A medical presentation about the complications of snake envenomation in child.

1. COMPLICATIONS
OF SNAKE
ENVENOMATION
DR. JEBA SHARON

2. INTRODUCTION
 Of the 1·8 million people envenomed by snakes every year, up to 125 000
die, while hundreds of thousands survive only to suffer with life‐changing
long‐term morbidity.
 Consequently, snakebite is one of the world's most severe neglected tropical
diseases.
 Every hour wasted between bite and antivenom administration is strongly
associated with sharp increases in mortality and the development of chronic or
permanent sequelae including amputation, disfigurement, PTSD, blindness, kidney
injury, infections, and partial or complete loss of function of the bitten limb

4. ACUTE/ LIFE THREATENING COMPLICATIONS
 Tissue necrosis and Compartment syndrome
 Acute Kidney Injury
 Hypotension due to hypovolaemia or direct vasodilatation or direct
cardiotoxicity
 Neuroparalysis
 Hemostatic abnormalities (VICC, DIC)
 Pituitary Insufficiency, neurological deficit (ADEMS, GBS)Rarely

5.  Chronic renal failure
 Chronic panhypopituitarism
 Chronic neurological deficits
 Malignant transformation of ulcers
CHRONIC COMPLICATIONS

6. TISSUE NECROSIS AND COMPARTMENT
SYNDROME
 Local tissue necrosis results from the direct action of
myotoxins and cytotoxins,
 Ischaemia caused by thrombosis,
 compression of blood vessels by first-aid methods such as tight
tourniquets or
 Swelling of envenomed muscle within such tight fascial
compartments could result in an increase in tissue pressure
above the venous pressure, resulting in compartment
syndrome

9. Compartment syndrome (6 P'S)
 Pain on passive stretching
 Pain out of proportion
 Pulselessness
 Pallor
 Parasthesia
 Paralysis
 6 Ps with significant swelling in the limb with obvious tenseness on
palpation can lead to the conclusion that the intracompartmental pressure
is above 40 mm of mercury and thus requires a fasciotomy.

10. Local and extensive necrosis resulting from venom action may
necessitate debridement of necrotic tissue.
Criteria for fasciotomy in snake-bitten limbs
(WHO)
• Haemostatic abnormalities have been corrected (antivenom with
or without clotting factors)
• Clinical evidence of an intracompartmental syndrome
• Intracompartmental pressure >30mmHg (varies with age and
clinical status of the child)
•Early treatment with antivenom remains the best way of
preventing irreversible muscle damage.

12. HYPOTENSION AND SHOCK
CAUSES
1o Anaphylaxis
Vasodilatation
Cardiotoxicity
Hypovolaemia
2o Antivenom reaction
Respiratory failure
Acute pituitary/ adrenal insufficiency
Septicaemia

13.  There is no conclusive trial evidence to support a preference for
colloids or crystalloid
 Treatment is by means of plasma expanders and raising the foot of
the bed.
 In addition fresh frozen plasma or factors present a possibility in
order to boost volume and restore factors.
 In many areas, particularly in developing countries, the only
available alternative will be fresh blood.
 In cases where generalised capillary permeability has been
established a vasoconstrictor such as dopamine can be used.
Dosing is 2.5- 5μg/kg/minute.

14. RENAL FAILURE
 A common complication of species such as Russell's Viper.
 Patient's presents with loin pain, haematuria, oliguria/anuria, symptoms and signs
of acute kidney injury/ uraemia (acidotic breathing, hiccups, nausea, pleuritic chest pain.
 The contributory factors are intravascular haemolysis, DIC, direct nephrotoxicity,
hypotension and rhabdomyolysis
 Renal damage can develop very early in cases of Russell’s viper bite and even when
the patient arrives at hospital soon after the bite, the damage may already have
been done.

15.  In patients with AKI, serum/plasma urea, creatinine and
electrolytes should be monitored daily until renal failure is
resolving.
 If the patient is passing dark brown urine, it is suggestive of
rhabdomyolysis or intravascular haemolysis.
 To minimise the risk of renal damage from excreted myoglobin
and/or haemoglobin:
< correct hypovolaemia and maintain urine output of 200-300ml/hr
< correct s evere acidosis with bicarbonate
< Promote alkalinise diuresis (urine pH > 6.5)
o < continue these measures until there is evidence that
rhabdomyolysis is decreasing (CK level <5000 U).

