|Year : 2018 | Volume
| Issue : 2 | Page : 61-64
Neurotoxicity following snakebite and the challenges of management in an urban area—a case report
Hamza Muhammad1, Sadiq Halilu2, Muzammil M Yakasai2, Ibrahim M Nashabaru1, Abdulrazaq G Habib1
1 Department of Medicine, CHS, Bayero University Kano; Department of Medicine, Aminu Kano Teaching Hospital, Kano, Nigeria
2 Department of Medicine, Aminu Kano Teaching Hospital, Kano, Nigeria
|Date of Web Publication||1-Nov-2018|
Department of Medicine, Bayero University, Kano/Aminu Kano Teaching Hospital, Kano
Snakebites disproportionately affect the lower socioeconomic segments of the society, people with poorly constructed houses, and those with limited access to education and health care. Cases of snakebite are rare in urban areas. Therefore, health centers located in urban areas are sometimes unprepared for managing cases of snakebite. Potent snake antivenoms are not available, and most healthcare workers lack basic training needed for the management of snakebite. Here, we report a case of 28-year-old cleric who was rushed to the accident and emergency unit of an urban tertiary hospital on account of snakebite injury involving the left forearm. At presentation, there was history of persistent vomiting and hypersalivation. However, there was no history of bleeding from the site of bite, hematemesis, hematuria, or bleeding from any orifice. He later became confused with altered level of consciousness, developed bilateral ptosis, and broken neck sign. The patient survived after receiving intravenous polyvalent snake antivenom (EchiTab-plus; Instituto Clodomiro Picado, Costa Rica), which was incidentally purchased for laboratory experiment and not for patient care. The case highlights the challenges frequently encountered in the management of snakebite victims, especially in nonendemic areas; it also stresses the need for urban health centers to stock snake antivenom in their pharmacy and train healthcare workers in the management and care of snakebite victims.
Keywords: Challenges, management, neurotoxicity, snakebite
|How to cite this article:|
Muhammad H, Halilu S, Yakasai MM, Nashabaru IM, Habib AG. Neurotoxicity following snakebite and the challenges of management in an urban area—a case report. Sub-Saharan Afr J Med 2018;5:61-4
|How to cite this URL:|
Muhammad H, Halilu S, Yakasai MM, Nashabaru IM, Habib AG. Neurotoxicity following snakebite and the challenges of management in an urban area—a case report. Sub-Saharan Afr J Med [serial online] 2018 [cited 2018 Nov 19];5:61-4. Available from: http://www.ssajm.org/text.asp?2018/5/2/61/243939
| Introduction|| |
Snakebite envenoming (SBE) is a major underappreciated medical and public health problem causing significant mortality and morbidity among rural dwellers throughout the tropics. Despite urbanization and destruction of their natural habitat, venomous snakes remain a constant component of the ecosystem in most parts of Africa. No country is free from the risk of snakebite, and in some rural areas, such as the Benue Valley of Northern Nigeria, snakebite is a leading cause of morbidity and mortality among farmers, pastoralists, hunters, and children. However, as cases of snakebite are rare in urban areas, health centers located in urban areas are sometimes unprepared for managing cases of snakebite. Potent antivenoms are not available, and most healthcare workers lack basic training to handle cases of snakebite.
Cobras are not only found around and inside houses and near water bodies, but also in rain forest and desert areas. Moreover, they can be found near human dwellings even in urban areas. The venoms of cobras and most other elapid species contain neurotoxins that induce a descending flaccid neuromuscular paralysis, which can include life-threatening blockade of bulbar and respiratory muscles. Two main types of neurotoxins are found in snake venoms: α-neurotoxins and β-neurotoxins. α-Neurotoxins belong to the threefinger toxin family and exert their action postsynaptically at neuromuscular junctions. They bind with high affinity to the cholinergic receptors at the motor end plate, thereby inhibiting the binding of acetylcholine and provoking flaccid paralysis. In contrast, β-neurotoxins are typically phospholipase A2 (PLA2s) that act at the presynaptic nerve terminal of neuromuscular junctions. Upon binding to their targets, neurotoxic PLA2s induce enzymatic hydrolysis of phospholipids at the nerve terminal plasma membrane, which causes neurotoxicity.
