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Electronic letters to:
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Electronic letters published:
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Metabolic considerations in managing autonomic dysreflexia.
Re: Anisocoria at autonomic dysreflexia
Reply to Drs. Cakmak and Muslumanoglu
Drug therapy for autonomic dysreflexia
Anisocoria at autonomic dysreflexia
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Richard G Fiddian-Green None
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richardfg{at}hotmail.com Richard G Fiddian-Green
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Tissue pH might vary greatly in patients with spinal cord injuries especially if they have some degree of renal dyfunction or recurrent urinary tract infections (1). Might these variations in ambient tissue pH contribute to the occurrence of autonomic dysreflexia? Alkalinization elicits neuropeptide release from superfused rat cerebrocortical synaptosomes in part by conventional exocytosis and largely by an external Ca2+-independent mechanism. It releases noradrenaline entirely by conventional exocytosis(2). The release is likely to be the consequence of perturbations in tissue energetics caused by the downregulation of oxidative phosphorylation by the decrease in the protonmotive force driving ATP resynthesis in mitochondria (3) and/or the stimulation of anaerobic glucolysis in the cytosol (4). The perturbations in pH might also be the product of the physical effect of perturbations in body temperature (5). The therapeutic benefits ascribed to nifedipine and ACE inhibitors are consistent with this possiblity. If an increase in tissue pH and/or rapid change in tissue pH are causes of autonomic dysreflexia treatment would be most rationally directed at preventing the changes. Urinary tract infections and changes in renal function are the most likely causes of changes in tissue pH. An abnormal fall in gastric intramucosal pH, which might precipitate the translocation of endotoxin and bacteria, and cytokine and free radical release, is a common finding in patients with chronic renal failure and could be missed if gastric intramucosal pH was not measured because arterial blood gases are commonly normal (6). Managing these precipitating disorders effectively with the aid of measurements of gastric intramucosal pH would seem, therefore, to be the management priority. Failure to control gastric intramucosal pH might be an indication of recurrent and possibly occult urinary tract infections and/or accompanying alterations in renal function. Pharmacological therapy should be administered with these considerations in mind. 1. Fiddian-Green RG. Gastric intramucosal pH, tissue oxygenation and acid-base balance. Br J Anaesth. 1995 May;74(5):591-606 2. Gemignani A, Paudice P, Longordo F, Raiteri M. External pH changes affect NMDA-evoked and spontaneous release of cholecystokinin, somatostatin and noradrenaline from rat cerebrocortical nerve endings. Neurochem Int. 2004 Oct;45(5):677-85. 3. Reid RA, Moyle J, Mitchell P. Synthesis of adenosine triphosphate by a protonmotive force in rat liver mitochondria. Nature. 1966 Oct 15;212(59):257-8. 4. 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. 5. 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. 6. Diebel L, Kozol R, Wilson RF, Mahajan S, Abu-Hamdan D, Thomas D. Gastric intramucosal acidosis in patients with chronic kidney failure. Surgery. 1993 May;113(5):520-6. Conflict of Interest:Tonometric patents issued in my name |
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Lianne M Hunt
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lmhunt{at}doh.health.nsw.gov.au Lianne M Hunt
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I have been working with spinal cord injury rehabilitation now for 6 years and have seen anisocoria in association with painful upper trapezius muscle in a C4 tetraplegic on manipulation during therapy with resolution of pupillary dilatation on the ipsilateral side with cessation of intervention. No intracranial pathology was identified and the patient otherwise well. In addition we also identified alternating pupillary dilatation in a C3 incomplete tetraplegic patient who had MRI evidence of syrinx formation and pupillary changes varied with postural change and presumed syrinx pressure change. Conflict of Interest:None declared |
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Jeff Blackmer The Rehabilitation Centre, Ottawa, Ontario
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jblackmer{at}ottawahospital.on.ca Jeff Blackmer
