Management should be started immediately on admission to the hospital irrespective of first aid given. Cardiopulmonary resuscitation may be needed, including administration of oxygen and establishment of intravenous access. Assessment of vital parameters and establishment of vital functions; airway (A), breathing (B) and circulation (C) must be done immediately. The level of consciousness must be assessed. Firstly, the deranged vital functions should be attended to. The severity of envenoming and initial clinical features might vary as follows. They may appear normal and healthy or in a state of severely compromised and near fatal cardiac or respiratory function. Airway must be made patent by removing vomitus and secretions in the mouth, pharynx and nose. The patient should be kept in left lateral position to prevent aspiration of vomitus. Respiratory arrest needs endotracheal intubation and mechanical ventilation whilst cardiac arrest should be managed with external cardiac massage, drugs and defibrillation. Venous blood samples are collected for initial investigations. The following are examples of clinical situations which might require urgent resuscitation.
ABC assessment of vital parameters and establishment of vital functions, airway(A), breathing(B) and circulation(C), must be done immediately.
Following the initial resuscitation (ABC) the patient should be assessed for signs of envenoming especially by focusing upon the vital parameters such as radial pulse, blood pressure, respiratory rate, tidal volume of respiration and level of consciousness. A respirometer is needed for the measurement of tidal volume and if it is not available, the respiratory drive should be assessed by asking the patient to count up to the maximum numerical number in a single breath (one breath count). At the outset, establishment of baseline parameters would help in the early detection of complications of envenoming that may be fatal if untreated.
Furthermore, a detailed history and thorough clinical examination are needed to arrive at a diagnosis and to recognize the offending snake type. A precise history of time and the place where the snake bite had taken place is important. Diagnosis is not difficult if the offending snake is produced. However, the availability of dead specimens of snakes varies between 21% to 40% and hence, circumstantial evidence has a major role to play with the knowledge of epidemiology of snake bite in the locality for clinical diagnosis. Moreover, in many instances the offending snake escapes from being killed or captured but the victim or a person nearby recognizes it. In such a situation showing specimens of snakes preserved in formalin in glass jars or pictures of snakes would help the patient or the witness to recognize the offending snake which facilitates the judgment of the clinician. Examination of the bitten part and distribution of fang marks may help in the diagnosis. A more reliable method of identifying the offending snake is the detection of venom antigen through immunodiagnosis such as ELISA. However, this procedure is time consuming and expensive and hence not suitable for routine use in the hospital practice of Sri Lanka.
The clinician must detect the evidence of envenoming early as it governs the decision of administering antivenom therapy, which in turn has a direct impact on the prognosis. These observations and physical signs are based on local and systemic manifestations of envenoming. Since the manifestations of specific patterns of envenoming are snake specific, the identification of the offending snake would help the clinician to look for particular clinical signs and evidence. Properties of snake venom depend mainly on the species of the snake but geographical factors could further modify it. Thus it is prudent to look for features of envenoming as a whole with an open mind.
Haematotoxicity (coagulation defect or coagulopathy and intravascular heamolysis)
Early detection of this complication is impossible without doing a WBCT20. This test is simple, fast and easy to carry out and doesn’t need laboratory assistance. A sample of 2ml of venous blood is put into a clean small glass test tube and rotated well to achieve good surface contact. It is kept standing for 20mins at room temperature for clotting. However, the glass tube should be examined gently at every 5 min interval to detect early clotting. Twenty minutes is the cut-off point and incoagulable blood (hypofibrinogenemia as a result of venom-induced consumption coagulopathy) at this point is considered a positive test. Clinically, obvious coagulation defect usually occurs in severe envenoming where the patient develops spontaneous bleeding from mucous membranes. These features include haematuria (red cells in urine), bleeding gums, haematemesis (vomiting blood), melaena (altered blood producing black stools) and haemoptysis (coughing out blood). Occasionally spontaneous bleeding could occur within the skin producing petechiae, purpura, ecchymoses or bruises and also into mucosae and the muscles or internal organs such as brain. Intracranial haemorrhage is suggested by lateralising neurological signs, asymmetrical pupils, convulsions or impaired consciousness and subarachnoid haemorrhage produce meningism. Intravascular haemolysis produces heamoglobinuria (red urine that becomes black on standing.
