- Email: [email protected]
Superior mesenteric artery injury: a case report
124
Injury, 8, 124-I
26
Superior mesenteric artery injury: a case report R. A. M. Myers Trauma Unit, Johannesburg General Hospital, and Department of Surgery, University of the Witwatersrand
Summary
A case of blunt trauma to the upper abdomen with multiple organ injury is described. The lesion involving the superior mesenteric artery was undiagnosed at operation. The subsequent diagnosis and handling of the case is described with a review of the literature on blunt injury to this vessel. INTRODUCTION THE FIRSTsuccessful repair of a superior mesen-
teric artery injury was reported in 1954 by Ulvestad. Since then there have been some 30 reported cases with a mortality rate of over 40 per cent. The majority of cases are due to penetrating injuries, namely gunshot and stab injuries, and a number are the result of iatrogenic injuries during pancreatic resection. Blunt injuries account for only 4 reported cases. Survival from this injury is uncommon, as is borne out by reports of several authors of a combined series of over 3000 cases of arterial injury from World War II and the Korean War, where no mention is made of superior mesenteric artery injury (Ficara, 1944; Ferguson et al., 1961; Drapanas et al., 1970). CASE REPORT A man aged 28 was admitted following a motor vehicle accident in which the steering wheel was driven against the lower chest and upper abdomen. On admission the patient was severely shocked and showed definite evidence of intraperitoneal injuries. Following immediate resuscitation he was taken to theatre where, at laparotomy, the following injuries were found: 1. A transverse tear of the left rectus abdominis muscle.
2. Laceration of the spleen. 3. Transection of the duodenojejunal flexure with the laceration extending into the mesentery exposing the superior mesenteric artery and vein with bleeding venous radicles. There was unrecognized blunt injury to the superior mesenteric artery. (Intimal tear or contusion and subsequent thrombosis.) 4. A further transection of the jejunum and mesentery, 25 cm from the duodenojejunal flexure. 5. Multiple seromuscular tears in the left colon. Splenectomy was performed, haemostasis secured and 1 m of jejunum resected from the duodenojejunal flexure. Bleeding was not brisk, but peristalsis was present. An end-to-end duodenojejunal anastomosis was performed and the seromuscular tears of the colon were closed in 2 layers. Sodium cephalothin intravenously and Garamycin (gentamicin) intramuscularly were given at operation. During the immediate postoperative period there was a large volume of nasogastric aspirate. Hyperalimentation with Intralipid and Amigen 800 was begun on day 1. Faeces and flatus were passed on day 5 and a serous discharge was noted at the drainage sites. On day 8, a severe bloody diarrhoea developed with a noticeably increasing jaundice. The patient also developed a pyrexia and attempts at isolating an organism were unsuccessful. Colicky abdominal pains had developed and the patient passed a jelly-like mass of blood and mucus. Histology showed necrotic tissue with acute inflammatory exudates. Barium meal and small-bowel follow-through
Myers: Mesenteric Artery Injury examination on day 19 showed a grossly abnormal small-bowel pattern suggestive of diffuse infarction. This was followed 2 days later by an aortogram and selective inferior mesenteric artery angiogram which showed an occlusion of the superior mesenteric artery 5 cm distal to its origin from the aorta, with retrograde filling of the artery distal to the occlusion from the inferior mesenteric artery via the marginal artery of Drummond. There was then a delayed filling of the bowel arterioles. The superior mesenteric vein and portal vein were both patent. In view of these findings oral feeds were discontinued. Hyperalimentation was begun using a central venous catheter. An Arnigen-dextrose mixture was used with added vitamins, and electrolytes were given as indicated by repeated studies of the patient’s urea and electrolytes. A 72-hour stool specimen showed a daily fat excretion of 12.9 g and nitrogen content of 47.8 g, in accordance with the gross malabsorption occurring with oral feeding. A Crosby capsule biopsy, however, showed a