CASE REPORT ON SNAKE BITE INDUCED NEPHROTOXICITY

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www.wjpps.com Vol 9, Issue 3, 2020. 1530 Anilet al. World Journal of Pharmacy and Pharmaceutical Sciences

CASE REPORT ON SNAKE BITE INDUCED NEPHROTOXICITY

Anina Anil^1*, Sawmya Sabu² and Dr. Jyothi Susan George³

1,26^th Year Pharm D Students, Nazareth College of Pharmacy, Othera, Thiruvalla.

3Clinical Pharmacist, Nephrology Department, Believers Chruch Medical College Hospital, Thiruvalla.

ABSTRACT

Acute kidney injury (AKI) is an important complication and major cause of mortality in patients with snake bites. Here we are discussing about an adult male patient who presented with a history of snake bite and developed acute kidney injury following the envenomation.

KEYWORDS: Snake bite, acute kidney injury, disseminated intravascular coagulation, glomerulonephritis.

INTRODUCTION

Snake bites are common and frequently devastating environmental and occupational hazard, especially in rural areas of tropical developing countries. Acute kidney injury (AKI) is an important complication and major cause of mortality in patients with snake bites. Although bites from all the venomous snakes are known to cause AKI, a substantial proportion of these cases results from viper bites.

In 2009, snakebite was recognized for the first time by the World Health Organization (WHO) as a neglected tropical disease and considered more attention.^[1] Accurate estimates of snake bite–related global morbidity and mortality are not available. As per a recent annual estimate, approximately 81,000 to 138,000 deaths occur from approximately 1.8 million to 2.7 million snake envenomings throughout the world.^[2] There are about 3500 known species of snakes in the world, of which less than 350 species are venomous.^[3] These types of snakes have front fangs that make them capable of injecting venom during the bite. These venomous snakes belong to four families: elapidae, viperidae, hydrophiidae, and colubridae.^[4]

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Volume 9, Issue 3, 1530-1535 Case Study ISSN 2278 – 4357

*Corresponding Author Anina Anil

6^th Year Pharm D Students, Nazareth College of Pharmacy, Othera, Thiruvalla.

Article Received on 14 Jan. 2020,

Revised on 03 Feb. 2020, Accepted on 23 Feb. 2020 DOI: 10.20959/wjpps20203-15761

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Elapids are land snakes, the venom of which contains a high concentration of neurotoxins.

The elapids, encountered in Africa and Asia include cobras, kraits, mambas, and coral snakes.

Renal involvement is uncommon in victims of bites from members of this family.^[3,4]

Vipers include the Russell's viper, Echis carinatus (sawscaled viper), puff adder, pit vipers, and rattlesnakes. The vipers are the most widely distributed species and are labelled the most dangerous snake in the world. The factors contributing to its deadliness are its widespread distribution, abundance in farming areas, diurnal habits, good camouflage, and its highly toxic venom. Renal lesions are seen in this condition.

Hydrophid or sea snake bites are primarily myotoxic.

Colubrids are usually harmless to humans but are occasionally known to cause serious and fatal poisoning.^[3,4]

CASE PRESENTATION

A 70 year old male patient presented to the emergency department with complaints of snake bite (viper) over the right hand over the fourth ring finger. Patient came to the hospital after one day of the bite. He was a known case of systemic hypertension and osteoarthritis. After the incident, he developed multiple episodes of vomiting and did not pass urine or stool, and had swelling over the right ring finger. There were no symptoms of headache, ptosis and bleeding manifestations.

On initial examinations he was conscious oriented, BP:140/90 mm, not dyspnoic, tachycardic and chest was clear . His laboratory investigations showed anemia (haemoglobin -9.3 mg/dl), leukocytosis, thrombocytopenia, deranged liver function tests, RFT (Serum creatinine -4.5, serum urea – 70.7), prothrombin time (14.5sec) /INR levels (1.11) were elevated, APPT level was found to be 39’.4”. His bleeding time was 1’30” and clotting time was 4’00”at the time of admission and whole blood clottting time was 22’40”. Urine analysis showed albumin 2+

and neumorous RBCs.