Neuromuscular transmission block leads to paralysis of muscles of varying severity. The worst is the paralysis of respiratory muscles which require artificial ventilation for survival. Severity of neuromuscular paralysis (degree of envenoming) could be graded as follows:
1. Mild: heavy eyelids, ptosis and external ophthalmoplegia, paralysis of facial muscles
2. Moderate: weakness of bulbar and neck muscles but does not require assisted ventilation
3. Severe: those requiring assisted ventilation due to paralysis of respiratory muscles
Any feature given above could be the earliest sign of envenoming. Paralysis of respiratory muscles is detected by measuring the tidal volume using a respirometer at regular intervals. Normal tidal volume of an adult range from 400 – 500ml which correlates directly with the body size. Intubation and assisted ventilation are needed if tidal volume falls below half of the predicted value. However, this depends on the rapidity of respiratory paralysis. Slowly developing respiratory paralysis may not need intubation even when reduced by 50% of tidal volume. Patients with profound generalized flaccid paralysis from neurotoxic envenoming may be fully conscious provided they are adequately ventilated. However, direct neurotoxic effect on brain could produce alteration of level of consciousness ranging from drowsiness to deep coma. Paraesthesiae, abnormalities of taste and smell, visual blurring, aphonia, dysphagia with accumulation of saliva in the mouth are the early features of neurotoxicity.
Venom toxin could damage the kidneys either directly or indirectly. Indirect damage occurs due to deposition of haemoglobin or myoglobin in renal tubules and dehydration is another contributory factor for such damage. Clinically the patient develops oliguria, dark coloured urine, oedema, loin pain and clinical features of ureamia (acidotic breathing, hiccups, nausea). Rising blood urea and serum creatinine, development of metabolic acidosis, hyperkalaemia, microscopic haematuria and casts in urine are biochemical markers of renal damage. Hyperkalaemia is best confirmed by the presence of tall peaked T waves in the ECG.
The effects of venom on the heart could occur through four different mechanisms: (1) direct myocardial damage, (2) effects on coronary arteries, (3) autonomic dysfunctions and (4) fluctuation of serum potassium level (hyperkalaemia or hypokalaemia). Clinical manifestations are usually tachy or brady arrhythmias, rapid thready pulse, hypotension or hypertension, chest pain and pulmonary oedema. The ECG is a useful investigation which might show abnormalities such as tall T waves, T inversion and ST segment changes.
The effects of venom on muscle produce generalized muscle pain, stiffness, trismus and tenderness (rhabdomyolysis) leading to myoglobinaemia and myoglobinuria. Patient voids dark red urine which could be tested for myoglobin. Rhabdomyolysis leads to hyperkalaemia and it gets worsen further due to acute renal failure secondary to myoglobinuria.
Acute pituitary and adrenal insufficiency could rarely manifest due to Russell’s viper bite. This leads to shock and hypoglycaemia.
Local symptoms and signs in the bitten part
The degree of local damage varies depending on the snake, for example, majority of cobra bites produce extensive skin necrosis which finally needs surgical excision and skin grafting. On the contrary, Russell’s viper could produce varying degree of local swelling, usually mild to moderate and rarely extensive necrosis. Furthermore, propagation of local swelling could occur over several days from the time of bite which may produce pain and discomfort and may end up in compartment syndrome. Sometimes, local necrosis could be fatal due to secondary bacterial toxaemia. Severity of local damage could be graded as:
(a) Mild- swelling at the site of bite without necrosis,
(b) Moderate- swelling involving half the limb without necrosis
© Severe- swelling with necrosis or swelling involving the whole limb.
