INTRODUCTION
• Snakebite isan acute life threatening time limiting medical emergency
• Causes significant mortality
• Treatable
3.
Epidemiology
• >2000 speciesof snakes in the world
• In India about 236 species of snakes (52 are venomous)
• The venomous snakes found in India belong to 3 families
Viperidae (Hemotoxic)
a. Russel’s viper
b. Saw scaled viper
c. Hump-nosed Pit viper
Hydrophidae
(Myotoxic)
a. Sea Snakes
Elapidae (Neurotoxic)
a. Cobra
b. King Cobra
c. Common Krait
4.
• 99% oftotal snake bite in India due to 4 venomous species
• These big 4’s are
1) Indian Cobra ( naja naja)
2) Common Krait (bungarus caruleus)
3) Russell Viper (daboia russeli)
4) Saw Scaled Viper (echis carinatus)
5.
• Male weremore affected than female .
• 97% snake bites occur in rural area .
• A peak in incidence is found during summer and rainy season.
6.
Venom
Modified saliva containingzootoxins from modified salivary
glands
Used by snakes to immobilize and digest prey or to serve as a
defence mechanism against a potential predator
Most of the snakes inject 10% of available venom in a single
strike
(Russel’s viper injects 75%)
7.
• Proteolytic enzymes(metalloproteinases, endopeptidases or hydrolases)
-Increase vascular permeability
• Zinc metalloproteinases & haemorrhagins (snake venom metalloproteinases-
SVMPs):
-Degrade basement membrane components
-Leading to endothelial cell damage
• Procoagulant enzymes: (venoms of Viperidae and few Elapidae)
-Cause consumption coagulopathy
8.
• Hyaluronidase:
-Increase permeability- promotes the spread of venom through tissues & contribute to
tissue damage
• Venom polypeptide toxins (“neurotoxins”)
Postsynaptic (α) neurotoxins (α-bungarotoxin and cobrotoxin)
- They bind to acetylcholine receptors at the motor endplate.
Presynaptic (β) neurotoxins (β-bungarotoxin)
-Damage the nerve endings, prevent further release of acetylcholine
Acetylcholinesterases: (elapid venoms)
-Cause fasciculation
1. Non –VenomRelated
2. Venom Related
Dry Bite
• Bites by venomous species are not always accompanied by the injection of venom
(dry bites)
• Symptoms (+) due to anxiety and sympathetic overactivity
CLINICAL PRESENTATION
11.
Non Venom RelatedSymptoms
• Palpitations
• Sweating
• Tremoulessness
• Tachycardia
• Tachypnoea
• Elevated Blood Pressure
• Cold Extremities
• Paraesthesia
• These patients may have dilated pupils suggestive of sympathetic over activity
Onset of typicalsymptoms :-
• within 30 min to 6 hours ----- Cobra bite
• 6 – 24 hours ------ Krait bite
(however, ptosis in Krait bite have been recorded as late as 36 hours after
hospitalization)
15.
Chronological order ofappearance of symptoms –
Furrowing of forehead
• Ptosis (drooping of eyelids)
• Diplopia (double vision),
• Dysarthria (speech difficulty),
• Dysphonia (pitch of voice becomes less)
• Dyspnoea (breathlessness)
• Dysphagia (inability to swallow)
16.
1. Diminished /absentdeep tendon reflexes
2. Head lag
Bedside identification of impending respiratory failure
A. Single breath count – number of digits counted in one exhalation - >30 normal
B. Breath holding time – breath held in inspiration –> 45 sec normal
C. Ability to complete a single sentence in one breath.
• Cry in a child whether loud or husky can help in identifying impending respiratory failure.
Signs of impending respiratory
failure
17.
Bleeding
(Haemotoxic or Vasculotoxic)– Viperine envenomation
A. LOCAL MANIFESTATIONS
Russel’s viper bite >>> Saw scaled viper .
Least seen -Pit Viper
• Local swelling, bleeding, blistering, and necrosis.
• Pain at bite site and severe swelling leading to compartment
syndrome.
