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Research Article | Volume 11 Issue 12 (December, 2025) | Pages 461 - 463
Role of Prolonged High-Dose Neostigmine in Residual Neuro-paralysis Following Common Krait Bite: A Case Report
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1
Assistant Professor, Anaesthesia, Adesh medical college and Hospital, Mohri, Shahbad, kurukshetra, Haryana,
2
Senior Resident, DM Nephrology Christian medical College and hospital Ludhiana
3
Assistant Professor, Anaesthesia , Adesh medical college and Hospital, Mohri, Shahbad, kurukshetra, Haryana
4
Assistant Professor, Anaesthesia, Adesh medical college and Hospital, Mohri, Shahbad, kurukshetra, Haryana
5
DNB Anaesthesia, (Post diploma) resident, Sir Gangaram hospital, New Delhi
6
PG Resident, Anaesthesia, Adesh medical college and hospital, Mohri, Shahbad, kurukshetra, Haryana
7
Senior Resident, Anaesthesia, Mahavir sansthan cancer hospital, patna
8
PG Resident, Anaesthesia, Adesh medical college and Hospital, Mohri, Shahbad, kurukshetra, Haryana.
Under a Creative Commons license
Open Access
Received
Nov. 10, 2025
Revised
Nov. 27, 2025
Accepted
Dec. 5, 2025
Published
Dec. 24, 2025
Abstract
Background: Snakebite envenomation remains a major public health problem in India, with the common krait (Bungarus caeruleus) causing severe neuroparalysis through presynaptic β-bungarotoxin–mediated blockade. While antivenom neutralizes circulating venom, it does not reverse established presynaptic damage, making recovery prolonged. Although neostigmine is traditionally viewed as ineffective for purely presynaptic toxicity, emerging evidence shows benefit in selected patients, particularly when a neostigmine test is positive. We report a middle-aged male who presented seven days after a krait bite with persistent paralysis despite receiving adequate antivenom and ventilatory support. On admission, he had ptosis, quadriparesis (2/5 power), and areflexia, but no respiratory compromise. A positive neostigmine sensitivity test prompted initiation of high-dose neostigmine with atropine cover, resulting in steady neurological improvement over one week, including recovery of limb power from 2/5 to 4/5, resolution of ptosis, and return of reflexes. He was discharged with near-complete recovery and achieved full strength at 10-day follow-up. This case demonstrates that neostigmine can significantly enhance neuromuscular recovery in selected krait envenomation patients—even in delayed presentations—and that a positive neostigmine test is a valuable predictor of therapeutic responsiveness
Keywords
INTRODUCTION
Snakebite continues to be a major public health problem in India, with the common krait (Bungarus caeruleus) responsible for severe neurotoxic envenomation. Its venom contains presynaptic β-bungarotoxin, which inhibits acetylcholine release and can produce profound neuromuscular paralysis lasting days to weeks. While antivenom neutralizes circulating venom, it does not reverse established presynaptic blockade. Traditionally, neostigmine is considered less effective for pure presynaptic toxicity; however, emerging evidence suggests benefit in some patients, especially when the neostigmine test is positive, indicating a partially reversible postsynaptic component. This case highlights a patient who presented one week after a krait bite, already treated with ASV and mechanical ventilation elsewhere, and who continued to exhibit partial ptosis and severe quadriparesis. The patient demonstrated dramatic recovery with prolonged high-dose neostigmine therapy, emphasizing its potential role even in delayed residual paralysis. CASE REPORT A middle-aged male farmer presented to our tertiary-care hospital seven days after a snake bite. The bite occurred at night while the patient was sleeping on the floor. He experienced a sharp pricking sensation on his left lower limb, after which two fang marks were noticed. There was no local pain, swelling, or redness, consistent with common krait envenomation. Within hours, he developed bilateral ptosis, progressive weakness of all four limbs, and respiratory difficulty. At the local hospital, he received polyvalent anti-snake venom (ASV) and subsequently required intubation and mechanical ventilation for five days. A repeat