normal proximal jejunum. Over the next 21 days the patient had diarrhoea with a stool volume ranging between 1 and 2 litres daily. The postoperative period was further complicated by the development of a fungal septicaemia with a Candida albicans-like organism. Torulopsis glabrata was cultured from all orifices, blood stream, sputum and urine. This responded well to Fungisone (amphotericin-B) and 5 flurocytosine. This therapy was continued for 6 weeks. In order to maintain his hydration and nutrition a Schribner shunt was inserted into the right leg for hyperalimentation and fungal treatment. By day 56 the patient was able to take oral feeds and tolerated them well with a daily stool frequency of 2 to 3. Follow-up barium meals showed improvement with a more normal distal ileum. His 72-hour stool specimen showed a marked improvement. The patient was then discharged and followed-up as an out-patient. During his period of hyperalimentation the patient maintained his weight at 53 kg. The total period of hyperalimentation was 40 days. DISCUSSION In reviewing the management of trauma to the superior mesenteric artery near its origin, several initial requirements are apparent. 1. Awareness of the possibility of such injury and knowledge of the anatomy of the area. 2. The ability to provide massive blood
125 replacement and vascular control, including aortic occlusion. 3. Careful exploration of all haematomas in the base of the small-bowel mesentery and particularly all mesenteric haematomas if they are expanding. 4. Appreciation of the fact that such injuries are rarely isolated. 5. Awareness that bowel ischaemia may show either immediate or delayed infarction or malabsorption. The bowel supplied by the superior mesenteric artery is intermediate in its ability to withstand ischaemia (compared to nerve tissue and extremities). The exact period of tolerable ischaemia is not known. In experimental animals, acute occlusion of the superior mesenteric artery is poorly tolerated-a 3-hour occlusion has a 25 per cent mortality rate; Chour occlusion has a 75 per cent rate. Reduction of the intestinal bacterial flora with the use of antibiotics reduces this 75 per cent mortality rate to 25 per cent. With the use of heparin preoperatively a similar reduction in mortality is found (Nelson and Kremen, 1950). Shirkey (1967) reported a Chour occlusion with survival followed by disruption of the arterial repair. Secondary revascularization was successful but intestinal malabsorption followed. The safe ischaemic time of human bowel is not known but is probably about 90 minutes (Ikard and Merendino, 1970). Fullen et al. (1972) in their classification of anatomical siting of lesions, have shown that occlusion of more distal segments of the superior mesenteric artery results in less ischaemia and in ischaemia to shorter segments of bowel than in proximal injury. Mucosal infarction may not be prevented but early re-establishment of arterial inflow may augment mucosal regeneration. This regeneration normally occurs within 5 days so that protracted malabsorption is unlikely. However, if the slough is deep enough, regeneration which normally occurs from the crypts fails. Retrograde filling from the ileocaecal artery may be sufficient to keep only the muscularis and serosa viable. Regeneration then is in a lateral manner from normal proximal jejunum to abnormal distal jejunum, taking its blood supply with it. A similar mechanism operates in a retrograde manner distally. Patients with bowel ischaemia have a complicated postoperative course and hyperalimentation is essential (Ledgerwood and Lucas, 1974). This case fully demonstrated this need With severe and continuous diarrhoea and
Injury: the British Journal of Accident Surgery Vol. ~/NO. 2