• Tender enlargement of local draining lymph node
18.
B.SYSTEMIC MANIFESTATIONS –
•Visible systemic bleeding ( due to haemorrhagins )
• Continuous bleeding from the bite site
• The skin and mucous membranes - petechiae, purpura
ecchymosis, blebs and gangrene.
• Acute abdominal tenderness -gastrointestinal or retro
peritoneal bleeding.
• Localizing neurological symptoms - intracranial bleeding
(eg :-asymmetrical pupils)
19.
LIFE THREATENING COMPLICATIONS
Renal involvement.
• Bilateral renal angle tenderness.
• Passage of discolored urine (reddish or dark brown)
• Acute Kidney Injury (Russell’s viper & Saw scale Viper)
-declining or no urine output,
-deteriorating renal signs such as serum creatinine, urea or potassium.
• Hypotension due to hypovolaemia or direct vasodilatation or direct cardiotoxicity
aggravates acute kidney injury.
Renal failure, ARDS, Refractory shock.
20.
• Rare disorder
•Dreaded complication of russel viper bite
• A/w morbidity and mortality.
• Males >> Females
• Characterized by episodes of
severe hypotension,
hypoalbuminemia,
hemoconcentration without albuminuria
Capillary leak syndrome
21.
• Due toprofound derangement of the vascular endothelium
resulting in leakage of plasma and proteins into the
interstitial compartment
• Manifestations like parotid swelling, conjunctival chemosis,
myalgia and severe thirst
• Increased Hct
• Leukocytosis
• Pleural effusion
Early
laboratory
&
radiological markers
22.
• Long termsequelae
- Pituitary insufficiency ( with Russell’s viper )
- Sheehan’s syndrome or amenorrhea in females
23.
Painful Progressive Swelling(PPS)
• Russel’s viper bite >>> Saw scaled viper bite > Cobra bite
• Indicative of local venom toxicity.
• This is associated with
Local necrosis -rancid smell.
Limb is swollen and the skin is taut and shiny.
Blistering with reddish black fluid at and around the bite site.
Skip lesions around main lesion
Ecchymosis
24.
• Significant painfulswelling potentially involving the whole
limb and extending onto the trunk.
• Compartment syndrome.
• Regional tender enlarged lymphadenopathy
25.
Myotoxic
• a /wSea snake bite.
Patient presents with:
Muscle aches, muscle swelling
Involuntary contractions of muscles
Passage of dark brown urine
Compartment syndrome
Cardiac arrhythmias due to hyperkalaemia
Acute kidney injury due to myoglobinuria
Subtle neuroparalytic signs.
26.
• A/w kraitbite
• Krait has nocturnal habitat and has fine slender teeth.
• Bite marks usually cannot be identified even on close
examination.
• Victims often has no history of snakebite & no local signs.
Occult Snakebite
27.
• Typical presentinghistory
Patient was healthy at night,
In the morning - severe epigastric/umbilical pain with vomiting persisting for
3 – 4 hours
Typical neuroparalytic symptoms- ptosis & sudden onset of acute flaccid paralysis- within
next 4- 6 hours.
High degree of suspicion is required for diagnosis Esp in Endemic Areas
28.
FIRST AID MEASURES/PRIMARYTREATMENT
“ Do it R.I.G.H.T ”
• Reassurance
• Immobillisation of limb - like a fractured one
• Go to Hospital immidiately
• Tell doctor of symptoms in details and any progression
Vigorous washing incision, suction, application of tourniquet ,cryotherapy, venom stone etc. are absolutely
contraindicated.
29.
At A HealthCare Facility
• All victims of snakebite (confirmed /suspected ) - Admit & keep
under observation for min 24 hours.
• ABCDE – Airway Protection, Breathing , Circulation,
Disability(level of consciousness),Exposure
• If Tight tourniquet (+) - to be removed carefully .
Apply a BP cuff above the tourniquet and inflate it just above
systolic blood pressure and reduce the pressure gradually
(to prevent rapid of release of poison from bite site which might
lead to sudden worsening of symptoms & Hypotension )
30.
