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Baroreceptor dysfunction during carotid artery surgery
- Richard G Fiddian-Green (27 September 2006)
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Substrate depletion in locoregional carotid surgery?
- Chritopher H E Imray, Jon Morgan, Patrick Doyle, Denny Levett, Mike Stroud, Mike Grocott, PaulGunning, Kay Mitchell, Chris van Tulleken,Hugh Montgomery, Mark Wilson (27 September 2006)
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Manipulating rCOD and rCOC : a false clinical meme complex?
- Richard G Fiddian-Green (11 September 2006)
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Chronic cerebral ischaemia: the primary cause of neuropsychiatric complications from carotid surgery
- Richard G Fiddian-Green (11 September 2006)
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Re: On reducing the metabolic need for cerebral blood flow in carotid surgery.
- Christopher H E Imray (22 August 2006)
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On reducing the metabolic need for cerebral blood flow in carotid surgery.
- Richard G Fiddian-Green (8 August 2006)
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Richard G Fiddian-Green, FRCS, FACS None
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Hypertension is an important cause of strokes as might be hypotension and accompanying hypoperfusion as Imray et al suggest (1). Bove et al defined the lability of the blood pressure known to be associated with carotid endarterectomy in a study of 100 consecutive endarterectomies (2). They concluded that, "postendarterectomy hypotension and hypertension appear to represent transient baroreceptor dysfunctions". Variations in blood pressure of this degree are known to impair cerebral oxygenation, certainly in patients with autonomic failure (3), and are a possible cause of neurological complications associated with carotid endarterectomy. What then might cause baroreceptor dysfunction in carotid surgery? Carotid artery baroreceptors are under central control (4). The sensitivity of the baroreceptors may be altered by the central action of angiotensin II. In a small animal study the sensitivity or curvature coefficient of the baroreceptor curve was increased by 36% by the administration of the angiotensin II receptor antagonist losartan (5). This is of relevance to baroreceptor dysfunction for the splanchnic hemodynamic response to circulatory shock is characterized by a selective vasoconstriction of the mesenteric vasculature mediated largely by the renin-angiotensin axis (6). The tissue alkalosis in the carotid arteries caused by the sudden expose to the hypocarbic hyperoxic environment in air would seem the most likely cause of baroreceptor dysfunction. Any cooling of the arterial wall that might occur concurrently during open carotid surgery should also elevate the pH by a purely physical action (7,8). Changes in interstitial pH are accompanied by changes in ionized [Ca++] and even [K+], changes that could alter synaptic function and even nerve conduction. The biochemical changes would be transient for they should be restored to normality, and the pH might even overshoot to abnormally low levels after surgery if there has been a compensatory fall in [HCO3-], when the wound is closed. The sudden changes in pH should be accompanied by sudden changes in tissue pO2 and presumably free radical release because of the high pO2 in air. Among these changes might well be the primary cause of any baroreceptor dysfunction during and after carotid surgery. Regional changes in tissue energy metabolism may be secondary to systemic changes. In the absence of Doppler-optimized fluid management (9) and/or gastrointestinal tonometry (10) another cause of the lability of the blood pressure might, therefore, be the variation in the ability of anaesthetists to administer fluids in a manner that maintains a normal gastric interstitial pH and intracerebral pH. The risks of major surgery are greatly reduced by preventing a fall in gastric intramucosal pH with supplementary infusions of Hetastarch. But infusions of hydroxyethyl starch may cause anaphylactoid reactions (11). This and the potential for fluid overload are of concern for "Doppler-optimized fluid management" is redundant in the some 50% of patients who do not develop an intramucosal acidosis and do not develop complications. If used in the absence of tonometric monitoring Doppler-optimized fluid management may fail to maintain a normal intramucosal pH and potentially to prevent the associated complications in as many as 15 % of patients. Doppler-optimized fluid management might be more effectively and safely applied with tonometric