We have a clinical problem with a patient with GBS treated promptly with IVIGS. The EMG examination talks about acute motor sensory axonal polineuropathy (AMSAN) with deteriorating clinical course from the first EMG examination. Now the patient is on mechanical ventilation and has no acute infections. At the moment, they have disautonomy and tetraparesia. 21 days ago they received 2 gr/kg in five days of IVIGS. What would you do now?
Nothing,
A second course of IVIGS,
Plasmapheresis?
Thanks for all your opinions, but the Guidelines on the Use of Therapeutic Apheresis in Clinical Practice (Journal of Clinical Apheresis 28: 145-284 (2013) says with GRADE methodology that is 2C ( very weak)...
In spite of the GRADE of the methodology, I think that Plasmapheresis is a good option.
If you give IVIG and plasmapheresis a few days after, I think you are doing opposite things...
We just had a very similar patient, with GBS - and the second dose of IVIG helped.
He seems to have done it.
A second course of IVIG may be helpful. However the response of AMSAN to IVIG is not very good. As regards plasmapheresis i agree with Dr Victor lopez
Knowing my post is not connected to the initial question but:
Information added with regard to actuality (hass been reported today in Austrian Newspaper for the first time):
MEYER SAUTEUR PM et al:
Research Article
Mycoplasma pneumoniae triggering the Guillain-Barré syndrome: A case-control study
Annals of Neurology, Volume 80, Issue 4 October 2016
Pages 566–580
First published: 26 August 2016
DOI: 10.1002/ana.24755
http://onlinelibrary.wiley.com/doi/10.1002/ana.24755/abstract
For convenience only:
Abstract
Objective
Guillain-Barré syndrome (GBS) is an acute postinfectious immune-mediated polyneuropathy. Although preceding respiratory tract infections with Mycoplasma pneumoniae have been reported in some cases, the role of M. pneumoniae in the pathogenesis of GBS remains unclear. We here cultured, for the first time, M. pneumoniae from a GBS patient with antibodies against galactocerebroside (GalC), which cross-reacted with the isolate. This case prompted us to unravel the role of M. pneumoniae in GBS in a case-control study.
Methods
We included 189 adults and 24 children with GBS and compared them to control cohorts for analysis of serum antibodies against M. pneumoniae (n = 479) and GalC (n = 198).
Results
Anti–M. pneumoniae immunoglobulin (Ig) M antibodies were detected in GBS patients and healthy controls in 3% and 0% of adults (p = 0.16) and 21% and 7% of children (p = 0.03), respectively. Anti-GalC antibodies (IgM and/or IgG) were found in 4% of adults and 25% of children with GBS (p = 0.001). Anti-GalC-positive patients showed more-frequent preceding respiratory symptoms, cranial nerve involvement, and a better outcome. Anti-GalC antibodies correlated with anti–M. pneumoniae antibodies (p < 0.001) and cross-reacted with different M. pneumoniae strains. Anti-GalC IgM antibodies were not only found in GBS patients with M. pneumoniae infection, but also in patients without neurological disease (8% vs 9%; p = 0.87), whereas anti-GalC IgG was exclusively found in patients with GBS (9% vs 0%; p = 0.006).
Interpretation
M. pneumoniae infection is associated with GBS, more frequently in children than adults, and elicits anti-GalC antibodies, of which specifically anti-GalC IgG may contribute to the pathogenesis of GBS. Ann Neurol 2016;80:566–580
IVIG 2nd course should be considered after taking sample for Ig G levels. We too have treated eight patients with 2nd course after two to three weeks in view of mechanical ventilation and found encouraging results with 2nd course IVIG.
Plasmapheresis may decrease Ig G levels further, may not benefit the pt.
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