A case report on Guillain–Barré Syndrome
Christina Rajathi1, Subadhra Devi2, Maha Lakshmi3
1Nursing Incharge, Kauvery Hospital, Cantonment, Trichy, Tamil Nadu
2Nurse Educator Kauvery Hospital, Cantonment, Trichy, Tamil Nadu
3Nursing Superintendent, Kauvery hospital, Cantonment, Trichy, Tamil Nadu
Abstract
Guillain–Barré syndrome (GBS) is a potentially life-threatening postinfectious disease characterized by rapidly progressive, symmetrical weakness of the extremities. About 25% of patients develop respiratory insufficiency and many show signs of autonomic dysfunction. Diagnosis can usually be made on clinical grounds, but lumbar puncture and electrophysiological studies can help to substantiate the diagnosis and to differentiate demyelinating from axonal subtypes of GBS. Molecular mimicry of pathogen-borne antigens, leading to generation of cross reactive antibodies that also target gangliosides, is part of the pathogenesis of GBS; the subtype and severity of the syndrome are partly determined by the nature of the antecedent infection and specificity of such antibodies. Intravenous immunoglobulin and plasma exchange are proven effective treatments but many patients have considerable residual deficits. Discrimination of patients with treatment-related fluctuations from those with acute-onset chronic inflammatory demyelinating polyneuropathy is important, as these conditions may require different treatments. Novel prognostic models can accurately predict outcome and the need for artificial ventilation, which could aid the selection of patients with a poor prognosis for more-individualized care. This review summarizes the clinical features of and diagnostic criteria for GBS, and discusses its pathogenesis, treatment and prognosis.
Background
Guillain-Barré Syndrome (GBS) is a rare but serious autoimmune neurological disorder in which the body’s immune system mistakenly attacks the peripheral nervous system. First described in 1916 by French physicians Georges Guillain, Jean Barré, and André Strohl, the condition typically begins with weakness, tingling, or numbness in the limbs, which can progress to muscle paralysis. GBS is often preceded by an infection, such as a respiratory or gastrointestinal illness, and is considered a medical emergency due to the risk of rapid progression and respiratory failure. With timely treatment, most patients recover, though the course of recovery can be slow and may involve long-term rehabilitation.
Case presentation
A patient presented to the emergency department with a 3-day history of bilateral lower limb weakness, followed by bilateral upper limb weakness. The patient had a recent history of Varicella and was on regular medication. Upon arrival, the patient’s Glasgow Coma Scale (GCS) score was 15/15 with quadriparesis noted on clinical examination. Based on the clinical presentation, Guillain-Barré Syndrome (GBS) was considered a likely diagnosis. Cardiac evaluation was normal, while nerve conduction studies (NCS) showed features suggestive of demyelinating neuropathy predominantly affecting the lower limbs. Blood investigations revealed elevated protein levels.
The patient was treated with 5 doses of intravenous immunoglobulin (IVIG) and showed partial improvement in symptoms. A general physician’s opinion was obtained to manage glycemic control, and relevant orders were carried out. Additionally, the patient was treated with antiviral medications and antiplatelet agents as part of the comprehensive management plan.
Allergies
No known medicine or environmental allergies
Past medical history
The patient had been affected with chicken pox 15 days before and has known cases of diabetes mellitus for 10 years and hypertension since 10 years on irregular treatment.
Physical examination
Vitals signs T – 99F, HR-68/min, BP- 110/70 mmhg, SPO2 – 92% on 40% Fio2, RR- 36/min
Airway – On NIV Support
Breathing- B/L adequate chest, diminished breath sounds.
Circulation – all peripheral pulse +
Disability – GCS 15/15, Neck flexion 5\5 present and grade one power of both lower limb 0/5 his tone had reduced in all 4 limbs.
E: No pressure injury and no other external injury noted
Investigations
Echocardiogram
- Normal chambers dimension
- No RWMA
- Good LV systolic function
- Grade I LV diastolic dysfunction
- Sclerotic AV
- Other valves normal
- Septae intact
- No pericardial effusion / clot
- Poor ECHO window
Markable investigations
| Albumin, Serum | 4.20 g/dl |
| Alkaline Phosphatase | 73.6 U/L |
| Aspartate Aminotransferase (AST/SGOT) | 41.3 U/L |
| Bicarbonate | 21 |
| Chloride | 103 mmol/L |
| Chloride Blood | 101 mEq/L |
| Creatinine | 0.59 mg/dL |
| Glucose | 251 mg/dL |
| HbA1c | 10.4 % |
| HCO3(c) | 12.1 mmol/L |
| Homocystine - Serum | 10.83 µmol/L |
| Indirect Bilirubin | 0.23 mg/dL |
| K + | 3.4 mmol/L |
| Potassium | 4.2 mmol/L |
| Sodium | 129 mmol/L |
| Total Protein | 8.50 g/dl |
| Urea Serum | 23.54 mg/dL |
| Albumin Urine | Present(+++) |
| Platelet Count | 316000 cells/µl |
| Test (APTT) | 27.0 Seconds |
| Test (PT) | 81.2 Seconds |
| Total RBC Count | 4.64 10^9/cmm |
| Total WBC Count | 8060 Cells/Cumm |
| Absolute Basophil Count (ABC) | 30 cells/µl |
| Eosinophil | 1.5 % |
| INR | 7.33 . |
| CA++(7.4) | 1.03 mmol/L |
| Direct Bilirubin | 0.17 mg/dL |
| Total Bilirubin | 0.57 . |
Imaging examination
NCS Report: Nerve conduction study showed features suggestive of demyelinating & axonal neuropathy. Predominantly affecting lower limbs.
