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The treatment of acute polyradiculoneuritis with respiratory paralysis
GUEST LECTURES
The Treatment of Acute Polyradiculoneuritis with Respiratory Paralysis Wu Hu-Sheng, MD, Yei Qi-Fen, MD, Liu Tian-Ci MD and Zhang Wu-Chang, MD
This paper reports 504 cases admitted with acute polyradiculoneuritis (AP) to Beijing Children's Hospital from 1975 through 1984. 343 of the 504 cases (68.1%) with AP had respiratory paralysis and in 198/504 (39.3%), tracheotomy was performed. In this study, none of the patients received steroids. We attempted to assess the grades of respiratory paralysis and established the criteria for tracheotomy. We also must perform the following procedures: 1) Artificial ventilation must be used correctly, 2) The secretion should be aspirated regularly in order to maintain a clear airway, 3) Sterilization must be strictly conducted to prevent cross infection. As a result, of 504 cases with AP 9 died, the mortality rate being 1. 79%. The study suggests tracheotomy should be performed early and it is one of the most important procedures in the treatment of AP with respiratory paralysis. Key words: Polyradiculoneuritis, respiratory paralysis, tracheotomy. Wu H-S, Yei Q-F, Liu T-C, Zhang W-c. The treatment of acute polyradiculoneuritis with respiratory paralysis. BrainDev 1988;10:147-9
Acute polyradiculoneuritis (AP) is a neurological disease that is more commonly seen in China. Much evidence supporting an immunologic basis for this disease exists [1] . Immunosuppressive drugs and plasmapheresis have been employed, but their value has not yet been proven [1] . In this study, we emphasized the treatment of respiratory paralysis in AP, and attempted to assess the grades of respiratory paralysis and established the criteria for tracheotomy. The purpose of this study was to decrease the mortality due to the disease. MATERIALS AND METHODS
We reviewed 504 patients with AP admitted to Beijing Children's Hospital from 1975 through 1984. It was possible to detect mild cases not admitted to the hospital. All the 504 cases fulfilled the currently accepted criteria for AP [1] . The male to female ratio was 3:2 . The patients were aged from 13 months to 14 years, the peak incidence of the disease being from 3 to 6 years of age. Area distribution: 472 patients (93.6%) were from the countryside,
From the Beijing Children's Hospital, Beijing. Correspondence address: Dr. Wu Hu-Sheng, Beijing Children's Hospital, Nan J"i She Rood, Beijing, People's Republic of China.
and only 32 (6.4%) were from Beijing City. Months of onset: patients can be seen all year round, but 450 patients (89.3 %) were seen from June through October. Preceding infections were found in 198 patients (Table 1), fever of unknown origin ranking first and upper respiratory infection and gastroenteritis second. Symptoms and Signs: All patients had weakness of the extremities. The 9th and 10th cranial nerves were particularly affected, that is in 50.4% of the patients. The 7th cranial nerve was affected in 34.5% of the patients. 343 of the 504 cases (68.1 %) with AP had respiratory paralysis, and in 198/504 (39.3%), tracheotomy was performed. Grading scale for respiratory paralysis is based on the manifestation of clinical symptoms, signs and chest X-rays. It was divided into 3 grades (Table 2). Grade 1 included a mild weak voice, weak cough and dyspnea, and weakness of intercostal muscle and/or diaphragm movements during respiration, as seen on X-raying, but without a paradoxical pattern of breathing. A paradoxical pattern of breathing can be seen in grade 2 on deep breathing and in grade 3 on quiet breathing. 92 patients were in grade 1, 81 in grade 2 and 170 in grade 3, i.e., about 50% of the total number. In this study, none of the patients received steroids. The study was divided into two different periods, 130 patients in period 1 and 213 in period 2. No significant difference was found in the severity of respiratory paralysis between the two different periods (Table 3).
