Histamine release in mesenteric traction syndrome during abdominal aortic aneurysm surgery: prophylaxis with H1 and H2 antihistamines

Duda, D.; Lorenz, W.; Çelik, I.

doi:10.1007/pl00012418

Cited by 21 publications

(12 citation statements)

References 19 publications

(37 reference statements)

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“…Between the two groups there was no significant difference in systolic blood pressure. One of the study finding was that the frequency of arrhythmias and the requirement for vasopressor medications during MT was lower in patient's receiving anti-histamines pre-operatively than in patients who were not medicated with anti-histamine [5]. This finding may point out to the role of histamine in the etiology of MTS.…”

Section: What Are the Mediators Of Mesenteric Traction Syndrome?mentioning

confidence: 99%

“…In 2002 a study conducted by Duda D et al [5] hypothesized that MTS was mediated by degranulation of mast cells resulting in histamine release. This study focused on 17 male patients undergoing AAA repair, in which half of the patients received an H1 receptor antagonist (dimetindene) and an H2 receptor antagonist (cimetidine) preoperatively while the other half of the participants received placebo.…”

Section: What Are the Mediators Of Mesenteric Traction Syndrome?mentioning

confidence: 99%

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Untitled

2017

JACCOA

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The first time I heard of mesenteric traction syndrome was three years into my training as an anesthesia resident. This first time was unfortunately intraoperatively while my patient was acutely unstable and mesenteric traction syndrome was part of my anesthesia team's differential diagnosis. Following this event I set out to educate myself about mesenteric traction syndrome and was shocked to find there was very little mention of it in the anesthesia literature, especially common textbooks that I had used throughout my residency to educate myself. The goal of this article is to present the literature on mesenteric traction that I encountered during my research and to provide a thorough review of the consensus on the etiology, pathophysiology, prevention and treatment of mesenteric traction syndrome. At the end of the review, I examine areas of mesenteric traction that need further investigation in order to fully understand mesenteric traction syndrome and what we can do, as anesthesiologists, to prevent it and appropriately treat it.

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Section: What Are the Mediators Of Mesenteric Traction Syndrome?mentioning

confidence: 99%

Section: What Are the Mediators Of Mesenteric Traction Syndrome?mentioning

confidence: 99%

Untitled

2017

JACCOA

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“…Eight patients received preoperatively HI and H2 receptor antagonists (dimentidene and cimetidine, respectively), whereas the remaining nine patients received a placebo. The plasma levels ofhistamine were higher in the placebo group, but the difference did not reach statistical significance (1). Arrhythmias occurred only in the placebo group but, facial and neckline flushing was mainly observed in the group that received the antihistamines, leading the authors to conclude that the flushing is not related to histamine (1).…”

Section: Autacoidsmentioning

confidence: 99%

“…The most prominent symptoms occur approximately 15 min. after the eventration of the small intestine (1). MTS was first reported by Seeling et al in 1986 as "eventration syndrome" (2).…”

mentioning

confidence: 99%

Mesenteric Traction Syndrome or Gut in Distress

Avgerinos

Theoharides

2005

Int J Immunopathol Pharmacol

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The mesenteric traction syndrome (MTS) remains, seventeen years after its first designation as a distinct pathologic entity, an aspect of surgical practice that has received limited attention. Apart from its symptomatology, there is mostly speculation about its exact causes and pathophysiologic mechanisms.Even though full-blown MTS is rather rare, the advent of laparoscopic surgery has indicated that there are different stages of stress associated with open abdominal surgery. Some evidence points to the involvement of mast cell derived vasoactive mediators and suggests possible pharmacologic management.MTS has been observed during many types of abdominal surgical procedures, shortly after eventration, manipulation and operation on the intestines. Symptoms of the syndrome include the characteristic triad of hypotension, tachycardia and facial flushing (Tab. I). The most prominent symptoms occur approximately 15 min. after the eventration of the small intestine (1). MTS was first reported by Seeling et al. in 1986 as "eventration syndrome" (2). However, the association between traction of the abdominal mesentery and decreases in systemic blood pressure had been reported in textbooks and review articles earlier (3-6). The initial opinion regarding the cause ofthis syndrome focused on afferent sympathetic stimulation that results in vasodilation of the splanchnic vessels (3, 5-6). The subsequent venous pooling was thought to result in decreased venous return, decreased stroke volume and cardiac output. Seltzer et al. (7) studied the hemodynamic changes associated with the traction of the abdominal mesentery in twenty patients who underwent an aortic operation. In all patients, there was a significant decrease in the mean arterial pressure accompanied by profound tachycardia, whereas 15 patients developed marked flushing of the skin in the head and neck (7). These results were in direct contrast with the previous stated opinions that the syndrome is due to a decrease in the cardiac output. AutacoidsSeeling et al. (1) first associated MTS with liberation of prostacyclin. They measured plasma levels ofprostaglandins (PG) and thromboxane in 13 patients undergoing infrarenal aortic bypass operation under neuroleptic anesthesia, after eventration of the gut. In 9 patients, an immediate increase in the levels of o-keto-Pfif', (a metabolite of prostacyclin) was observed, accompanied by a significant decrease in the partial pressure of arterial oxygen. The fact that plasma levels of 6-kPGF z remained normal, indicated that there was no general prostaglandin secretion, but rather local intestinal release of prostacyclin. The authors concluded that eventration of the intestines causes liberation of prostacyclin due to the involved manipulation or to the impairment of intestinal circulation (2). Subsequent studies also supported the role of 0394-6320 (2005) Copyright© by BIOLIFE,s.a.s. This publicationand/orarticle is for individualuse only and may not be further reproducedwithout writtenpermissionfrom the copyrightholder. ...

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“…The impact of perioperative measures such as different prophylactic measures and surgical procedures on the intraoperative course and especially on the postoperative outcome [6] has always been of interest to both surgeons and anaesthetists [7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Antibiotic prophylaxis influences cardiovascular stability in complicated surgery

Çelik¹,

Stinner

Thiel³

et al. 2004

Inflamm. res.

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The stability and reproducibility of this model clearly demonstrated the concept of a 'clinic modelling randomised trial' as a useful tool. Antibiotic prophylaxis influences the organism's capability to cope with intraoperative bleeding and fluid resuscitation problems. Indeed antibiotic prophylaxis may be beneficial. These effects of antibiotics could only be demonstrated in complex surgical models. Thus new antibiotics should be investigated in complex animal models prior to prospective randomised clinical trials or usage in clinical practice.

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Histamine release in mesenteric traction syndrome during abdominal aortic aneurysm surgery: prophylaxis with H1 and H2 antihistamines

Cited by 21 publications

References 19 publications

Untitled

Untitled

Mesenteric Traction Syndrome or Gut in Distress

Antibiotic prophylaxis influences cardiovascular stability in complicated surgery

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