ASSESSMENT
• Treating physicianshould not start treatment or get biased only by
identification of the offending snake.
Primary assessment –
a) Level of consciousness
b) Local site of bite - wound for pain, swelling, necrosis
c) Vitals
d) Bleeding manifestations
e) Neurological signs
31.
Inspection of localsite of bite
• Examine the bite site and look for fang marks
• Any signs of local envenomation.
• Fang mark or their patterns have no role to determine whether the biting
species was venomous or non venomous or amount of venom injected,
severity of systemic poisoning and nature of poisoning .
• Some species like Krait may leave no bite marks
32.
Inspection of localsite of bite can also help to identify snake’s species :-
• Local swelling, bleeding, blistering, necrosis ------ Cobra bite.
• Minimum local changes ------ Krait bite.
• Local bleeding ------- Russel’s viper bite.
• Pain in abdomen and hyper peristalsis indicates Krait bite
33.
Physical examination
Check forand monitor
• Pulse rate,
• Respiratory rate,
• Blood pressure
• 20 minutes Whole Blood clotting test (20 WBCT)
• Check distal pulses and monitor (if there is increasing edema)
• W/O for development of compartment syndrome.
every hourly for first 3
hours
&
every 4 hourly for
remaining 24 hours.
34.
LAB INVESTIGATIONS
• 20minute whole blood clotting test (20 WBCT): – It is a bedside test
• If clotted, the test should be carried
out every 1 h from admission for
three hours and then 6 hourly for 24
hours.
• In case test is non-clotting, repeat 6
hour after administration of loading
dose of ASV.
35.
• Following teststo be done as early as possible -
Complete hemogram :- hb - hemoconcentration (transient)
hb - hemolysis (viper envenomation)
Neutrophilic leucocytosis- Systemic envenoming
Thrombocytopenia- (viper envenomation)
P/S - fragmented red cells (“helmet cell”, schistocytes) - microangiopathic haemolysis
Liver function test - SGOT, SGPT, ALP
Renal function test- S.Cr - AKI (viper and sea snakebite)
Electrolyte :- patients with respiratory paralysis and systemic symptoms
36.
Coagulation profile –BT ,CT ,PT,INR & aPTT prolongation - viper bite
Low fibrinogen & elevated FDP –DIC
Urine examination & microscopy - colour/proteinuria/ rbc/ haemoglobinuria/
myoglobinuria
Serum creatinine phosphokinase (CPK) - muscle damage
S .Amylase ------ Pancreatic injury
ECG – 12 leads
(nonspecific ECG changes such as bradycardia and atrioventricular block with ST-T
changes may be seen )
37.
Chest X-Ray –PleuralEffusion ,ARDS
Abdominal ultrasound (identification of bleeding)
Neuroimaging if intracranial hemorrhage is suspected.
38.
Specific Ix -Tertiary Health Care Centre
In Vasculotoxic Envenomation
• Cardiotoxicity- CPK-MB, 2D Echo, BNP
• Myotoxicity – CPK, SGOT, Urine myoglobin, Compartment Pressure
• Infection- Serum procalcitonin, culture and sensitivity (blood, urine, wound)
In Neuroparalytic Envenomation
• Arterial blood gases -pH show evidence of respiratory or metabolic acidosis
• Pulmonary function tests assess respiratory function (presenting with neuroparalytic
syndrome)
39.
GENERAL MANAGEMENT
• Cleanthe bitten site with povidone-iodine solution, but do not apply any
dressings
• Administer booster dose of Tetanus toxoid injection
• Antibiotic is not used routinely .
In presence of cellulitis and necrosis ,
Inj. Amoxyclav (1.2gm ) i.v. tds is used for 7 days followed by
tab.amoxyclav(625) - tds for 3-7 days
Inj.metronidazole (400mg ) i.v. tds for 7 days is also used.
40.