Table I Preceding infection fliness Fever of unknown origin Upper respiratory infection Gastroenteritis Bacillary dysentery Mumps Chicken-pox
Table 2 Grading scales of respiratory paralysis No
%
82 55 51 5 3
41.4 27.8 25.7 2.5 1.6 0.5 0.5
Post-immunization
Weak voice Weak cough Dyspnea
Grade 1
Grade 2
Grade 3
Mild Mild
Mod
Severe Severe
None/mild
Mod Mod
None
On deep breathing
Mild
Mod
Paradoxical pattern of breathing X-ray findings*
Severe On quiet breathing Severe or no movement
* The weakness of intercostal muscle and/or diaphragm movements as seen on X-raying. The first period was from 1975 through 1977 and there were 130 cases with respiratory paralysis, in 68 of which (52.3%) tracheotomy was performed. In order to reduce the possibility of pulmonary infection due to tracheotomy, we performed repeated intratracheal aspiration instead of tracheotomy. The second period was from 1978 through 1984 and there were 213 cases with respiratory paralysis. In 130 of the 213 cases (61.0%) tracheotomy was performed. In this period, we established the following criteria of tracheotomy: 1) grade 3 of diaphragm paralysis, 2) grade 2 of respiratory paralysis complicated by both the 9th and 10th cranial nerves being affected, 3) grade 2 of respiratory paralysis complicated by pneumonia and/or pulmonary atelectasis, and 4) rapidly progressive diaphragm paralysis to grade 3 24-48 hours after onset. In 190 of the 198 patients mechanical ventilation was performed after tracheotomy. We used intermittent positive pressure ventilation (IPPV), Type Volume Circle, I for the patients with AP. The number of days on the ventilator ranged from 2 to 92 days (average, 28 days). Days extubated ranged from 10 to 163 days (average, 53 days). Extubation was performed when the patients could cough and protect the airway, and had a minute volume that was adequate for gas exchange.
RESULTS The outcome of respiratory paralysis was compared between the two different periods (Table 4); in period 1, 11 cases suddenly suffered from asphyxia, due to tracheal aspiration and hypoxia; 4 died and 7 survived. The other 5 cases died of acute myocarditis or other causes. In period 2, only 2 cases suffered from asphyxia and there were no deaths. We must perform the following procedures: 1) artificial ventilation must be used correctly, 2) the secretion should be aspirated ragularly in order to maintain a clear airway, 3) sterilization must be strictly conducted to prevent cross infection, and 4) the patients should be observed carefully by both doctors and nurses, to present accidents. As a result, of the 504 cases with AP 9 died,
148 Brain & Development, Vol 10, No 3,1988
Table 3 The comparison on the severity of respiratory paralysis between 2 different periods Period
No
Grade 1 %
Grade 2 No %
Grade 3 No %
Period 1 (1975-1977)
39
30
23
17.7
68
52.3
Period 2 (1978-1984)
53
24.9
58
27.2
102
47.9
Table 4 The compairson on the outcome of patients with respiratory paralysis between 2 different periods Period
Noo! patients
Noo! tracheotomy
Noo! asphyxia
Noo! death
1975-1977
130
68
11
4 (5*)
1978-1984
213
130
2
0
* The other 5 cases died of acute myocarditis or other causes.
the mortality rate being 1 .79%. The study suggests tracheotomy should be performed early and it is one of the most important procedures in the treatment of AP with respiratory paralysis.
DISCUSSION Although it is one of the most common diseases of the peripheral nervous system, the precise pathologic mechanism of inflammatory polyneuropathy or Guillain-Barre syndrome (GBS) remains unknown [2]. In the 100 years since its description advances in electrophysiology have broadened diagnostic techniques and modern immunology has led to new treatments and research methods [2]. Despite modern intensive care, up to 5% of patients still die of acute polyradiculoneuritis (AP) [3] . Using the population of the United States in 1970 as a standard, the average annual age - adjusted incidence of GBS was 0.75 per lOS persons [4]. When age-specific
rates were analyzed, two peaks were observed; a high peak for patients over 60 years of age, and another peak for the first 5 years of life [4]. The age -specific incidence of GBS might be explained in terms of endogenous (immune response) and exogenous (antecedent illness) factors that are thought to contribute to the pathogenesis of GBS [5]. The GBS cases were quite evenly distributed, both seasonally and geographically, and no clusters or epidemic peaks were noted [4]. Fewer cases appear during the summer months when colds and other infections are less frequent [6]. However, in this paper, seasonal and area distribution variations have been noted. 