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Polyneuropathy in Critically Ill Patients J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.47.11.1223 on 1 November 1984. Downloaded from Journal of Neurology, Neurosurgery, and Psychiatry 1984;47: 1223-1231 Polyneuropathy in critically ill patients CHARLES F BOLTON, JOSEPH J GILBERT, ANGELIKA F HAHN, WILLIAM J SIBBALD From Departments ofClinical Neurological Sciences, Pathology and Medicine, and The Critical Care/Trauma Unit, Victoria Hospital, University of Western Ontario, London, Ontario, Canada SUMMARY Five patients developed a severe motor and sensory polyneuropathy at the peak of critical illness (sepsis and multiorgan dysfunction complicating a variety of primary illnesses). Difficulties in weaning from the ventilator as the critical illness subsided and the development of flaccid and areflexic limbs were early clinical signs. However, electrophysiological studies, espe- cially needle electrode examination of skeletal muscle, provided the definite evidence of polyneuropathy. The cause is uncertain, but the electrophysiological and morphological features indicate a primary axonal polyneuropathy with sparing of the central nervous system. Nutritional factors may have played a role, since the polyneuropathy improved in all five patients after total parenteral nutrition had been started, including the three patients who later died of unrelated causes. The features allow diagnosis during life, and encourage continued intensive management since recovery from the polyneuropathy may occur. guest. Protected by copyright. During a four year period five patients developed a beds, admits 1,300 patients a year, is located in an 860 bed severe polyneuropathy within one month of admis- teaching hospital, and has a referral base of 1-2 million sion to a critical care unit. Although two patients persons. The voluminous charts were reviewed, particu- gradually recovered from the polyneuropathy, three larly regarding events in the first month, since these might later died of unrelated causes. Systematic analysis of theoretically have been of aetiological significance in the clinical data, and development of the polyneuropathy. Day 1 was designated neuropathological studies of both as the first day of admission to the critical care units of central and peripheral nervous systems, failed to either Victoria Hospital or the referring hospital (the first reveal a cause. Nonetheless, we suggest the features 18 and 16 days of patients 2 and 3, respectively.) of this unusual polyneuropathy form a distinctive Initially, all patients received standard intravenous solu- pattern which allows diagnosis during life. It is our tions to ensure haemodynamic stability. Tube feeding purpose, therefore, to document the clinical, elec- (Ensure, Ross (Abbott) Laboratories, Montreal, Canada) trophysiological and morphological characteristics, was given at varying times and rates. When provided, the discuss possible causes and suggest future total parenteral nutrition formula was: 10% Travasol, approaches to management. 250 ml/l; 13-5% dextrose, 750 ml/I; Na 40, K 20, Mg 2-5, Ca 5-0, Cl 30 and acetate 37-5 mg/l; and a 10 ampule of Methods multivitamins: vit C-1000 mgm, vit A-10,000 IU, vit D-1000 IU/UI, vit E- 10 IU/UI, thiamine HCL-45 mg, Because of their unusual nature, the five patients were riboflavin-10 mg, niacinamide-100 mg, pyradoxine- recalled from the many seen in the Victoria Hospital criti- 12 mg, and d pantothenic acid-26 mg. Supplements were: folate 5 mg, vit K- 10 mg, vit B12- 100 mg twice weekly; care unit between 1977 and 1981. This unit has 18 http://jnnp.bmj.com/ cal trace elements (zn-2 mg, Mn-i mg, Cu-1 mg, Cr- 2 gg, 1-120 ,ug) once weekly; intralipid 10%, 500 ml Supported in part by The Muscular Dystrophy Association of thrice weekly, and albumin hydroxine gel alternating with Canada. magnesium and aluminium hydroxide 30 ml every two hours, maxeran 10 mg every eight hours by nasogastic A preliminary report of these observations was presented at the tube, and cimetidine 300 mgm every six hours IV as International Congress of Neuromuscular Diseases, Marseille, required to maintain gastric pH >5-0. France, September 12-18, 1982. All patients had full neurological examination, initially and in follow-up. Address for reprint requests: Dr CF Bolton, Victoria Hospital Electrophysiological studies were per- on September 26, 2021 by Corporation, South St Campus, 375 South St, London, Ontario, formed on patients 1 to 4, using surface electrodes for Canada N6A 4G5. nerve conduction studies and concentric needle electrodes for electromyography;' -3 isolation procedures prevented Received 6 January 1984 and in revised form 3 May 1984. such studies in patient 5. Phrenic nerve conduction4 was Accepted 5 May 1984 studied in patient 3. 