126 malabsorption, hyperalimentation was essential for survival. This was complicated by a fungal septicaemia which responded to antifungal therapy. The dilemma faced was that hyperalimentation was essential but had surely contributed to the fungal infection. The removal of the central infusion line would greatly facilitate treatment of the fungal septicaemia but the patient would not have been able to maintain himself nutritionally. For this reason a Schribner shunt was inserted into his right leg and a 3-way attachment introduced into the circuit. Via this the hyperalimentation and amphotericin were given daily with excellent results and complete recovery from the fungaemia. The shunt allows a rapid flow rate which prevents the fungi from colonizing on the foreign material of the shunt. Antibiotics given at the operation and afterwards may well have contributed to the fungaemia but were of value in reducing the intestinal flora count and thence the likelihood of death. An associated venous injury must be repaired to reduce the engorgement of the bowel and to prevent sequestration of blood in bowel. However,
if the vein is severely damaged it can be sacrificed, but the artery must be repaired or revascularized by a graft if bowel integrity is sought (Ficara, 1944; Ferguson et al., 1961; Patman et al., 1964; Drapanas et al., 1970; Perry et al., 1971). Furthermore, experimental work has demonstrated that arterial occlusion is tolerated for a longer period than is venous occlusion (Nelson and Kremen, 1950; Lillehei et al., 1959). Marston (1963) has documented the sequential effects of experimental mesenteric arterial occlusion. There is progressive destruction of bowel from the mucosa outwards. Following one hour of occlusion, the tips of the intestinal villi begin to slough and form a membrane of necrotic material and bacteria. The blood volume has been observed to contract at a rate of 5 per cent per hour (mostly plasma) and this has been attributed to back-flow in the portal system even though the portal venous pressure was not raised. In conclusion it may be asked why a more aggressive approach was not taken once the diagnosis had been confirmed on day 21 after injury and operation. The matter was discussed at length with the’vascular surgeons, who felt that the patient had survived up to that time, was recovering from severe trauma (Crosby capsule biopsy result) and had developed a collateral Requeslsforreprintsshouldbeaddressedio: R. A. M. Myers, School, Hospital Street, Johannesburg, South Africa.
circulation (the artery of Drummond). Intervention may actually compromise the situation and with the severe trauma to the base of the mesentery the operation might be technically very difficult. Thus it was decided against reconstructive surgery. Acknowledgements Thanks are due to Dr J. McMurdo, Superintendent of the Hospital,for permission to publish the case and to Professor C. G. Bremner for assistance in preparation of the article. REFERENCES Drapanas T., Hewitt R. L. and Weichert R. F. (1970) Civilian vascular injuries; a critical appraisal of three decades of management. Ann. Surg. 172, 351. Ferguson I. A., Byrd W. M. and McAfee D. K. (1961) Experience in the management of arterial injuries. Ann. surg. 153, 980. Ficara B. J. (1944) Mesenteric vascular occlusion. A presentation of i5 cases. Am. J. Surg. 66,168. Fullen W. D.. Hunt J. and Altemeier W. A. (1972) The clinical spectrum of penetrating injury‘ to SMA circulation. J. Trauma 12,656.
Ikard R. and Merendino K. A. (1970) Accidental excision of the superior mesenteric artery. Surg. Clin. North Am. 50, 1075. Ledgerwood A. and Lucas C. E. (1974) Survival following proximal superior mesenteric artery occlusion from trauma. J. Trauma 14, 622. Lillehei R. C., Goott B. and Miller F. A. (1959) The physiological response of the small bowel of the dog to ischaemia including prolonged in vitro preservation of the bowel with successful replacement and survival. Ann. Surg. 150,543. Marston A. (1963) Causes of death in mesenteric arterial occlusion. 1. Local and general effects of devascularization of the bowel. Ann. Surg. 158, 952. Nelson L. E. and Kremen A. J. (1950) Experimental occlusion of the superior mesenteric vessels with special role of intravascular thrombosis and its prevention by heparin. Surgery 28, 819. Patman R. D., Poulos E. and Shires G. T. (1964) The management of civilian arterial injuries. Surg. Gynecol. Obstet. 118, 725.
Perry M. O., Thai E. R. and Shires G. T. (1971) Management of arterial injuries. Ann. Surg. 173, 403. Shirkey A. L., Quast D. C. and Jordaan G. L. (1967) Superior mesenteric artery division and intestinal function. J. Trauma 7, 7. Ulvestad L. E. (1954) Repair of laceration of superior mesenteric artery acquired by non-penetrating injury to abdomen. Ann. Surg. 140, 752.
