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1.Meena AK, Khadilkar SV, Murthy JM. Treatment guidelines for Guillain-Barré Syndrome. Ann Indian
Acad Neurol. 2011;14. 73-81.!
2. Lesch, D. Gullaine-Barre Syndrome. [PowerPoint]. Louisville, KY: Bellarmine University Doctor of
Physical Therapy Program; 2014. !
3. Van doorn PA, Ruts L, Jacobs BC. Clinical features, pathogenesis, and treatment of Guillain-Barré
syndrome. Lancet Neurol. 2008;7(10):939-50.!
4.Khan F. Rehabilitation in Guillian Barre syndrome. Aust Fam Physician. 2004;33(12):1013-7.!
5. Harms M. Inpatient management of guillain-barré syndrome. Neurohospitalist. 2011;1(2):78-84.!
6. Ranjani P, Khanna M, Gupta A, Nagappa M, Taly A, Haldar P. Prevalence of fatigue in Guillain-Barre
syndrome in neurological rehabilitation setting. Annals Of Indian Academy Of Neurology [serial
online]. July 2014;17(3):331-335. !
7. Nicholas R, Playford E, Thompson A. A retrospective analysis of outcome in severe Guillain-Barre
syndrome following combined neurological and rehabilitation management. Disability & Rehabilitation
[serial online]. July 10, 2000;22(10):451-455.!
8. Guillain-Barré Syndrome, CIDP and Variants: Guidelines for Physical and Occupational
Therapy.GBS/CIDP Foundation International.!
9. Tuckey J, Greenwood R. Rehabilitation after severe Guillain-Barré syndrome: the use of partial body
weight support. Physiotherapy Research International [serial online]. June 2004;9(2):96-103.](https://image.slidesharecdn.com/25a0f528-dfe9-4d00-8665-075009930e61-150227085443-conversion-gate01/75/Guillain-Barre-Syndrome-final-26-2048.jpg)
Guillain-Barre Syndrome final
- 1. Guillain-Barre Syndrome Epidemiology, prognosis,medical and rehabilitation treatment ! ! Laura Stigler ! Bellarmine University ! 2014 ! ! ! https://www.youtube.com/watch?v=zLs0MLxfgYU
- 2. Prevalence Likelihood of acquiringGBS is 1: 1,000. 1! North America and Europe: Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP)- 90% of cases. 1! China and Japan: Acute Motor Axonal Neuropathy (AMAN) most common. 1! Peak incidence between June-July and September- October.1! Occurs in all ages: Most common in young adults and white males. 2
- 3. Epidemiology Correlation between recentinfection and onset of GBS: infection-induced aberrant immune response that damages peripheral nerves. 3! 1/4 of GBS patients have gad a recent C. Jejuni infection-AMAN form most common. 1! About two-thirds of patients have symptoms of an infection in the 3 weeks before the onset of weakness. 3! Up to 60% have a preceding upper respiratory illness. 4! 27% have no preceding illness. 4! Infection with cytomegalic virus (CMV) and Campulobacter jejuni- associated with axonal form of GBS. 4! Associated with: diabetes, alcohol abuse, exposure to heavy metals, epidural aesthetic, and drug abuse. 4
- 4. Disease ProcessImmune response attacksmyelin- producing Schwann cells which are destroyed by macrophages- AIDP! Underlying axon left intact ! Affects both motor and sensory
- 5. Diagnosis Form of GBSCharacteristics Acute inflammatory demyelinating polyradiculoneuropathy Motor, bilateral facial and pharyngeal, occasional sensory, and autonomic disturbances. Acute motor axonal neuropathy Only motor Miller fisher syndrome Ophthalmoplegia, ataxia, areflexia. 1
- 6. Clinical Features Ascending motor symmetrical,flaccid areflexia paralysis! Parathesias and hypersthesias! Cranial nerve involvement ! Autonomic dysfunction: sinus tachycardia or less often bradycardia, fluctuating blood pressure, loss of sweating! History of flu-like illness! Recovery after 2-4 weeks of plateau of the disease process. https://indianclinicalknowledgedotnet1.wordpress.com/tag/gbs/