Neurotoxic envenomation tends to occur following bites by black and green mambas, neurotoxic nonspitting cobras (Naja haje, N. annulifera, N. anchietae, N. melanoleuca, and N. nivea) and berg adder. Bites by neurotoxic snakes cause some local swelling, but tissue necrosis does not occur. Classical neurotoxic symptoms appear as early as 30 min after the bite and can evolve into fatal respiratory paralysis within 2 to 16 h of the bite.,, Transient paresthesia of the tongue and lips, impairment of taste and smell sensation, heaviness of the eyelids, excessive salivation or a dry mouth, nausea, and vomiting may occur. These are followed by progressive, descending paralysis: bilateral ptosis, pupillary abnormalities, external and internal ophthalmoplegia, paralysis of the facial muscles, jaw, tongue, neck flexors (causing the “broken neck” sign) and other muscles innervated by the cranial nerves. Other symptoms include pooling of secretions in the pharynx, dysphonia, loss of gag reflex, declining ventilatory capacity, paradoxical abdominal respiration, use of accessory muscles of respiration and cyanosis, all of which are signs of impending bulbar and respiratory paralysis. The victim is unable to open the mouth, clench the jaws, protrude the tongue, swallow or protect the airway from secretions, unable to speak or extend the neck, and eventually cannot breathe. Respiratory distress increases, the patient becomes anxious, sweaty, and cyanosed, and will die unless ventilated artificially.
Antivenom is efficacious in decreasing the likelihood of dying and is the main treatment for SBE.,, But poor access, poor quality, and delay in administration following envenoming often results in loss of lives or debilitating complications. The few effective antivenoms in sub-Saharan Africa are scarce, locally unaffordable, and inaccessible where they are most needed. For these reasons, antivenom utilization has drastically declined to a very small fraction of indicated need., Antivenom administration can reverse postsynaptic neurotoxicity, and if given early, prevent or limit presynaptic neurotoxicity. Management of neurotoxic envenoming requires polyspecific antivenom; trial of anticholinesterase therapy; monitoring of respiratory function, intubation, and assisted ventilation when necessary.
| Case report|| |
Here, we report a case of 28-year-old cleric who was rushed to the accident and emergency unit of an urban tertiary hospital on account of snakebite injury involving the left forearm of about 10-h duration. This was reported to have occurred in the evening while the man was in his generator room trying to put on the electric generator. He subsequently developed pain at the site of the bite with swelling of the forearm. There was history of persistent vomiting and hypersalivation. However, there was no history of bleeding from the site of bite, no hematemesis, hematuria, or bleeding from any orifice. He later became confused with altered level of consciousness. No history of seizure or headache, and no trauma head was noticed. He had associated history of breathlessness, but there no sign of cough, palpitation, and orthopnea or paroxysmal nocturnal dyspnea. Review of the other systems was not contributory. He had no history of hypertension or diabetes in addition to alcohol ingestion or cigarette smoking. He was married and had children.
On examination, we found no evidence of pallor, cyanosis, jaundice, dehydration, or edema. He had normal cardiovascular functions. He was suffering with confusion and had a Glasgow Coma Score of 11/15. He was unable to hold his neck upright and had bilateral ptosis. Pupils were measured as 3 mm, equal and reactive to light. Hypotonia was diagnosed in all the limbs, and strength was difficult to ascertain due to the impaired level of consciousness. Chest and abdominal examination findings were normal. Twenty-minute whole blood clotting test was normal.
An assessment of snakebite with neurotoxicity was made. Serum electrolytes, urea, and creatinine were essentially normal. His packed cell volume was 36%. He received 20 ml (two vials) of intravenous polyvalent snake antivenom (EchiTab-plus). He was transferred to the intensive care unit (ICU) for close monitoring, though he was not intubated. His symptoms and signs, including ptosis, improved, and the patient regained consciousness. He was discharged on the 5th day of admission.
| Discussion|| |
Snakebite is uncommon in urban areas; however, cobra can be found near human dwellings in urban areas. Most of the time snakes hide behind logs of wood or farm produce and are transported unknowingly to urban areas. The fact that cobras are known to breed near human dwelling means incidences of snakebite envenomation can occur in urban areas as reported in the index case. The victim presented with typical features of neurotoxicity, that is, ptosis, confusion, and inability to control the neck (broken neck sign) [Figure 1].
The snake responsible for the bite in the index case was brought to the hospital alive by a snake charmer, and close examination of the snake showed features closely similar to Naja senegalensis as shown in [Figure 2] and [Figure 3]. These snakes are found in the savannah region of Africa, belong to the class of elapids/nonspitting cobras, and are known to cause neurotoxic envenomation.
