Guillain-Barré syndrome (GBS) in Sub-Saharan Africa: Experience from a tertiary level hospital in Burkina Faso
Alfred Anselme Dabilgou, Raphael Kaboré, Alassane Dravé, Julie Marie Adeline Kyelem, Maniènon Mariette Kambiré, Christian Napon, Athanase Millogo, Jean Kaboré
Corresponding author: Alfred Anselme Dabilgou, Department of Neurology, University Hospital Yalgado Ouedraogo, Ouagadougou, Burkina Faso
Received: 08 Oct 2021 - Accepted: 06 Jan 2022 - Published: 21 Jan 2022
Domain: Neuromuscular Medicine
Keywords: Guillain-Barré syndrome, clinical feature, cerebrospinal fluid, prognosis
©Alfred Anselme Dabilgou et al. PAMJ Clinical Medicine (ISSN: 2707-2797). This is an Open Access article distributed under the terms of the Creative Commons Attribution International 4.0 License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Cite this article: Alfred Anselme Dabilgou et al. Guillain-Barré syndrome (GBS) in Sub-Saharan Africa: Experience from a tertiary level hospital in Burkina Faso. PAMJ Clinical Medicine. 2022;8:15. [doi: 10.11604/pamj-cm.2022.8.15.31957]
Available online at: https://www.clinical-medicine.panafrican-med-journal.com//content/article/8/15/full
Case series
Guillain-Barré syndrome (GBS) in Sub-Saharan Africa: Experience from a tertiary level hospital in Burkina Faso
Guillain-Barré syndrome (GBS) in sub-Saharan Africa: experience from a tertiary level hospital in Burkina Faso
Alfred Anselme Dabilgou1,&, Raphael Kaboré2, Alassane Dravé3, Julie Marie Adeline Kyelem1, Maniènon Mariette Kambiré1, Christian Napon4, Athanase Millogo5, Jean Kaboré1
&Corresponding author
Guillain-Barré Syndrome (GBS) is an acute inflammatory disorder of peripheral nerves. This was a cross-sectional retrospective study of patients admitted to the neurology department of Yalgado Ouedraogo University Teaching Hospital for GBS from September 01, 2003 to July 31, 2020. Medical records were reviewed according to the clinical criteria of Asbury and Cornblath. Thirty-five patients with GBS were included in the study. Most of the patients were female gender (60%). The mean age of the patients was 27.9 years. The most common initial symptom was weakness in the extremities (91.4%) and paresthesia (42.9%). Motor deficit was progressive and symmetrical in 94.3% and ascending in all the patients (100%). The most common predisposing factors were pregnancy and post-partum in 10 (28.6%) patients. The pattern of paralysis was distal and proximal (42.9%), distal in (34.3%) and proximal (22.8%). Lumbar puncture was performed in 88.5%, and albuminocytologic dissociation of cerebro-spinal fluid was found in 42.3% of case. Routine nerve electrophysiology was performed in 17.14% of patients. GBS etiology has been undetermined in 77.1% of patients. The treatment was mainly based on steroids (80%) and vitamin therapy (65.7%). Supportive treatment consisted of physiotherapy (45.71%) and oxygen supplies (11.42%). The length of hospital stay was 21.25 days. The most common complication was pneumonia 17.14%). The mortality rate was 11.4%. Guillain-Barré Syndrome is rare in Burkina Faso. Steroids are the main treatment with high mortality.
Guillain-Barré Syndrome (GBS) is an acute inflammatory disorder of peripheral nerves characterized by rapidly progressive, symmetric weakness, and areflexia. Respiratory insufficiency develops in about 25% of cases, rendering mechanical ventilation crucial and long-term hospital admission necessary [1]. The annual incidence of GBS ranges from 0.81 to 1.89 cases per 100,000 population increasing linearly with age with a sex ratio of 1.5 [1]. Acute respiratory failure develops in 20-30% of patients [2]. Admission to the ICU is recommended for patients with GBS who have imminent respiratory insufficiency, severe autonomic dysfunction with cardiovascular instability, severe swallowing dysfunction and/or diminished cough reflex or rapidly progressive weakness [3]. Management of GBS requires a multidisciplinary approach including supportive medical care and immunotherapy. Intravenous immunoglobulin and plasma exchange are proven and equally effective treatments for GBS [4]. In Sub Saharan Africa, studies on GBS are rare. To our knowledge, the first study on GBS in Burkina Faso published in 2004 by Millogo focused on Guillain-Barré Syndrome in HIV-infected patients [5]. Since then, no further study has been carried out on GBS in Burkina Faso. The objective of our study was to determine the epidemiological, clinical and therapeutic profile of Guillain-Barré Syndrome GBS admitted in neurology department of a tertiary hospital in Burkina during the last 18 years.
