Annals of the Royal College of Surgeons of England (1992) vol. 74, 356-359
Intestinal ischaemia in the unconscious intensive care unit patient Sina Dorudi
BSc Surgical Registrar
FRCS*
Peter M Lamont
MD FRCS Reader and Consultant Surgeon
Nuffield Department of Surgery, John Radcliffe Hospital, Oxford
Key words: Acute intestinal ischaemia; Intensive
care
unit
This paper highlights the difficulties of diagnosing intestinal ischaemia in unconscious patients on an intensive care unit. We have analysed the clinical details and investigations of eight such patients in whom a preoperative diagnosis of intestinal ischaemia was made on clinical grounds. Intestinal ischaemia was confirmed at laparotomy in only four cases (50%). These patients showed no significant differences in any of the commonly accepted parameters of intestinal ischaemia from the four patients who had a negative laparotomy. In particular, ali patients exhibited a metabolic acidosis with fever and a leucocytosis. There was a mean delay of 13.6 h between surgical opinion and laparotomy in the four patients with ischaemia, only one of whom was salvaged. There was no morbidity associated with the laparotomy in this smali series. It is suggested that, in the intensive care setting, early laparotomy should be performed immediately the clinical suspicion of intestinal ischaemia arises.
The early diagnosis of acute intestinal ischaemia is difficult, even in the conscious and alert patient (1,2). The reported mortality of 80-90% associated with bowel infarction has not altered significantly over the last decade (2). Severe abdominal pain with a relative paucity of abdominal signs and a systemic response of fever and leucocytosis have been stressed as useful clinical features (1-3). In addition, a metabolic acidosis that persists after adequate resuscitation has long been recognised to be a constant positive finding
in
ischaemia (2,5,6). However, there are significant problems associated with its interpretation, particularly with non-occlusive ischaemia (2,5). Critically ill patients in the intensive care unit are prone to haemodynamic disturbances, both central and visceral, which can cause intestinal ischaemia even in the absence of arterial obstruction (7). The pathogenesis of such non-occlusive ischaemia remains unclear but includes hypovolaemia, poor cardiac output, splanchnic vasoconstriction or the use of positive inotropic drugs
(8). Clinical assessment of the abdomen in unconscious and ventilated patients in the intensive care unit is difficult and of limited value. Mesenteric angiography on such patients is often impractical. Thus it is more often persisting evidence of sepsis, in the absence of an obvious extra-abdominal focus of infection, that raises the possibility of intestinal ischaemia. There are currently no clearly defined indications for laparotomy in such patients.
Patients and results During a 6-month period between July and December 1990, a clinical diagnosis of intestinal ischaemia was made in eight unconscious patients on the intensive care unit. Brief clinical summaries are presented below.
patients with acute intestinal
ischaemia (3,4). Arteriography remains the only investigation of proven value in the diagnosis of acute intestinal * Current address: ICRF Colorectal Cancer Unit, St Mark's Hospital, City Road, London Correspondence to: Mr P M Lamont, Nuffield Department of Surgery, John Radcliffe Hospital, Headington, Oxford OX3 9DU
Case reports Case I-age 58 years Admitted to the intensive care unit in respiratory failure after thoracotomy and left lower lobectomy. At 15 h after admission to the unit he became hypotensive and acidotic, which persisted despite appropriate resuscitation. The intensivist raised the diagnosis of intestinal ischae-
Intestinal ischaemia in the unconscious ICU patient mia and a surgical opinion was sought. The abdomen was soft and not distended but bowel sounds were absent. The patient did not respond to the abdominal examination and was therefore observed for another 9 h but failed to make any progress. After repeated requests from the intensivist a laparotomy was performed, at which extensive infarction of the small bowel was found. No resections were performed and the patient died.