17. INDICATIONS FOR DIALYSIS
a. Absolute value of Blood urea >130 mg/dl (BUN 100 mg/dl), Sr. Creatinine
> 4 mg/dl OR evidence of hypercatabolism in the form of daily rise in blood
urea 30 mg/dL (BUN > 15), Sr. Creatinine > 1 mg/dL, Sr. Potassium > 1
mEq/L and fall in bicarbonate >2 mmol/L
b. Fluid overload leading to pulmonary oedema
c. Hyperkalaemia (>7 mmol/l (or hyperkalaemic ECG changes)
d. unresponsive to conservative management.
e. Uremic complications – encephalopathy, pericarditis. nausea, vomiting,
hiccups, fetor, drowsiness, confusion, coma, flapping tremor, muscle
twitching, convulsions, pericardial friction rub, signs of fluid overload

18. NEUROPARALYSIS
Neuroparalytic snakebite patients presents with progressive weakness
• In chronological order of appearance of symptoms –
 Furrowing of forehead, Ptosis (drooping of eyelids) occurs first
 Diplopia (double vision),
 Dysarthria (speech difficulty),
 Dysphonia (pitch of voice becomes less) followed by Dyspnoea
 Dysphagia (Inability to swallow) occurs.
 All these symptoms are related to 3rd, 4th, 6th and lower cranial nerve paralysis.
Finally, paralysis of intercostal and skeletal muscles occurs in descending manner.
• Other signs of impending respiratory failure are diminished or absent deep tendon
reflexes and head lag; stridor, ataxia may also be seen.

19.  Toxin- alpha neurotoxin; Binds
specifically to acetylcholine receptors,
preventing the interaction between
acetylcholine and receptors on
postsynaptic membrane.
 It prevents the opening of the sodium
channel associated with the acetylcholine
receptor and results in neuromuscular
blockade
 On ASV administration, there is rapid
reversal of paralysis- causing dissociation
of the toxin-receptor complex, which
leads to reversal of paralysis
 Anticholinesterases reverse the
COBRA - POSTSYNAPTIC
ACTION

20.  Toxin- Beta bungarotoxin- Phospholipases A2
Inhibiting the release of acetylcholine from the
presynaptic membrane
 Presynaptic nerve terminals exhibits signs of
irreversible physical damage and are devoid of
synaptic vesicles
 Hence antivenoms and anticholinesterases are
of no effect
 paralysis lasts for several weeks and frequently
requires prolonged mechanical ventilation
 Recovery is dependent upon regeneration of
axon terminals
KRAIT- PRESYNAPTIC
ACTION

23.  The muscles flexing the neck may be paralysed, giving the “broken neck
sign”
 secretions accumulating in the pharynx, an early sign of bulbar paralysis.
 Ask the patient to take deep breaths in and out."Paradoxical respiration”(
abdomen expands rather than the chest on attempted inspiration)
indicates that the diaphragm is still contracting but that the intercostal
muscles and accessory muscles of inspiration are paralysed
Do not assume that snake-bitten patients are unconscious or even irreversibly
“brain dead” just because their eyes are closed, they are unresponsive to painful
stimuli, are areflexic, or have fixed dilated pupils.
They may merely be paralysed! They may be severely paralysed and lack motor
responses or spontaneous eye movements mimicking coma (locked-in syndrome).
Check pulse, heart sounds and, if possible, ECG.

25.  Death may result from aspiration, airway obstruction or respiratory failure.
 A clear airway must be maintained.
INDICATIONS FOR INTUBATION [INSERTION OF
ENDOTRACHEAL TUBE (ETT) OR OTHER AIRWAY]:
a. Imminent respiratory arrest (breathing is absent or inadequate)
b. Neck muscle weakness with shallow respiration or paradoxical
breathing
c. Upper airway obstruction with stridor (secondary to anaphylaxis)
d. Oxygen saturation <90% (equivalent to Pa02 <60 mmHg) despite high
flow oxygen
e. Blood gas measurement showing respiratory acidosis (hypoxia PaO2 <
60 mm Hg with PaCO2 > 45 mm Hg)

26. HAEMOSTATIC ABNORMALITIES
 coagulopathy is one of the most common complications of snakebites
 Haemorrhage caused by snake venom is often complicated and exacerbated by
patients presenting with blood clotting disturbances as the result of
venom‐induced consumption coagulopathy (VICC).
 VICC, a disseminated intravascular coagulation (DIC)‐like syndrome, is characterised
by low or undetectable levels of fibrinogen, resulting in incoagulable blood
 It manifested as prolonged INR, hypofibrinogenemia, thrombocytopenia, and
increased fibrin degradation products in laboratory studies
 In majority of cases timely use of anti venom will stop bleeding.