- 7. Frequency of featuresin acute GBS Features Frequency in fully developed cases 4 Weakness in legs 95% Weakness in arms 90% Areflexia 90% Parasthaesia 85% Sensory loss 75% Oropharyngeal weakness 50% Pain 30% Respiratory failure 30% Opthalmoparesis 15% Ataxia 15% Sphincter involvement 5%
- 8. Differential Diagnosis • Brainstem encephalitis! • Meningitis carcinomatosis ! • Vitamin B1 deficiency ! • Botulism ! • Polymytosis! • Dermatomyotosis! • Acute rhabdomyolysis 3! • Spinal cord compression ! • Transverse myelitis! • Myasthenia gravis! • Vasculitis neuropathy ! • Paraneoplastic neuropathy 4
- 9. Differential Diagnosis Red FlagsRaising Other Diagnostic Possibilities - Fever at onset - Severe pulmonary dysfunction with limited weakness at onset - Severe sensory signs with limited weakness at onset - Persistent bladder or bowel dysfunction, or dysfunction at onset. - Sharp sensory level - Marked persistent asymmetry of weakness - Increased number of mononuclear cells in CSF
- 10. Tests and Measures Electrodiagnosis:demonstrates demyelination. 1 ! Sural sparing: normal Sural sensory nerve response ! CSF analysis: Elevated CSF protein, fever than 10 cells/3mm. 4! CSF examination helps to rule out other causes of weakness- lyme disease, HIV related radiculitis. 3 http://intensivecarehotline.com/clinical-pictures/guillain-barre- syndrome/
- 11. Medical Treatment Clinical SignManagement Respiratory Failure Ventilator (2-6 weeks) Dysautonomia Possible pacemaker placement for bradycardia Hyperoxygenation during suction Short lived antihypertensives Treatment of dysmotility Hyponatremia Electrolyte replacement Deep Vein Thrombosis Prophylaxis Nutrition Nasogastric or gastric tube High energy and high protein- prevent muscle wasting and promote ventilator weaning Immunity Plasmapheresis Immunotherapy (IVIg)
- 12. Plasmapheresis vs Intravenous Immunoglobulins Plasmapheresis(PE) and Intravenous Immunoglobulin (IVIg) therapy are both utilized ! IVIg more convenient- greater availability ! Neither treatment found to be more effective 1! Higher incidence of relapse after IVIg treatment 4! Few cost analyses though PE may be more cost effective than IVIg! Not more effective when combined. 1
- 13. Plasmapheresis Meta-analysis showed patientstreated with plasmapheresis at onset were at a reduced risk for developing respiratory failure. 1! Patients treated with PE have better secondary outcomes including: ! Decreased time to recover walking without an AD! Reduced necessity and duration of ventilator use! Full muscle strength recover after 1 year. 1
- 14. Plasmapheresis Adverse effects ofPE include: ! hypotension! septicemia! pneumonia! abnormal clotting! hypocalcemia. 1! Contraindications to using PE: ! hemostatic disorder, unstable cardiovascular state, active infection, and pregnancy. 1 http://www.giveplasma.ca/plasmapheresis
- 15. Intravenous Immunoglobulins Side effectsof IVIg include: ! CHF! Stroke! Myocardial ischemia! Renal failure! Thrombocytopenia! Hemolysis! Anaphylatic shock. 5
- 16. Prognosis Rehabiliation can take upto 1 year, though residual effects can be present 3-6 years. ! Patient disability is seen in 20%-30%. 1 Clinical features associated with poorer outcomes • Older age • Requirements for respiratory support • Abnormal nerve function • No plasmapheresis is performed • Primary axonal degeneration • Patients with rapid onset • Progression to quadriplegia • Respiratory dependence • Severe disease at presentation • Campylobacter jeuni infection • Patients showing no improvement at 3 weeks of plateau of disease
- 17. Clinical Picture Progression: fromdistal to proximal 1! Recovery: from proximal to distal 1! Where do we start???! Proximally- train muscles as they recover! AAROM arms, sitting balance, core strengthening. ! Progress to sliding board transfers- once there is recovery of UE strength. https://www.youtube.com/watch?v=VwQzjj9aQnQ