Case 2-age 73 years Admitted to the intensive care unit with renal and respiratory failure after oversewing of a perforated duodenal ulcer. At 8 h after admission to the unit the patient remained hypotensive and acidotic despite vigorous resuscitation. The abdomen was distended and silent and a surgical opinion was sought as intestinal ischaemia was suspected by the intensivist. In view of the non-specific clinical findings the patient was observed for another 12 h after which a laparotomy was performed as the condition of the patient had not improved. At laparotomy the entire small bowel and proximal colon were infarcted. No resections were performed and the patient died. Case 3-age 62 years Admitted to the intensive care unit after elective repair of an abdominal aortic aneurysm. The patient developed a persistent acidosis 16 h after admission to the unit. A surgical opinion was sought as the intensivist strongly suspected a diagnosis of intestinal ischaemia. The abdomen was not distended and bowel sounds were present but reduced. The patient did not respond to the examination and was therefore observed for another 18 h. At this time the patient became hypotensive and more acidotic. After repeated requests from the intensivist a laparotomy was performed, at which there was extensive infarction of the entire small bowel. No resections were performed and the patient died.
Case 4-age 68 years Admitted to the intensive care unit after bilateral renal artery endarterectomy. Within 12 h of admission the patient became hypotensive and acidotic which persisted despite appropriate resuscitation. In addition, the abdomen distended so a surgical opinion was sought. The patient did not respond to the examination and bowel sounds were absent. After a 6 h period of further observation it was decided to perform a laparotomy as the patient's condition was unaltered and a diagnosis of intestinal ischaemia was suspected. At laparotomy a 30 cm segment of infarcted proximal ileum was resected in conjunction with a thrombectomy of the superior mesenteric artery. The patient made a full recovery. Case 5-age 69 years Admitted to the intensive care unit after repair of a ruptured abdominal aortic aneurysm. At 24 h after
357
admission the patient developed a persistent acidosis. In view of this, the intensivist raised the possibility of intestinal ischaemia and a surgical opinion was sought. The abdomen was distended and silent but the patient did not respond to the examination so it was elected to observe the patient. After 12 h the acidosis persisted and a laparotomy was performed to exclude intestinal ischaemia, at which the findings were consistent with recent aortic surgery with no evidence of bowel infarction. The patient subsequently made a full recovery.
Case 6-age 72 years Admitted to the intensive care unit in respiratory and cardiac failure following a myocardial infarction. An acidosis was present on admission to the unit and persisted thereafter. The patient developed a distended abdomen 12 h after admission and a surgical opinion was sought to exclude the possibility of intestinal ischaemia The examination revealed a soft, distended abdomen with absent bowel sounds. The patient was observed for a further 10 h at which time a laparotomy was performed as the patient's condition had not altered. At laparotomy there were no abnormal findings. The patient made a full recovery. Case 7-age 60 years Admitted to the intensive care unit in septic shock after Hartmann's operation for faecal peritonitis. At 72 h after admission to the unit, by which time the patient's general vital signs had stabilised, the patient became hypotensive and acidotic. A surgical opinion was sought on the basis of a putative diagnosis of intestinal ischaemia. The abdomen was soft and not distended, though bowel sounds were absent. The patient did, however, appear to respond to the abdominal palpation. After a 10 h period of observation a laparotomy was performed as the situation remained unaltered. At laparotomy there was no evidence of bowel ischaemia or residual sepsis. The patient's condition subsequently deteriorated and he died 10 days later from multiple system failure. Case 8-age 48 years Admitted to the intensive care unit with septicaemia secondary to acute bacterial endocarditis and metastatic cerebral abscesses. Five days after admission to the unit the patient developed a persistent acidosis. A surgical assessment was arranged by the intensivist as a diagnosis of intestinal ischaemia was strongly suspected. The abdomen was soft and not distended and the patient made no apparent response during the examination. After a 24 h period of observation a laparotomy was performed after strong pressure from the intensivist, at which there were no abnormal findings. The patient made a full recovery. The results of those investigations which are commonly associated with small bowel infarction are listed in
358
S Dorudi and P M Lamont
Table I. Investigations in patients undergoing positive laparotomy for small bowel infarction compared with patients undergoing negative laparotomy. Results expressed as mean and (range) Positive laparotomy
WCC pH
Negative laparotomy
21.4 (9.3-35.8) 17.2 (12.4-16.6) 7.23 (7.05-7.30) 7.26 (7.20-7.32)
Base excess (negative) 10.6 (7.20-15.6) 7.5 (5.6-10.3) Phosphate (normal range: 0.8-1.45 mmol/1) 1.42 (0.96-1.91) 1.47 (0.92-1.83) Table I. There were no other differences in any of the clinical features, haematology or biochemistry between the patients having a positive laparotomy compared with those with a negative laparotomy. Plain abdominal radiography and ultrasound examination of the abdomen were non-contributory. Of four positive laparotomies only one patient was salvaged. A small bowel resection was performed in conjunction with a superior mesenteric artery thrombectomy and the patient recovered (Case 4). In the remaining three positive laparotomies the extent of bowel infarction precluded any chance of survival. In these three cases the abdomen was closed and the patients subsequently died. In addition to these mortalities there was one death in the negative laparotomy group. This occurred on the 10th postoperative day in a patient with multiple system failure (Case 7). The mean delay between surgical opinion and laparotomy was 13.6 h in the positive group and 14 h in the negative group. All the patients studied were receiving positive inotropic agents at the time of diagnosis.