monitoring. Moreover maintaining a normal gastric intramucosal pH might be particularly important because of the importance of the liver, which is supplied with arterial blood from the coeliac axis, in dealing with the metabolic byproducts of anaerobiosis (12). Splanchnic vasoconstriction is a compensatory haemodynamic response to shock of the degree that might well occur during carotid surgery and be evident from a fall in gastrointestinal intramucosal pH regardless of whether the blood pressure has fallen or not. The release of angiotensin II has been implicated in the pathogenesis of the multiple organ dysfunction that may complicate other forms of major surgery. The brain, seemingly the canary of the body in awake patients, might well be a target. In which case the effects might be prevented by administering an angiotensin II receptor antagonist. This may not suffice if ischaemic mucosal injury, endotoxin translocation and cytokine release have occurred. That perioperative complications including neurological complications might be the product of a regional or systemic energy deficit is supported by the beneficial effects of pre-operative oral carbohydrate loading reported in patients having abdominal surgery (13). It is also supported by the beneficial effects of hypocapnia in the evolution of mesenteric ischemia-reperfusion injury (14). That perioperative supplemental oxygen administration might also be beneficial in these circumstances (15) might be due to upregulation of oxidative phosphorylation by the lowering of the interstitial pH, as suggested in my earlier communication on this subject. Additionally or alternatively the beneficial effects of oxygen might be due to enhancement of bacterial killing by the neutrophils and macrophages recruited to the wound site and their release of reactive oxygen species by respiratory burst (16). That neurological complications appear to have occurred four times more often in the Oxford study than in comparable US practices might be dismissed, because they are different studies, were it not that similar differences were found in patients undergoing major non-cardiac surgery and followed prospectively in the USA (n = 1056) and the UK (n = 1539) (17). The possibility that the difference in outcomes from carotid surgery might reflect differences in surgical and/or anaesthetic skills has been considered (18). What has not been considered is that the differences in outcomes might reflect differences in case selection. Current criteria for patient selection for carotid surgery may well be as poorly sensitive and specific, and therefore as variable between clinicians, institutions and countries, as conventional clinical criteria are in the case of chronic gastrointestinal ischaemia. Indeed it has taken exercise tonometry to reveal the full extent of that uncertainty of in the case of chronic gastrointestinal ischaemia. 1. C. H. E. Imray, A. J. Thacker, M. K. Mead, R. G. Fiddian-Green, and M. D. Stoneham Oxygen administration can reverse neurological deficit following carotid cross-clamping Br. J. Anaesth. 2005; 95: 274-275 2. Bove EL, Fry WJ, Gross WS, Stanley JC. Hypotension and hypertension as consequences of baroreceptor dysfunction following carotid endarterectomy. Surgery. 1979 Jun;85(6):633-7. 3. Hunt K, Tachtsidis I, Bleasdale-Barr K, Elwell C, Mathias C, Smith M. Changes in cerebral oxygenation and haemodynamics during postural blood pressure changes in patients with autonomic failure. 1: Physiol Meas. 2006 Sep;27(9):777-85. 4. McDowall LM, Horiuchi J, Killinger S, Dampney RA. Modulation of the baroreceptor reflex by the dorsomedial hypothalamic nucleus and perifornical area. Am J Physiol Regul Integr Comp Physiol. 2006 Apr;290(4):R1020-6 5. Huang C, Yoshimoto M, Miki K, Johns EJ. The contribution of brain angiotensin II to the baroreflex regulation of renal sympathetic nerve activity in conscious normotensive and hypertensive rats. J Physiol. 2006 Jul 15;574(Pt 2):597-604. 6. Reilly PM, Bulkley GB. Vasoactive mediators and splanchnic perfusion. Crit Care Med. 1993 Feb;21(2 Suppl):S55-68. 7. Product of a tissue alkalosis induced by hypocarbia? Richard G Fiddian-Green (6 March 2005) eLetter re: T Tsubo, T Kudo, A Matsuki, and T Oyama Decreased glucose utilization during prolonged anaesthesia and surgery Can J Anesth 1990; 37: 645-649 8. Severinghaus JW, Astrup P, Murray JF. Blood gas analysis and critical care medicine. Am J Respir Crit Care Med. 1998 Apr;157(4 Pt 2):S114-22. 9. Noblett SE, Snowden CP, Shenton BK, Horgan AF. Randomized clinical trial assessing the effect of Doppler-optimized fluid management on outcome after elective colorectal resection. Br J Surg. 2006 Sep;93(9):1069-76. 