Presence of fang marks, pain, bleeding, bruising, lymphangitis, lymphadenitis, and inflammations are some more faetures of local effects in the bitten part.
Abdominal pain, pruritus
Important features of envenoming, but anxiety could cause also abdominal pain.
What is antivenom?
Antivenom is an immunoglobulin, usually an enzyme refined fragment of IgG purified from the serum or plasma of a horse or sheep that has been immunized with snake venom. Monovalent antivenom neutralises only the venom of one species and polyvalent antivenom neutralises the venom of several species of snakes. However, cross-neutralising activity could exist among antivenoms.
Antivenom available in Sri Lanka
Antivenom serum currently available in Sri Lanka is polyvalent equine serum manufactured in India (Haffkine Laboraratories, Mumbai; Serum Instutute of India,Pune; Vins Bioproduct Limited, Mumbai) which is effective against the venoms of cobra, Russell’s viper, common krait and saw-scaled viper. It is not effective against the venom of the hump-nosed viper. Also it is more effective than a monovalent AVS-Polonga-Tab that is prepared specifically to use against the venom of the Sri Lankan Russell’s viper. Furthermore, it is recommended that polyvalent antivenom is better suited than monovalent antivenom, because precise identification of the offending snake is not possible in most of the cases.
Indications for antivenom treatment
AVS should be started at the earliest sign of systemic envenoming and it is quite effective in reversing the clotting defect (WBCT20) that follows Russell’s viper bite. Its efficacy in reversing the established neuromuscular paralysis is doubtful, but has the ability of neutralizing venom antigens in the circulation before binding to neuromuscular junction. Therefore, in krait bite the administration of AVS as early as possible is worthwhile as it produces pure neurotoxicity. Standard initial dose of AVS is 10 vials, but higher doses (20 –30 vials) are required in Russell’s viper bite depending on the severity of the coagulation defect and the deranged clinical states. However, the initial dose of AVS should be 20 vials if Vins Bioproduct is used due to doubtful efficacy. Furthermore, repetitive doses may be required in Russell’s viper bite until the coagulation defect is corrected but not in envenoming due to other snakes (i.e. Common krait, Ceylon krait and Cobra) where the first dose of 10 vials would be adequate.
The first evidence of systemic envenoming might appear at anytime from the time of bite and therefore, the patients should be monitored continuously to detect it. In the case of suspected Russell’s viper bite where there are no physical signs of envenoming such as ptosis, ophthalmoplegia, bleeding tendency or moderate to severe local swelling, WBCT20 is a very important marker of first evidence of envenoming. In such a situation while anticipating a positive result one must repeat WBCT20 on an hourly basis till it becomes positive during first six hours from the time of bite. Positive WBCT20 is an indication to administer the first dose of AVS therapy. Thereafter, successive WBCT20s are performed at 2hour intervals up to 12th hour and 6 hour intervals thereafter. If it remains positive, 2nd and 3rd doses of AVS (10 vials) should be administered to achieve normal coagulation. Ninety eight percentage (98%) of Russell’s viper bites produce definitive envenoming. Occasionally, it could produce acute renal failure as the only manifestation and detection of this might take time. Hence, all proven Russell’s viper bites with definitive fang marks should receive antivenom before development of signs of envenoming. AVS may reverse systemic envenoming even when this has persisted for several days or, in case of haemostatic abnormalities for two weeks. However, repetitive administration of antivenom beyond two days doesn’t contribute much to the prognosis. Polyvalent antivenom is available in dry powder form, which has a long life span, provided it is stored under the manufacturer specified instructions. It is recommended that each vial of AVS be dissolved in 10 ml of distilled water and added to an infusion medium such as normal saline (i.e. 10 vials of AVS dissolved in 100 ml of distilled water and added to 400ml of normal saline). The volume of infusion is reduced according to the body size and the state of hydration of the patient. An initial higher dose of AVS (more than 10 vials) is needed in acute severe disseminated intravascular coagulation due to Russell’s viper bite. AVS infusion should be given over a period of one hour at a slower rate during the first 15 mins to detect adverse reactions. Signs of itching, urticaria, rigors, sweating, cough, pulmonary rhonchi and monitoring pulse, BP, are important during the infusion for the early detection of allergy and anaphylaxis.