Study location
Burkina Faso is a French speaking country located in West Africa without access to the sea. It covers an area of 274,200km² and its population was estimated in 2016 at 19,034,397 inhabitants. Ouagadougou is its capital and the largest city of the country. The city has public health infrastructures such as the Yalgado Ouédraogo University Teaching Hospital, Tingandogo University Teaching Hospital, Charles De Gaule Pediatric University Hospital, Bogodogo Hospital and many private health infrastructures. The department of neurology has been in existence since March 2003. It has a capacity of 23 beds. The neurology department welcomes all patients suffering from peripheral neuropathies, myasthenia gravis and myopathies. The department does not have an electroneuromyography machine, a key examination for the diagnosis of peripheral neuropathies.
Study profile
We conducted a cross-sectional study whose data collection covered the period from September 1, 2003 to July 31, 2020 (18 years old).
Population study
The study was based on data from adult patients (> 15 years of age) admitted in the Neurology department for GBS in the period from 2003 to 2020. GBS diagnosis was based on Asbury and Cornblath criteria [6]: (1): progressive motor weakness, (2): areflexia. Patients with incomplete or missing medical data were excluded from the study.
Data collection and analyzed
Data was collected from clinical records, hospitalization and discharge registers, and from patients´ death registers. The study included socio-demographic data (age, sex, professional category, residence, level of education, marital status), clinical data (history, presence or absence of inaugural events, functional signs, installation mode, results of the neurological examination, hospital stay), paraclinical data (detection of a biological inflammatory syndrome, results of the cerebrospinal fluid (CSF) analysis, electroneuromyography results). The data obtained were entered and analyzed on a microcomputer using Epi info software version 7.2.2.6. The graphs were produced with Excel 2010 software. The results were expressed as a percentage and as an average.
Ethical approval and consent to participate
This study was approved by the Ethical board of medical school of Joseph Ki Zerbo University and the local ethical Committee of Yalgado Ouedraogo University Teaching hospital. The confidentiality of patient's data was taken into account.
Frequency
Our study included 35 patients with Guillain-Barré Syndrome, as 1.9 cases per year.
Socio-demographic characteristics
The majority of patients were female (60%). The mean age of the patients was 27.9 years with extremes of 15 and 68 years. Patients under the age of 35 years of age accounted for 60 percent of the study population. Table 1 shows the patients with GBS age distribution.
Clinical characteristics
The most common initial symptom was weakness in the extremities in 32 patients (91.4%) and paresthesia in 15 (42.9%) patients. Motor deficit involved four limbs in 21 patients (65.6%) and both lower limbs in 14 patients (11.4%). The mode of onset was progressive in all the patients. The motor deficit was symmetrical in 33 (94.3%) patients, asymmetrical limb weakness in 2 (5.7%) and ascending in all the patients (100%). The most common predisposing factors were pregnancy and post-partum in 10 (28.5%) patients. History of infection was present in 5 (14.2%) patients. The patient admission time was 14 days with extremes of 4 and 28 days. Fourteen patients (40%) were hospitalized during the extension of paralysis phase and 21 (60%) during the plateau phase. The mean duration of the extension and plateau phase was 7.6 days and 46.4 days, respectively. The neurological examination on admission revealed lower limbs paralysis with abolition of tendon reflexes in all patients. Flaccid tretaplegia was noted in 15 patients, trauma in 12 (34.3%) patients and paraplegia in 4 (11.4%). The pattern of paralysis was proximo-distal in 15 (42.9%) patients, distal in 12 (34.3%) patients and proximal in 8 (22.8%) patients. The other abnormalities were represented by neuro-vegetative disorders in 34 patients and objective sensitivity disorders in 25 patients. Clinical manifestations of GBS at the time of presentation were listed in the Table 2. The pattern of paralysis was proximo-distal in 15 (42.9%) patients, distal in 12 (34.3%) patients and proximal in 8 (22.8%) patients. The other abnormalities were represented by neuro-vegetative disorders in 34 patients and objective sensitivity disorders in 25 patients. Clinical manifestations of GBS at the time of presentation were listed in the Table 2. The pattern of paralysis was proximo-distal in 15 (42.9%) patients, distal in 12 (34.3%) patients and proximal in 8 (22.8%) patients. The other abnormalities were represented by neuro-vegetative disorders in 34 patients and objective sensitivity disorders in 25 patients. Clinical manifestations of GBS at the time of presentation were listed in the Table 2.
