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Anticipating Mechanical Ventilation in Guillain-Barré Syndrome
Nicholas D. Lawn, FRACP;
Dade D. Fletcher, MD;
Robert D. Henderson, FRACP;
Troy D. Wolter, MS;
Eelco F. M. Wijdicks, MD
Arch Neurol. 2001;58:893-898.
ABSTRACT
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Context The combination of multiple clinical factors culminates in neuromuscular
respiratory failure in up to 30% of the patients with Guillain-Barré
syndrome (GBS). Although guidelines exist as to when to proceed with intubation,
early indicators of subsequent progression to respiratory failure have not
been established.
Objectives To identify clinical and respiratory features associated with progression
to respiratory failure and to examine patterns of respiratory decline in patients
with severe GBS.
Design Retrospective survey.
Setting Tertiary care hospital.
Patients One hundred fourteen consecutive patients with severe GBS admitted to
the intensive care unit between January 1, 1976, and December 31, 1996.
Main Outcome Measures Early markers of impending respiratory failure, requirement for mechanical
ventilation, and patterns of respiratory decline.
Methods The clinical and electrophysiologic features of 60 patients receiving
mechanical ventilation were compared with 54 patients with severe GBS who
did not receive mechanical ventilation. Daily preventilation maximal inspiratory
and maximal expiratory respiratory pressures and vital capacity were analyzed.
Multivariate predictors of the necessity for mechanical ventilation were assessed
using logistic regression analysis.
Results Progression to mechanical ventilation was highly likely to occur in
those patients with rapid disease progression, bulbar dysfunction, bilateral
facial weakness, or dysautonomia. Factors associated with progression to respiratory
failure included vital capacity of less than 20 mL/kg, maximal inspiratory
pressure less than 30 cm H2O, maximal expiratory pressure less
than 40 cm H2O or a reduction of more than 30% in vital capacity,
maximal inspiratory pressure, or maximal expiratory pressure. No clinical
features predicted the pattern of respiratory decline; however, serial measurements
of pulmonary function tests allowed detection of those at risk for respiratory
failure.
Conclusions While inherently unpredictable, the course of patients with severe GBS
can, to some extent, be predicted on the basis of clinical information and
simple bedside tests of respiratory function. These data may be used in the
decisions regarding admission to the intensive care unit and preparation for
elective intubation.
INTRODUCTION
THE MANAGEMENT of patients with Guillain-Barré syndrome (GBS)
can be intimidating. The unpredictable course and potential for rapidly producing
life-threatening respiratory failure may prompt admission to an intensive
care unit (ICU). However, it is clearly unnecessary to transfer every patient
with GBS to the ICU based on the potential for deterioration alone. At present,
only limited data are available to provide guidance in this situation. Although
many studies have identified factors that are associated with the need for
ventilation (severe generalized weakness, bulbar involvement, or rapid disease
progression), these factors were variably analyzed prior to intubation.1, 2, 3, 4, 5
It is, therefore, difficult to know how to use this information in the assessment
of a patient before the point of respiratory failure as many of the clinical
findings identified may have occurred after intubation.
In their observational series of 19 patients, Ropper and Kehne6 established strict criteria for intubation in GBS
based on previously defined clinical and respiratory factors.7
Patients were intubated when clinical evidence of fatigue or severe oropharyngeal
weakness resulting in aspiration occurred. They also intubated when vital
capacity (VC) measurements fell below 15 mL/kg or if PO2 values
were less than 70 mm Hg on room air.6 Many
textbooks have since reiterated the guidelines for intubation adhered to in
this article.8, 9, 10
These clinical and respiratory factors are accurate in determining when to
proceed with intubation but do not provide guidance for the early respiratory
management of patients with GBS.
Serial measurements of respiratory function are frequently advocated
in patients with GBS.8, 9, 10
However, there is little detailed clinical information in the literature on
the patterns of decline of neuromuscular respiratory function and the respiratory
values at which preemptive measures are warranted.11
Respiratory management would be simplified and guidelines for the use of elective
intubation and admission to the ICU could be developed if accurate predictors
of respiratory failure could be identified early in the course of the disease.