Indications for antivenom
Contraindications to antivenom
There are no absolute contraindications. But precautions should be taken with patients who have a strong history of atopic diseases (bronchial asthma), drug allergy and allergy to serum products.
Allergic and anaphylactic or anaphylactoid reactions to antivenom are common and their incidence range from 48%- 81% despite its improvement in purity and the introduction of monovalent antivenom. There were many premedications tested to reduce these acute adverse reactions which include promethazine, chlorpheniramine (H1antihistamine) and hydrocortisone without a proven benefit. However, the use of low dose subcutaneous adrenaline immediately before administration of antivenom serum has shown to reduce acute adverse reactions significantly. The major concern regarding the use of adrenaline is the risk of intracerebral heamorrhage in some patients. Additionally, there are also limitations to the use of adrenaline, for example in children, during pregnancy and in patients with heart disease. Thus, treating an established anaphylactic reaction promptly is important in current practice. However, it has been observed that giving an intravenous bolus of chlorpheniramine 10mg five minutes after commencement of AVS infusion and a hydrocortisone infusion reduces the reaction rate significantly. However, infusion of hydrocortisone in large doses (approximately 1000mg) on its own in parallel to AVS infusion has no proven benefit against the occurrence of reactions. Consensus of opinion is to commence hydrocortisone 1000 mg in 300 ml of normal saline infusion 5 min before AVS infusion and to continue for 30 min after antivenom. A 400mg of hydrocortisone bolus could be given at the outset. Additionally, chlorpheniramine 10 mg intravenous bolus dose should be given 5 min after the commencement of antivenom.
With the onset of a reaction it is prudent to stop the AVS infusion for a few minutes until anti-allergy treatment is instituted. The clinical management depends on the severity of the reactions at the outset. Proper monitoring and recognizing the clinical features of allergy help to assess the degree of severity. The reactions could be categorized into three groups: mild, moderate and severe.
1. Mild reaction include fever, rigor, sweating, itching, urticaria, abdominal pain and increased body temperature.
2. The presence of cough, rhonchi, dyspnoea, lowering of blood pressure below 80/60 mmHg and tachycardia above 120/ min in addition to the above constitute a moderate reaction.
3. Severe cases on the other hand would display a cold clammy skin, central cyanosis, tachycardia above 120/min, low volume pulse, and hypotension below 80/60 mmHg
Treatment of a mild reaction: chlorpheniramine 10mg iv and hydrocortisone 400mg iv bolus. If the patient has vomiting, metoclopramide 10mg iv is recommended. In a moderate reaction adrenaline 0.5ml (1:1000) is given subcutaneously followed by other medications as in the mild reaction. In a severe reaction the route of adrenaline administration is intramuscular immediately. The dose of adrenaline could be repeated whilst carefully monitoring pulse and blood pressure. Normalization of blood pressure and pulse occurs almost immediately and other features of reaction recover within 30 mins.
Once the reactions are treated, the AVS infusion should be restarted slowly. It is rare for reactions to recur. Similarly, the occurrence of reactions to a second dose of AVS is rare. Hence, AVS should not be withheld due to an undue fear of adverse reactions. Severe reactions could be fatal unless treated promptly. It is recommended that the emergency drug trolley must be available at close proximity during AVS administration.
Reassurance is very important as fear of death could produce a false clinical picture such as a hysterical state or pseudo-coma. Furthermore, agitation and excitement produce rapid absorption of venom. The doctor in attendance should talk to the patient sensibly to get rid of the fear of death. It is prudent to allow a relative or a friend to stay with the patient as a bystander.