Discussion The diagnosis of the acute abdomen in the unconscious patient on an intensive care unit can be difficult. In such patients the combination of haemodynamic instability with increasing reliance on inotropic support raises the possibility of sepsis (9). In the absence of an obvious source of extra-abdominal infection, sequential organ failure is often a valid sign of occult intra-abdominal sepsis (9). A persistent metabolic acidosis, a raised serum phosphate level and a leucocytosis have all been proposed as diagnostic markers of early acute intestinal ischaemia (1,3,4,10). In our series of eight ventilated patients, it was the combination of the clinical context described above, together with the positive findings of a metabolic acidosis and a raised white cell count that led to a putative diagnosis of acute intestinal ischaemia. Intestinal ischaemia was confirmed at laparotomy in four of the eight cases. Those patients undergoing negative laparotomy did not differ significantly in any of the commonly accepted parameters of intestinal ischaemia from patients with bowel infarction. All our patients were acidotic,
febrile and exhibited a leucocytosis. We found no correlation between elevated serum phosphate and gut ischaemia in our patients. It is of interest that there was a mean delay of 13.6 h between surgical opinion and laparotomy in the four patients with ischaemia, only one of whom was salvaged. This delay occurred despite a strong argument for laparotomy from the intensivist looking after the patient in each case, as there was either a lack of significant progress in the patient's state or a deterioration had occurred, despite maximal supportive therapy. Surgeons are often reluctant to operate on such sick patients in the intensive care unit; however, it is well established that support of organ function without definitive treatment of an intra-abdominal source of sepsis is only palliative (9). Furthermore, laparotomy assumes more importance both in diagnosis and as a therapeutic intervention in intensive care patients with intestinal ischaemia, as there are no clear non-invasive radiological methods of evaluation in this condition (11,12). The significant delay between surgical opinion and laparotomy may well have contributed to the high mortality (three out of four patients) in the four patients with intestinal ischaemia. These three patients may still not have been salvaged with earlier laparotomy but at least prolonged and expensive life-support therapy could have been withdrawn earlier, saving both relatives and clinical staff from the emotional rollercoaster so often associated with a sick patient on the intensive care unit. Laparotomy was clinically valuable even when negative, as a life-threatening condition was excluded and the staff of the intensive care unit were better able to pursue alternative sources of sepsis without feeling that they were fighting a losing battle with the spectre of gangrenous bowel. There was no immediate morbidity associated with laparotomy in this small series. The death in the negative laparotomy group occurred on the 10th postoperative day in a patient with multiple organ failure. It has been suggested that intestinal tonometry, which involves an indirect assessment of mucosal pH, is of predictive value in the early diagnosis of acute intestinal ischaemia (13,14). This technique is not widely available at the present time and clearly requires further evaluation in the particular setting of the unconscious patient in the intensive care unit. The diagnosis of intestinal ischaemia is recognised to be difficult in the conscious and co-operative patient (2). This problem is further compounded in the unconscious and ventilated intensive care patient who cannot complain of abdominal pain and may exhibit signs of sepsis with no clear-cut focus. The established clinical and laboratory criteria of intestinal ischaemia are not reliable indicators of its presence or absence. Haemodynamic instability, metabolic acidosis, hyperphosphataemia and leucocytosis are all non-specific markers of severe infection and do not always indicate bowel infarction. It is suggested that laparotomy remains the only certain method of diagnosis in the intensive care setting and early laparotomy has proved valuable in the patient
Intestinal ischaemia in the unconscious ICU patient with haemodynamic instability and metabolic acidosis but no obvious focus of infection. A high negative exploration rate may have to be accepted as a consequence of early laparotomy which has a low morbidity if negative and allows earlier definitive therapy when positive.
