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Year : 2019  |  Volume : 8  |  Issue : 1  |  Page : 302-304  

A rare case of quadriparesis

1 Department of Neurology, Vivekananda Polyclinic and Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
2 Department of Radiodiagnosis, Vivekananda Polyclinic and Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication31-Jan-2019

Correspondence Address:
Swati Sharma
A-4 Laurie Road, P.O. New Forest, Forest Research Institute, Dehradun, Uttarakhand - 248 006
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jfmpc.jfmpc_293_17

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Snakebite is a public health problem. Common krait is nocturnally active with painless bite. Patients exhibit neuromuscular weakness.

Keywords: Neurology, neuromuscular, neurotoxicology, venoms

How to cite this article:
Pandey AK, Sharma S, Upadhyay V. A rare case of quadriparesis. J Family Med Prim Care 2019;8:302-4

How to cite this URL:
Pandey AK, Sharma S, Upadhyay V. A rare case of quadriparesis. J Family Med Prim Care [serial online] 2019 [cited 2021 Sep 17];8:302-4. Available from: https://www.jfmpc.com/text.asp?2019/8/1/302/251165

  Background Top

Snakebite is an occupational hazard causing considerable morbidity and mortality worldwide, particularly in tropical countries such as India. An estimated 50,000 Indians die due to venomous snakebite yearly, 70% of whom are males between the ages of 20 and 50 years.[1] They are hematotoxic, neurotoxic, and myotoxic. Over 2000 species of snakes are known worldwide, of which around 400 are poisonous. These snakes belong to the families Elapidae, Viperidae, Hydrophiidae, and Colubridae. Indian cobra (Naja naja) and Common Indian krait (Bungarus caeruleus) are the two important species of elapid snakes found in India and are responsible for most of the cases of neurotoxic snakebite.[2] Kraits of Southeast Asia are elapid snakes represented by 12 species. Common krait is nocturnally active and its bite is painless. Patients exhibit ptosis, exophthalmoplegia, dysphagia, dyspnea, and neuromuscular weakness.[3]

  Case Presentation Top

A 30-year-old married female presented with sudden onset upper abdominal pain and vomiting 7 h back followed by inability to speak, dysphagia, dyspnea, choking, drooping of eyelids, and weakness of all four limbs within half an hour. On further enquiry, attendants told that patient had gone for a festival celebration and dinner in the night in village and after half an hour of returning back, the problem occurred but other people who ate the dinner had no complaints. She had two children with history of eclampsia in last child birth.

She was unconscious with pulse 64/min, blood pressure 100/60 mmHg, and oxygen saturation 50% which was decreasing and was intubated. On further examination, bilateral ptosis with complete ophthalmoplegia on oculocephalic reflex testing, quadriparesis with power 0/5 in all muscle groups was present, plantar reflex and deep tendon reflexes were absent. Chest, cardiac, and abdominal examinations were normal. Blood and urine investigations were normal. Chest X-ray, MRI brain [Figure 1], and spine [Figure 2] were normal. Neostigmine test was negative. Tests for porphyrias were negative. High degree of suspicion of snakebite was considered but attendants gave no history and no bite mark was found at first but later, a mark on right ear [Figure 3] was seen and attendants told that it was not present before. Patient was given polyvalent antivenom urgently and after 2 days, she was conscious, ptosis decreased, muscle power increased to 1-2/5. After 4 days, patient was successfully extubated. She was whispering earlier, slowly speech became normal. After 12 days, she could walk with support, ptosis disappeared, and was discharged.
Figure 1: Axial T2-weighted MR image of the brain showing the normal parenchymal signal intensity

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Figure 2: Sagittal T2 weighted MR image of the cervico-dorsal spine showing normal contour and signal intensity of the spinal cord

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Figure 3: Mark of snake bite on ear

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  Discussion Top

Unexplained unresponsiveness in a previously healthy person in areas where snakebites are common should create the suspicion of possibility of snakebite even in the absence of history of snakebite or definite fang mark on clinical examination. Polyvalent antisnake venom (ASV) is relatively safe, and allergic reactions after ASV injection can be prevented by premedication with adrenaline, intravenous hydrocortisone, and histamines. Therefore, suspected snake envenomation should be treated empirically with intravenous polyvalent ASV, and simultaneously should be investigated for differential diagnosis and etiology of unresponsiveness.[4] Abdominal pain is the initial symptom of krait bite and may mimic surgical abdomen. Patient may also present with vomiting and at times diarrhea. Our patient had recurrent vomiting along with pain abdomen mimicking botulinum poisoning. This is followed by drooping of eyelids, double vision, weakness of limbs, and breathing difficulty progressing to neuromuscular paralysis. In an unknown scenario, patient gets up at night, with colicky abdominal pain and may be misdiagnosed as acute abdomen. Kraits may have painless bites and negligible local swelling.[5]