PATIENTS, MATERIALS, AND METHODS
The medical records of 114 patients with GBS admitted to the ICU between
January 1, 1976, and December 31,1996, were reviewed. Standard diagnostic
criteria for GBS were used.9, 12
All patients were examined by a neurologist. The clinical, biochemical, and
electrophysiologic features of 60 of these patients with GBS who received
mechanical ventilation were compared with a group of 54 patients with GBS
who were admitted to the ICU but who did not receive mechanical ventilation.
These patients were admitted for many reasons including autonomic dysfunction,
bulbar weakness, comorbid disease, systemic complications, and importantly,
concerns regarding progression of disease and development of respiratory dysfunction.
DATA COLLECTION
All data were collected before ventilation or to peak disability in
patients who had received mechanical ventilation and those who did not, respectively.
Demographic features analyzed were age, sex, time to peak disability, presence
of pulmonary comorbidity (chronic obstructive airways disease, asthma, or
pulmonary fibrosis), and antecedent event, in particular, preceding gastrointestinal
illness (diarrhea or abdominal pain). Time to peak disability was defined
as time to intubation (patients who underwent ventilation), or time to worst
score on the Hughes disability scale (patients who did not undergo ventilation),
from onset of neuropathic symptoms.8 The use
of specific treatment with intravenous immunoglobulin or plasma exchange was
also analyzed. Clinical features analyzed were presence of bilateral facial
weakness, upper limb paralysis (complete absence of movement in the upper
limbs), autonomic dysfunction (unexplained blood pressure or heart rate fluctuations
or significant bladder or bowel dysfunction), and bulbar weakness (dysarthria,
dysphagia or impairment of the gag reflex). The results of cerebrospinal fluid
examination (protein level and cell count) and chest radiographs performed
prior to peak disability were analyzed. The compound muscle action potential
(CMAP) was analyzed on the first nerve conduction study performed at the Mayo
Clinic, Rochester, Minn. Low CMAP amplitude was defined as less than 20% of
the lower limit of normal.13 Inexcitable nerves
were defined as CMAP amplitude absent in all nerves tested or present in only
1 nerve with a CMAP amplitude less than 10% of the lower limit of normal and
absent in all other nerves tested.14
Serial respiratory function tests including VC (measured in milliliters
per kilograms), maximal inspiratory pressure (PImax), maximal expiratory
pressure (PEmax) (measured in centimeters of water), and arterial blood gases
were analyzed daily. For PImax, negative values are usually measured, but
in this article, these values are expressed, for simplicity, as positive (eg,
PImax of –50 cm H20 is recorded as 50 cm H20).
Respiratory factors were measured by a respiratory therapist using standard
techniques. For those with facial weakness, the lips would be held sealed
by the respiratory technician or an anesthesia mask would be used. When multiple
respiratory measurements were recorded, the best score was analyzed. We also
reviewed the patterns of respiratory decline in each patient. The time of
day at which intubation occurred was analyzed and, for each patient, it was
determined whether this was an elective or urgent procedure.
STATISTICAL ANALYSIS
Characteristics between patients with GBS who received mechanical ventilation
and those who did not were assessed for comparability using the Wilcoxon rank
sum test for continuous variables and the Fisher exact test for categorical
variables. Multivariate predictors of ventilation were assessed using logistic
regression analysis with a backward elimination procedure of nonsignificant
variables. In this model, mechanical ventilation (yes vs no) was the dependent
variable and all variables with a univariate P<.10
were included as potential independent predictors. All predictors were entered
into the model at the first step. The least significant variable was then
removed, with all remaining variables entered into the model at the second
step. This procedure was repeated until all variables remaining in the model
contributed significantly (P<.05) to the prediction
of ventilation. Owing to the amount of missing data for some variables, we
also used a multivariate analysis in which missing data were imputed with
the mean values of the respective variables from the available data. Only
variables with data values missing in no more than 25% of the patients were
imputed for the multivariate analysis. Variables with data missing in more
than 25% of the patients were omitted from the multivariate analysis. Odds
ratios and corresponding 95% confidence intervals for variables found to be
multivariately predictive of ventilation were calculated.