10. Mythen MG, Webb AR. Perioperative plasma volume expansion reduces the incidence of gut mucosal hypoperfusion during cardiac surgery. Arch Surg. 1995 Apr;130(4):423-9. 11. Brian A. Hall, Evangelo Frigas, Damir Matesic, Michael D. Gillett, and Juraj Sprung. Case report: Intraoperative anaphylactoid reaction and hydroxyethyl starch in balanced electrolyte solution (Hextend(R): Can J Anesth 2006;53 989-993 12. Should screening for occlusive coelic axis disease be included in goal-directed therapy? Richard G Fiddian-Green (5 March 2006) eLetter re: Stephen Trzeciak, R. Phillip Dellinger, Nicole L. Abate, Robert M. Cowan, Mary Stauss, J. Hope Kilgannon, Sergio Zanotti, and Joseph E. Parrillo Translating Research to Clinical Practice: A 1-Year Experience With Implementing Early Goal-Directed Therapy for Septic Shock in the Emergency Department,* Chest 2006; 129: 225-232 13. Noblett SE, Watson DS, Huong H, Davison B, Hainsworth PJ, Horgan AF. Pre-operative oral carbohydrate loading in colorectal surgery: a randomized controlled trial. Colorectal Dis. 2006 Sep;8(7):563-9. 14. Might hypocapnia up-regulate ATP resynthesis and down-regulate free radical generation? Richard G Fiddian-Green CJA Online, 3 Apr 2005 eLetter re: Michelle Duggan, Doreen Engelberts, Robert P. Jankov, Jordan M. A. Worrall, Rong Qu, Gregory M. T. Hare, A. Keith Tanswell, J. Brendan Mullen, and Brian P. Kavanagh. Hypocapnia attenuates mesenteric ischemia-reperfusion injury in a rat model: Can J Anesth 2005; 52: 262-268 15. Garcia-Botello SA, Garcia-Granero E, Lillo R, Lopez-Mozos F, Millan M, Lledo S. Randomized clinical trial to evaluate the effects of perioperative supplemental oxygen administration on the colorectal anastomosis. Br J Surg. 2006 Jun;93(6):698-706. 16. Sen CK, Khanna S, Babior BM, Hunt TK, Ellison EC, Roy S. Oxidant- induced vascular endothelial growth factor expression in human keratinocytes and cutaneous wound healing. J Biol Chem. 2002 Sep 6;277(36):33284-90 17. Bennett-Guerrero E, Hyam JA, Shaefi S, Prytherch DR, Sutton GL, Weaver PC, Mythen MG, Grocott MP, Parides MK. Comparison of P-POSSUM risk -adjusted mortality rates after surgery between patients in the USA and the UK. Br J Surg. 2003 Dec;90(12):1593-8. 18. Re: improving surgical training Richard G Fiddian-Green (7 May 2003) eLetter re: David Carter The surgeon as a risk factor BMJ 2003; 326: 832-833 Conflict of Interest:Tonometric patents issued in my name |
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Chritopher H E Imray, Reader in Surgery Warwick Medical School, Jon Morgan, Patrick Doyle, Denny Levett, Mike Stroud, Mike Grocott, PaulGunning, Kay Mitchell, Chris van Tulleken,Hugh Montgomery, Mark Wilson
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Dear Sir, We read with interest Fiddian-Green’s further contribution to the cerebral dysfunction during loco-regional carotid endarterectomy (LA-CEA) debate1,2,3. His suggestion of using a Paratrend 7 Monitor to assess substrate depletion during LA-CEA raises certain important ethical questions. With only approximately 1 in 40 patients requiring an intra- operative shunt for neurological obtundation during LA-CEA, the risk of inserting the Paratrend probes ‘directly into representative regions of the brain’2,3 unnecessarily in 39 out of 40 patients cannot, in our opinion be justified. Urgent placement of the probe at the time of patient deterioration during surgery is too late. Whilst Fiddian-Green’s contribution to the debate is of great theoretical interest, we feel it currently offers little in terms of practical contribution to the management of what should be a relatively simple procedure. LA-CEA takes 60-90 minutes, the patient should be ready for discharge within 24-48 hours of surgery and the major complication rate including ‘cerebral cognitive dysfunction’ should be of the order of 1-3%. We feel that the use of the Paratrend 7 will contribute little to the evaluation of the chronic post-operative cognitive dysfunction related to this acute setting in what clearly appears to be a substrate delivery problem. As previously suggested, further study in the neuro-ITU setting would appear to be a more fruitful line of investigation. Yours, Chris Imray, Consultant Surgeon ( www.carotidsurgeon.com ), Patrick Doyle, Consultant Anaesthetist, Mark Wilson, Neurosurgical SPR, Paul Gunning, Consultant Anaesthetist, Jon Morgan, Anaesthetist and IFMGA Mountain Guide Denny Levett, Anaesthetic SPR, KayMitchell,ITUSister, Chris van Tulleken, SHO ITU Mike Stroud., Consultant Gastroenterologist Mike Grocott, Consultant Intensivist, Hugh Montgomery, Consultant Intensivist. Xtreme Everest, Cho Oyu Advance Base Camp, 5700m, Tibet. 1. C. H. E. Imray, A. J. Thacker, M. K. Mead, R. G. Fiddian-Green, and M. D. Stoneham. Oxygen administration can reverse neurological deficit following carotid cross-clamping Br. J. Anaesth. 2005; 95: 274-275 2. R.G. Fiddian-Green "Chronic cerebral ischaemia: the primary cause of neuropsychiatric complications from carotid surgery" Br. J. Anaesth. 2006; e-letter 4th September 3. R.G. Fiddian-Green. "Manipulating rCOD and rCOC : a false clinical meme complex?" Br. J. Anaesth. 2006; e-letter 4th September Conflict of Interest:None declared |