References I Jamieson WG, Marchuk S, Rowsum J, Duran D. The early diagnosis of massive intestinal ischaemia. Br J Surg 1982; 69:552-3. 2 Marston A. Acute intestinal ischaemia. BrMedJ 1990;301: 1174-5. 3 Sarr MG, Bulkley GB, Zuidema GD. Preoperative recognition of intestinal strangulation obstruction. Am J Surg 1983;145: 176-81. 4 Brooks DH, Carey LC. Base deficit in superior mesenteric artery occlusion: An aid to early diagnosis. Ann Surg 1973;177:352-6. S Williams LF. Mesenteric ischemia. Surg Clin North Am 1988;68:331-53. 6 Boley SJ, Sprayregen S, Siegelmann SS, Veith FJ. Initial results from an aggressive approach to acute mesenteric ischemia. Surgery 1977;82:848-55.
359
7 Gottlieb JE, Menashe PI, Cruz E. Gastrointestinal complications in critically ill patients: The intensivists' overview. AmJ7 Gastroenterol 1986;81:227-38. 8 Brandt LJ, Boley SJ. Ischemic intestinal syndromes. In: Maclean LD ed. Advances in Surgery, Vol. 15. Chicago: Year Book Publishers, 1981:1-45. 9 Polk HG, Shields CL. Remote organ failure: A valid sign of occult intra-abdominal infection. Surgery 1977;81:310-13. 10 Jamieson WG, Lozon A, Duran D et al. Changes in serum phosphate levels associated with intestinal infarction and necrosis. Surg Gynecol Obstet 1975;140:19-21 11 Sinanan M, Maier RV, Carrico J. Laparotomy for intraabdominal sepsis in patients in an intensive care unit. Arch Surg 1984;119:652-8. 12 Glick PL, Pellegrini CA, Stein S et al. Abdominal abscess: A surgical strategy. Arch Surg 1983;118:646-50. 13 Fiddian-Green RG, Amelin PM, Herrmann JB et al. Prediction of the development of sigmoid ischemia on the day of aortic operations. Arch Surg 1986;121:654-8. 14 Poole JW, Sammartano RJ, Boley SJ. The use of tonometry in the early diagnosis of mesenteric ischemia. Curr Surg 1987;44:21-6.
Received 31 December 1991
Invited comment This paper illustrates very clearly a real clinical problem. The specialist who works every day in the intensive care unit becomes familiar with this picture. The surgeon one of a number on call-is asked to consider such a patient only rarely and is in a difficult situation; one cannot overlook the fact that one-half of the patients who might, on their signs, have intestinal ischaemia will prove at laparotomy to have no evidence of sepsis. However, with present methods there is no way round this dilemma save by laparotomy, negative laparotomy has proved to be relatively harmless, and it can eliminate various sources of intra-abdominal sepsis in the most conclusive way. These can only be pursued, in the absence of a laparotomy, by more fallible investigations, and the certainty of the findings of even a negative laparotomy are of great value to the intensivist. What this paper emphasises is a truth which has not received much recognition in the British medical press.
Polk has for some years called attention to the fact that 'organ failure may indicate the presence of otherwise occult intra-abdominal infection in postoperative patients. Support of organ function without definitive correction of underlying infection is only palliative' (1). He has recently re-emphasised this clinical observation (2). The outcome reported in patient No. 4 in this paper shows what can be achieved by timely intervention. PETER F JONES
FRCS
Aberdeen
References I Polk HC, Shields CL. Remote organ failure: a valid sign of occult intra-abdominal infection. Surgery 1977;81:3 10-13. 2 Polk HC. Concealed progress in the management of severe surgical infection. Am J Surg. 1991;162:195-6.