Pain at the site of bite could be severe, specially in cobra bite. Mere reassurance would relieve the pain. Drugs such as aspirin and other NSAID should be avoided as they might interfere with clotting and might produce bleeding into the gastrointestinal tract. Paracetamol is safer in therapeutic doses.
All patients should have a intravenous line placed with minimum trauma. Intramuscular and subcutaneous injections should be avoided as it might produce local haematomas. Oxygen is needed for patients who have hypotension and impending respiratory paralysis.
The site of bite is cleaned with an antiseptic solution and allowed to dry without dressings. Incision on the site of bite and applying strong irritant antiseptics should be avoided. It is necessary to clean the whole limb with clean water including foot and toe webs. Applying oil based antibiotic ointments or olive oil on the skin (except on the bitten site) would prevent cracks otherwise drying of skin would facilitate development of infections as the local swelling gets worsen. If there are rings or bangles in the bitten limb, these should be removed to prevent pressure effects due to local swelling.
The patient should avoid taking solid foods and large amounts of liquids during the first 24h as reactions to antivenom may produce vomiting, which may lead to aspiration especially in the presence of neuromuscular paralysis. In the case of severe neurotoxicity, a nasogastric tube should be inserted for free drainage rather than feeding. In subjects with minimum envenoming or non-envenoming, oral feeding is allowed after 24hrs. Potassium containing liquids or food such as oranges and king coconut should be avoided during the first week especially following a viper bite.
The value of antibiotics for local swelling is doubtful. It was believed that contamination of the bitten site may occur with the bacterial flora in the oral cavity of the snake at the time of bite. However, recent research has shown that parenteral benzyl penicillin and metronidazole were not beneficial in reducing the local swelling. Hence, prophylactic antibiotics are not recommended routinely. However, secondary infections should be treated with appropriate antibiotics (Amoxycillin or a cephalosporin plus a single dose of gentamicin plus metronidazole). To prevent renal damage in patients with myoglobinuria or haemoglobinuria needs correction of hypovolaemia with saline to produce diuresis. Furthermore, diuresis could be achieved by giving a single dose of mannitol over 30 minutes provided the patient doesn’t have pulmonary oedema. Intravenous frusemide is indicated in pulmomary oedema and in achieving diuresis. Correction of severe acidosis with bicarbonate is indicated.
Fresh blood transfusion is indicated in severe intravascular haemolysis to correct anaemia.
Initial assessment should be followed by further assessment at regular intervals. The aims of assessment are to:
The frequency and duration of assessment of parameters should be individualized according to the clinical status of the patient.
The parameters of assessment are as follows:
Radial pulse rate, blood pressure, status of the peripheries (warm or cold), cyanosis, respiratory rate, tidal volume (one breath count), level of consciousness (normal, drowsy, semi-coma, coma, deep coma or Glasgow coma scale), systemic physical signs (3rd, 4th, 6th, 7th and bulba cranial nerves, motor power of neck muscles, motor power of limbs), urine output, urine colour, spontaneous bleeding (skin and mucous membrane), WBCT20, status of bitten site (degree of swelling, necrosis and gangrene), laboratory parameters (blood urea, creatinine, electrolytes such as sodium and potassium, Hb%, platelet count, prothrombin time, fibrinogen levels, fibrinogen degradation products, liver enzymes, serum albumin, cardiac enzymes such as CPK-MB or troponine T levels, myoglobin in blood and urine) and ECG.
The use of all the above mentioned parameters are not practical and rational in each and every patient. Therefore, the clinician would have to decide what parameters are useful to a particular patient depending on the type of snake bite and the anticipated complications.