RESULTS
Baseline demographic and clinical characteristics of patients with severe
GBS who received mechanical ventilation and those who did not are listed in Table 1. Patients requiring mechanical
ventilation tended to have more severe disease evidenced by the presence of
bulbar dysfunction (P<.001), autonomic dysfunction
(P = .009), and bilateral facial palsy (P = .03). In addition, the requirement for mechanical ventilation was
associated with a shorter time to peak disability following the onset of neuropathic
symptoms (P = .01). No significant differences were
noted between those patients who received ventilation and those who did not
for age, sex, and the presence of a preceding gastrointestinal illness, upper
limb paralysis, or pulmonary disease. Results of cerebrospinal fluid analysis
were similar in both groups. Nerve conduction studies were comparable in both
groups; however, this analysis was limited because only 18 patients who received
mechanical ventilation and 26 patients who did not receive mechanical ventilation
had an electromyogram prior to peak disability. No patient in either group
had evidence of inexcitable nerves prior to peak disability. In this series
the lack of treatment with intravenous immunoglobulin or plasma exchange was
not associated with intubation and mechanical ventilation.
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Table 1. Baseline Demographics and Clinical Features of 114 Patients
With Guillain-Barré Syndrome*
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Baseline and subsequent respiratory measures are summarized in Table 2. Patients requiring mechanical
ventilation had lower baseline VCs (P = .007) on
hospital admission, lower baseline PImax (P = .01),
and lower baseline PO2 (P = .01) compared
with patients who did not receive mechanical ventilation. In addition, patients
requiring ventilation were more likely to have a VC decrease to lower than
20 mL/kg at some stage following admission (P<.001)
or a reduction in VC of at least 30% from baseline (P<.001).
They were also more likely to have a reduction from baseline by 30% in PEmax
(P = .002) and PImax (P
= .003). Additionally, PImax less than 30 cm H20 and PEmax less
than 40 cm H20 were strongly associated with eventual requirement
for ventilation (P<.001 and P = .007, respectively).
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Table 2. Respiratory Features*
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We also analyzed the temporal patterns of decline in VC. Of 32 patients
with severe GBS who received mechanical ventilation for whom complete data
were available, 23 had a greater than 30% decline in VC. Fifteen patients
experienced a rapid decompensation (over <24 hours) whereas 8 patients
were noted to have a more gradual decline (over >24 hours) in VC. Nine patients
had no appreciable decline prior to intubation. Three of these patients had
an initial VC less than 20 mL/kg and were intubated soon thereafter. The other
6 patients were intubated for airway protection because of bulbar weakness
or significant hypoxia related to superimposed pneumonia. Of the 42 patients
with severe GBS who did not receive mechanical ventilation for whom comprehensive
data were available, 36 (86%) had either no decline or an improvement in their
serial VC measurements during the course of their admission. Only 6 patients
had a decline in VC. All but 1 had an absolute VC greater than 20 mL/kg at
their nadir. Forty-eight percent of patients were intubated between the hours
of 6 PM and 8 AM, although most of these seemed to be semielective procedures.
Urgent ("crash") intubation, necessitated by respiratory or cardiac arrest
or extreme respiratory distress, occurred in 16% of patients.
Radiographic abnormalities on chest x-ray films were more commonly seen
in patients who required ventilation (49% of the patients who received ventilation
vs 29% of the patients who did not receive ventilation, P = .06). Patients usually had a combination of radiographic abnormalities
including pulmonary infiltrates, atelectasis, and pleural effusion. These
were often multifocal in distribution without any preponderance of right lower
lobe changes despite the high frequency of significant bulbar weakness and
risk for aspiration.
Clinical and respiratory features found to be predictive on univariate
analysis were included in the model for multivariate analysis. Owing to missing
more than 25% of the data, PO2 and the percentage of reduction
variables for VC, PImax, and PEmax were excluded from the model. The presence
of bulbar dysfunction (P<.001) and having a VC
less than 20 mL/kg at some time during hospitalization (P<.001) were found to be independently predictive of the requirement
for mechanical ventilation. Odds ratios and 95% confidence intervals for these
predictors are given in Table 3.
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Table 3. Multivariate Predictors of Mechanical Ventilation
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Results from the analysis on the data that included only the patients
with complete data (ie, patients with missing data were omitted, missing data
were not imputed) were comparable (bulbar dysfunction, P<.001; VC <20 mL/kg, P<.001). Owing
to missing data, the effective total sample size for this analysis was reduced
to only 68 patients. The proportion of patients omitted from this analysis
in the group who received mechanical ventilation was significantly higher
compared with the group who did not receive mechanical ventilation (33 patients
who received ventilation and 13 patients who did not receive ventilation, P = .001).