Intestinal ischaemia in the unconscious intensive care unit patient Sina Dorudi
BSc Surgical Registrar
FRCS*
Peter M Lamont
MD FRCS Reader and Consultant Surgeon
Nuffield Department of Surgery, John Radcliffe Hospital, Oxford
Key words: Acute intestinal ischaemia; Intensive
care
unit
This paper highlights the difficulties of diagnosing intestinal ischaemia in unconscious patients on an intensive care unit. We have analysed the clinical details and investigations of eight such patients in whom a preoperative diagnosis of intestinal ischaemia was made on clinical grounds. Intestinal ischaemia was confirmed at laparotomy in only four cases (50%). These patients showed no significant differences in any of the commonly accepted parameters of intestinal ischaemia from the four patients who had a negative laparotomy. In particular, ali patients exhibited a metabolic acidosis with fever and a leucocytosis. There was a mean delay of 13.6 h between surgical opinion and laparotomy in the four patients with ischaemia, only one of whom was salvaged. There was no morbidity associated with the laparotomy in this smali series. It is suggested that, in the intensive care setting, early laparotomy should be performed immediately the clinical suspicion of intestinal ischaemia arises.
The early diagnosis of acute intestinal ischaemia is difficult, even in the conscious and alert patient (1,2). The reported mortality of 80-90% associated with bowel infarction has not altered significantly over the last decade (2). Severe abdominal pain with a relative paucity of abdominal signs and a systemic response of fever and leucocytosis have been stressed as useful clinical features (1-3). In addition, a metabolic acidosis that persists after adequate resuscitation has long been recognised to be a constant positive finding
in
ischaemia (2,5,6). However, there are significant problems associated with its interpretation, particularly with non-occlusive ischaemia (2,5). Critically ill patients in the intensive care unit are prone to haemodynamic disturbances, both central and visceral, which can cause intestinal ischaemia even in the absence of arterial obstruction (7). The pathogenesis of such non-occlusive ischaemia remains unclear but includes hypovolaemia, poor cardiac output, splanchnic vasoconstriction or the use of positive inotropic drugs
(8). Clinical assessment of the abdomen in unconscious and ventilated patients in the intensive care unit is difficult and of limited value. Mesenteric angiography on such patients is often impractical. Thus it is more often persisting evidence of sepsis, in the absence of an obvious extra-abdominal focus of infection, that raises the possibility of intestinal ischaemia. There are currently no clearly defined indications for laparotomy in such patients.
Patients and results During a 6-month period between July and December 1990, a clinical diagnosis of intestinal ischaemia was made in eight unconscious patients on the intensive care unit. Brief clinical summaries are presented below.
patients with acute intestinal
ischaemia (3,4). Arteriography remains the only investigation of proven value in the diagnosis of acute intestinal * Current address: ICRF Colorectal Cancer Unit, St Mark's Hospital, City Road, London Correspondence to: Mr P M Lamont, Nuffield Department of Surgery, John Radcliffe Hospital, Headington, Oxford OX3 9DU
Case reports Case I-age 58 years Admitted to the intensive care unit in respiratory failure after thoracotomy and left lower lobectomy. At 15 h after admission to the unit he became hypotensive and acidotic, which persisted despite appropriate resuscitation. The intensivist raised the diagnosis of intestinal ischae-
Intestinal ischaemia in the unconscious ICU patient mia and a surgical opinion was sought. The abdomen was soft and not distended but bowel sounds were absent. The patient did not respond to the abdominal examination and was therefore observed for another 9 h but failed to make any progress. After repeated requests from the intensivist a laparotomy was performed, at which extensive infarction of the small bowel was found. No resections were performed and the patient died.