Lumbar puncture performed in 31 (88.5%) patients demonstrated albuminocytologic dissociation in 15 patients or 48.38% of cases. Routine nerve electrophysiology was performed in six (17.14%) patients. Of them, four (66.7%) patients had demyelinating forms and two (33.3%) mixed forms. The etiology of GBS was undetermined in 27 (77.1%), HIV infection in 3 (8.6%), viral hepatitis B in 3 (8.6%) patients and helicobacter pylori in 2 (5.7%) patients.
Treatment
The treatment consisted of high dose corticosteroid therapy first injectable (500 mg to 1g per day) then oral (80%). Vitamin therapy was use only or in association in 65.71% of patients. No patient was treated with intravenous immunoglobulin or plasma exchange. Supportive treatment consisted of physiotherapy (45.71%), low-molecular-weight heparin (37.14%) and of oxygen therapy (11.42%).
Clinical outcome
The average length of hospital stay was 21.25 days. The severity of the disease ranged from grade 3 to grade 5 of GBS disability score. Complications during hospitalization were pneumonia in 6 (17.14%) patients, urinary tract infection in 2 (5.71%) and deep vein thrombosis in a patient (2.85%). Five cases of death were recorded (14.3%). One case of death was recorded during the extension phase (2.8%) and three cases (8.6%) during the plateau phase. One patient was transferred to intensive care for respiratory decompensation. On discharge, complete functional recovery was noted in one (2.6%) patient and partial in 17 (48.6%) patients.
This cross-sectional study described the epidemiological, clinical and therapeutic profile of GBS admitted in neurology department in Burkina Faso during the last 18 years. The frequency of GBS in our context was very low, only 1.9 cases per year. This situation could be explained by the lack of neurologists and neurophysiologist in the country. The mean age of patients with GBS was 27.9 years, comparable to that found by Basse in Senegal (33.9 years) [7]and Saisha in Zambia (33.6 years) [8]. Young adults were more affected than the older patients [9]. Our study showed a predominance of women (60%), in line with the study of Basse in Senegal (69.23%) but in contrast with most studies who reported a clear male predominance [4]. About 14.2% of patients had experimented infectious disease prior to their admission in neurology department. According to the literature, more than two-thirds of GBS cases are preceded by acute infection within 3-4 weeks [10].
This low history of infections could be explained by the long wait times for patients to be hospitalized. Pregnancy and postpartum were present in 28.5% of patients, in lower percentage than that found by Basse in Senegal (63.6%) [7]. The risk of GBS is lower during pregnancy and increases post-delivery particularly in the first 2 weeks after delivery [11]. Diagnosis of GBS is based on the patient history and neurological, electrophysiological and cerebrospinal fluid (CSF) examinations [6] but in resource limited settings, the diagnosis is usually made clinically with the support of a few laboratory investigations. Lumbar puncture was performed in 88.5% of cases but electromyogram was available in few patients (17.1%). The low rate of completion of electromyogram could be explained by the limited number of devices (two in total for the whole country), the high cost of this examination (30,000 fcfa) and the severity of the patients. An albinuno-cytological dissociation was found in 42.8% of cases, approaching the rate found by Basse et al. in Senegal (45.4%) [7].
The study of cerebrospinal fluid can be normal in the first week but shows albuminocytologic dissociation after two weeks [12]. The electromyogram showed demyelinating lesions in 66.7% of cases and axono-myelinic in 33.3% of cases. The preponderant myelinic involvement is in favor of AIDP which constitutes the most frequent form of GBS (75 to 80%) [13] . In the majority of cases, the causes of GBS were undetermined linked to the lack of financial resources.
