenal ulcers. Fifteen per cent of the patients had combined gastroduodenal ulceration, and less than one per cent had ulceration elsewhere in the gastrointestinal tract. The primary complication of these burned patients with Curling's ulcers was massive hemorrhage. Approximately 10 per cent of these ulcers required surgery for control of bleeding, with a survival rate of less than 50 per cent. Of great interest was the gross pathological description of the ulcer, as simple "punched-out" areas without the surrounding areas of induration so commonly found with chronic peptic ulcer. In a more recent report from this large burn center, Pruitt et al. 30 found Curling's ulcer in 11. 7 per cent of 2772 patients. Forty-two of the 323 patients with this complication of burns required surgery, and 27 of these patients died. The overall survival of the entire group of 323 patients with Curling's ulcer was only 23 per cent, indicating the seriousness of both the underlying disease process and this complication. In 1970 O'Neil28 reported upon some mechanisms of ulcer production in the burned patient. In this clinical study involving the burned patient there was no evidence of hypersecretion of highly acid gastric juice. In addition, in experimental dogs with Heidenhain pouches, burn injury did not produce hypersecretion. Indeed, burn injury is more often associated with a decrease in the production of gastric hydrochloric acid. There is some evidence to indicate that perhaps the burn injury causes a decrease in the rate of renewal of the gastric mucous barrier and thus lays the groundwork for ulcer production. In an interesting autopsy study in 81 burn patients, primarily children, Law et al. 22 found the incidence of erosive lesions of the esophagus, stomach, and duodenum to be 46.9 per cent. A larger number of esophageal erosions were found and attributed to the prolonged use of the nasogastric tube. In 11 of the 81 patients studied, clinically significant hemorrhage was present during life. We do not have sufficient data to know whether or not a patient with a past history of "garden variety" duodenal ulcer will have a greater tendency to hemorrhage when a burn injury is sustained. A priori we might think that this indeed would be the case, and it is, therefore, important to note in the admission history whether or not such a past condition has existed in this acutely injured patient. Reasonable treatment
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of these seriously ill patients appears to be conservative, with the use of antacids and atropine-like drugs. The high mortality rate associated with surgical intervention is undoubtedly due to the fact that these patients are badly depleted before surgery is considered. In addition, we are dealing with a group of severely burned patients who have all the metabolic deficits associated with severe burns. Since such a high percentage of burned patients have gastroduodenal ulceration, it would appear wise that all severely burned patients in the intensive care unit be put on a modified ulcer regimen in that they should be offered a bland diet with frequent feedings and supplements of milk and antacids.
GASTROINTESTINAL COMPLICATIONS OF RESPIRATORY DISEASE The association of acute gastrointestinal disorders with both acute and chronic respiratory problems has been observed for many years. 21 With the segregation of patients with respiratory insufficiency into special care units such as intensive care units or respiratory care units, this association has become even more noticeable. Skillman31 reported massive gastrointestinal hemorrhage occurring in 8 of the 150 patients admitted to a respiratory intensive care unit at the Beth Israel Hospital in Boston. In this group of well-studied patients, multiple superficial gastric ulcerations were found to be confined to the fundus of the stomach and ranged from 0.2 to 4.0 cm. in size. All these patients had had tracheostomies performed and were on respiratory assistance to insure adequate ventilation. Study of these patients failed to reveal any increase of hydrochloric acid secretion. The only members of this group that were considered to have abnormal increase in hydrochloric acid production were those patients who had intracranial lesions or who had undergone intracranial surgery. Only 1 patient out of 8 survived this complication. Again it must be realized that these patients were those in which other severe pathological processes were present, and recovery was extremely doubtful even before this complication of hemorrhage from the gastrointestinal tract developed. The European literature lO • 12 notes the high incidence of peptic ulcer formation in patients with chronic respiratory disease, with figures varying from 20 to 35 per cent. This high incidence of peptic ulceration in patients with respiratory insufficiency may be related to the medication being administered for the respiratory disease, namely, the cortisone group of drugs. In the Lateran Hospital in Rome,t2 4 of 151 patients with chronic pUlmonary disease had major gastrointestinal hemorrhage; all 4 died. In the Salvatore Hospital 1o in France, among the 1500 patients with severe pulmonary insufficiency, 30 had acute abdominal problems. The most common crisis was gastrointestinal hemorrhage, and half of these patients recovered following surgical intervention. The French 10 propose the theory that emphysema and peptic ulcer
1280
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represent a common genetic disorder of the mucous glands of both respiratory and digestive tract, accounting for the high incidence of peptic ulcer problems in erythematous patients. " Another frequently cited theory is that hypoxia and hypercarbia of the respiratory insufficient patient leads to increased gastric hydrochloric acid production; this is moderated by an anticholinesterase effect, which in turn leads to increased vagal tone, causing increased production of acetylcholine; this results in increased secretion of hydrochloric acid by the gastric mucous membrane. This ingenious theory has not been documented by critical human or animal experiments. Indeed, the careful work performed by Skillman et al. 31 documents the fact that acute ulceration of the gastroduodenal area will take place in those patients in whom hypoxia and hypercarbia are prevented by means of mechanical ventilation assistance, and as noted previously these patients also do not exhibit gastric hypersecretion. We can thus see that the patients admitted to the intensive care unit with respiratory insufficiency, either as an exacerbation of a chronic underlying pulmonary disorder or as a consequence of an acute injury, must be carefully observed for evidence of gastrointestinal hemorrhage. The treatment of the hemorrhage, once it occurs, is difficult since these patients are critically ill and, secondly, the usual types of surgery may not control the hemorrhaging area.