FRCS (Ed.), Department of Surgery, University of Witwatersrand Medica
Injury, 8, 124-I
26
Superior mesenteric artery injury: a case report R. A. M. Myers Trauma Unit, Johannesburg General Hospital, and Department of Surgery, University of the Witwatersrand
Summary
A case of blunt trauma to the upper abdomen with multiple organ injury is described. The lesion involving the superior mesenteric artery was undiagnosed at operation. The subsequent diagnosis and handling of the case is described with a review of the literature on blunt injury to this vessel. INTRODUCTION THE FIRSTsuccessful repair of a superior mesen-
teric artery injury was reported in 1954 by Ulvestad. Since then there have been some 30 reported cases with a mortality rate of over 40 per cent. The majority of cases are due to penetrating injuries, namely gunshot and stab injuries, and a number are the result of iatrogenic injuries during pancreatic resection. Blunt injuries account for only 4 reported cases. Survival from this injury is uncommon, as is borne out by reports of several authors of a combined series of over 3000 cases of arterial injury from World War II and the Korean War, where no mention is made of superior mesenteric artery injury (Ficara, 1944; Ferguson et al., 1961; Drapanas et al., 1970). CASE REPORT A man aged 28 was admitted following a motor vehicle accident in which the steering wheel was driven against the lower chest and upper abdomen. On admission the patient was severely shocked and showed definite evidence of intraperitoneal injuries. Following immediate resuscitation he was taken to theatre where, at laparotomy, the following injuries were found: 1. A transverse tear of the left rectus abdominis muscle.
2. Laceration of the spleen. 3. Transection of the duodenojejunal flexure with the laceration extending into the mesentery exposing the superior mesenteric artery and vein with bleeding venous radicles. There was unrecognized blunt injury to the superior mesenteric artery. (Intimal tear or contusion and subsequent thrombosis.) 4. A further transection of the jejunum and mesentery, 25 cm from the duodenojejunal flexure. 5. Multiple seromuscular tears in the left colon. Splenectomy was performed, haemostasis secured and 1 m of jejunum resected from the duodenojejunal flexure. Bleeding was not brisk, but peristalsis was present. An end-to-end duodenojejunal anastomosis was performed and the seromuscular tears of the colon were closed in 2 layers. Sodium cephalothin intravenously and Garamycin (gentamicin) intramuscularly were given at operation. During the immediate postoperative period there was a large volume of nasogastric aspirate. Hyperalimentation with Intralipid and Amigen 800 was begun on day 1. Faeces and flatus were passed on day 5 and a serous discharge was noted at the drainage sites. On day 8, a severe bloody diarrhoea developed with a noticeably increasing jaundice. The patient also developed a pyrexia and attempts at isolating an organism were unsuccessful. Colicky abdominal pains had developed and the patient passed a jelly-like mass of blood and mucus. Histology showed necrotic tissue with acute inflammatory exudates. Barium meal and small-bowel follow-through
Myers: Mesenteric Artery Injury examination on day 19 showed a grossly abnormal small-bowel pattern suggestive of diffuse infarction. This was followed 2 days later by an aortogram and selective inferior mesenteric artery angiogram which showed an occlusion of the superior mesenteric artery 5 cm distal to its origin from the aorta, with retrograde filling of the artery distal to the occlusion from the inferior mesenteric artery via the marginal artery of Drummond. There was then a delayed filling of the bowel arterioles. The superior mesenteric vein and portal vein were both patent. In view of these findings oral feeds were discontinued. Hyperalimentation was begun using a central venous catheter. An Arnigen-dextrose mixture was used with added vitamins, and electrolytes were given as indicated by repeated studies of the patient’s urea and electrolytes. A 72-hour stool specimen showed a daily fat excretion of 12.9 g and nitrogen content of 47.8 g, in accordance with the gross malabsorption occurring with oral feeding. A Crosby capsule biopsy, however, showed a normal proximal jejunum. Over