• Mild pain- Paracetamol 500-1000 mg Q6H P.O (in children 10-15 mg/kg)
• Severe pain - Tab. Tramadol 50 mg or Inj. Tramadol 50 mg IV (in adults)
Do not use aspirin or other NSAIDs.
• Maintain hydration and nutrition.
• Local spreading edema – slightly elevate the affected limb and allow it to rest on a sand bag.
• For hypotension - Normal Saline (30ml/kg ) is used followed by 5% albumin if response is
inadequate.
• If hypotension persists after adequate fluid administration, then start ionotrope
(Inj. Dopamine at 5 – 10 mcg/min)
41.
• Watch outfor development of Compartment syndrome
Intra-compartmental pressure >40 mmHg of normal saline (in adults)
This can be confirmed by vascular Doppler and rising CPK in
thousands
• Clinical features of a compartmental syndrome (5 ‘P’): •
Pain (severe)
Pallor
Paraesthesia
Pulselessness
Paralysis or weakness of compartment muscle.
• Fasciotomy is indicated if compartment syndrome is present
42.
Specific Mx
• Antisnakevenom (ASV) is the only specific treatment for snake bite
• Should be given as soon as it is indicated.
• 2 types of anti snake venoms
• Monovalent antivenom - neutralises the venom of only one species of snake.
• Polyvalent antivenom - neutralises the venoms of several different species of
snakes
Indian Polyvalent ASV
• Cobra
• Common krait
• Russell’s viper
• Saw - scaled viper
Does not cover
• Pit viper
• King Cobra
• Sea snakes
• Others
43.
Administration of ASV
ASVinfusion and dosage schedule
• Initial dose is 10 vials
• 10 vials of ASV dissolved in 100 ml of distilled water
and added to 400ml of normal saline
• Infuse at a rate of 10-15 drops/min for first 15min,if
no reaction infuse rest i.v over one hour
• Monitor vitals at 5min interval for 30min & at 15min
interval for 2hrs.
44.
REPEAT DOSE INHEAMATOTOXIC ENVENOMATION
• After initial 10 vials of ASV
Repetition of dose in hemotoxic bite :
If active bleeding present after 1 hour or
WBCT remain positive after 6 hours
[liver unable to replace clotting factors in under 6 hrs]
• Then give 2nd dose of 10 vials of ASV
• Upto maximum 30 vials.
45.
REPEAT DOSE INNEUROTOXIC ENVENOMATION
►After initial dose 10 vials given
►Repetition of dose in neurotoxic bite :
• If no improvement of symptoms or worsening of condition occurs after 1 hour ,
►Maximum dose of ASV neurotoxic envenomation- 20 vials
46.
Management Neurotoxic
(Neuroparalytic) Envenomation
ASVtreatment alone cannot save the life of a patient
In addition administer following
i. Oxygen
ii. Administer ‘Atropine Neostigmine (AN)’ schedule
iii. Assisted ventilation - bulbar or respiratory paralysis
47.
If signs ofneurotoxicity present (eg- Ptosis , Inability to maintain upward gaze)
Administer ‘Atropine-Neostigmine (AN)’ schedule
• Inj. Atropine (0.6mg) followed by Inj. Neostigmine(1.5mg ) i.v. stat
Repeat dose of neostigmine 0.5 mg with atropine (0.6) every 30 minutes for 5
doses
• Thereafter to be given as tapering dose at 1 hour, 2 hour, 6 hours and 12 hour
Dose for pediatric age group :-
Inj.Atropine 0.05 mg/kg and Inj.Neostigmine 0.04 mg/kg and repeat dose 0.01 mg/kg every 30 minutes for 5 doses
48.
• Improvement isfirst noted by improvement of ptosis after 30 min.
50% or more ptosis improves by 1 hour.
• Majority of patients improve within first 5 doses
There is also improvement of
a) single breath count
b) Uncovered area of iris
c) Upper and lower incisor distance
d) Maintenance of upward gaze
e) FEV1 or FVC (if available)
• Improvement by atropine neostigmine (AN) indicates Cobra bite (Postsynaptic
neurotoxin )
49.