472 patients (93.6%) were from the countryside, and 450, patients (89.3%) were seen from June through October, but so far the reasons for this have not been determined. The care of the GBS patient involves acute and rehabilitative aspects. Treatment is first approached symptomatically. Because of the unpredictable course in the first weeks, initial meticulous evaluation of function must be made in order to gauge clinical changes [2]. In the acute phase, the patient is closely monitored, generally in an intensive care unit (lCU). The immediate concerns are respiratory failure and autonomic dysfunction [2] . GBS is not always a mild disease with a good prognosis; 10-23% require tracheotomy [7]. However, the criteria for intubation, mechanical ventilation, weaning, extubation and tracheostomy are uncertain, and have been determined by local practice [8] . A series of patients were managed using easily applicable bedside signs and chest X-rays, that we have found useful. We established the criteria for tracheotomy, and reviewed our experience. Thirty-one patients (61 %) had trunk weakness (including respiratory muscles) and there was respiratory insufficiency in 18 (35%). Artificial respiration was necessary in seven patients (14%) [9]. One-third of our patients were on ventilators, but only six for over 2 months. Thirteen of our patients were on ventilators for under 2 months (mean, 19 days) [10]. The frequency of respiratory paralysis was much higher in our cases, and the number of patients who needed artificial respiration was high, there was also a considerably higher frequency of cranial nerve damage. These differences indicate that GBS was more severe in our patients. Arterial blood gases are determined to detect hypoxia before clinical signs of respiratory insufficiency appear. Hypoxia reflects small regions of atelectasis due to loss of spontaneous high volume signs [2] . PC02 is not a sensitive guide for mechanical respiratory failure because impaired CO 2 exchange occurs when the vital capacity falls to 10 ml/kg. Current practice suggests that tracheostomy be performed if intubation is anticipated beyond 2 weeks [2] . There is no convincing evidence supporting the use of steroids in the treatment of acute inflammatory polyneuropathy [lJ . Most reports showed that corticosteroids
do not significantly alter the course of the disease and suggest that the complications of corticosteroid therapy prevent their safe usage. For these reasons, no firm policy for corticosteroid use has been developed [7, 11, 12] . The results of a controlled trial of prednisolone in acute polyneuropathy provide no grounds for the use of steroids in the management of acute inflammatory neuropathy since the prognosis is not improved, the rate of recovery is slowed and the chance of relapse may be increased [7] . As mentioned above, in this study, none of the patients received steroids. Respiratory support and other measures were maintained until no longer needed, the other measures including hydration, nutrition, and maintenance of cardiovascular and renal function where necessary, as well as routine nursing care as to pressure areas, eyes, bowels, etc [11]. Chest physical therapy and frequent positional changes are the most important care factors in GBS [2]. We did not use bronchoscopy to clear secretions in patients with major atelectasis, but instead relied on vigorous chest physical therapy and tracheal suctioning. In other words, good nursing care and physiotherapy are very important for the severely affected patient, both to avoid complications and to lessen the long-term disability.
REFERENCES 1. Parke JT. Para-infectious neurologic syndromes. In: Fishman MA, ed. Pediatric neurology. Houston: Grune & Stratton, 1986: 232.{i. 2. Griswold K, Mckenna M, Ropper AH. An approach to the care of patients with Guillain-Barre syndrome. Heart Lung 1984;13:66-72. 3. Leibowitz S, Hughes RAC. Immunology of the nervous system. London: Edward Arnold, 1983:101-25. 4. Soffer D, Feldman S, Alter M. Epidemiology of GuillainBarre syndrome. Neurology 1978;7:686-9. 5. Kaplan JE, Schonberger LB, Hurwitz ES, et al. GuillainBarre syndrome in the United States, 1978-1981: additional observations from the national surveillance system. Neurology 1983;33: 633-6. 6. Mcfarland HR, Heller GL, Arbor A, et aI. Guillain-Barre disease complex. Arch Neurol 1966; 14: 196-201. 7. Hughes RA, Newson-Davies JM, Perkin GD, et al. Controlled trial of prednisolone in acute polyneuropathy. Lancet 1978; 2: 750-3. 8. Ropper AH, Kehne SM, Guillain-Barre syndrome: management of respiratory failure. Neurology 1985;35: 1662-5. 9. Bak P.- Guillain-Barre syndrome in a Danish county. Neurology 1985; 35: 207 -11. 10. Ropper AH. Severe acute Guillain-Barre syndrome. Neurology 1986;36:429-31. 11. Moore P, James O. Guillain-Barre syndrome: incidence, management and outcome of major complications. Crit Care Med 1981;9:549-54. 12. Goodall JA, Kosmidis JC, Geddes AM. Effect of corticosteroids on course of Guillain-Barre syndrome. Lancet 1974; 1:524-6.