21 vials of antisnake venom (ASV) were given. Patient was immediately managed with 0.5 ml tetanus toxoid, and other supportive measures. He was catheterized for hourly urine output examination. In view of acute kidney injury and anuria he was taken for haemodialysis 2 hours post ASV. Conservative management of the ring finger was adopted with limb elevation and use of antibiotics (Inj.piperacillin +tazobactam). His ultrasound report showed

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features suggestive of acute renal injury and multiple renal cortical cysts. Haemodialysis sessions were continued as the patient was anuric.

During the hospital stay he developed disseminated intravascular coagulation (DIC)and was treated with fresh frozen plasma and packed red blood cells. In total the patient had received 4 Fresh Frozen Plasma and 11 units of packed red blood cells. Serial investigations were made. Daily haemodialysis was then changed to alternate days and urine output was monitored closely. Patient developed recurrent episodes of pulmonary edema for which ECHO was taken and this revealed poor LV function (query of venom induced myocardial damage). Patient continued to be dialysisis dependent with no significant improvement in urine output and continued to be oligoanuric. For this renal biopsy was taken which showed acute cortical necrosis, global glomerulosclerosis, tubulointerstitial nephritis, thrombotic microangiopathy and hypertensive vascular changes. He was managed with antibiotics, proton pump inhibitos, calcium supplements and other supportive measures. Patients laboratory parameters imporved at the time of discharge but needed to continue haemodialysis.

DISCUSSION

Snake venom is a complex mixture of multiple enzymes and proteins. The venom can affect multiple organ systems and tissues of the victim instantaneously, resulting in incapacitation and death.^[2] Snake venom shows its effect through the cascades of proteins and enzymatic components of toxins. They are neurotoxin, myotoxin, nephrotoxin and necrotoxin.

Acute kidney injury (AKI) is an important complication of snake bite and is one of the major cause of mortality. AKI is common after bites from myotoxic or hemotoxic snakes. These snakes are Russell’s viper, saw-scaled viper, hump-nosed pit viper, green pit viper, and sea- snake. Renal pathologic changes include tubular necrosis, cortical necrosis, interstitial nephritis, glomerulonephritis, and vasculitis.

Incidence of complications is directly proportional to the duration of venom in the blood prior to neutralization by ASV. The early institution of ASV is beneficial in preventing complications however severe is the systemic envenomation.^[5]

Some of the risk factors associated with development of AKI in snake bite are native treatment, bite to needle time more than 2 h, age, bite to hospital/ASV time, black or brown

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urine, bleeding manifestations, hypotension/shock, cellulitis, regional lymphadenopathy, abdominal pain/tendernes and vomiting, 20 WBCT > 20 min, prolonged bleeding time, prolonged prothrombin time, low hemoglobin, high WBC count, low serum albumin, and a high serum bilirubin, Creatinine Kinase > 2000 U/L, albuminuria, intravascular hemolysis, DIC, complications of septicaemia.^[6]

Hemodynamic alterations caused by vasoactive mediators and cytokines and direct nephrotoxicity can lead to the development of nephropathy.^[7] Haemorrhage, hypotension, disseminated intravascular coagulation (DIC), intravascular hemolysis, and rhabdomyolysis enhance renal ischemia leading to AKI. The incidence of AKI caused by these snakes varies from 5% to 29% depending on the species of snake and the severity of envenomation. The onset of AKI is can occur from a few hours to as late as 96 h after the bite. The duration of AKI after snake bite generally ranges from 2 to 3 week. Tubular necrosis is an important pathological correlate of AKI.

Prolonged AKI with oligoanuria after snake bite is indicative of cortical necrosis or acute tubular necrosis associated with interstitial nephritis or extracapillary glomerulonephritis.