Assessment to detect the earliest evidence of envenoming
Institution of specific treatment is based on the earliest evidence of envenoming. Clinical evidence of envenoming such as signs of neurotoxicity (double vision, external opthalmoplegia, etc.), red coloured urine (due to haematuria, haemoglobinuria), tidal volume, respiratory rate, severe local effects and WBCT20 are useful parameters. Frequency of assessment is as follows:
First 6h (after bite) - clinical parameters half hourly, WBCT20 hourly
® 6th to 12th hour- clinical parameters hourly and WBCT20 two hourly
® 12th to 24th hour- clinical parameters 2 hourly and WBCT20 six hourly
® 24th to 48th hour - six hourly assessment and the patient could be discharged in the absence of envenoming.
To monitor response to antivenom and to decide on repeated administration
With an effective antivenom (eg:- currently available polyvalent) the first dose alone is adequate to reverse haematotoxicity in 50% of patients. However, a 2nd or 3rd dose is needed in others. The recovery of haematotoxicity is best detected by WBCT20 which should be done 6 hourly and administration of 2nd or 3rd dose based on its results. Clinical neurological features take a few days to recover and hence are not useful guides to repeat doses of AVS. In the absence of haematotoxicity but in the presence of other signs of envenoming the first dose of antivenom is adequate. However, WBCT20 should be performed 6 hourly to detect late development of haematotoxicity. Nevertheless, knowledge about the offending snake is important as snakes such as krait don’t produce haematotoxicity where the first dose alone is adequate and doing WBCT20 is unnecessary.
Complications could arise as a result of severe envenoming or as a reaction to the treatment (anaphylaxis to antivenom). Regular monitoring of previously mentioned clinical parameters are necessary to detect early complications.
Acute respiratory paralysis
Difficulty in swallowing saliva is an early sign of bulbar paralysis. Abdominal respiration indicates intercostals muscles paralysis. Weakness of the flexion of neck has direct correlation to the paralysis of respiratory muscles.
The useful parameters are respiratory rate, tidal volume, respiratory minute volume (respirometer), one breath count (maximum number the patient can count for a breath holding), PEF, FEV1, FVC (peak flow meter, spirometer), cyanosis of mucous membrane and weakness of neck flexors. Or else, the patient can be asked to blow into the tube of a sphygmomanometer to record the maximum expiratory pressure (mmHg). Connecting the patient to a pulse oxymeter to monitor percentage of oxygen saturation in the haemoglobin (Sa02 %). Blood gas estimation (Pa02 , PaCo2) is complimentary for early intervention. Monitoring of appropriate parameters should be done at 15 min intervals during the first 6 hrs after bite and then at 30 min intervals up to 12 hours followed by hourly monitoring up to 24 hours. This should be modified based on the type and severity of the snake bite.
Acute severe coagulopathy
This complication occurs within 6 hours after the bite and should be suspected in the presence of spontaneous and severe bleeding from oral cavity, haemoptysis, haematemesis, red urine due to haematurea, bleeding per rectum, bleeding from venepuncture sites and positive WBCT20. Monitoring pulse, blood pressure, WBCT20, platelet count, urine output are important in such cases. Measurement of fibrinogen level and fibrinogen degradation products (FDP) may confirm the diagnosis.
Sub acute severe coagulopathy
Repeatedly WBCT20 may remain positive despite antivenom therapy. This complication should be suspected if the very first WBCT20 was short (less than 5 min). Hump-nosed viper bite could produce this complication lasting for 4 to 6 days but recovers uneventfully. However, it may also deteriorate to severe coagulopathy (DIC) leading to multiple organ dysfunction. Multiple organ dysfunction carries high mortality. Monitoring pulse, blood pressure, WBCT20, bleeding time, prothrombin time, platelet count, urine output, liver enzymes, fibrinogen level and fibrinogen degradation products are important.