AN dosage isStopped if :-
a. Patient has complete recovery from neuroparalysis.
b. No improvement after 3 doses.
c. Patient shows side effects in form of bradycadia or fasciculation
If there is No improvement after 3 doses of atropine neostigmine -Krait
bite
(affects pre-synaptic fibres )
• For krait bite
Inj. Calcium gluconate 10 ml slow i.v. over 10 minutes can be given
every 6 hourly and continue till neuroparalysis recovers .
Neuroparalysis in krait bite takes 5-7 days for complete recovery.
50.
RESPONSE TO ASV-RECOVERY PHASE
• General- feels better
(Nausea, headache and generalized aches and pains disappear very quickly)
• Spontaneous systemic bleeding stops within 30 minutes
• Blood coagulability usually restored in 3-9 hrs
(20 minute WBCT becomes negative in 6 hours )
• Neurotoxic Envenomation Signs -
Cobra bite (post synaptic type) may begin to improve 30 min to several hrs,
Krait bite (pre synaptic type) usually takes hours to days to improve
51.
Patients Inshock, BP increase within the first 30-60 min & arrhythmias such as
sinus bradycardia may resolve
Active haemolysis & rhabdomyolysis -cease in few hrs & urine returns to normal
colour within few hrs - days
52.
PERSISTENT COAGULOPATHY
• ProlongedPT/INR - FFP
• FFP administration -more rapid restoration of clotting function
• FFP is given at a dose of 10-15 ml /kg over 30 -60 min within 4 hours of ASV administration
• Normalization of coagulation profile defined as INR < 2.0 after 6 hrs of FFP administration.
• Elevated PT / aPTT , Low fibrinogen and high FDP – Suspect DIC
• Rx- 10-15U of cryoprecipitate for every 2-3U of FFP to correct homeostasis
(or 1-2 bags of cryoprecipitate /10kg BW)
53.
PARAMETERS
S .Creatinine >4 mg/dl or rise by 1 mg/dl/day
Blood urea >130 mg/dl or rise by 30 mg/dl/day
S. Potassium 7 mmol/dl or rise by 1 mmol/dl/day
Hyperkalemic ECG Changes
Bicarbonate Daily fall >2 mmol/L
Uremic complications encephalopathy, pericarditis
ABG metabolic acidosis
Evidence of Pulmonary edema –Fluid Overload
INDICATION OF HEMODIALYSIS –
54.
COMPLICATIONS OF ASV& Mx
• ASV can cause
a) Early anaphylactic reaction
b) Pyogenic reaction
c) Late reaction (serum sickness like)
• Any new sign or symptom after initiation of ASV should be suspected as reaction
• Premedication with inj. Adrenaline (epinephrine) 0.25 mg of 0.1% solution i.e
1mg/ml (1:1000) s/c prevents most reactions
55.
EARLY ANAPHYLACTIC REACTIONS
•Within 10–180 min
• Characterized by :- itching, urticaria, dry cough,
nausea and vomiting, abdominal colic, diarrhoea,
tachycardia, and fever
• Minority may develop severe life-threatening
anaphylaxis, hypotension, bronchospasm and
angiooedema
56.
If reaction occurs, following measures are taken –
i. Stop ASV infusion temporarly
ii. Moist O2 inhalation
iii. Inj. Adrenaline (1 in 1,000 solution ) – 0.5mg (0.5 ml) I.M. Is life saving.
iv. Inj. Adrenaline is repeated if no response occurs within 15 minutes.
v. 500 ml Normal Saline is infused using a new transfusion set.
vi. Inj. Hydrocortisone - 100 mg & antihistaminic injection like promethazine 25mg or
chlorpheniramine maleate 10mg is given.
57.
Once thepatient recovers ,
ASV is started slowly for 10 – 15 minutes keeping the patient under
close observation
If no reaction occurs , then give at normal flow rate .
58.
Pyrogenic reactions
• Contaminationof the ASV with pyrogens during the manufacturing process
• 1–2 h after treatment.