Wu et al: Treatment ofpolyradiculoneuritis 149
The Treatment of Acute Polyradiculoneuritis with Respiratory Paralysis Wu Hu-Sheng, MD, Yei Qi-Fen, MD, Liu Tian-Ci MD and Zhang Wu-Chang, MD
This paper reports 504 cases admitted with acute polyradiculoneuritis (AP) to Beijing Children's Hospital from 1975 through 1984. 343 of the 504 cases (68.1%) with AP had respiratory paralysis and in 198/504 (39.3%), tracheotomy was performed. In this study, none of the patients received steroids. We attempted to assess the grades of respiratory paralysis and established the criteria for tracheotomy. We also must perform the following procedures: 1) Artificial ventilation must be used correctly, 2) The secretion should be aspirated regularly in order to maintain a clear airway, 3) Sterilization must be strictly conducted to prevent cross infection. As a result, of 504 cases with AP 9 died, the mortality rate being 1. 79%. The study suggests tracheotomy should be performed early and it is one of the most important procedures in the treatment of AP with respiratory paralysis. Key words: Polyradiculoneuritis, respiratory paralysis, tracheotomy. Wu H-S, Yei Q-F, Liu T-C, Zhang W-c. The treatment of acute polyradiculoneuritis with respiratory paralysis. BrainDev 1988;10:147-9
Acute polyradiculoneuritis (AP) is a neurological disease that is more commonly seen in China. Much evidence supporting an immunologic basis for this disease exists [1] . Immunosuppressive drugs and plasmapheresis have been employed, but their value has not yet been proven [1] . In this study, we emphasized the treatment of respiratory paralysis in AP, and attempted to assess the grades of respiratory paralysis and established the criteria for tracheotomy. The purpose of this study was to decrease the mortality due to the disease. MATERIALS AND METHODS
We reviewed 504 patients with AP admitted to Beijing Children's Hospital from 1975 through 1984. It was possible to detect mild cases not admitted to the hospital. All the 504 cases fulfilled the currently accepted criteria for AP [1] . The male to female ratio was 3:2 . The patients were aged from 13 months to 14 years, the peak incidence of the disease being from 3 to 6 years of age. Area distribution: 472 patients (93.6%) were from the countryside,
From the Beijing Children's Hospital, Beijing. Correspondence address: Dr. Wu Hu-Sheng, Beijing Children's Hospital, Nan J"i She Rood, Beijing, People's Republic of China.
and only 32 (6.4%) were from Beijing City. Months of onset: patients can be seen all year round, but 450 patients (89.3 %) were seen from June through October. Preceding infections were found in 198 patients (Table 1), fever of unknown origin ranking first and upper respiratory infection and gastroenteritis second. Symptoms and Signs: All patients had weakness of the extremities. The 9th and 10th cranial nerves were particularly affected, that is in 50.4% of the patients. The 7th cranial nerve was affected in 34.5% of the patients. 343 of the 504 cases (68.1 %) with AP had respiratory paralysis, and in 198/504 (39.3%), tracheotomy was performed. Grading scale for respiratory paralysis is based on the manifestation of clinical symptoms, signs and chest X-rays. It was divided into 3 grades (Table 2). Grade 1 included a mild weak voice, weak cough and dyspnea, and weakness of intercostal muscle and/or diaphragm movements during respiration, as seen on X-raying, but without a paradoxical pattern of breathing. A paradoxical pattern of breathing can be seen in grade 2 on deep breathing and in grade 3 on quiet breathing. 92 patients were in grade 1, 81 in grade 2 and 170 in grade 3, i.e., about 50% of the total number. In this study, none of the patients received steroids. The study was divided into two different periods, 130 patients in period 1 and 213 in period 2. No significant difference was found in the severity of respiratory paralysis between the two different periods (Table 3).