Case 2-age 73 years Admitted to the intensive care unit with renal and respiratory failure after oversewing of a perforated duodenal ulcer. At 8 h after admission to the unit the patient remained hypotensive and acidotic despite vigorous resuscitation. The abdomen was distended and silent and a surgical opinion was sought as intestinal ischaemia was suspected by the intensivist. In view of the non-specific clinical findings the patient was observed for another 12 h after which a laparotomy was performed as the condition of the patient had not improved. At laparotomy the entire small bowel and proximal colon were infarcted. No resections were performed and the patient died. Case 3-age 62 years Admitted to the intensive care unit after elective repair of an abdominal aortic aneurysm. The patient developed a persistent acidosis 16 h after admission to the unit. A surgical opinion was sought as the intensivist strongly suspected a diagnosis of intestinal ischaemia. The abdomen was not distended and bowel sounds were present but reduced. The patient did not respond to the examination and was therefore observed for another 18 h. At this time the patient became hypotensive and more acidotic. After repeated requests from the intensivist a laparotomy was performed, at which there was extensive infarction of the entire small bowel. No resections were performed and the patient died.
Case 4-age 68 years Admitted to the intensive care unit after bilateral renal artery endarterectomy. Within 12 h of admission the patient became hypotensive and acidotic which persisted despite appropriate resuscitation. In addition, the abdomen distended so a surgical opinion was sought. The patient did not respond to the examination and bowel sounds were absent. After a 6 h period of further observation it was decided to perform a laparotomy as the patient's condition was unaltered and a diagnosis of intestinal ischaemia was suspected. At laparotomy a 30 cm segment of infarcted proximal ileum was resected in conjunction with a thrombectomy of the superior mesenteric artery. The patient made a full recovery. Case 5-age 69 years Admitted to the intensive care unit after repair of a ruptured abdominal aortic aneurysm. At 24 h after
357
admission the patient developed a persistent acidosis. In view of this, the intensivist raised the possibility of intestinal ischaemia and a surgical opinion was sought. The abdomen was distended and silent but the patient did not respond to the examination so it was elected to observe the patient. After 12 h the acidosis persisted and a laparotomy was performed to exclude intestinal ischaemia, at which the findings were consistent with recent aortic surgery with no evidence of bowel infarction. The patient subsequently made a full recovery.
Case 6-age 72 years Admitted to the intensive care unit in respiratory and cardiac failure following a myocardial infarction. An acidosis was present on admission to the unit and persisted thereafter. The patient developed a distended abdomen 12 h after admission and a surgical opinion was sought to exclude the possibility of intestinal ischaemia The examination revealed a soft, distended abdomen with absent bowel sounds. The patient was observed for a further 10 h at which time a laparotomy was performed as the patient's condition had not altered. At laparotomy there were no abnormal findings. The patient made a full recovery. Case 7-age 60 years Admitted to the intensive care unit in septic shock after Hartmann's operation for faecal peritonitis. At 72 h after admission to the unit, by which time the patient's general vital signs had stabilised, the patient became hypotensive and acidotic. A surgical opinion was sought on the basis of a putative diagnosis of intestinal ischaemia. The abdomen was soft and not distended, though bowel sounds were absent. The patient did, however, appear to respond to the abdominal palpation. After a 10 h period of observation a laparotomy was performed as the situation remained unaltered. At laparotomy there was no evidence of bowel ischaemia or residual sepsis. The patient's condition subsequently deteriorated and he died 10 days later from multiple system failure. Case 8-age 48 years Admitted to the intensive care unit with septicaemia secondary to acute bacterial endocarditis and metastatic cerebral abscesses. Five days after admission to the unit the patient developed a persistent acidosis. A surgical assessment was arranged by the intensivist as a diagnosis of intestinal ischaemia was strongly suspected. The abdomen was soft and not distended and the patient made no apparent response during the examination. After a 24 h period of observation a laparotomy was performed after strong pressure from the intensivist, at which there were no abnormal findings. The patient made a full recovery. The results of those investigations which are commonly associated with small bowel infarction are listed in
358
S Dorudi and P M Lamont
Table I. Investigations in patients undergoing positive laparotomy for small bowel infarction compared with patients undergoing negative laparotomy. Results expressed as mean and (range) Positive laparotomy
WCC pH
Negative laparotomy
21.4 (9.3-35.8) 17.2 (12.4-16.6) 7.23 (7.05-7.30) 7.26 (7.20-7.32)
Base excess (negative) 10.6 (7.20-15.6) 7.5 (5.6-10.3) Phosphate (normal range: 0.8-1.45 mmol/1) 1.42 (0.96-1.91) 1.47 (0.92-1.83) Table I. There were no other differences in any of the clinical features, haematology or biochemistry between the patients having a positive laparotomy compared with those with a negative laparotomy. Plain abdominal radiography and ultrasound examination of the abdomen were non-contributory. Of four positive laparotomies only one patient was salvaged. A small bowel resection was performed in conjunction with a superior mesenteric artery thrombectomy and the patient recovered (Case 4). In the remaining three positive laparotomies the extent of bowel infarction precluded any chance of survival. In these three cases the abdomen was closed and the patients subsequently died. In addition to these mortalities there was one death in the negative laparotomy group. This occurred on the 10th postoperative day in a patient with multiple system failure (Case 7). The mean delay between surgical opinion and laparotomy was 13.6 h in the positive group and 14 h in the negative group. All the patients studied were receiving positive inotropic agents at the time of diagnosis.