the next 21 days the patient had diarrhoea with a stool volume ranging between 1 and 2 litres daily. The postoperative period was further complicated by the development of a fungal septicaemia with a Candida albicans-like organism. Torulopsis glabrata was cultured from all orifices, blood stream, sputum and urine. This responded well to Fungisone (amphotericin-B) and 5 flurocytosine. This therapy was continued for 6 weeks. In order to maintain his hydration and nutrition a Schribner shunt was inserted into the right leg for hyperalimentation and fungal treatment. By day 56 the patient was able to take oral feeds and tolerated them well with a daily stool frequency of 2 to 3. Follow-up barium meals showed improvement with a more normal distal ileum. His 72-hour stool specimen showed a marked improvement. The patient was then discharged and followed-up as an out-patient. During his period of hyperalimentation the patient maintained his weight at 53 kg. The total period of hyperalimentation was 40 days. DISCUSSION In reviewing the management of trauma to the superior mesenteric artery near its origin, several initial requirements are apparent. 1. Awareness of the possibility of such injury and knowledge of the anatomy of the area. 2. The ability to provide massive blood
125 replacement and vascular control, including aortic occlusion. 3. Careful exploration of all haematomas in the base of the small-bowel mesentery and particularly all mesenteric haematomas if they are expanding. 4. Appreciation of the fact that such injuries are rarely isolated. 5. Awareness that bowel ischaemia may show either immediate or delayed infarction or malabsorption. The bowel supplied by the superior mesenteric artery is intermediate in its ability to withstand ischaemia (compared to nerve tissue and extremities). The exact period of tolerable ischaemia is not known. In experimental animals, acute occlusion of the superior mesenteric artery is poorly tolerated-a 3-hour occlusion has a 25 per cent mortality rate; Chour occlusion has a 75 per cent rate. Reduction of the intestinal bacterial flora with the use of antibiotics reduces this 75 per cent mortality rate to 25 per cent. With the use of heparin preoperatively a similar reduction in mortality is found (Nelson and Kremen, 1950). Shirkey (1967) reported a Chour occlusion with survival followed by disruption of the arterial repair. Secondary revascularization was successful but intestinal malabsorption followed. The safe ischaemic time of human bowel is not known but is probably about 90 minutes (Ikard and Merendino, 1970). Fullen et al. (1972) in their classification of anatomical siting of lesions, have shown that occlusion of more distal segments of the superior mesenteric artery results in less ischaemia and in ischaemia to shorter segments of bowel than in proximal injury. Mucosal infarction may not be prevented but early re-establishment of arterial inflow may augment mucosal regeneration. This regeneration normally occurs within 5 days so that protracted malabsorption is unlikely. However, if the slough is deep enough, regeneration which normally occurs from the crypts fails. Retrograde filling from the ileocaecal artery may be sufficient to keep only the muscularis and serosa viable. Regeneration then is in a lateral manner from normal proximal jejunum to abnormal distal jejunum, taking its blood supply with it. A similar mechanism operates in a retrograde manner distally. Patients with bowel ischaemia have a complicated postoperative course and hyperalimentation is essential (Ledgerwood and Lucas, 1974). This case fully demonstrated this need With severe and continuous diarrhoea and
Injury: the British Journal of Accident Surgery Vol. ~/NO. 2
126 malabsorption, hyperalimentation was essential for survival. This was complicated by a fungal septicaemia which responded to antifungal therapy. The dilemma faced was that hyperalimentation was essential but had surely contributed to the fungal infection. The removal of the central infusion line would greatly facilitate treatment of the fungal septicaemia but the patient would not have been able to maintain himself nutritionally. For this reason a Schribner shunt was inserted into his right leg and a 3-way attachment introduced into the circuit. Via this the hyperalimentation and amphotericin were given daily with excellent results and complete recovery from the fungaemia. The shunt allows a rapid flow rate which prevents the fungi from colonizing on the foreign material of the shunt. Antibiotics given at the operation and afterwards may well have contributed to the fungaemia but were of value in reducing the intestinal flora count and thence the likelihood of death. An associated venous injury must be repaired to reduce the engorgement of the bowel and to prevent sequestration of blood in bowel. However,