• Chills and rigors, fever, and hypotension.
59.
LATE (SERUM SICKNESS–TYPE)REACTIONS
• 1–12 days (mean 7 day ) after treatment.
• Clinical features include fever, nausea, vomiting, diarrhoea, itching, recurrent
urticaria, arthralgia, myalgia, lymphadenopathy,
• Rarely Glomerulonephritis (immune complex nephritis) and Encephalopathy
Rx
• Inj. Chlorpheniramine maleate 2 mg in adults Q6H for 5 days
• In patients who fail to respond within 24–48 h
A 5-day course of Prednisolone -5 mg Q6H in adults given
SCORPION STING
• Arachinoids,that feed on small arthropods and lizard
• Nocturnal
• Tip of the tail- stinger- venom ( neurotoxic)
• Mech- venom is situated near tail tip
• 3 main effects
• neurotoxic- cause Na channels remain to open
• increased excitability of tissue
• Autonomic excitation- SLUDGE( PARASYMPATHETIC)
• SYMPATHETIC – VASOCONSTRICTION-
• LOCAL effect- necrosis is very rare
• Pain- due to serotonin in the venom
62.
CLINICAL FEATURES
• LOCALEFFECTS-
• Pain at the site
• Erythema
• Ascending paraesthesia and hyperesthesia( tap test-worsens on
tapping the affected side)
• Necrosis and swelling – rare
63.
NEUROLOGIC
SYMPATHETIC PARASYMPATHETIC
HYPERTHERMIA BRONCHOSPASM
PrPR, BP, RR HR, BP
DIAPHORESIS SLUDGE
ARRYTHMIA MIOSIS
PULMONARY EDEMA DYSPHAGIA
PILO ERECTION PRIAPISM
SEIZURES LOSS OF BOWEL AND BLADDER CONTROL
RESTLESSNESS GENERALISED WEAKNESS
COLD ECTREMITIES SWEATING- SKIN DIARRHEA
64.
• CRANIAL NERVEPALSIES
• Blurring of vision, ptosis, dysphagia, dysarthria,mydriasis
• GIT-nausea, vomiting, toxic hepatitis, acute pancreatitis
• last phase- catecholamines get depleted ---- hypotension,
bradycardia
Bee sting
• Beeinjects venom into the skin through its stinger
• CLINICAL FEATURES- local-
• Pain, redness and swelling,itching
• signs of anaphylaxis- dyspnea, dysphagia, palpitations, wide spread
rashes beyond sting site, dizziness confusion
• Treatement- remove the stinger immediately if visioble
• wash the area with soap and water
• Ice pack – to reduce pain and swelling
• Pain- paracetamol
• Antihistamines for itching
• anaphylaxis- steroid and adrenaline
Editor's Notes
#3 There are more than 2000 species of snakes in the world
In India about 236 species of snakes (52 are venomous)
Elapidae (Neurotoxic) -Cobra ,King Cobra ,Common Krait
#6 Most of the snakes inject 10% of available venom in a single strike
Russel’s viper injects 75% of stored venom in a single bite
#7 Venom contains
increase vascular permeability causing oedema, blistering, bruising and necrosis at the site of the bite.
degrade basement membrane components, leading to endothelial cell damage and contributing to spontaneous systemic bleeding
enzymes that are thrombin-like or activate factors V, X, prothrombin and other clotting factors. (“consumption coagulopathy”). \
#8
Hyaluronidase:Increase permeability - promotes the spread of venom through tissues & contribute to tissue damage
Acetylcholinesterases: although found in most elapid venoms, may cause fasciculation.
#9 they damages mitochondria, red blood cells, leucocytes, platelets, peripheral nerve endings, skeletal muscle, vascular endothelium, and other membranes, producing presynaptic neurotoxic activity, cardiotoxicity, myotoxicity, necrosis, hypotension, haemolysis, haemorrhage, plasma leakage
#10 2 types of symptoms
Non –Venom Related symptoms (anxiety and sympathetic overactivity)
Even in case of dry bite, symptoms due to anxiety and sympathetic overactivity
#13 – These symptoms can be remembered as 5 Ds and 2 Ps.