COMMENT
The results of our study suggest that a decline in neuromuscular respiratory
function and progression to mechanical ventilation should be anticipated in
patients with severe GBS who have bulbar dysfunction or a VC of less than
20 mL/kg. The presence of bilateral facial palsy, autonomic dysfunction, and
rapid disease progression were also associated with an increased likelihood
of mechanical ventilation. Upper limb paralysis was identified in a higher
proportion of patients who subsequently received mechanical ventilation, but
this did not reach statistical significance. Patient-dependent factors such
as age and the presence of preexisting chronic pulmonary disease did not predict
the progression to mechanical ventilation.
Our study confirms that serial measurements of respiratory factors are
an important component of the assessment of patients with severe GBS and clearly
contribute to respiratory management.7, 11, 15
Chevrolet and Deleamont11 studied serial VC
in 10 patients, 5 of whom received mechanical ventilation. They identified
that a decline in VC of 50% from baseline was associated with subsequent ventilation
within 36 hours and a drop in VC to an absolute value less than 1 L was associated
with ventilation within 18 hours. Conversely, the serial VC measurements were
stable and greater than 40 mL/kg in all patients who did not receive mechanical
ventilation.11 Our findings are comparable,
but on detailed analysis of day-to-day changes we found that a 30% reduction
in VC, PImax, or PEmax was highly correlated with a subsequent progression
to respiratory failure and intubation. In addition, certain "threshold" respiratory
values were identified that indicate that progression to respiratory failure
was highly likely to occur. These were as follows; VC less than 20 mL/kg,
PImax less than 30 cm H20, and PEmax of less than 40 cm H20. The use of these data ("20/30/40 rule") may allow identification
of patients at risk of respiratory failure early and the institution of preemptive
measures such as admission to the ICU.16 This
may avoid waiting until critical values are reached where respiratory failure
is established and urgent intubation under suboptimal circumstances is necessary.
A proposed guideline for the use of clinical data and respiratory function
tests in the management of GBS is shown in Figure 1.
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Proposed flowchart for the use of clinical and respiratory factors
in the management of Guillain-Barré syndrome. Hughes disability scale
score of less than 3 indicates that the patient is able to walk unassisted
more than 5 m. Hughes disability scale score of 3 or more indicates that the
patient is unable to walk more than 5 m or less (ie, bedridden or receiving
mechanical ventilation). VC indicates vital capacity; PImax, maximal inspiratory
pressure (expressed as positive values for simplicity, see "Patients, Materials,
and Methods" section in the text); PEmax, maximal expiratory pressure; and
ICU, intensive care unit.
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Serial measurement of respiratory factors revealed the following 3 patterns:
gradual decline (>30% reduction in VC over >24 hours), rapid decline (>30%
reduction in VC in <24 hours), and no decline. The vast majority of patients
(86%) without a decline in VC did not require ventilation. The patients who
received mechanical ventilation but who did not have a decline in VC were
primarily intubated for bulbar weakness and airway protection or because of
low baseline respiratory function test results. No clinical features predicted
those at risk of a decline in VC. However, gradual decline should allow elective
intubation. Rapid decompensation, which occurred in a significant number of
patients, was only detected by serial measurements combined with clinical
examination. Because rapid decompensation can occur, even in those with a
seemingly predictable course, ICU admission should be considered when the
above threshold respiratory values are reached, or if there is significant
bulbar weakness. The optimal frequency of VC measurement was not specifically
addressed by this study. However, we believe it is reasonable to recommend
that respiratory function tests be performed at least 3 times daily during
the period of disease progression to enable detection of significant decline.