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Thank you for your eLetter describing a very interesting clinical case. I have not encountered the phenomenon you describe during my clinical practice. My suspicion would have also been an intracranial bleed but the resolution of the problem with no intervention would obviously not be in keeping with this. The only vaguely relevant case in the literature I could find was: Edwards A, Andrews R. A case of Brown-Sequard syndrome with associated Horner's syndrome after blunt injury to the cervical spine. Emerg Med J. 2001 Nov;18(6):512-3. However, this case does not involve dysreflexia. If I come across any more information I will send it along. Sorry I could not be of more assistance. Conflict of Interest:None declared |
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Hubert A. Anton Division of Physical Medicine and Rehabilitation, University of British Columbia
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hanton{at}pacificrehab.net Hubert A. Anton
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November 13, 2003 To the editors: We commend the CMAJ for its decision to publish a series of articles on topics in rehabilitation medicine. The article by Dr. Blackmer on autonomic dysreflexia was a useful review of an important and poorly understood topic.1 Dr. Blackmer appropriately identifies non- pharmacologic measures as the first (and usually only) step needed in acute treatment. He also refers to the use of pharmacologic agents, including immediate release nifedipine. There are few published studies evaluating antihypertensive therapy for autonomic dysreflexia. Because of several reports of serious adverse reactions occurring after immediate- release nifedipine, the Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure has discouraged use of this drug.2 Faced with this problem, we evaluated the use of captopril as an alternative to nifedipine in the treatment of hypertensive emergencies associated with autonomic dysreflexia.3 We have found captopril to be both safe and effective in that setting. We continue to rely on non- pharmacologic interventions as first line therapy for treatment of autonomic dysreflexia, but consider captopril the first choice in those situations where drug therapy is required. Hugh Anton Andrea Townson G.F. Strong Rehab Centre Division of Physical Medicine and Rehabilitation University of British Columbia Vancouver, BC 1. Blackmer J. Rehabilitation medicine: 1. Autonomic dysreflexia. CMAJ 2003; 169: 931-5. 2. Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure. The sixth report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. Arch Intern Med 1997;157:2413-45. 3. Esmail Z, Shalansky KF, Sunderji R, Anton H, Chambers K, Fish W. Evaluation of captopril for the management of hypertension in autonomic dysreflexia: a pilot study. Arch Phys Med Rehabil 2002;83:604-8. Conflict of Interest:None declared |
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Aysegul Cakmak Istanbul University, Istanbul Medical Faculty, Department of Physical Medicine and Rehabilitation
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cakmakaysegul{at}hotmail.com Aysegul Cakmak
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As a physiatrist, we frequently encounter with autonomic dysreflexia as a complication in patients with high-level spinal cord injuries in our department. We are interested to receive your comments about an additional sign of a patient. We admitted the patient in our PM&R Department on September 9th. The diagnosis was incomplete tetraplegia due to C5-C6 anterior dislocation after a fall on July 10th 2003. The patient had been operated on July 19th in another hospital. At admission to our unit, muscle strength was about 4+/5 to 5/5 in left upper extremity and 3/5 in right upper extremity. After three weeks, the patient had symptoms of autonomic dysreflexia attacks like, headache, palpitations, shaking, shortness of breath, nausea, unsteadiness and hot flushes. At the 3rd attack anisocoria (R>L) was observed. With the consultation of Neurology Department, suspected to subdural hematoma or intracerebral haemorrhage, MRI evaluation was requested. Next day anisocoria disappeared, so MRI cancelled. Afterwards, we didn't encounter any autonomic dysreflexia attack and anisocoria in the patient. The patient's general condition was good and we have continued the rehabilitation program. We couldn't find any information in our textbooks and Pubmed about this sign. During our search we have seen your very valuable, brief and specific review. Therefore we decided to ask your opinion concerning this case. Aysegul Cakmak MD. Ass. Prof. Lutfiye Muslumanoglu MD. Prof. Istanbul University, Istanbul Medical Faculty, Department of Physical Medicine and Rehabilitation, Istanbul, Turkey Conflict of Interest:None declared |
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