#15 Ptosis (drooping of eyelids) occurs first
Followed by
Finally, paralysis of intercostal and skeletal muscles occurs in descending manner
#16
Other signs of impending respiratory failure are :-
impending respiratory failure can b identified by following bedside tests
#17
They can have local manifestations as well as systemic manifestations
Local manifestations –
these are more prominent in Russel’s viper bite followed by Saw scaled viper and least in Pit viper bite.
Local manifestations are in form of:
• Local swelling, bleeding, blistering, and necrosis.
• Pain at bite site and severe swelling leading to compartment syndrome.
• Tender enlargement of local draining lymph node
#18 • Visible systemic bleeding
e.g. gingival bleeding, epistaxis,, hematemesis, hemoptysis, bleeding per rectum, subconjunctival haemorrhages
from the action of haemorrhagins
Bleeding or ecchymosis at the injection site is a common finding in Viper bites.
The skin and mucous membranes may show evidence of petechiae, purpura ecchymoses, blebs and gangrene.
Acute abdominal tenderness may suggest gastro-intestinal or retro peritoneal bleeding.
Lateralizing neurological symptoms such as asymmetrical pupils may be indicative of intracranial bleeding.
Consumption coagulopathy detectable by 20WBCT, develops as early as within 30 minutes from time of bite but may be delayed
#19
treatening complications are due to renal involvement
Patient presents with
. Some species e.g.) Russell’s viper (Daboia sp) and Saw scale vipers (Echis sp frequently cause acute Kidney Injury.
#20 It is seen in more commonly in males as compared to females.
manifestations like parotid swelling, conjunctival chemosis, myalgia, thirst and systemic hypotension observed in patients of Daboia russelii bite indicate capillary leak syndrome.
It is seen in more commonly in males as compared to females.
#21 Hemoconcentration
effusion are early laboratory and radiological markers of capillary leak syndrome
#22 : Haemorrhagic infarction of the anterior pituitary resulting in Sheehan’s-like syndrome (pan-hypopituitarism) after Russell’s viper bite
#23 It is prominent in Russel’s viper bite, Saw scaled viper bite and Cobra bite.
indicative of local venom toxicity.
This is associated with
Local necrosis which often has a rancid smell.
Limb is swollen and the skin is taut and shiny.
Blistering with reddish black fluid at and around the bite site.
Skip lesions around main lesion are also seen.
Ecchymosis due to venom action destroying blood vessel wall.
#26 Hence bite marks usually cannot be identified even on close examination.
#27 In the morning gets up with severe epigastric/umbilical pain with vomiting persisting for
3 – 4 hours
Followed by typical neuroparalytic symptoms- ptosis & sudden onset of acute flaccid paralysis- within next 4- 6 hours.
#28 Reassure the patient as around 70% of all snakebites are from non-venomous species.
Immobilize the limb in the same way as a fractured limb.
Use bandages or cloth to hold the splints (wooden stick), but do NOT block the blood supply or apply pressure
If victim is expected to reach the hospital in more than 30 minutes but less than 3 hours crepe bandage may be applied by qualified medical personnel till the patient is shifted to the hospital. The bandage is wrapped over the bitten area as well as the entire limb with the limb placed in a splint. It should be capable of admitting a finger beneath it
#29
ABC – airway protection, breathing and circulation are to be taken care on arrival
Tourniquet on a 43-year-old woman presenting at a rural health
#30 The physician shud do assessment of – level of consiousness
#33 –
Pain on passive movement, pallor, pulseless limb, hypoaesthesia over the sensory nerve passing through the compartment are suggestive of compartment syndrome.