Various procoagulant enzymes are found in viper venoms, which activate different steps of the clotting cascade resulting in a state of DIC. Bleeding tendencies can also cause severe blood loss resulting in hypotension, further adding to the renal insult. Fibrin thrombi in renal microvasculature glomerular capillaries, microangiopathic hemolytic anemia and thrombocytopenia in patients with cortical necrosis strongly suggest that DIC plays a major pathogenetic role in snake bite-induced cortical necrosis. Thus, bleeding tendencies secondary to DIC are a major factor in the development of AKI in patients of snake bite, especially those involving vipers.

The therapeutic approach for acute renal failure in patients bitten by snakes is the same as that for acute renal failure of any other cause. Early administration of antivenom is the first therapeutic measure. Blood coagulability generally is restored within 6 hours of an adequate dose of antivenom, but repeated doses sometimes are indicated until the blood clots normally.

Tests for coagulability should be repeated for at least 3 days to detect the recurrence of coagulation defects due to delayed absorption of venom from the bite area. Antivenom should be given to patients with uncoagulable blood, even several days after the bite.

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Lost blood should be replaced with fresh blood, because bleeding is the consequence of consumptive coagulopathy and thrombocytopenia. Other therapeutic measures include maintenance of electrolyte balance, administration of tetanus immune globulin, and treatment of pyogenic infection with antibiotics.^[4] In patients with intravascular hemolysis, maintenance of a high urine output by increasing fluid intake and giving a diuretic, as well as rendering the urine alkaline early in the course of the disease may prevent renal damage.^[6,8]

Snake bite-induced AKI can be catabolic with rapid rise in blood urea and serum creatinine levels, hyperkalemia and severe metabolic acidosis. Early and frequent peritoneal dialyses and hemodialyses are life saving for AKI.

CONCLUSION

Acute renal failure complicates in 5% to 30% of victims of severe viper poisoning. The exact mechanism causing acute renal failure after viper bite is unknown . However, viper venom induces several clinical abnormalities that can favor the development of acute renal failure.

Clinical manifestations of systemic envenoming by snakes include acute kidney injury, haematological manifestations, and other organ involvement, in some cases leading to death.

Snake envenomation leading to acute kidney injury is a major health issue due to delay in reaching to the hospital after the envenomation, referral to the appropriate care centre. Early referral to specified care centre can reduce mortality and morbidity, but lack of patient education on need for treatment after snake bite, social and cultural, especially, financial constraints of the patients are some of the major hindrances.

CONFLICT OF INTREST NIL.

CONSENT

Written informed consent was obtained from the patient for publication of this case report.

REFERENCES

1. P Mukhopadhyay, R Mishra, D Mukherjee R Mishra, M Kar; Snakebite mediated acute kidney injury, prognostic predictors, oxidative and carbonyl stress: A prospective study Indian journal of nephrology, 2016; 26(6): 427-433.

2. Gopalakrishnan N; Snake Envenoming─ An Underreported Cause of Acute Kidney Injury Kidney International Reports ;Kidney International reports, 2019; 4: 643–646.

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3. Venomous stings and bites; V V Pillai; Modern medical toxicology;Jaypee brothers medical publishers; fourth edition, 137-153.

4. K. S. Chrugh; Snake-bite-induced acute renal failure in India; Kidney International, 1989;

35: 891-907.

5. Narvencar K. Correlation between timing of ASV administration and complications in snake bites. J Assoc Physicians India, 2006; 54: 717-719.

6. Vikrant S, Jaryal A, Parashar A; Clinicopathological spectrum of snake bite-induced acute kidney injury from India; World Journal of Nephrology, 2017; 6(3): 150–161.

7. ShivanthanM, Yudhishdran M, Navinan R, Rajapakse S; Hump-nosed viper bite: an important butunder-recognized cause of systemic envenoming; Journal of Venomous Animals and Toxins including Tropical Diseases, 2014; 20: 24.

8. Kanjanabuch T, Sitprija V. Snakebite nephrotoxicity in Asia; Semin Nephrol, 2008; 28:

363-372.