Compared with Gelofusine, the perioperative pulmonary function of patients treated with HES after abdominal aortic aneurysm surgery was better.

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Background: Gastric intramucosal pH (pHi), a surrogate marker of splanchnic oxygenation, falls following abdominal aortic aneurysm surgery. Aim: To investigate the effects of volume expansion with hydroxyethyl starch (eloHAES) on splanchnic perfusion compared to another colloid such as gelofusine. Patients and methods: Twenty-two consecutive patients undergoing AAA repair were randomised to receive either eloHAES or gelofusine as plasma expanders. Tissue oxygenation was monitored (10 gelofusine and 12 eloHAES) indirectly by measuring pHi using a nasogastric tonometer. Results: Compared to the eloHAES group, the fall in pHi was significantly greater in the gelofusine group at clamp release (7.29 vs 7.33, P = 0.003) and at 4 h following clamp release (7.29 vs 7.33, P= 0.03). There was a good inverse correlation between the lowest pHi and the peak serum interleukin-6 ( rs= −0.47, P= 0.03). By multivariate analysis, the only factor that influenced the pHi was the type of colloid used ( F= 5.54. P= 0.005). The eloHAES treated patients required significantly less colloid on the first postoperative day (3175±175 vs 4065±269 ml, P=0.01). Conclusion: In patients undergoing abdominal aortic aneurysm repair, plasma expansion with eloHAES improves microvascular perfusion and splanchnic oxygenation.

Correspondence caused by the application of an Esmarch bandage to the fracture site. In other words, we were not attempting to achieve the complete exsanguination usually associated with elective surgery.A simple method to ensure that venous pressures stay well below cuff pressures is to connect an anaeroid arterial pressure gauge, (e.g. Pressurveil) between the syringe and venous cannula via a three way tap. Venous pressures cannot exceed injection pressure, which is closely controlled.We are sorry to hear your resident is entering the Iron Man contest. The injections in our experiments were performed manually by one of our investigators, who regularly represents the Gloucester rugby fifteen.Finally, the purpose of the 10-second injection was to demonstrate the pressures generated, consequent to injudiciously attempting to inject as fast as possible, in order to reach the parts other Biers (sic) fail to reach! University of Natal. E.G. LAWES lntracranial pressure after phenoperidineThe case report by Grummitt and Goat (Anaesthesia 1984; 39 565). is interesting. There have been no reports of the effects of phenoperidine alone on cerebral blood flow but there was no change when it was given to the human in combination with dehydrobenzperidol' and, as the authors reported, this same combination produced only minor changes in intracranial pressure (ICP) in humans with normal cerebrospinal fluid pathThere may be situations when narcotic drugs can activate the electrocencephalogram with, presumably, increases in ICP but arterial hypertension usually accompanies these c h a n g e~.~ I have observed transient rises in ICP accompanied by arterial hypotension following the administration of phenoperidine to patients in intensive care units and 1 have attributed this to histamine release. It is possible that the patient's intracranial volume/pressure relationship was such that a small increase in volume caused a large increase in 1CP and in this circumstance the increase could have been prolonged for thirty minutes.I agree that arterial hypotension could have been aggravated by volume depletion. It perturbs me, when reading the anaesthetic literature, that clinicians still subject patients with head injury to fluid restrictions. Except when there is inappropriate secretion of antidiuretic hormone it is important to maintain adequate hydration of the patients and to make regular checks of fluid balance and plasma electrolytes. A replyI thank Dr Barker for his comments on our case report. It is possible that both the cardiovascular changes seen and the increase in intracranial pressure could have resulted from histamine release, although no other clinical stigmata of this phenomenon were evident in this case.