#34 False positive – plastic ,glass vessel cleaned with detergent
False negative – In patients with mild degree of coagulopathy
#35 Transient rise in hb
ANEMIA
Prothrombin time (PT) and activated partial thromboplastin time (aPTT) –
Electrolyte determinations: these tests are necessary for patients with respiratory paralysis and systemic symptoms
#38 2d echo –to monitor LVEF in hypotensive nd shock patient
resp aciodis – resp failure – neurotoxic envenomation
Metabolic acidosis- renal failure a/w russels viper ,sea snake
Arterial blood gases and urine examination should be repeated at frequent intervals during the acute phase to assess progressive systemic toxicity
#39 Administer booster dose of Tetanus toxoid injection, if not vaccinated earlier or vaccination history is not reliable after correction of coagulopathy
#40 For mild pain, in adults Paracetamol 500-1000 mg (in children 10-15 mg/kg) every 4-6 hourly orally. Do not use aspirin or other non steroidal anti-inflammatory drugs (NSAIDs). In case of severe pain in adults, Tab. Tramadol 50 mg or Inj. Tramadol 50 mg IV
Shock due toASV TREATED WITHH NOR AD- 8-12 MCG/MIN ………TITRATE……………. MAINTAINACE 2-4 MCG/MIN IV
preferrably
#41 Monitor the intra compartmental pressure bedside - intracompartmental pressure monitoring device
Blood flow , patency of arteries and veins assessed using doppler
Pain on passive movement
#42 - signs and symptoms of envenomation with or without evidence of laboratory tests
#44 Initial blood test reveals coagulation abnormality – 10 vials of ASV
is repeated and used upto maximum 30 vials.
#45 If no improvement of symptoms or worsening of condition occurs after 1 hour , then another and final dose of 10 vials of ASV is given.
Maximum dose of ASV neurotoxic envenomation- 20 vials
#46 Some patients go into a deep coma state but recover completely. Hence, diagnosis of brain death should not be considered. Do not give AN in case of confirmed krait bite.
Assisted ventilation. If the patient has evidence of bulbar or respiratory paralysis,
#47 Neostigmine - anticholinesterase
Prolongs the life of Ach
Reverse neurotoxic symptoms & respiratory failure
Postsynaptic neurotoxin (Cobra)
Krait & Russells Viper(presynaptic) - ? Use
Followed by
Dose for pediatric age group is Inj.Atropine 0.05 mg/kg and Inj.Neostigmine 0.04 mg/kg and repeat dose 0.01 mg/kg every 30 minutes for 5 doses
#49 If there is no improvement after 3 doses of atropine neostigmine, this indicates probable Krait bite.
Krait affects pre-synaptic fibres where calcium ion acts as neurotransmitter. Give Inj. Calcium gluconate 10ml IV (in children 1-2 ml/kg (1:1 dilution) slowly over 5-10 min every 6 hourly and continue till neuroparalysis recovers which may last for 5-7 days
#50 Observation of the response to adequate dose of anti snake venom
#52 FFP administration after ASV administration results in more rapid restoration of clotting function
Prolonged CT, PT, aPTT Low fibrinogen and high FDP will require fibrinogen/FFP supplementation
FFP- whole coagulation factors ,vWF, plasma protein ,protein c&S
Cryo- fibrinogen ,factor 8 ,vWF
FFP is given at a dose of 10-15 ml /kg over 30 -60 min within 4 hours of ASV administration
#55 occurs within 10–180 min of start of therapy
Premedication with inj. Adrenaline (epinephrine) 0.25 mg of 0.1% solution s/c Prevents most reactions.
#56 ( for children = 0.01 mg/kg)
( for children = hydrocortisone 2 mg/kg , promethazine 0.5 mg/kg).
#58 develop 1–2 h after treatment.
Symptoms include chills and rigors, fever, and hypotension.
These reactions are caused by contamination of the ASV with pyrogens during the manufacturing process
#59 (In children 0.25 mg/kg/day)
6 hourly
develop 1–12 (mean 7) days after treatment.
Clinical features include fever, nausea, vomiting, diarrhoea, itching, recurrent urticaria, arthralgia, myalgia, lymphadenopathy,
#60 Specific ASV for sea snake and Pit viper bite is not available in India. However, available ASV may have some advantage by cross reaction