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Richard G Fiddian-Green, FRCS, FACS None
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Imray et al observed that, "Clinical measurement of the balance between rCOD and rCOC is difficult, as patients undergoing awake carotid surgery rarely have jugular venous lines inserted. Cerebral near infrared spectroscopy , whilst having limitations in terms of absolute measurements,7 may give continuous non-invasive assessments of the rCOD–rCOC balance" (1). That is not at all the same as monitoring the availability of ATP or energy charge which, I submit, is only relevant variable. As Guyton and Hall observe in the most recent issue of their textbook on physiology pO2t only becomes a rate limiting variable in the synthesis of ATP by mitochondrial oxidative phosphorylation when it falls below 1mmHg. It is the availability of ADP that is the rate limiting variable as clearly shown in an accompanying figure shown in their textbook (2). Their conclusion is supported by the effects of carbon monoxide (CO) which when inhaled in low concentrations competes with oxygen for binding by haemoglobin and in effect causes some degree of desaturation. This inhalation of CO is cytoprotective having an inflammmatory action and inhibiting ischaemia/reperfusion injury (3). There would seem, therefore, no benefit to be derived from increasing pO2 even by hyperbaric means unless haemoglobin is severely desaturated. The issue, therefore, is how best to monitor the availability of ATP or energy charge during carotid surgery. I submit is with measurements of pH (4) possibly made directly with Paratrend probes inserted directly into representative regions of the brain. The risk of inserting these small probes, which should be as easy to do at the bedside as inserting a catheter into the ventricles, should be no greater than that of one of these catheters which is said to be no greater than that of a central line especially if withdrawn shortly after surgery. Microdialysis is another option but lactate is not a good end-point for its production would seem to depend upon the ambient pH (5). Measuring ATP degradation products by this means should, however, increase the specificity of any changes in pH. 1. C. H. E. Imray, A. J. Thacker, M. K. Mead, R. G. Fiddian-Green, and M. D. Stoneham Oxygen administration can reverse neurological deficit following carotid cross-clamping Br. J. Anaesth. 2005; 95: 274-275 2. Guyton & Hall: Textbook of Medical Physiology 11th edition 2005. 3. Schober P, Koch A, Zacharowski K, Loer SA. Carbon monoxide: toxic molecule with antiinflammatory and cytoprotective properties. Anasthesiol Intensivmed Notfallmed Schmerzther. 2006 Mar;41(3):140-9. 4. Richard G Fiddian-Green Irreversible shock, gastric intramucosal pH and energy charge. http://adc.bmjjournals.com/cgi/eletters/78/2/155#1417, 12 Mar 2005 5. Cain SM. pH effects on lactate and excess lactate in relation to O2 deficit in hypoxic dogs. J Appl Physiol. 1977 Jan;42(1):44-9. Conflict of Interest:None declared |
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Richard G Fiddian-Green, FRCS, FACS None
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Might the primary cause of the neurological abnormalities that can develop so acutely during awake carotid surgery, even those ascribed to macro-embolization, be chronic cerebral ischaemia? In other words might the precipitating event, be it hypotension, cross clamping the carotid or the belief that an embolus might have been dislodged, be the last straw that breaks the camel's back? it is an important consideration for if true management could be changed to avert the problems. The rate of ATP turnover in the brain must be very, very high for the brain accounts for 20% of global oxygen consumption and represents just 2% of total body weight. ATP may be particularly important for synaptic transmission for synaptic vesicles concentrate ATP [100nM] almost as much as they concentrate the catecholamines, dopamine, norepinephrine and epinephrine [400nM] (1) and presumably release them and possibly even act together. An acute decline in availability of ATP could, therefore, have a profound influence not only upon ATPase