eMedicine Specialties > Emergency Medicine > Neurology

Guillain-Barre Syndrome: Treatment & Medication

Author: Andrew C Miller, MD, Chief Resident and Clinical Assistant Instructor, Departments of Emergency Medicine and Internal Medicine, State University of New York Downstate Medical Center, Kings County Hospital Center
Coauthor(s): Razi M Rashid, MD, MPH, Intern, Department of Internal Medicine, St John's Hospital and Medical Center, Detroit, Michigan; Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Contributor Information and Disclosures

Updated: Jul 1, 2009

Treatment

Prehospital Care

  • ABCs, IV, oxygen, and assisted ventilation may be indicated.
  • Monitor for cardiac arrhythmias.
  • Transport expeditiously.

Emergency Department Care

  • ABCs, IV, oxygen, and assisted ventilation may be indicated.
  • Intubation should be performed on patients who develop any degree of respiratory failure. Clinical indicators of the need for intubation include hypoxia, rapidly declining respiratory function, poor or weak cough, and suspected aspiration. Typically, intubation is indicated when the FVC is less than 15 mL/kg.30
  • Patients who have, or are suspected of having, Guillain-Barré syndrome (GBS) should be monitored closely for changes in blood pressure, heart rate, and other arrhythmias.
    • Treatment rarely is needed for tachycardia.
    • Atropine is recommended for symptomatic bradycardia.
    • Because of the lability of dysautonomia, hypertension is best treated with short-acting agents, such as a short-acting beta-blocker or nitroprusside.
    • Hypotension of dysautonomia usually responds to intravenous fluids and supine positioning.
    • Temporary pacing may be required for patients with second-degree and third-degree heart block.

Consultations

  • Consult a neurologist if any uncertainty exists as to the diagnosis.
  • Consult the ICU team for evaluation of need for admission to the unit.

Medication

Only plasma exchange (PE) therapy and intravenous immune serum globulin (IVIG) have proven effective for Guillain-Barré syndrome (GBS). Both therapies have been shown to shorten recovery time by as much as 50%. IVIG is easier to administer and has fewer complications than plasma exchange.31  The cost and efficacy of the 2 treatments are comparable.

Randomized trials in severe disease show that IVIG started within 4 weeks from onset hastens recovery as much as plasma exchange.32,33,34,35  Combining plasma exchange and IVIG neither improved outcomes nor shortened the duration of illness.36  IVIG has also been proven safe and effective in the treatment of pediatric GBS.36,37  Additionally, IVIG is the preferential treatment in hemodynamically unstable patients and in those unable to ambulate independently.38,36  
Corticosteroids are ineffective as monotherapy.2,5 Limited evidence shows that oral corticosteroids significantly slow recovery from GBS.33 Substantial evidence shows that intravenous methylprednisolone alone does not produce significant benefit or harm. In combination with IVIG, intravenous methylprednisolone may hasten recovery but does not significantly affect the long-term outcome.33,39

Immunoadsorption is an alternative that is still in the early stages of investigation. A small prospective study showed no difference in outcome between patients treated with immunoadsorption and those treated with plasma exchange.40

Interferon beta was not associated with significant clinical improvement compared with controls in a small randomized control trial.41

Simple analgesics or nonsteroidal anti-inflammatory drugs may be tried but often do not provide adequate pain relief. Single, small randomized controlled trials support the use of gabapentin or carbamazepine in the intensive care unit for the treatment of pain in the acute phase of GBS. Adjuvant therapy with tricyclic antidepressant medication, tramadol, gabapentin, carbamazepine, or mexiletine may aid in the long-term management of neuropathic pain.42

Time to development of deep vein thrombosis (DVT) or pulmonary embolism varies from 4-67 days following symptom onset.42 DVT prophylaxis with gradient compression hose and subcutaneous low molecular weight heparin (LMWH) may cause a dramatic reduction in the incidence of venous thromboembolism, one of the major sequela of extremity paralysis.42

True gradient compression stockings (30-40 mm Hg or higher) are highly elastic, providing a gradient of compression that is highest at the toes and gradually decreases to the level of the thigh. This reduces capacity venous volume by approximately 70% and increases the measured velocity of blood flow in the deep veins by a factor of 5 or more.

The ubiquitous white stockings known as antiembolic stockings or thromboembolic disease (TED) hose produce a maximum compression of 18 mm Hg and rarely are fitted in such a way as to provide adequate gradient compression. They have not been shown to be effective as prophylaxis against thromboembolism.

Blood product derivatives

These agents are used to improve the clinical and immunologic aspects of the disease. They may decrease autoantibody production and increase solubilization and removal of immune complexes.


Intravenous immune globulin (IVIG, Gammagard S/D)

May neutralize circulating myelin antibodies through anti-idiotypic antibodies and down-regulate proinflammatory cytokines, including interferon-gamma (INF-gamma). In addition, may block the complement cascade and promote remyelination.