If values are low, the tests should be repeated, ensuring full patient cooperation,
prior to any major change in management. The frequency of monitoring is in
accord with that used by Chevrolet and Deleamont.11
More frequent measurements may result in unnecessary fatigue17, 18
Nocturnal decompensation was frequently seen and resulted in semielective
intubation either late at night or in the early morning hours in a significant
proportion of these patients. This most likely was due to a combination of
poor pulmonary mechanics while the patient was in the supine position, which
can result in up to 50% reduction in VC, and impairment of central respiratory
drive.17, 18 There was no correlation
between long-term outcome and urgency of intubation but whether any short-term
morbidity occurs remains to be determined.19
Noninvasive methods of respiratory support such as continuous or bilevel
positive airway pressure have a limited role in patients with severe GBS with
borderline pulmonary mechanics.15, 20
In patients with bulbar weakness, the use these modalities is particularly
limited as upper airway collapse may significantly increase airway resistance.21 Additionally, continuous positive airway pressure
does not provide any airway protection from secretions that are often difficult
for these patients to control. The use of these measures to prevent nocturnal
decompensation in patients without bulbar dysfunction and relatively preserved
VC may warrant further study.
We acknowledge that the amount of missing respiratory data is potentially
a limitation of this study. However, the subgroup of patients with comprehensive
data available were representative of the group as a whole as suggested by
the comparability with the imputed data. Analysis of the contribution of electrophysiologic
variables in predicting progression to respiratory failure was also limited
by the amount of missing data. Low CMAP and more recently inexcitable nerves
have been associated with an adverse outcome, but these have not been evaluated
specifically in regard to predicting ventilation.14, 19
Inexcitable nerves were eventually detected on subsequent electromyograms,
after intubation, in 7 patients who received mechanical ventilation. None
of the patients who did not receive mechanical ventilation developed inexcitable
nerves at any stage. Evaluation of phrenic nerve conduction and diaphragmatic
electromyograms have been shown to predict the need for ventilation, but this
technique is not universally available and was performed prior to ventilation
in very few of our patients.22, 23
Bifacial palsy occurred in more than 50% of our patients and could have confounded
measurement of pulmonary function tests. However, because the decisions for
intubation were based largely on the interpretation of serial measurements
in the same patient, a poor seal, if any, should not be a major factor. Intubation
remains an arbitrary decision, based on multiple factors and important clinical
considerations including physician experience and comfort level, which would
not have been recorded in the medical records, and cannot be assessed by this
study. The finding that a low VC or bulbar dysfunction was associated with
a high likelihood of progression to respiratory failure should be analyzed
in the context of the study design. Both of these are reasons to intubate
and are, therefore, inextricably linked to the institution of mechanical ventilation.
Nevertheless, the findings identified in our study can be used in early management
decisions in patients with GBS. Moreover, this study has also demonstrated
that a 30% reduction in respiratory factors and certain threshold values were
associated with subsequent intubation. These values may provide early warning
signs of significant respiratory decline, which are independent of values
that necessitate intubation, allowing opportunity for intervention or closer
observation.
While no single factor can be established that encompasses all patients,
our data can be synthesized as follows: an admission VC or fall in VC to less
than 20 mL/kg, a decrease of VC, PImax, and/or PEmax more than 30% from baseline
and evidence of bulbar dysfunction should alert the physician that progression
to respiratory failure is highly likely to occur. The presence of these factors
alone or in combination may not necessitate immediate support with mechanical
ventilation but may be used in the decision to admit the patient to the ICU
and prepare for elective intubation. Regular assessment of the patient with
these simple bedside measurements should continue until a clear and sustained
improvement is observed.
AUTHOR INFORMATION
Accepted for publication August 14, 2000.
Presented in part at the 51st Annual Meeting of the American Academy
of Neurology, Toronto, Ontario, April 22, 1999.
From the Departments of Neurology, Neurocritical Care Unit (Drs Lawn,
Henderson, and Wijdicks), Physical Medicine and Rehabilitation (Dr Fletcher),
and Biostatistics (Mr Wolter), Mayo Clinic, Rochester, Minn.
Corresponding author: Eelco F. M. Wijdicks, MD, Department of Neurology,
Mayo Clinic–W8A, 200 First St SW, Rochester, MN 55905 (e-mail: wijde{at}mayo.edu).
REFERENCES
| |
1. McKhann GM, Griffin JW, Cornblath DR, Mellits ED, Fisher RS, Quaskey SA for the Guillain-Barré Syndrome Study Group. Plasmapheresis and Guillain-Barré syndrome: analysis of prognostic
factors and the effect of plasmapheresis. Ann Neurol. 1988;23:347-353.
FULL TEXT
|
ISI
| PUBMED
2. Winer JB, Hughes RA, Osmond C. A prospective study of acute idiopathic neuropathy, I: clinical features
and their prognostic value. J Neurol Neurosurg Psychiatry. 1988;51:605-612.