CUSHING'S ULCER-CENTRAL NERVOUS SYSTEM DISEASE This eponym is applied to acute gastrointestinal hemorrhages which occur in patients who have had surgery or the central nervous system lesions described by Cushing in 1932.6 Globus and Ralston 17 were also able to collect cases of "Cushing's ulcers" in many types of neurological disorders. There appears tobe some evidence that this complication is related to hypersecretion of gastric acid, although it is often difficult to document this fact. Injury to the central nervous system may increase vagal tone, which leads to hypersecretion. The possibility of severe gastrointestinal hemorrhage should always be kept in mind when dealing with a patient admitted to the intensive care llilit either as a postoperative neurological patient or a patient with any acute neurological disorder or injury. Small amounts of coffee-ground material may often times herald the fact that the patient has acute gastric dilatation secondary to filling of the stomach with blood. Evacuation of the stomach of blood, determination of the amount of blood lost, and prompt replacement of blood are essential in this condition. Continued hemorrhage will make surgical intervention mandatory.
STRESS ULCERS There remains a relatively large group of patients who have massive gastrointestinal bleeding or perforation following serious illness, severe
ACUTE GASTROINTESTINAL PROBLEMS IN THE INTENSIVE CARE UNIT
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trauma, or major surgery of any sort. The problem is described by a number of terms: Dieulafoy's ulcer,9 stress ulcer, acute gastritis, gastroduodenal malacia, etc. Indeed, precisely what is bleeding in the gastrointestinal tract is often times difficult to evaluate in the literature. While some authors such as Fogelman and Garvey15 describe a single ulcer in over two thirds of their patients, others 1B . 24. 25. 27 describe multiple bleeding points in the stomach and duodenum. This issue is important, as it will determine the rationale for therapy to be described later. There is much confusion in the literature as to what a "stress ulcer" is, or indeed if ulcer is the name that should be applied at all. Careful examination of numerous case reports indicate that there are several pathological processes involved. If we define an ulcer as a localized, deeply penetrating area of inflammation surrounded by tissues exhibiting chronic inflammatory changes with evidence of repair, it is quickly apparent that "stress ulcers" do not all conform to such a description. Indeed all studies of the problem of "stress ulcer" make a great effort to differentiate this type of disease from the usual peptic ulcer. Such terms as a "simple punched-out" ulcer, multiple superficial ulcers, gastric erosions, and gastromalaciaB give the impression that we are not dealing with a single pathological entity, but rather a complex of conditions involving the integrity of the gastroduodenal wall- sometimes superficially, sometimes quite deeply, sometimes in a single location, sometimes in multiple locations. At the moment all that we can do is to describe the outward manifestations of the "stress ulcer" syndrome, namely, hemorrhage and perforation. 15. lB. 24 Autopsy studies by Fletcher and Harkins,t4 Grosz and WU,19 and Mears 26 give an incidence of 0.5 to 5.0 per cent of acute gastroduodenal ulceration in large general hospital autopsy series. One gets the impression that the more carefully one searches for superficial erosions, the more one will see them. However, it is quite difficult to separate postmortem autolysis from premortem changes in many instances. When hemorrhage or perforation calls attention to the gastroduodenal area, we undoubtedly make the diagnosis of "stress ulcer" with greater certainty.