Table I Preceding infection fliness Fever of unknown origin Upper respiratory infection Gastroenteritis Bacillary dysentery Mumps Chicken-pox
Table 2 Grading scales of respiratory paralysis No
%
82 55 51 5 3
41.4 27.8 25.7 2.5 1.6 0.5 0.5
Post-immunization
Weak voice Weak cough Dyspnea
Grade 1
Grade 2
Grade 3
Mild Mild
Mod
Severe Severe
None/mild
Mod Mod
None
On deep breathing
Mild
Mod
Paradoxical pattern of breathing X-ray findings*
Severe On quiet breathing Severe or no movement
* The weakness of intercostal muscle and/or diaphragm movements as seen on X-raying. The first period was from 1975 through 1977 and there were 130 cases with respiratory paralysis, in 68 of which (52.3%) tracheotomy was performed. In order to reduce the possibility of pulmonary infection due to tracheotomy, we performed repeated intratracheal aspiration instead of tracheotomy. The second period was from 1978 through 1984 and there were 213 cases with respiratory paralysis. In 130 of the 213 cases (61.0%) tracheotomy was performed. In this period, we established the following criteria of tracheotomy: 1) grade 3 of diaphragm paralysis, 2) grade 2 of respiratory paralysis complicated by both the 9th and 10th cranial nerves being affected, 3) grade 2 of respiratory paralysis complicated by pneumonia and/or pulmonary atelectasis, and 4) rapidly progressive diaphragm paralysis to grade 3 24-48 hours after onset. In 190 of the 198 patients mechanical ventilation was performed after tracheotomy. We used intermittent positive pressure ventilation (IPPV), Type Volume Circle, I for the patients with AP. The number of days on the ventilator ranged from 2 to 92 days (average, 28 days). Days extubated ranged from 10 to 163 days (average, 53 days). Extubation was performed when the patients could cough and protect the airway, and had a minute volume that was adequate for gas exchange.
RESULTS The outcome of respiratory paralysis was compared between the two different periods (Table 4); in period 1, 11 cases suddenly suffered from asphyxia, due to tracheal aspiration and hypoxia; 4 died and 7 survived. The other 5 cases died of acute myocarditis or other causes. In period 2, only 2 cases suffered from asphyxia and there were no deaths. We must perform the following procedures: 1) artificial ventilation must be used correctly, 2) the secretion should be aspirated ragularly in order to maintain a clear airway, 3) sterilization must be strictly conducted to prevent cross infection, and 4) the patients should be observed carefully by both doctors and nurses, to present accidents. As a result, of the 504 cases with AP 9 died,
148 Brain & Development, Vol 10, No 3,1988
Table 3 The comparison on the severity of respiratory paralysis between 2 different periods Period
No
Grade 1 %
Grade 2 No %
Grade 3 No %
Period 1 (1975-1977)
39
30
23
17.7
68
52.3
Period 2 (1978-1984)
53
24.9
58
27.2
102
47.9
Table 4 The compairson on the outcome of patients with respiratory paralysis between 2 different periods Period
Noo! patients
Noo! tracheotomy
Noo! asphyxia
Noo! death
1975-1977
130
68
11
4 (5*)
1978-1984
213
130
2
0
* The other 5 cases died of acute myocarditis or other causes.
the mortality rate being 1 .79%. The study suggests tracheotomy should be performed early and it is one of the most important procedures in the treatment of AP with respiratory paralysis.
DISCUSSION Although it is one of the most common diseases of the peripheral nervous system, the precise pathologic mechanism of inflammatory polyneuropathy or Guillain-Barre syndrome (GBS) remains unknown [2]. In the 100 years since its description advances in electrophysiology have broadened diagnostic techniques and modern immunology has led to new treatments and research methods [2]. Despite modern intensive care, up to 5% of patients still die of acute polyradiculoneuritis (AP) [3] . Using the population of the United States in 1970 as a standard, the average annual age - adjusted incidence of GBS was 0.75 per lOS persons [4]. When age-specific
rates were analyzed, two peaks were observed; a high peak for patients over 60 years of age, and another peak for the first 5 years of life [4]. The age -specific incidence of GBS might be explained in terms of endogenous (immune response) and exogenous (antecedent illness) factors that are thought to contribute to the pathogenesis of GBS [5]. The GBS cases were quite evenly distributed, both seasonally and geographically, and no clusters or epidemic peaks were noted [4]. Fewer cases appear during the summer months when colds and other infections are less frequent [6]. However, in this paper, seasonal and area distribution variations have been noted. 