Discussion The diagnosis of the acute abdomen in the unconscious patient on an intensive care unit can be difficult. In such patients the combination of haemodynamic instability with increasing reliance on inotropic support raises the possibility of sepsis (9). In the absence of an obvious source of extra-abdominal infection, sequential organ failure is often a valid sign of occult intra-abdominal sepsis (9). A persistent metabolic acidosis, a raised serum phosphate level and a leucocytosis have all been proposed as diagnostic markers of early acute intestinal ischaemia (1,3,4,10). In our series of eight ventilated patients, it was the combination of the clinical context described above, together with the positive findings of a metabolic acidosis and a raised white cell count that led to a putative diagnosis of acute intestinal ischaemia. Intestinal ischaemia was confirmed at laparotomy in four of the eight cases. Those patients undergoing negative laparotomy did not differ significantly in any of the commonly accepted parameters of intestinal ischaemia from patients with bowel infarction. All our patients were acidotic,
febrile and exhibited a leucocytosis. We found no correlation between elevated serum phosphate and gut ischaemia in our patients. It is of interest that there was a mean delay of 13.6 h between surgical opinion and laparotomy in the four patients with ischaemia, only one of whom was salvaged. This delay occurred despite a strong argument for laparotomy from the intensivist looking after the patient in each case, as there was either a lack of significant progress in the patient's state or a deterioration had occurred, despite maximal supportive therapy. Surgeons are often reluctant to operate on such sick patients in the intensive care unit; however, it is well established that support of organ function without definitive treatment of an intra-abdominal source of sepsis is only palliative (9). Furthermore, laparotomy assumes more importance both in diagnosis and as a therapeutic intervention in intensive care patients with intestinal ischaemia, as there are no clear non-invasive radiological methods of evaluation in this condition (11,12). The significant delay between surgical opinion and laparotomy may well have contributed to the high mortality (three out of four patients) in the four patients with intestinal ischaemia. These three patients may still not have been salvaged with earlier laparotomy but at least prolonged and expensive life-support therapy could have been withdrawn earlier, saving both relatives and clinical staff from the emotional rollercoaster so often associated with a sick patient on the intensive care unit. Laparotomy was clinically valuable even when negative, as a life-threatening condition was excluded and the staff of the intensive care unit were better able to pursue alternative sources of sepsis without feeling that they were fighting a losing battle with the spectre of gangrenous bowel. There was no immediate morbidity associated with laparotomy in this small series. The death in the negative laparotomy group occurred on the 10th postoperative day in a patient with multiple organ failure. It has been suggested that intestinal tonometry, which involves an indirect assessment of mucosal pH, is of predictive value in the early diagnosis of acute intestinal ischaemia (13,14). This technique is not widely available at the present time and clearly requires further evaluation in the particular setting of the unconscious patient in the intensive care unit. The diagnosis of intestinal ischaemia is recognised to be difficult in the conscious and co-operative patient (2). This problem is further compounded in the unconscious and ventilated intensive care patient who cannot complain of abdominal pain and may exhibit signs of sepsis with no clear-cut focus. The established clinical and laboratory criteria of intestinal ischaemia are not reliable indicators of its presence or absence. Haemodynamic instability, metabolic acidosis, hyperphosphataemia and leucocytosis are all non-specific markers of severe infection and do not always indicate bowel infarction. It is suggested that laparotomy remains the only certain method of diagnosis in the intensive care setting and early laparotomy has proved valuable in the patient
Intestinal ischaemia in the unconscious ICU patient with haemodynamic instability and metabolic acidosis but no obvious focus of infection. A high negative exploration rate may have to be accepted as a consequence of early laparotomy which has a low morbidity if negative and allows earlier definitive therapy when positive.