MRI Brain taken, it showed post traumatic gliosis changes in the left anterior temporal region. Age related cerebral atrophy. CT Brain showed gliosis changes in the left anterior temporal region. Age related cerebral atrophy.
Management
He was treated with immunoglobulins 40 mg for 6 days and connected to a noninvasive mechanical ventilator. After 4 days weaned, and on facemask. He was on antibiotics, anti-hypertensive, corticosteroids, analgesics, vitamin tablets and bronchodilators and physiotherapy
Outcome and prediction of outcome
Guillain-Barré syndrome is still a life-threatening disorder with frequent morbidities, even with the best treatment available. Mortality rates in Europe and North America vary between 3% and 7%, and more widely in other countries where data are available. Patients can die in the acute progressive stage, most probably because of ventilatory insufficiency or pulmonary complications, or from autonomic dysfunction including arrhythmia.
However, death can occur at a late stage when a patient is discharged from an ICU to a general neurology ward, which further shows the importance of prolonged accurate monitoring and general care. Emergency situations can occur after delayed diagnosis, especially in young children. Patients who survive Guillain-Barré syndrome frequently have residual complaints and deficits, which can have a substantial effect on daily activities and quality of life. About 20% of patients with Guillain-Barré syndrome cannot walk unaided 6 months after onset.
Most patients have residual pain and fatigue, which can in part be attributed to persistent axonal loss. Many patients have to change their work and daily activities, even after reaching a good functional level. Most improvement happens in the first year, but patients might show further recovery even after 3 or more years.
To improve the outcome of Guillain-Barré syndrome, more effective treatments and good outcome assessments are needed. However, the clinical course and outcome of the disease is highly variable and early recognition of patients with poor outcome is needed to personalize and improve treatment. Prognostic models could help to identify patients who need additional treatment and monitoring. Patient characteristics consistently related to poor prognostic outcome in Guillain-Barré syndrome are higher age (aged 40 years and over), preceding diarrhea, and high disability at nadir.
The EGOS, which is based on these three clinical characteristics, can be used 2 weeks after admission to predict the ability of the patient to walk at 6 months. The mEGOS requires the Medical Research Council (MRC) Scale for muscle strength score instead of disability and can predict outcome as soon as one week after admission, when therapeutic interventions are probably even more effective.
The risk of respiratory failure is associated with rate of disease progression, severity of limb weakness, peroneal nerve conduction block, and low vital capacity. This risk can be predicted for individual patients using EGRIS; based on the severity of weakness (expressed as MRC sum score); onset of weakness; and facial palsy, bulbar weakness, or both. These models need to be We assessed the patient’s Muscle strength and reflex assessment. Daily twice physiotherapy advised, hourly Monitored Vital Signs
Respiratory Management
Monitor Respiratory Status: Assess for signs of respiratory distress or difficulty breathing, particularly if the diaphragm or other respiratory muscles are involved. Incentive Spirometry: Encouraging deep breathing exercises to prevent atelectasis and promote lung expansion.
Immune Therapy
Corticosteroids were added to reduce inflammation.
Pain Management: Analgesics were prescribed for pain control.
Physical Therapy
Positioning: Proper positioning and padding can help to prevent discomfort and injury caused by muscle weakness.
Nutrition Support
Parenteral Nutrition: Feeding has started through oral
Psychosocial Support
Encourage Family Involvement: Family members should be educated on the course of the disease, expected recovery trajectory, and how they can help care for the patient.
Patient education and discharge planning
During discharge he was conscious and oriented, muscle power upper limb – 3, lower limb – 4
Rehabilitation
Advised limb physiotherapy and medication follow up
Respiratory Monitoring
Education has been provided to patients and relatives, regarding how to do spirometry effectively. Along with breathing and coughing exercise.
Follow up treatment
| Tab. Pan | 40 MG |
| Tab. Dolo | 650 MG |
| Tab. Clonozep | 0.5 MG |
| Tab. Silodal - d | 8 MG |
| Tab. Gabablu - nt | 400/10 |
| Syp. Ascoril - ls | 10 ML |
| Syp. Potassium chloride | 10 ML |
| Syp. Duphalac | 15 ML |
Follow up: He has to review in OPD after 15 days in the Neurology department.
Conclusion
Early cranial nerve and respiratory involvement in patients presenting with GBS are associated with poor outcomes warranting immediate critical care involvement. It is imperative to recognize these symptoms, identify the subtype of GBS, and rapidly implement treatment. Validated for use in children and patients with axonal forms of Guillain-Barré syndrome.
Patients treated with IV Ig. Both PLEX and IV Ig had similar functional outcomes. Given the variability of infection, disease, and triggers in different populations, further prospective clinical trials with a well-defined population will help us evaluate the impact of different treatment modalities on this disease.