MECHANISMS OF ULCERATION It has been impossible thus far to produce a satisfactory experimental model that will explain the various aspects of the acute ulcerative process occurring in the gastrointestinal tract secondary to sepsis, shock, burn injury, central nervous system injury, and a host of other factors that may be at work in the acutely ill patient seen in the intensive care unit. Experiments in rabbits by Harjola and Sivula20 describe the development of areas of anemic infarct in the gastric mucosa when the animal was made hypotensive by hemorrhage. With restoration of the blood volume these areas in the gastric mucosa showed petechial formation with local hemorrhage. These findings, however, were inconstant and could not be demonstrated in all the animals in the study.
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Friesen 16 postulated that hemoconcentration in burn patients resulted in ischemia of the gastric mucosa, which was thought to be the underlying factor in the production of erosive gastritis. This has not been substantiated by clinical or laboratory work. Deficient mucin production in the acutely injured patient has been cited as a possible cause of these ulcerations. Detailed histological studies have failed to demonstrate mucin deficiency24 in acutely traumatized patients. Boley et al,2 did experimental studies in which there was created decreased blood flow in the superior mesenteric artery which resulted in increased gastric blood flow. This was thought to lead to increased acid production by the stomach and acute gastric ulceration. However we do not have good evidence that there is decreased blood flow in the superior mesenteric artery in human beings during acute stress situations, and we must consider this an isolated and interesting finding in one animal species rather than a theory we could relate to the human situation.
TREATMENT It is obvious that acute gastric bleeding appearing in a patient who is already in the intensive care unit because of another severe problem does not lend itself to a standard method of management. The initial efforts are, and should be, conservative ones. Specifically, treatment should be aimed at replacement of blood volume, keeping the stomach empty by means of suction, discontinuance of steroid administration if possible, and perhaps iced gastric lavage. Recently, endoscopic means have become available to diagnose the number and position of the bleedingpoints. When hemorrhage cannot be controlled by conservative means, one is forced to perform an operation of some sort to control the bleeding. Ferguson and Clarke 13 recommend vagotomy and pyloroplasty for these problems. This operation is described as inadequate by other authors,3, 25, 27 who reason that, in general, hypersecretion is not the mechanism of production of "stress ulceration," Indeed, Menguey et al. 27 state that total or near total gastrectomy will be needed to control hemorrhage. While one would hesitate to perform such radical surgery in a desperately ill patient, diffuse bleeding from the gastric wall will require it. On the other hand, should surgical exploration reveal solitary ulcers in the distal stomach or duodenum, lesser surgical procedures will suffice.
SUMMARY An attempt has been made to describe an important complication of the gastrointestinal tract of patients admitted to the intensive care unit of a large general hospitaL The most important syndrome, namely, the stress ulcer, has been described and discussed. It has been emphasized
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that we recognize this condition only by two of its sequelae-hemorrhage and perforation. Hemorrhage, by far, is the more frequent sign that points to the presence of a "stress ulcer." How often such "stress ulcer" exists in the intensive care unit patient without hemorrhage is an unanswerable problem. We have pointed to the four large groups of patients in whom stress ulcers appear. The lack of understanding of such ulcer production is obvious when the numerous theories relating to genesis are considered. Treatment of this problem has been quite unsatisfactory, and often, tot?J or near total gastrectomy may be necessary.
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26. Mears. F. B.: Autopsy survey of peptic ulcer associated with other diseases. Surgery. 34: 640,1953. 27. Menguey, R., Gadaez, T., and Zalctrick, R.: The surgical management of acute gastric mucosal bleeding: Stress ulcer, acute erosive gastritis and acute hemorrhagic gastritis. Arch. Surg., 99: 198, 1969. 28. O'Neil, J. A.: The influence of thermal burns on gastric secretion. Surgery, 67:207, 1970. 29. O'Neil, J. A., Pruitt, B. A., and Moncrief, J. A.: Surgical treatment of Curling's ulcer. Surg. Gynec. Obstet., 126:40, 1968. 30. Pruitt, B. A., Foley, F. D., and Moncrief, J. A.: Curling's ulcer: A clinical-pathological study of 323 cases. Ann. Surg., 172:523, 1970. 31. Skillman, J. J., Bushnell, L. S., Goldman, H., and Silen, W.: Respiratory failure, hypotension, sepsis and jaundice: A clinical syndrome associated with lethral hemorrhage from acute stress ulceration of the stomach. Amer. J Surg., 117:523, 1969. 32. Swan, J: Case of severe burn. Edinburg, M. S. J., 19:344, 1823. The Presbyterian Hospital in The City of New York 622 West 168th Street New York, New York 10032