dose of ASV was administered at the hospital. After partial improvement in respiratory function, he was extubated but continued to have profound generalized weakness, prompting referral to our centre. Condition on Arrival • Conscious, oriented, vitally stable • Partial bilateral ptosis • Quadriparesis (2/5 muscle power in all four limbs) • Deep tendon reflexes: absent • Plantars: mute • Sensory exam: normal • Fang marks on left leg with no local reaction • No respiratory distress Routine investigations including hemogram, electrolytes, LFT, RFT, and WBC were normal. MANAGEMENT Since the patient had already received adequate ASV at the peripheral centre, no further ASV was administered. Neostigmine Sensitivity Test A neostigmine test was performed with atropine 0.6 mg IV premedication. Within minutes, the patient showed improvement in neck flexor strength and limb movement, indicating a positive test, suggesting partial responsiveness to anticholinesterase therapy. Day-wise Treatment and Neuromuscular Improvement in ICU Table 1: Progress Chart of Limb Power Response Day Treatment Upper Limb Power (UL) Lower Limb Power (LL) Day 0 Inj. Neostigmine + Glycopyrrolate 1.5 mg q12hrly started 2/5 2/5 Day 2 Inj. Neostigmine + Glycopyrrolate 1.5 mg q12hrly 4/5 2/5 Day 3 Inj. Neostigmine + Glycopyrrolate 1.5 mg q12hrly 4/5 3/5 Day 4 Inj. Neostigmine + Glycopyrrolate 2.5 ml q12hrly 4/5 4/5 Day 5 Neostigmine + Glycopyrrolate stopped; Tab. Neostigmine 15 mg q12hrly started 4/5 4/5 Day 6 Tab. Neostigmine 15 mg q12hrly Tab. Glycopyrrolate 1 mg q24hrly added 4/5 4/5 Day 7 (Discharge) Tab. Neostigmine 15 mg q12hrly Tab. Glycopyrrolate 1 mg q24hrly 4/5 (maintained) 4/5 (maintained) Clinical Progress • Progressive improvement in neuromuscular function • Limb power improved from 2/5 → 3/5 → 4/5 → maintained 4/5 • Ptosis gradually resolved • Deep tendon reflexes reappeared • No cholinergic side effects due to adequate atropine cover The patient was able to walk independently and was discharged with near-complete neurological recovery. Pt was managed with multidisciplinary approach and was advised for follow up in medicine OPD. On follow up, Patient presented to OPD after 10 days with power 5/5 in all 4 limbs
DISCUSSION
Common krait venom contains potent presynaptic neurotoxins causing structural damage to nerve terminals. Recovery requires regeneration, which may take days to weeks. Therefore, even after ASV neutralizes circulating venom, patients can continue to exhibit severe paralysis. Although neostigmine is classically considered ineffective for purely presynaptic toxicity, responsiveness in some cases can be explained by: 1. Mixed pre- and postsynaptic involvement allowing partial reversibility 2. Residual partially functional presynaptic terminals that respond to increased acetylcholine availability 3. Positive neostigmine test, which is a reliable predictor of response regardless of delay in presentation This patient, despite presenting 7 days after the bite, showed significant improvement with high-dose neostigmine, emphasizing its role in selected cases.
CONCLUSION
Prolonged high-dose neostigmine can be highly effective in selected krait envenomation patients, even in late presentations. A positive neostigmine test should guide therapy. With proper monitoring, neostigmine is safe and can significantly accelerate neuromuscular recovery.
REFERENCES
1. Gupta S, Smilie R, et al. Unusually prolonged neuromuscular weakness caused by krait (Bungarus caeruleus) bite: Two case reports. Toxicon. 2021;193:1–5. 2. Ranawaka UK, Lalloo DG, de Silva HJ. Neurotoxicity in snakebite — the limits of our knowledge. PLoS Negl Trop Dis. 2013;7(10):e2302. 3. Irshad VS, Godhiwala P, Kumar S, et al. Role of neostigmine in neurotoxic snake bite. J Evolution Med Dent Sci. 2021;10(15):1095–1097. 4. Silva A, Johnstone B, et al. Neuromuscular Weakness and Paralysis Produced by Snakebite Envenoming: Mechanisms and Proposed Standards. Toxins (Basel). 2023;15(1):49. 5. Kularatne SA. Neostigmine in the treatment of snakebite. Lancet. 2002;360:883–884. 6. Anil A, Singh S, Bhalla A, et al. Role of neostigmine and polyvalent antivenom in Indian common krait (Bungarus caeruleus) bite. J Infect Public Health. 2010;3(2):83–87.
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