However, our study was to highlight certain causes. About eight percent of patients (8.6%) were HIV positive, lower than that found in the study of Millogo in 2004 (20%) [5] and Saisha in Zambia in 2015 (82%) [8]. According to Thornton, HIV infection is more frequent cause of GBS in sub-Saharan Africa [14]. Viral hepatitis B was also noted in 5.7% of patients, in agreement with several data from the literature [15]. The presence of HBs Ag is found in the CSF of some patients with GBS [16]. Gastrointestinal infection with Helicobacter pylori was identified in 5.7% of patients. To our knowledge, we have not been able to identify any cases in the literature. Therapeutically, corticosteroid therapy was the main treatment for GBS in our setting (80%), in agreement with the study by Basse in Senegal (53.4%) [7]. This is due to the high cost of immunoglobulins, the treatment of choice for GBS. Corticosteroids were recommended in treating patients with refractory or severe GBS as immunosuppressants [17].
Physiotherapy was performed in 45.71% of patients but some authors argued that there was no evidence of the impact of physiotherapy in the management of GBS patients (44-46). Functional reduction be considered for patients with a GBS [2]. The mortality rate recorded in our series (14.3%) was comparable to that recorded by Basse in Senegal (10.2%) [7]. This mortality was high compared to that reported in North America and Europe (1-5%) [18]. This high mortality rate in our context could be explained by the presence of severe forms early in hospitalization (tetraplegia, damage to the bulbar nerves, respiratory failure) and the lack of intensive neurological care. The causes of death are notably linked to respiratory complications and ventilatory support is necessary in 15 to 20% of cases [19]. Most patients with GBS require admission to an intensive care unit (ICU) under the care of physicians who are familiar with the medical complications that develop in paralyzed Intensive Care Unit patients [20]. A patient was transferred in resuscitation unit, lower than in the study of Basse (20.5%) [7] due to low reception capacity of the service.
Limitations of the study
Our study has several limitations. This is a retrospective study with inherent biases in this study profile (incomplete or not found files; lack of data on the course of the disease after the patients have been discharged). This hospital based study included patients with severe GBS, explaining the low number of patients included. Electromyogram was performed in few patients who did not allow us to specify the electrophysiological forms of GBS.
Guillain-Barré Syndrome was infrequent in Burkina Faso. Steroids were the main treatment with high mortality. It is necessary to develop medico-technical skills.
What is known about this topic
- Guillain-Barré Syndrome (GBS) is an acute inflammatory disorder of peripheral nerves with respiratory insufficiency, severe autonomic dysfunction, severe swallowing dysfunction and rapidly progressive weakness;
- Intravenous immunoglobulin and plasma exchange are proven and equally effective treatments for GBS.
What this study adds
- Our study addresses all aspects of the management of Guillain-Barré Syndrome, namely the epidemiological, diagnostic, therapeutic and outcome aspects;
- Our study gives 17 years of experience in an African hospital in the management of Guillain-Barré Syndrome;
- Our study could enrich African literature because the data are scarce and often old.
The authors declare no competing interests.
AAD, AD, RK, MMK and JMAK had contributed to the data collection or processing, analysis or interpretation, literature research and writing. CN, KK and JK had contributed to concept and design of the study All the authors read and approved the final manuscript.
I want to thank Mrs Zongo L Carine Patricia for translation.