Other differential diagnoses were human botulism, Guillain-Barre syndrome (GBS), myasthenia gravis, periodic paralyses, and porphyria. Human botulism is a rare, serious, potentially fatal disease. It is an intoxication caused by ingestion of potent neurotoxins in contaminated foods. Early symptoms are marked fatigue, weakness, and vertigo, usually followed by blurred vision, ophthalmoplegia, dry mouth, and dysphagia and speaking. Vomiting, diarrhea, constipation, and abdominal swelling may also occur. It can progress to weakness in neck and arms, after which respiratory muscles and muscles of lower body are affected. The paralysis may make breathing difficult. There is no fever and unconsciousness.[6] The progression to complete quadriparesis and respiratory paralysis is not that fast (within hours) as happened in our case. People with GBS usually experience their most significant weakness within 2–4 weeks after symptoms begin. Recovery usually begins 2–4 weeks after weakness plateaus. Guillain-Barre syndrome (GBS) often begins with tingling and weakness starting in feet and legs and spreading to upper body parts including arms. A core clinical feature of all GBS subtypes is the characteristic disease time course. In 90% patients, this is monophasic, although up to 10% develop recurrent or relapsing GBS. The time interval between onset of neurological symptoms and nadir ranges between 12 h and 28 days and is usually followed by subsequent clinical plateau or improvement.[7] Myasthenia gravis patients progress from mild to severe disease over weeks to months. Weakness tends to spread from ocular to facial to bulbar muscles and then to truncal and limb muscles. On the other hand, symptoms may remain limited to extraocular and eyelid muscles for years. Rarely, patients with severe generalized weakness may not have associated ocular muscle weakness.[8] Periodic paralyses is characterized by episodes of flaccid muscle weakness occurring at irregular intervals. Most of the conditions are hereditary and more episodic than periodic.[9] It usually recovers very fast and ophthalmoplegia and respiratory paralysis is rare. Major manifestations of acute hepatic porphyrias are neurologic including neuropathic abdominal pain, peripheral motor neuropathy, ophthalmoplegia, and mental disturbances, with attacks often precipitated by dieting, certain drugs, and hormonal changes. Acute porphyria should be suspected in patients with neuro-visceral symptoms after puberty, such as abdominal pain, and when the initial clinical evaluation does not suggest another cause.[10]

  Conclusion Top

There should be high suspicion of snake (krait) bite in cases of sudden onset quadriparesis and respiratory failure even if the local signs of painless bite are absent. Patient's life can be saved if the possibility is timely considered and appropriate management started accordingly.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Menon JC, Joseph JK, Whitaker RE. Venomous snake bite in India - Why do 50,000 Indians die every year? J Assoc Physicians India 2017;65:78-81.  Back to cited text no. 1
Pandey PC, Bajaj S, Srivastava A. A Clinico-epidemiological profile of neuroparalytic snake bite: Using low dose ASV in a tertiary care centre from North India. J Assoc Physicians India 2016;64:16-20.  Back to cited text no. 2
Prasarnpun S, Walsh J, Awad SS, Harris JB. Envenoming bites by kraits: The biological basis of treatment-resistant neuromuscular paralysis. Brain 2005;128:2987-96.  Back to cited text no. 3
Prakash S, Mathew C, Bhagat S. Locked-in syndrome in snakebite. J Assoc Physicians India 2008;56:121-2.  Back to cited text no. 4
Aftab Alam HM, Hussain Zaidi SB. Envenomation in pregnancy by common krait (Bungarus caeruleus). J Coll Physicians Surg Pak 2014;24(Special Supplement 2):S144-6.  Back to cited text no. 5
Available from: www.who.int/mediacentre/factsheets/fs270/en/. [Last accessed on 2017 Sep 05].  Back to cited text no. 6
Available from: www.mayoclinic.org/diseases-conditions/guillain-barresyndrome/basics/symptoms. [Last accessed on 2017 Sep 06].  Back to cited text no. 7
Engel AG. Acquired autoimmune myasthenia gravis. In: Engel AG, Franzini-Armstrong C, editors. Myology: Basic and Clinical. 2nd ed; 1994. p. 1769-97.  Back to cited text no. 8
Available from: http://emedicine.medscape.com/article /1171678-overview#a4. Periodic Paralyses. [Last accessed on 2017 Sep 10].  Back to cited text no. 9
Desnick RJ, Balwani M. The Porphyrias. Harrison's Principles of Internal Medicine. 19th ed. 2015. p. 2521.  Back to cited text no. 10


  [Figure 1], [Figure 2], [Figure 3]


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