catalyzed enzymatic actions and the degree of openess of K(atp) but also synaptic transmission. The acute decline could, however, be caused not only by an impairment of the rate of ATP resynthesis brought about by, for example, carotid clamping but also by an increase in the rate of ATP utilization. The changes in fMRI induced by mental stress raise the possibility that the demand for ATP might, for example, be increased by intraoperative stress especially in an awake patient. Our measurements of gastric intramucosal pH made before and after revascularisation in patients with chronic visceral ischaemia (2) and of sigmoid intramucosal pH measured during abdominal aortic surgery in patients who developed endoscopic evidence of ischaemic colitis after surgery (3), both of which have since been confirmed by other investigators, shed some light on the relevant issues. We found it impossible to assess the adequacy of intestinal perfusion and its consequences, judged from measurements of intramucosal pH, from vascular anatomy alone. To my surprise stenosis of the celiac axis alone has emerged as the commonest cause of chronic gastrointestinal ischaemia. Stenosis of the celiac axis alone, rather than stenosis of the celiac axis and SMA, was also the most responsive to surgical correction both in terms of improvement of the intramucosal pH achieved and the relief of symptoms(4). Stress tests improved the diagnostic accuracy of the measurements of intramucosal pH. In those patients having abdominal aortic surgery "The average minimum intraoperative [sigmoid intramucosal] pHI and its duration were the best predictors for the development of ischemic colitis [after surgery, the presence or absence of which was established by endoscopy] ...Intraoperative pHI dropped below 6.86 in all three patients in whom severe ischemic colitis developed. Mild colitis developed in seven patients whose minimum pH was 6.99 +/- 0.12 (mean +/- SD). No colitis developed in the remaining 24, whose minimum pH was 7.21 +/- 0.13.. Ligation of a patent IMA did not increase the likelihood of ischemic colitis". Importantly in the context of carotid endarterectomy " IMA stump pressure criteria for predicting ischemic colitis were absent in nine of the ten patients in whom ischemic colitis developed and were present in five of the 24 in whom it did not develop ". The lower statistical limit of normality in the study of patients having aortic surgery was a sigmoid intramucosal pH of 6.86. In the stomach the lower limit of normality was a gastric intramucosal pH of 7.32. Gastric dysfunction, namely the inability to secrete acid in response to pentagastrin, occurs when the gastric intramucosal pH falls below 7.32 in the critically ill (5). The gastric dysfunction is associated with gastrointestinal feeding-related complications (6). In a small animal model potassium efflux did not occur until the pH measured on the surface of the liver had fallen below 7.20 (Personal communication from the department of physiology in Erlangen). There is also a direct correlation between the degree of intramyocardial acidosis and the degree of myocyte apoptosis seen " in cardiac samples obtained both from human patients undergoing cardiac surgery and porcine subjects maintained on cardiopulmonary bypass simulating cardiac surgery" (7). Thus the risk of apoptosis would appear to increase progressively as the tissue interstitial pH falls below 7.32 but might not be accompanied by the naked eye evidence of haemorrhagic necrosis unless the pH has fallen below 6.86. In monitoring human cerebral metabolism with Paratrend 7 sensors 0.5 mm in diameter inserted into the brain during surgery Charbel et al found the "normal" range of the intracerebral pH to be 7.19 +/- 0.11 and the critical level below which ischaemia was present to be 6.8. The cerebral interstitial pH two standard deviations below their mean, the usual definition of the lower limit of abormality, is a little higher: 6.97 (8). In a seperate study the same investigators identified preoperatively, "A compromised cerebral circulation.. in 8 of 14 patients by single photon emission computed tomography (SPECT) scan, cerebral angiography, and transient ischemic episodes. Under baseline conditions with isoflurane anesthesia and normal blood gases intracerebral pH (7.16 +/- 0.08) was decreased in both noncompromised, which were used as controls, and the compromised patients (6.82 +/- 0.21; P < 0.05) patients. Critical tissue value for the identification of ischemia in this study was said to have been pH 7.0 close to their lower statisitical limit of normality pH=6.97 (9). In 10 other patients with subarachnoid haemorrhage (SAH) the same investigators inserted a