Adult

0.4 g/kg/d IV for 5 d

Pediatric

Administer as in adults

Documented hypersensitivity; IgA deficiency and anti-IgE/IgG antibodies

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Check serum IgA level before IVIG (use an IgA-depleted product, eg, Gammagard S/D); infusions may increase serum viscosity and thromboembolic events; infusions may increase risk of migraine attacks, aseptic meningitis (10%), urticaria, pruritus, or petechiae (2-30 d postinfusion)
Increases risk of renal tubular necrosis in elderly patients and in patients with diabetes, volume depletion, and preexisting kidney disease; laboratory result changes associated with infusions include elevated antiviral or antibacterial antibody titers for 1 mo, 6-fold increase in ESR for 2-3 wk, and apparent hyponatremia


Albumin (Albuminar, Albumisol, Albunex, Albutein)

Used in plasma exchange when the patient's plasma is exchanged with a plasma substitute. May remove autoantibodies and immune complexes from serum. Plasma exchange is carried out with albumin (50 mL/kg) over a 10-d period. Has been shown to decrease recovery time by 50%. May aid in removing cytotoxic constituents from serum.

Adult

Remove 3-4 L of the patient's plasma and substitute with albumin; administered IV

Pediatric

<16 years: Not established
>16 years: Administer as in adults

Pulmonary edema; renal insufficiency

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

While theoretically attractive, no proven benefit of colloid resuscitation over isotonic crystalloids exists

Fractionated low molecular weight heparins

These agents are used in the prophylaxis of DVT. Fractionated LMWH first became available in the United States as enoxaparin (Lovenox). LMWH has been used widely in pregnancy, although clinical trials are not yet available to demonstrate that it is as safe as unfractionated heparin.

Reversible elevation of hepatic transaminase levels occurs occasionally. Heparin-associated thrombocytopenia has been observed with fractionated low molecular weight heparin.


Enoxaparin (Lovenox)

Enhances the inhibition of factor Xa and thrombin by increasing antithrombin III activity. Also slightly affects thrombin and clotting time and preferentially increases the inhibition of factor Xa. Has a wide therapeutic window; prophylactic dose is not adjusted based on the patient's weight. Enoxaparin is safer and more effective than unfractionated heparin for prophylaxis of venous thromboembolism. Average duration of treatment is 7-14 d.

Adult

30 mg SC bid

Pediatric

Not established
The following doses have been suggested:
<2 months: 0.75 mg/kg/dose bid SC
>2 months to 18 years: 0.5 mg/kg/dose bid SC

Platelet inhibitors or oral anticoagulants such as dipyridamole, salicylates, aspirin, NSAIDs, sulfinpyrazone, and ticlopidine may increase risk of bleeding

Documented hypersensitivity; major bleeding and thrombocytopenia

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

If thromboembolic event occurs despite LMWH prophylaxis, discontinue drug and initiate alternate therapy; elevation of hepatic transaminase levels may occur but is reversible; heparin-associated thrombocytopenia may occur with fractionated LMWH; 1 mg of protamine sulfate will reverse effect of approximately 1 mg of enoxaparin if significant bleeding complications develop

More on Guillain-Barre Syndrome

Overview: Guillain-Barre Syndrome
Differential Diagnoses & Workup: Guillain-Barre Syndrome
Treatment & Medication: Guillain-Barre Syndrome
Follow-up: Guillain-Barre Syndrome
References
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Further Reading

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Keywords

Guillain-Barre syndrome, Guillain-Barré syndrome, GBS, nervous system, myelin sheath, neuropathy, nerves, causes, symptoms, treatment, viral infection, weakness, autoimmune disease, acute inflammatory demyelinating polyneuropathy, AIDP, acute motor axonal neuropathy, AMAN, acute motor-sensory axonal neuropathy, AMSAN, Miller-Fisher syndrome, MFS, acute panautonomic neuropathy, pharyngeal-brachial-cervical variant, pure sensory variant, Campylobacter jejuni, IVIG, plasmapheresis, acute flaccid paralysis

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Contributor Information and Disclosures

Author

Andrew C Miller, MD, Chief Resident and Clinical Assistant Instructor, Departments of Emergency Medicine and Internal Medicine, State University of New York Downstate Medical Center, Kings County Hospital Center
Andrew C Miller, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians, American Medical Association, Emergency Medicine Residents Association, Islamic Medical Association of North America, Medical Society of the State of New York, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Razi M Rashid, MD, MPH, Intern, Department of Internal Medicine, St John's Hospital and Medical Center, Detroit, Michigan
Disclosure: Nothing to disclose.

Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Edward A Michelson, MD, Program Director, Associate Professor, Department of Emergency Medicine, University Hospital Health Systems in Cleveland
Edward A Michelson, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM, Director of Emergency Services, Director of Chest Pain Center, Department of Emergency Medicine, Ft Sanders Sevier Medical Center
Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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