The victim in the index case received two vials (20 ml) of snake antivenom (EchiTab-plus: a polyvalent snake antivenom developed for managing envenomation caused by three most common Nigerian snakes: Echis ocellatus, Bitis arietans, and Naja spp.). Symptoms and signs of neurotoxicity resolved completely within 48 h.
The snake antivenom was out of stock when patient was presented in the tertiary health center. The managing team was however able to get two vials of snake antivenom (EchiTab-plus) that were primarily bought for laboratory experiment. Scarcity of potent and effective snake antivenom has been reported. Antivenom is the main intervention against snakebite envenomation, but is relatively scarce, unaffordable, and the situation has been compounded further by the recent cessation of production of effective antivenoms and marketing of inappropriate products.,This case highlights the need for healthcare facilities in urban areas to ensure availability of snake antivenom in their pharmacy. Snake antivenom minimizes the risk of death following neurotoxic envenomation. The victim was admitted to ICU, though he had no intubation/artificial respiration.
| Conclusion|| |
The case highlights the challenges frequently encountered in the management of snakebite especially in nonendemic areas. There is need for urban health centers to stock snake antivenom in their pharmacy and also ensure adequate training of healthcare workers in the management and care of snakebite victims. The patient survived after receiving intravenous polyvalent snake antivenom that was purchased with the sole aim of laboratory work.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Habib AG, Kuznik A, Hamza M, Abdullahi MI, Chedi BA, Chippaux JP et al.
Snakebite is under appreciated: Appraisal of burden from West Africa. PLoS Negl Trop Dis 2015;9:e0004088. doi: 10.1371/journal.pntd.0004088.eCollection2015
WHO. World Health Organization guidelines for the prevention and clinical management of snakebite in Africa. Brazzaville: WHO: Regional office for Africa; 2010.
Barber CM, Isbister GK, Hodgson WC. Alpha neurotoxins. Toxicon 2013;66:47-58.
Rossetto O, Montecucco C. Presynaptic neurotoxins with enzymatic activities. Handb Exp Pharmacol 2008;184:129-70.
Paoli M. Mass spectrometry analysis of the phospholipase A2 activity of snake pre-synaptic neurotoxins in cultured neurons. J Neurochem 2009;111:737-44.
Strover HM. Snakebite and its treatment. Cent Afr J Med 1961;7:84-7.
Warrell DA, Barnes HJ, Piburn MF. Neurotoxic effects of bites by the Egyptian cobra (Naja haje
) in Nigeria. Trans R Soc Trop Med Hyg 1976;70:78-9.
Blaylock RS, Lichtman AR, Potgieter PD. Clinical manifestations of Cape cobra (Naja nivea
) bites. A report of 2 cases. S Afr Med J 1985;68:342-4.
Gutiérrez JM, Calvete JJ, Habib AG, Harrison RA, Williams DJ, Warrell DA. Snakebite envenoming. Nat Rev Dis Primers 2017;3:17063.
Meyer WP, Habib AG, Onayade AA. First clinical experience with a new ovine Fab Echis ocellatus
snake bites antivenom in Nigeria. Randomized comparative trial with institute Pasteur Serum (IPSer) Africa antivenom. Am J Trop Med Hyg 1997;56:291-300.
Habib AG, Warrell DA. Antivenom therapy of carpet viper (Echis ocellatus) envenoming: Effectiveness and strategies for delivery in West Africa. Toxicon 2013;69:82-9. doi: 10.1016/j.toxicon.2013.01.002, PMID: 23339853.
Abubakar IS, Abubakar SB, Habib AG, Nasidi A, Durfa N, Yusuf PO et al.
, Nigeria-UK EchiTab Study Group. Randomised controlled double-blind non-inferiority trial of two antivenoms for saw-scaled or carpet viper (Echis ocellatus
) envenoming in Nigeria. PLoS Negl Trop Dis 2010;4:e767. doi: 10.1371/journal.pntd.0000767, PMID: 20668549.
Hamza M, Idris MA, Maiyaki MB, Lamorde M, Chippaux JP, Warrell DA et al.
Cost-effectiveness of antivenoms for snakebite envenoming in 16 countries in West Africa. PLoS Negl Trop Dis 2016;10:e0004568. doi: 10.1371/journal.pntd.0004568
Warrell DA. In: Campbell JR, Lamar WW, editors. Venomous reptiles of the Western Hemisphere. Ithaca, New York City, USA: Cornell University Press; 2004. pp. 709-61.
[Figure 1], [Figure 2], [Figure 3]