Neurotrend 7 probe ipsilateral to the region of the SAH. "In eight patients the probe was inserted during surgery for clipping the aneurysm and in two patients the probe was inserted in the neurosurgery ICU... Brain tissue pH was measured over 6-hour periods for 7 to 10 days until the termination of monitoring... Seven patients did not develop vasospasm during monitoring and were considered as controls. In this group pH remained between 7.1 and 7.2. In three patients who developed vasospasm during monitoring the pH decreased to 6.7" (10). During artery occlusion induced by clips during the course of cereovascular neurosurgery the interstitial pH fell below 7.0 (11) but, as we had observed in dogs, all collateral flow must be interupted for the pH to fall much below that. The intracerebral interstitial pH in those ambulatory patients whose perfusion was judged by the preoperative investigations to have been compromised was alarming low (6.82 +/- 0.21), as low as that seen in some patients with chronic gastric ischaemia. This suggests that there are people being submitted for carotid endarterectomy who might have had severely compromised cerebral tissue energetics long before cross clamping regardless of the pressure in the distal carotid artery or the presence of back flow. Those who develop symtoms and neurological deficits during or after surgery might well be resticted to these patients. If so being forewarned is to be forearmed. If the logisticical problems could be resolved by technological improvements nuclear magnetic responance (NMR), rather NIRS, might be the best noninvasive form of monitoring to use in evaluating patients having carotid surgery for it can measure ATP degradation in addition to measuring the mean ambient intracerebral pH. NMR is, however, unable to distinguish extracellular pH from cytosolic pH and they are very different. Furthermore fluid shifts between intracellular and extracellular compartments could confound the interpretation of the measurements of mean ambient pH. Measuring the interstitial pH with Paratrend 7 would seem, therefore, the most sensitive means of monitoring the adequacy of tissue energetics in the brain but the measurements are subject to the risk of measurement artefacts, electrode drift is used for extended periods, and the probes cannot be recalibrated in vivo. In patients who are given heparin during carotid endarterectomy the risk of intracranial haemorrhage might prove to be be unacceptably high but has not been a problem in the small group of patients that have had neurovascular surgery for hemodynamically significant intracranial lesions. The safest and most reliable means of intracranial monitoring might, therefore, be cortical tonometers possible made collar-stud-shaped with the gas-permeable siliconesensing surface confined to the cortical surface. Preliminary data obtained with a prototype in patients who have had head injuries suggest that the surface of the cortex may be a very appropriate sampling site (12). Occlusive cerebrovascular disease is likely to be the commonest cause of chronic cerebral ischaemia in patients sumitted for carotid endarterectomy. But malnutrition in the elderly and mitochondrial toxins contaminating food and water supplies, and cytokine release could all be contributing factors in the evolution of a chronic intracerebral energy deficit. Given the progressive nature of cerebrovascular atherosclerotic disease a good case can be made for keeping sensors in place for the reminder of a patient's life and monitoring them intermittently or even continuously. A prospective study is needed to establish the validity of the hypothesis that the commonest cause of the neuropsychiatric abnormalities complicating carotid endarterectomy might be chronic cerebral ischaemia. Knowing that was the case could have a profound effect not only upon introperative metabolic management but also upon case selection and postoperative management. 1. Neuroscience: Exploring the Brain - Bear, Connors & Paradiso, 2006.. 2. Fiddian-Green RG, Stanley JC, Nostrant T, Phillips D. Chronic gastric ischemia. A cause of abdominal pain or bleeding identified from the presence of gastric mucosal acidosis. J Cardiovasc Surg (Torino). 1989 Sep-Oct;30(5):852-9. 3. Schiedler MG, Cutler BS, Fiddian-Green RG. Sigmoid intramural pH for prediction of ischemic colitis during aortic surgery. A comparison with risk factors and inferior mesenteric artery stump pressures. Arch Surg. 1987 Aug;122(8):881-6. 4. Kolkman JJ, Mensink PB, van Petersen AS, Huisman AB, Geelkerken RH. Clinical approach to chronic gastrointestinal ischaemia: from 'intestinal angina' to the spectrum of chronic splanchnic disease. Scand J Gastroenterol Suppl. 