472 patients (93.6%) were from the countryside, and 450, patients (89.3%) were seen from June through October, but so far the reasons for this have not been determined. The care of the GBS patient involves acute and rehabilitative aspects. Treatment is first approached symptomatically. Because of the unpredictable course in the first weeks, initial meticulous evaluation of function must be made in order to gauge clinical changes [2]. In the acute phase, the patient is closely monitored, generally in an intensive care unit (lCU). The immediate concerns are respiratory failure and autonomic dysfunction [2] . GBS is not always a mild disease with a good prognosis; 10-23% require tracheotomy [7]. However, the criteria for intubation, mechanical ventilation, weaning, extubation and tracheostomy are uncertain, and have been determined by local practice [8] . A series of patients were managed using easily applicable bedside signs and chest X-rays, that we have found useful. We established the criteria for tracheotomy, and reviewed our experience. Thirty-one patients (61 %) had trunk weakness (including respiratory muscles) and there was respiratory insufficiency in 18 (35%). Artificial respiration was necessary in seven patients (14%) [9]. One-third of our patients were on ventilators, but only six for over 2 months. Thirteen of our patients were on ventilators for under 2 months (mean, 19 days) [10]. The frequency of respiratory paralysis was much higher in our cases, and the number of patients who needed artificial respiration was high, there was also a considerably higher frequency of cranial nerve damage. These differences indicate that GBS was more severe in our patients. Arterial blood gases are determined to detect hypoxia before clinical signs of respiratory insufficiency appear. Hypoxia reflects small regions of atelectasis due to loss of spontaneous high volume signs [2] . PC02 is not a sensitive guide for mechanical respiratory failure because impaired CO 2 exchange occurs when the vital capacity falls to 10 ml/kg. Current practice suggests that tracheostomy be performed if intubation is anticipated beyond 2 weeks [2] . There is no convincing evidence supporting the use of steroids in the treatment of acute inflammatory polyneuropathy [lJ . Most reports showed that corticosteroids
do not significantly alter the course of the disease and suggest that the complications of corticosteroid therapy prevent their safe usage. For these reasons, no firm policy for corticosteroid use has been developed [7, 11, 12] . The results of a controlled trial of prednisolone in acute polyneuropathy provide no grounds for the use of steroids in the management of acute inflammatory neuropathy since the prognosis is not improved, the rate of recovery is slowed and the chance of relapse may be increased [7] . As mentioned above, in this study, none of the patients received steroids. Respiratory support and other measures were maintained until no longer needed, the other measures including hydration, nutrition, and maintenance of cardiovascular and renal function where necessary, as well as routine nursing care as to pressure areas, eyes, bowels, etc [11]. Chest physical therapy and frequent positional changes are the most important care factors in GBS [2]. We did not use bronchoscopy to clear secretions in patients with major atelectasis, but instead relied on vigorous chest physical therapy and tracheal suctioning. In other words, good nursing care and physiotherapy are very important for the severely affected patient, both to avoid complications and to lessen the long-term disability.
REFERENCES 1. Parke JT. Para-infectious neurologic syndromes. In: Fishman MA, ed. Pediatric neurology. Houston: Grune & Stratton, 1986: 232.{i. 2. Griswold K, Mckenna M, Ropper AH. An approach to the care of patients with Guillain-Barre syndrome. Heart Lung 1984;13:66-72. 3. Leibowitz S, Hughes RAC. Immunology of the nervous system. London: Edward Arnold, 1983:101-25. 4. Soffer D, Feldman S, Alter M. Epidemiology of GuillainBarre syndrome. Neurology 1978;7:686-9. 5. Kaplan JE, Schonberger LB, Hurwitz ES, et al. GuillainBarre syndrome in the United States, 1978-1981: additional observations from the national surveillance system. Neurology 1983;33: 633-6. 6. Mcfarland HR, Heller GL, Arbor A, et aI. Guillain-Barre disease complex. Arch Neurol 1966; 14: 196-201. 7. Hughes RA, Newson-Davies JM, Perkin GD, et al. Controlled trial of prednisolone in acute polyneuropathy. Lancet 1978; 2: 750-3. 8. Ropper AH, Kehne SM, Guillain-Barre syndrome: management of respiratory failure. Neurology 1985;35: 1662-5. 9. Bak P.- Guillain-Barre syndrome in a Danish county. Neurology 1985; 35: 207 -11. 10. Ropper AH. Severe acute Guillain-Barre syndrome. Neurology 1986;36:429-31. 11. Moore P, James O. Guillain-Barre syndrome: incidence, management and outcome of major complications. Crit Care Med 1981;9:549-54. 12. Goodall JA, Kosmidis JC, Geddes AM. Effect of corticosteroids on course of Guillain-Barre syndrome. Lancet 1974; 1:524-6.
Wu et al: Treatment ofpolyradiculoneuritis 149