- 18. Rehab- Acute Care Whatis the patient experiencing?! Fear and anxiety ! Depression and guilt ! Pain http://www.oregonlive.com/health/index.ssf/ 2010/12/a_mysterious_disease_sends_por.html
- 19. Rehab: Acute Care- Evaluation Patient/caregiverinterview! Sensory assessment ! Skin inspection ! Joint ROM ! Muscle Testing Functional testing ! Mobility ! Respiration! Activity tolerance
- 20. Rehab: Acute Care Preventionof contractures and maintenance of posture and joint alignment 4,8! Family education: transfers, positioning, PROM 4,8 ! Reducing effects of prolonged immobilization: tilt tables for weight-bearing and positioning to prevent skin care issues and nerve palsies. 4! Densentitisation therapy for pain and depression. 4! Introduce breathing and coughing techniques 8! Anticipate rehab and AD needs 8
- 21. Acute Care- Rehabilitation ! Providegentle stretching and active or active assistive exercise at a level consistent with patient’s strength 2, 8! Don’t exercise to muscle fatigue- overuse or overstretch can impede recovery 2! Emphasize patient communication about fatigue and pain. Educate on signs of fatigue. 2! Teach energy conservation techniques 2,8! Introduce coughing and breathing exercises to insure good air exchange 2,8! Increase repetitions before resistance 2! Use PNF 2
- 22. Rehab: Sub-Acute Progress strengthening! Progress to ambulation- decrease assistance as patient progresses strength, balance and coordination! Emphasize proper mechanics and avoid substitutions! Continue to educate family on rehabilitation progress! HEP for patient and family members ! Rehab similar to incomplete spinal cord injured patient ! Partial body weight support treadmill training 9
- 23. Rehab- Chronic 12-week bicycleextensive training program has positive effects on fatigue, anxiety, depression, and functional outcome. 1! Pool therapy! Functional training ! Dynamic balance and strength training! Make it fun yet challenging.
- 24. Outcome Measures Modifed BarthelIndex,! Functional Independence Measure, ! Environmental Status Scale ! Handicap Assessment Scale 7
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- 26. Resources 1.Meena AK, KhadilkarSV, Murthy JM. Treatment guidelines for Guillain-Barré Syndrome. Ann Indian Acad Neurol. 2011;14. 73-81.! 2. Lesch, D. Gullaine-Barre Syndrome. [PowerPoint]. Louisville, KY: Bellarmine University Doctor of Physical Therapy Program; 2014. ! 3. Van doorn PA, Ruts L, Jacobs BC. Clinical features, pathogenesis, and treatment of Guillain-Barré syndrome. Lancet Neurol. 2008;7(10):939-50.! 4.Khan F. Rehabilitation in Guillian Barre syndrome. Aust Fam Physician. 2004;33(12):1013-7.! 5. Harms M. Inpatient management of guillain-barré syndrome. Neurohospitalist. 2011;1(2):78-84.! 6. Ranjani P, Khanna M, Gupta A, Nagappa M, Taly A, Haldar P. Prevalence of fatigue in Guillain-Barre syndrome in neurological rehabilitation setting. Annals Of Indian Academy Of Neurology [serial online]. July 2014;17(3):331-335. ! 7. Nicholas R, Playford E, Thompson A. A retrospective analysis of outcome in severe Guillain-Barre syndrome following combined neurological and rehabilitation management. Disability & Rehabilitation [serial online]. July 10, 2000;22(10):451-455.! 8. Guillain-Barré Syndrome, CIDP and Variants: Guidelines for Physical and Occupational Therapy.GBS/CIDP Foundation International.! 9. Tuckey J, Greenwood R. Rehabilitation after severe Guillain-Barré syndrome: the use of partial body weight support. Physiotherapy Research International [serial online]. June 2004;9(2):96-103.