1223 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.47.11.1223 on 1 November 1984. Downloaded from 1224 Bolton, Gilbert, Hahn, Sibbald Table 1 Cerebrospinal fluid results Patient Week* WBClmm3 RBClmm3 Protein (mgldl) Sugar (mg/dl) 1 3 0 0 10 78 2 4 0 0 38 78 9 0 0 80 112 3 5 1 8 31 56 4 2 90 11000 23 117 6 0 64 25 110 5 4 1 16 64 67 Normal <4 0 15-45 - *In Critical Care Unit. Neuropathological studies of the central and peripheral renal failure and pneumonia due to Staphylococcus aureus nervous system were performed on patients 3, 4 and 5. and Klebseilla pneumoniae was successful; cephalolithin Brain, spinal cord, muscle and nerve were fixed with 10% sodium and gentamycin were given. At 3 weeks she could buffered formaldehyde, processed and embedded in not be weaned from the respirator and complained of paraffin, according to standard techniques. Sections were numbness, tingling and burning of the hands and feet. stained with haematoxilin and eosin, solochrome R and Swallowing, tongue protrusion and biting were strong, but Bodian's stain for axis cylinders. Samples of nerve roots, neck, chest wall, abdomen and limb muscles were very peripheral nerves and muscle, obtained by surgical biopsy weak. All deep tendon reflexes were absent. Position sense or necropsy, were fixed in buffered glutaraldehyde, proces- and vibration sense were distally impaired, but pinprick sed and embedded in epon according to standard proce- was preserved. The CSF was unremarkable. (table 1). dures. Semithin sections were stained with toluidine blue; Electrophysiology (table 2) indicated a severe axonal selected thin sections were stained with uranyl acetate and degeneration of motor and sensory fibres, electromyogra- lead citrate and viewed with a Philips 201 electron micro- phy revealing numerous fibrillation potentials and positive scope. Samples of superficial peroneal nerve were teased in waves and absent voluntary unit activity in proximal and glycerine and the different fibre types assessed and distal limb muscles. Aetiological investigations of the guest. Protected by copyright. classified according to Dyck.5 Muscle histochemistry was polyneuropathy were negative (see below). After total done using haematoxylin and eosin, Gomori's trichrome, parenteral nutrition was started at 3 weeks, gradual recov- periodic-acid-shiff, fat stain, myosin ATPase at pH 4-3, ery occurred. She left hospital in a wheelchair at four and 4-6, 9-3 and oxidative enzyme stains. one half months, was still confined to a wheelchair at six months, but her linmbs were now moderately strong. The deep tendon reflexes were still absent. Vibration and post- Case reports ion sense were normal, but pain and temperature were impaired distally. Two-point discrimination was absent in Patient I the feet. Electrophysiology confirmed improvement (table A 56-year-old hypersensitive and mildly diabetic woman 2); abnormal spontaneous activity in muscle had almost experienced epigastric pain, vomiting, generalised weak- disappeared and voluntary motor unit activity had ness and a 20 lb (10 kg) weight loss. She was mildly con- returned, several units being highly polyphasic, indicating fused and feverish. Treatment in the critical care unit for reinnervation. At two years, she could walk independently phenformin-induced lactic acidosis, dehydration, transient but still had residual signs of polyneuropathy. Table 2 Nerve conduction studies Patient Month* Conduction velocities (mls) t Cap distal latencies (ms) Cap amplitudes F response latencies (ms) t Median Median Peroneal Sural Thenar Digital EDB Thenar Digital EDB Sural Median Peroneal motor sensory motor sensory muscle nerve muscle muscle nerve muscle nerve nerve nerve (mv) (Av) (mv) (Av) 1 1 - - 45-5 - 3-9 0 3-8 0-8 0 1-4 0 28-5 - http://jnnp.bmj.com/ 6 52-6 - 41-8 - 4-3 3-2 4-9 6-0 4 2-4 0 28-1 53-3 2 1 64-6 72-9 46-7 46-4 3-6 2-7 3-6 0-1 6 0-9 3 - - 2 53-2 57-9 39-4 41-9 5-7 3-2 3-9 0-7 7 1-2 6 33-4 46-3 3 51-9 48-4 39-1 40-8 5-1 2-5 4-2 1-5 12 1-1 6 32-1 53-5 3 1 48-0 55-2 - - 3-3 2-5 - 2-8 16 0 0 32-4 - 3 51-4 53-1 38-7 42-7 3-6 2-6 5-1 6-0 24 0-2 3 31-2 - 4 1 56-7 61-7 50-0 - 4-9 3-0 3-5 0-4 10 0-2 0 - - 3 - - - 34-7 - - - - - 0 5 - - Normal Mean 57-4 62-3 48-6 45-6 3-7 2-6 4-7 11-0 43 7-0 15 27-7 47-7 2SD 49-4 53-2 41-0 37-4 4-5 3-2 6-3 5-2 8 1-4 0 33-4 58-7 on September 26, 2021 by *In Critical Care Unit. tConduction velocity nerve segments: median-elbow to wrist, peroneal-knee to ankle, sural-midcalf to ankle. tF response stimulation sites: median-wrist, peroneal-ankle. Cap means compound action potential.
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