ABSTRACT
3. Hewer RL, Hilton PJ, Crampton Smith AC, Spalding JM. Acute polyneuritis requiring artificial ventilation. Q J Med. 1968;37:479-491.
4. Rantala H, Uhari M, Cherry JD, Shields WD. Risk factors of respiratory failure in children with Guillain-Barré
syndrome. Pediatr Neurol. 1995;13:289-292.
FULL TEXT
| PUBMED
5. Sunderrajan EV, Davenport J. The Guillain-Barré syndrome: pulmonary-neurologic correlations. Medicine (Baltimore). 1985;64:333-341.
PUBMED
6. Ropper AH, Kehne SM. Guillain-Barré syndrome: management of respiratory failure. Neurology. 1985;35:1662-1665.
FREE FULL TEXT
7. Pontippidan H, Geffin B, Lowenstein E. Acute respiratory failure in the adult (second of three parts). N Engl J Med. 1972;287:743-752.
8. Hughes RAC. Guillain-Barré Syndrome. In: Swash M, consulting ed. Clinical Medicine and
the Nervous System. London, England: Springer-Verlag; 1990.
9. Ropper AH, Wijdicks EFM, Truax BT. Guillain-Barré Syndrome. Philadelphia, Pa: FA Davis Co Publishers; 1991.
10. Parry GJ. Guillain-Barré Syndrome. New York, NY: Thieme Medical and Scientific Publishers; 1993.
11. Chevrolet JC, Deleamont P. Repeated vital capacity measurements as predictive parameters for mechanical
ventilation need and weaning success in the Guillain-Barré syndrome. Am Rev Respir Dis. 1991;144:814-818.
ISI
| PUBMED
12. Asbury AK, Cornblath DR. Assessment of current diagnostic criteria for Guillain-Barré
syndrome. Ann Neurol. 1990;27(suppl):S21-S24.
13. Cornblath DR, Mellits ED, Griffin JW, et al. Motor conduction studies in Guillain-Barré syndrome: description
and prognostic value. Ann Neurol. 1988;23:354-359.
FULL TEXT
|
ISI
| PUBMED
14. Hadden RD, Cornblath DR, Hughes RA, et al for the Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome
Trial Group. Electrophysiological classification of Guillain-Barré syndrome:
clinical associations and outcome. Ann Neurol. 1998;44:780-788.
FULL TEXT
|
ISI
| PUBMED
15. Hughes RA, Bihari D. Acute neuromuscular respiratory paralysis. J Neurol Neurosurg Psychiatry. 1993;56:334-343.
ISI
| PUBMED
16. Hughes RA. Management of acute neuromuscular paralysis. J R Coll Physicians Lond. 1998;32:254-259.
PUBMED
17. Borel CO, Guy J. Ventilatory management in critical neurologic illness. Neurol Clin. 1995;13:627-644.
PUBMED
18. Teitelbaum JS, Borel CO. Respiratory dysfunction in Guillain-Barré syndrome. Clin Chest Med. 1994;15:705-714.
ISI
| PUBMED
19. Fletcher DD, Lawn ND, Wolter TD, Wijdicks EF. Long-term outcome in patients with Guillain-Barré syndrome requiring
mechanical ventilation. Neurology. 2000;54:2311-2315.
FREE FULL TEXT
20. Polkey MI, Lyall RA, Moxham J, Leigh PN. Respiratory aspects of neurological disease. J Neurol Neurosurg Psychiatry. 1999;66:5-15.
FREE FULL TEXT
21. Vincken W, Elleker G, Cosio MG. Detection of upper airway muscle involvement in neuromuscular disorders
using the flow-volume loop. Chest. 1986;90:52-57.
FREE FULL TEXT
22. Zifko U, Chen R, Remtulla H, Hahn AF, Koopman W, Bolton CF. Respiratory electrophysiological studies in Guillain-Barré syndrome. J Neurol Neurosurg Psychiatry. 1996;60:191-194.
ABSTRACT
23. Gourie-Devi M, Ganapathy GR. Phrenic nerve conduction time in Guillain-Barré syndrome. J Neurol Neurosurg Psychiatry. 1985;48:245-249.
ABSTRACT
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