2004;(241):9-16. 5. Higgins D, Mythen MG, Webb AR. Low intramucosal pH is associated with failure to acidify the gastric lumen in response to pentagastrin. Intensive Care Med. 1994;20(2):105-8. 6. Hamilton MA, Chapman MV, Mutch M, Bennett-Guerrero E, Mythen MG. The relationship between a pentagastrin-stimulated gastric luminal acid production test (Gastrotest) and enteral feeding-related gastrointestinal complications in critically ill patients. Anesth Analg. 2005 May;100(5):1447-52. 7. Thatte HS, Rhee JH, Zagarins SE, Treanor PR, Birjiniuk V, Crittenden MD, Khuri SF. Acidosis-induced apoptosis in human and porcine heart. Ann Thorac Surg. 2004 Apr;77(4):1376-83. 8. Charbel FT, Hoffman WE, Misra M, Hannigan K, Ausman JI. Cerebral interstitial tissue oxygen tension, pH, HCO3, CO2. Surg Neurol. 1997 Oct;48(4):414-7. 9. Hoffman WE, Charbel FT, Edelman G. Brain tissue oxygen, carbon dioxide, and pH in neurosurgical patients at risk for ischemia. Anesth Analg. 1996 Mar;82(3):582-6 10. Charbel FT, Du X, Hoffman WE, Ausman JI. Brain tissue PO(2), PCO(2), and pH during cerebral vasospasm. Surg Neurol. 2000 Dec;54(6):432-7 11. Hoffman WE, Charbel FT, Gonzalez-Portillo G, Ausman JI. Measurement of ischemia by changes in tissue oxygen, carbon dioxide, and pH. Surg Neurol. 1999 Jun;51(6):654-8. 12. Yokota H, Yamamoto Y, Naoe Y, Fuse A, Sato H, Unemoto K, Kurokawa A. Measurements of cortical cellular pH by intracranial tonometer in severe head injury. Crit Care Med. 2000 Sep;28(9):3275-80 13. RP Simon, M Niro and R Gwinn Brain acidosis induced by hypercarbic ventilation attenuates focal ischemic injury. Pharmacology and Experimental Therapeutics Volume 267, Issue 3, pp. 1428-1431, 12/01/1993 Conflict of Interest:Tonometric patents issued in my name |
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Christopher H E Imray, Carotid Surgeon Warwick Medical School
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Dear Sir I read with interest R G Fiddian-Greene's response to our letter. I agree with his proposition that the neurological obtundation occasionally observed during the cross clamp phase of loco-regional anaesthesia carotid endarterectomy (LA CEA) could be due either to decreased local cerebral tissue oxygenation or alternatively as he suggests due to a local fall in substrate levels. However, I am unaware of a real time non-invasive technique for assessing substrate depletion that is suitable for use in theatre or in the field (the equivalent of NIRs for cerebral tissue oxygenation). An alternative way of assessing his hypothesis would be to trial a therapeutic intervention. The Oxford and the Coventry groups have succesfully shown that manipulating either blood pressure, FiO2 or FiCO2 will change will improve cerebral oxygenation or neurological status either in theatre or in the field. I suspect the ease/speed/safety by which substrate or pH manipulation could be achieved makes such an trial therapeutic intervention relatively complex. Consequently whilst substrate depletion may be a theoretical possibility I suspect it is unlikely to be demonstrated in practise during LA CEA. There may greater opportunity to assess the theory in ventilated patients in the neuro-ITU setting where measuring the arteial to jugular bulb differences could be more readily justified. Christopher Imray MB BS FRCS DiMM(UIAA) PhD Conflict of Interest:None declared |
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Richard G Fiddian-Green, FRCS, FACS None
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Imray et al observed that a rise in PaCO2 causes an increased rate and depth of respiration, increased cerebral blood flow, and right shift of the oxygen dissociation curve and that these mechanisms improve rCOD. The real question is whether this improves intracerebral energy demand/supply balance. The neurological response to increasing F1O2 to 100% raises the possibility that it might certainly in the short term. The assumption is, however, that it does so by increasing regional oxygen delivery rather than regional nutrient delivery. If clamping the carotid causes an intracerebral energy defict increasing nutrient delivery rather than oxygen delivery may be needed to meet an increased glycolytic need for nutrient imposed by the less efficient anaerobic metabolism. In which case upregulating oxidative phosphorylation by, for example, decreasing pH or increasing the efficiency of substrate utilization might be a more effective strategy(1). 1. Richard G Fiddian-Green ICP and cerebral oedema at high altitude. http://www.jnnp.com/cgi/eletters/75/6/813#438, 25 Mar 2005 Conflict of Interest:None declared |
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