if the vein is severely damaged it can be sacrificed, but the artery must be repaired or revascularized by a graft if bowel integrity is sought (Ficara, 1944; Ferguson et al., 1961; Patman et al., 1964; Drapanas et al., 1970; Perry et al., 1971). Furthermore, experimental work has demonstrated that arterial occlusion is tolerated for a longer period than is venous occlusion (Nelson and Kremen, 1950; Lillehei et al., 1959). Marston (1963) has documented the sequential effects of experimental mesenteric arterial occlusion. There is progressive destruction of bowel from the mucosa outwards. Following one hour of occlusion, the tips of the intestinal villi begin to slough and form a membrane of necrotic material and bacteria. The blood volume has been observed to contract at a rate of 5 per cent per hour (mostly plasma) and this has been attributed to back-flow in the portal system even though the portal venous pressure was not raised. In conclusion it may be asked why a more aggressive approach was not taken once the diagnosis had been confirmed on day 21 after injury and operation. The matter was discussed at length with the’vascular surgeons, who felt that the patient had survived up to that time, was recovering from severe trauma (Crosby capsule biopsy result) and had developed a collateral Requeslsforreprintsshouldbeaddressedio: R. A. M. Myers, School, Hospital Street, Johannesburg, South Africa.
circulation (the artery of Drummond). Intervention may actually compromise the situation and with the severe trauma to the base of the mesentery the operation might be technically very difficult. Thus it was decided against reconstructive surgery. Acknowledgements Thanks are due to Dr J. McMurdo, Superintendent of the Hospital,for permission to publish the case and to Professor C. G. Bremner for assistance in preparation of the article. REFERENCES Drapanas T., Hewitt R. L. and Weichert R. F. (1970) Civilian vascular injuries; a critical appraisal of three decades of management. Ann. Surg. 172, 351. Ferguson I. A., Byrd W. M. and McAfee D. K. (1961) Experience in the management of arterial injuries. Ann. surg. 153, 980. Ficara B. J. (1944) Mesenteric vascular occlusion. A presentation of i5 cases. Am. J. Surg. 66,168. Fullen W. D.. Hunt J. and Altemeier W. A. (1972) The clinical spectrum of penetrating injury‘ to SMA circulation. J. Trauma 12,656.
Ikard R. and Merendino K. A. (1970) Accidental excision of the superior mesenteric artery. Surg. Clin. North Am. 50, 1075. Ledgerwood A. and Lucas C. E. (1974) Survival following proximal superior mesenteric artery occlusion from trauma. J. Trauma 14, 622. Lillehei R. C., Goott B. and Miller F. A. (1959) The physiological response of the small bowel of the dog to ischaemia including prolonged in vitro preservation of the bowel with successful replacement and survival. Ann. Surg. 150,543. Marston A. (1963) Causes of death in mesenteric arterial occlusion. 1. Local and general effects of devascularization of the bowel. Ann. Surg. 158, 952. Nelson L. E. and Kremen A. J. (1950) Experimental occlusion of the superior mesenteric vessels with special role of intravascular thrombosis and its prevention by heparin. Surgery 28, 819. Patman R. D., Poulos E. and Shires G. T. (1964) The management of civilian arterial injuries. Surg. Gynecol. Obstet. 118, 725.
Perry M. O., Thai E. R. and Shires G. T. (1971) Management of arterial injuries. Ann. Surg. 173, 403. Shirkey A. L., Quast D. C. and Jordaan G. L. (1967) Superior mesenteric artery division and intestinal function. J. Trauma 7, 7. Ulvestad L. E. (1954) Repair of laceration of superior mesenteric artery acquired by non-penetrating injury to abdomen. Ann. Surg. 140, 752.
FRCS (Ed.), Department of Surgery, University of Witwatersrand Medica