References I Jamieson WG, Marchuk S, Rowsum J, Duran D. The early diagnosis of massive intestinal ischaemia. Br J Surg 1982; 69:552-3. 2 Marston A. Acute intestinal ischaemia. BrMedJ 1990;301: 1174-5. 3 Sarr MG, Bulkley GB, Zuidema GD. Preoperative recognition of intestinal strangulation obstruction. Am J Surg 1983;145: 176-81. 4 Brooks DH, Carey LC. Base deficit in superior mesenteric artery occlusion: An aid to early diagnosis. Ann Surg 1973;177:352-6. S Williams LF. Mesenteric ischemia. Surg Clin North Am 1988;68:331-53. 6 Boley SJ, Sprayregen S, Siegelmann SS, Veith FJ. Initial results from an aggressive approach to acute mesenteric ischemia. Surgery 1977;82:848-55.
359
7 Gottlieb JE, Menashe PI, Cruz E. Gastrointestinal complications in critically ill patients: The intensivists' overview. AmJ7 Gastroenterol 1986;81:227-38. 8 Brandt LJ, Boley SJ. Ischemic intestinal syndromes. In: Maclean LD ed. Advances in Surgery, Vol. 15. Chicago: Year Book Publishers, 1981:1-45. 9 Polk HG, Shields CL. Remote organ failure: A valid sign of occult intra-abdominal infection. Surgery 1977;81:310-13. 10 Jamieson WG, Lozon A, Duran D et al. Changes in serum phosphate levels associated with intestinal infarction and necrosis. Surg Gynecol Obstet 1975;140:19-21 11 Sinanan M, Maier RV, Carrico J. Laparotomy for intraabdominal sepsis in patients in an intensive care unit. Arch Surg 1984;119:652-8. 12 Glick PL, Pellegrini CA, Stein S et al. Abdominal abscess: A surgical strategy. Arch Surg 1983;118:646-50. 13 Fiddian-Green RG, Amelin PM, Herrmann JB et al. Prediction of the development of sigmoid ischemia on the day of aortic operations. Arch Surg 1986;121:654-8. 14 Poole JW, Sammartano RJ, Boley SJ. The use of tonometry in the early diagnosis of mesenteric ischemia. Curr Surg 1987;44:21-6.
Received 31 December 1991
Invited comment This paper illustrates very clearly a real clinical problem. The specialist who works every day in the intensive care unit becomes familiar with this picture. The surgeon one of a number on call-is asked to consider such a patient only rarely and is in a difficult situation; one cannot overlook the fact that one-half of the patients who might, on their signs, have intestinal ischaemia will prove at laparotomy to have no evidence of sepsis. However, with present methods there is no way round this dilemma save by laparotomy, negative laparotomy has proved to be relatively harmless, and it can eliminate various sources of intra-abdominal sepsis in the most conclusive way. These can only be pursued, in the absence of a laparotomy, by more fallible investigations, and the certainty of the findings of even a negative laparotomy are of great value to the intensivist. What this paper emphasises is a truth which has not received much recognition in the British medical press.
Polk has for some years called attention to the fact that 'organ failure may indicate the presence of otherwise occult intra-abdominal infection in postoperative patients. Support of organ function without definitive correction of underlying infection is only palliative' (1). He has recently re-emphasised this clinical observation (2). The outcome reported in patient No. 4 in this paper shows what can be achieved by timely intervention. PETER F JONES
FRCS
Aberdeen
References I Polk HC, Shields CL. Remote organ failure: a valid sign of occult intra-abdominal infection. Surgery 1977;81:3 10-13. 2 Polk HC. Concealed progress in the management of severe surgical infection. Am J Surg. 1991;162:195-6.