27.  DIC results from activation of clotting pathway and has a very high mortality.
 By contrast, VICC involves a different pathogenic process (specific enzyme
activation) and has a benign course than DIC.
 Procoagulant toxins cause rapid clot formation in vitro, but, in vivo, they cause
consumption of severe clotting factors therefore increase the risk of bleeding.
 The toxins in venom that cause VICC are classified by where they effect in the
clotting pathway, with the important ones being thrombin-like enzymes (also known
as fibrinogenase), prothrombin activators, factor V and X activators.

29.  strict bed rest to avoid even minor trauma including intramuscular
injections;
 transfusion of clotting factors and platelets; ideally, fresh frozen plasma
(FFP) or cryoprecipitate with platelet concentrates or, if these are not
available, fresh whole blood.
 The indications for these blood components are the same as those for
antivenom administration for bleeding tendency, but it is important to
recognize that, in the presence of un-neutralized circulating venom
procoagulant toxins, administered clotting factors will be rapidly
consumed, with the potential danger of formation of microthrombi.

30.  Heparin is ineffective against venom-induced thrombin and may cause
bleeding on its own account. It should never be used in cases of
snake-bite.
 Antifibrinolytic agents are not effective and should not be used in
victims of snakebite
 In patients with incoagulable blood, any injection (subcutaneous,
intramuscular) and, particularly venepuncture, carries a risk of persistent
bleeding and haematoma formation.
 Arterial puncture is contraindicated in such patients.

31. ACUTE PITUITARY FAILURE (SHEEHAN SYNDROME) A Rare case;
 A Previously healthy 21-year-old man was envenomed by a Russell's viper and treated
with antivenom.
 Ten hours after the bite, he developed persistent hypotension, which responded promptly
to intravenous dexamethasone.
 His hormone profiles were consistent with hypocortisolism secondary to acute pituitary
insufficiency. He also developed hypokalaemia.
 Analysis of urine and serum electrolytes suggested redistribution of potassium in to the
cells rather than renal loss.
 Hypotension and hypoglycaemic coma are life-threatening manifestations of acute
pituitary insufficiency.

33. Haemorrhagic infarction of
anterior pituitary resulting in
Sheehan's syndrome

34. ACUTE DEMYELINATING ENCEPHALOMYELITIS
 ADEM (rare complication) followed by Anti-venom therapy in Russel viper
bite, complicated by the development of immune complex mediated
demyelination.
 Presents as acute onset poly symptomatic neurological dysfunction
following triggering events such as infection or vaccination.
 Presents with
Encephalopathy( malaise, Irritability, coma)
Fever, nausea, vomiting
Meningeal signs
Weakness ( diffuse or focal), Cranial nerve palsy
Ataxia, Seizures

35.  Imaging shows multifocal white and grey matter lesions in brain and spinal
cord.
 Clinical examination, MRI and CSF Analysis are most useful in establishing
diagnosis.
 Corticosteroids are the mainstay of treatment.

37. GUILLAIN-BARRE SYNDROME FOLLOWING SNAKEBITE
 Guillain-Barre syndrome is an acute autoimmune-mediated polyneuropathy that
commonly presents with bilateral symmetrical ascending flaccid paralysis.
 Patient presents with Pain, progressive quadriparesis(LMN type), Parasthesia, areflexia,
autonomic dysfunction, hypotension, sphincter disturbance etc.
 EMG/NCS shows motor and sensory neuropathy-primarily suggestive of demyelination
with secondary axonal degeneration.
 cerebrospinal fluid (CSF) analysis shows cytoalbuminologic dissociation.
 cross-reactivity between venom proteins and neuronal GM2 gangliosides (molecular
mimicry), postulating a potential immunological basis for this association rather than
direct venom toxicity.

38. VENOM
TOXINS

41. PERSISTING RENAL DYSFUNCTION

42.  Patients with persistent tubular degenerative changes can shows
continuing albuminuria, hypertension and nocturia for many
months after the bite, despite apparent recovery in renal function.
 Patients referred to renal units with acute kidney injury following
Russell’s viper bite suffered oliguria for more than 4 weeks
suggesting the possibility of bilateral renal cortical necrosis and
the need for referral to a nephrologist.
 Patients with patchy cortical necrosis show delayed and partial
recovery of renal function but those with diffuse cortical necrosis
require regular maintenance dialysis and eventual renal
transplantation.

43. CHRONIC PANHYPOPITUITARISM
Chronic phase (months to years after the bite):
weakness, loss of secondary sexual hair, loss
of libido, amenorrhoea, testicular atrophy,
hypothyroidism etc

44. MALIGNANT TRANSFORMATION OF ULCERS
AND DISABILITY

45. THANK YOU !!!