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Critical illness polyneuropathy: reply to the letter by op de coul and verheul
Clinical Neurology and Neurosurgeq
ELSEVIER
Clinical
Neurology
and Neurosurgery
96
(1994)263
Letter to the Editor
Critical illness ~olyneuropathy: reply to the letter by Op de Coul and Verheul F.S.S. Leijten *, A.W. de Weerd Department
of’ Neurolog.~~, Westein& Received
Zirkmhuis,
28 March
19Y4; accepted
Deur Sit:
We thank Drs. Op de Coul and Verheul for their thoughtful remarks on our recent review article on critical illness polyneuropathy (CIP) [l]. However, they differ in their approach of the matter. This is exemplified most clearly by their use of the term critical illness ‘polyneurowtyopathy’, as we adhered to the original ‘polyneuropathy’. We felt that otherwise confusion might abound. No one will deny that myopathy is encountered in critically ill patients, especially when muscle biopsy is used [Z], but it is unclear whether the pathophysiology involved is the same as in CIP. Myopathy is associated with specific combinations of medicaments in mechanically ventilated patients, but we did not see why these cases without polyneuropathy should fall into a polyneuromyopathy concept. Thus, we would not consider the case of the boy [3], the neonates [4], the ophthalmoplegic [5], nor the asthmatic [6] as having CIP. None of them had signs of acute axonal polyneuropathy. More difficult is the role of muscle relaxants in CIP. In our experience and those of others, their concurrence is not obligatory. It is conceivable that prolonged effects of these medicaments on the neuromuscular synapse are in part due to underlying CIP, and not only the result of altered metabolism [7]. It has never been proven that pdncuronium or vecuronium can actually cause polyneuropathy. So far, there is no suitable animal model for CIP, nor
*Corresponding
author.
0303-84~7/94/$7.00 0 1994 Eisevier SSnlo3~3-8467(94)o~~l7-z
Science B.V. At1 rights
reserved
Lijnhuun 32, 2501 CK The Hague, 28 March
Tlw N~~therltmdv
1994
is prolonged mechanical vel~tilation possible in animals. Clinical studies remain most important for elucidating the pathophysiology of CIP, in which attention should also be directed towards patients who under critical circumstances do not develop polyneLlropathy. We agree with Op de Coul and Verheul that only little is known in this regard and hope that cooperative efforts may reveal answers to the many questions.
References 111Leijten.
F.S.S. and de Weerd, A.W. (1994) Critical illness polyncuropathy: a review of the literature, definition and pathophysiology. Clin. Neural. Neurosurg., 96: IO--19. 121Coakley. J.H., Nagendran, K., Honavar, M. and Hinds, C.J. (1993) Preliminary observations on the neuromuscular abnormalities in patients with organ failure and sepsis. Intensive Care Med., 19: 323.328. Ul Pascucci, R.C. (1990) Prolonged weakness after extended mechanical ventilation in a child. Crit. Care Med., 18: 1181. 1182. W.M. and Agostinelli, T. (1985) Muscle [41Torres. C.F., Maniscalco, weakness and atrophy following prolonged paralysis with pancuronium bromide in neonates. Ann. Neural.. 18: 403. B.C., Monpetit, V. and Reid, D. (1991) 151Sitwell, L.D.. Weinshenker, Complete ophthalmople~ia as a complication of acute corticosteroid- and pancuronium-associated myopathy. Neurology, 41: 921 2. PI Lacomis. D.. Smith, T.W. and Chad, D.A. (I 993) Acute myopathy and neuropathy in status asthmaticus: case report and lrterature review. Muscle Nerve, 16: 84 90. 171Segredo. V., Caldwell, J.E.. Matthay. M.A.. Sharma. M.L., Gruenke, L.D. and Miller. R.D. f 1992) Persistent paralysis in critically ill patients after long-term administration of vecuronium. U. Engl. J. Med., 327: 524-S.
ELSEVIER
Clinical
Neurology
and Neurosurgery
96
(1994)263
Letter to the Editor
Critical illness ~olyneuropathy: reply to the letter by Op de Coul and Verheul F.S.S. Leijten *, A.W. de Weerd Department
of’ Neurolog.~~, Westein& Received
Zirkmhuis,
28 March
19Y4; accepted
Deur Sit:
We thank Drs. Op de Coul and Verheul for their thoughtful remarks on our recent review article on critical illness polyneuropathy (CIP) [l]. However, they differ in their approach of the matter. This is exemplified most clearly by their use of the term critical illness ‘polyneurowtyopathy’, as we adhered to the original ‘polyneuropathy’. We felt that otherwise confusion might abound. No one will deny that myopathy is encountered in critically ill patients, especially when muscle biopsy is used [Z], but it is unclear whether the pathophysiology involved is the same as in CIP. Myopathy is associated with specific combinations of medicaments in mechanically ventilated patients, but we did not see why these cases without polyneuropathy should fall into a polyneuromyopathy concept. Thus, we would not consider the case of the boy [3], the neonates [4], the ophthalmoplegic [5], nor the asthmatic [6] as having CIP. None of them had signs of acute axonal polyneuropathy. More difficult is the role of muscle relaxants in CIP. In our experience and those of others, their concurrence is not obligatory. It is conceivable that prolonged effects of these medicaments on the neuromuscular synapse are in part due to underlying CIP, and not only the result of altered metabolism [7]. It has never been proven that pdncuronium or vecuronium can actually cause polyneuropathy. So far, there is no suitable animal model for CIP, nor
*Corresponding
author.
0303-84~7/94/$7.00 0 1994 Eisevier SSnlo3~3-8467(94)o~~l7-z
Science B.V. At1 rights
reserved
Lijnhuun 32, 2501 CK The Hague, 28 March
Tlw N~~therltmdv
1994
is prolonged mechanical vel~tilation possible in animals. Clinical studies remain most important for elucidating the pathophysiology of CIP, in which attention should also be directed towards patients who under critical circumstances do not develop polyneLlropathy. We agree with Op de Coul and Verheul that only little is known in this regard and hope that cooperative efforts may reveal answers to the many questions.
References 111Leijten.
F.S.S. and de Weerd, A.W. (1994) Critical illness polyncuropathy: a review of the literature, definition and pathophysiology. Clin. Neural. Neurosurg., 96: IO--19. 121Coakley. J.H., Nagendran, K., Honavar, M. and Hinds, C.J. (1993) Preliminary observations on the neuromuscular abnormalities in patients with organ failure and sepsis. Intensive Care Med., 19: 323.328. Ul Pascucci, R.C. (1990) Prolonged weakness after extended mechanical ventilation in a child. Crit. Care Med., 18: 1181. 1182. W.M. and Agostinelli, T. (1985) Muscle [41Torres. C.F., Maniscalco, weakness and atrophy following prolonged paralysis with pancuronium bromide in neonates. Ann. Neural.. 18: 403. B.C., Monpetit, V. and Reid, D. (1991) 151Sitwell, L.D.. Weinshenker, Complete ophthalmople~ia as a complication of acute corticosteroid- and pancuronium-associated myopathy. Neurology, 41: 921 2. PI Lacomis. D.. Smith, T.W. and Chad, D.A. (I 993) Acute myopathy and neuropathy in status asthmaticus: case report and lrterature review. Muscle Nerve, 16: 84 90. 171Segredo. V., Caldwell, J.E.. Matthay. M.A.. Sharma. M.L., Gruenke, L.D. and Miller. R.D. f 1992) Persistent paralysis in critically ill patients after long-term administration of vecuronium. U. Engl. J. Med., 327: 524-S.