Table 1: distribution of patients with GBS by age group at admission
Table 2: clinical manifestations of GBS at the time of presentation
- Van den Berg B, Walgaard C, Drenthen J, Fokke C, Jacobs BC, Pieter A van Doorn. Guillain-Barré Syndrome: pathogenis, diagnostics, treatment and prognosis. Nat Rev Neurol. 2014 Aug;10(8):469-82. PubMed | Google Scholar
- Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barré Syndrome. Lancet. 2016 Aug 13;388(10045):717-27. PubMed | Google Scholar
- Zhahirul Islam, Nowshin Papri, Gulshan Ara, Tanveen Ishaque, Arafat Alam U, Israt Jahan et al. Risk factors for respiratory failure in Guillain-Barré Syndrome in Bangladesh: a prospective study. Ann Clin. Transl Neurol. 2019 Jan 7;6(2):324-332. PubMed | Google Scholar
- Van Doorn PA, Ruts L, Jacobs BC. Clinical features, pathogenesis, and treatment of Guillain-Barré Syndrome. Lancet Neurol. 2008 Oct;7(10):939-50. PubMed | Google Scholar
- Millogo A, Sawadogo A, Lankoandé D, Sawadogo AB. Guillain-Barré Syndrome in HIV-infected patients at Bobo-Dioulasso Hospital. Rev Neurol. 2004; 160 (5pt 1): 559-62. PubMed | Google Scholar
- Asbury AK, Cornblath DR. Assessment of current diagnostic criteria for Guillain-Barré Syndrome. Ann Neurol. 1990;27 Suppl:S21-4. Google Scholar
- Basse AM, Boubacar S, Sow AD, Diagne NS, Diop MS, Gaye NM et al. Epidemiology of acute polyradiculoneuritis at Fann Department of Neurology Dakar, Senegal. Clin Neurol and Neurosci. 2017; 1 (4): 76-9. Google Scholar
- Joshua S, Margaret MM, Banda-Chalwe M, Nkhata LA, Kafumukache E, Simpamba M et al. The Prevalence of Guillian-Barré syndrome and the rate of physiotherapy referral at the University Teaching Hospital, Lusaka, Zambia. International Journal of Neurologic Physical Therapy. 2015;2(1):1-4. Google Scholar
- Howlett WP, Vedeler CA, Nyland H, Aarli. Guillain-Barré Syndrome in Northern Tanzania, a comparison of epidemiologic and clinical findings with Western Norway. Acta Neurol Scand. 1996;93(1):44-9. PubMed | Google Scholar
- Liu S, Dong C, Ubogu EE. Immunotherapy of Guillain-Barré Syndrome. Hum Vaccin Immunother. 2018;14(11):2568-2579. PubMed | Google Scholar
- Jiang GX, de Pedro-Cuesta J, StrigĂ„rd K, Olsson T, Link H. Pregnancy and Guillain-Barré Syndrome: a nationwide register cohort study. Neuroepidemiology. 1996;15(4):192-200. PubMed | Google Scholar
- Yuki N, Hartung H. Guillain-Barré Syndrome. N Engl J Med. 2012 Jun 14;366(24):22940-304. PubMed
- Jasti AK, Selmi C, Sarmiento-Monroy JC, Vega DA, Anaya JM, Gershwin ME. Guillain-Barré Syndrome: causes; immunopathogenic mechanisms and treatment. Expert Review of clin Immunol. 2016 Nov;12(11):1175-1189. PubMed | Google Scholar
- Thornton CA, Latif AS, Emmanuel, JC. Guillain-Barré Syndrome associated with human immunodeficiency virus infection in Zimbabwe. Neurology. 1991 Jun;41(6):812-5. PubMed | Google Scholar
- Yimam KK, Merriman RB, Frederick RT. A Rare Case of Acute Hepatitis B Virus Infection Causing Guillain-Barré Syndrome. Gastroenterology & Hepatology. 2013;9(2):121-3. PubMed | Google Scholar
- Ray G, Ghosh B, Bhattacharyya R. Acute hepatitis B presenting as Guillain-Barré Syndrome. Indian J Gastroenterol. Nov-Dec 2003;22(6):228. PubMed | Google Scholar
- Shahar E. Current therapeutic options in severe Guillain-Barré Syndrome. Clin Neuropharmacol. Jan-Feb 2006;29(1):45-51. PubMed | Google Scholar
- Alshekhlee A, Hussain Z, Sultan B, Katirji B. Guillain-Barré Syndrome: incidence and mortality rates in US hospitals. Neurology. 2008 Apr 29;70(18):1608-13. PubMed | Google Scholar
- Orlikowski D, Prigent H, Sharshar T, Lofaso F, Raphael JC. Respiratory dysfunction in Guillain-Barré Syndrome. Neurocrit Care. 2004;1(4):415-22. PubMed | Google Scholar
- Hughes RAC, Wijdicks EFM, Benson E, Cornblath DR, Hahn AF, Meythaler JM et al. Supportive care for patients with Guillain-Barré Syndrome. Arch Neurol. 2005 Aug;62(8):1194-8. PubMed | Google Scholar