Multiple organ failure (MOF)
In this condition, impaired tissue perfusion, microcirculatory abnormalities and defective oxygen utilization can damage vital organs. Severe coagulopathy (DIC) or extensive tissue necrosis and secondary infection may lead to MOF. Organ failure occurs over the weeks leading to ARDS, renal and liver failure, pancreatitis, ischaemic colitis, cerebral dysfunction and metabolic derangements. Demonstration of clinical and biochemical abnormalities of deranged organ function make the diagnosis.
Acute renal failure (ARF)
Reduced urine output (oliguria) or anuria is a strong marker of acute renal failure. Urine output should be monitored hourly in a patient with an indwelling catheter and two hourly in a patient without a catheter. Red coloured urine is a risk factor of ARF. Blood urea and serum creatinine are measured on admission and daily thereafter. Performing an ultrasound examination may show enlarged kidneys with abnormal parenchyma. Also, it would differentiate acute-on-chronic renal failure where kidneys are small and contracted. In established ARF, frequent monitoring of these parameters are needed. Russell’s viper and hump-nosed viper bite carries a higher risk of ARF.
This could be either dependent or independent of ARF. However, early detection of hyperkalaemia is important to prevent acute cardiac decompensation. Clinically, patient may become restless, tachypnoeic, confused, develop sweating and hypotension with a rapid thready pulse. Hyperkalaemia can be detected by doing an ECG in addition to the measurement of serum electrolytes (K+). Features of the ECG are tall peaked T waves, widened QRS complex, reduced amplitude of R wave and prolonged PR interval. These investigations should be done at regular intervals perhaps, twice daily or once a day depending on the clinical status of the patient. Hyperkalaemia is a silent killer in the recovery phase of Russell’s viper bite.
Acute Respiratory Distress Syndrome (ARDS)
The commonest cause for ARDS is nasal insufflation of oil or herbal liquids. It may also occur secondary to severe DIC, multiple organ failure, septicaemia and during mechanical ventilation. Chest X-ray shows bilateral perihilar congestion and shadowing which may occupy the whole lung field. Severe hypoxaemia may occur despite inhalation of a high concentration of oxygen. Regular monitoring of blood gases and clinical examination for respiratory distress and hypoxaemia are useful to suspect this condition early. X -ray is complimentary in early diagnosis.
Severe myalgia is suggestive of myotoxicity (rhabdomyolysis) of venom. In severe myotoxicity myoglobin appears in urine giving it a red colour. In mild cases urine may look normal and should be examined in laboratory for myoglobinuria. Myoglobin could damage renal tubules leading to acute renal failure.
Cardiac dysfunction and cardiogenic shock
Shock in snake bite may be neurogenic or due to a reaction to antivenom. After exclusion of these possibilities and the persistence of shock could be cardiac and vascular in origin. ECG might show rhythm abnormalities and ST segment and T wave changes. However, tall T wave in anterior lead is a benign feature in Russell’s viper bite. Blood pressure, pulse rate, capillary filling rate, temperature of peripheries and urine output are useful parameters for the detection and monitoring of shock. Troponin T level may increase if there is myocardial necrosis and an echocardiogram would help to assess cardiac functions.
Foetal loss and abortion
Foetal loss often occurs after snake bite either as an abortion or premature labour. Adverse reactions to antivenom may be responsible for foetal loss. However, the mother should not be deprived of any treatment in consideration of the risks for the foetus. Saving the mother’s life is the priority. Monitoring the pregnancy, foetal heart sounds should be done at regular intervals and seeking obstetric and gynaecological opinion is very essential. Ultrasound examination may help to confirm the diagnosis.
Severe local necrosis and compartment syndrome
Regular inspection of the bitten site for the extent of swelling, blister formation, dark discolouration of skin, necrosis, oozing, tenderness, warmth and gangrene of the digits are useful to detect the severity of local effects.
In compartment syndrome, pain is severe and tender to palpation, the bitten limb is cold and anaesthetic and arterial pulses may be weak or absent. Weakness and pain on passive stretching of intracompatmental muscles could be elicited. These observations should be done at least twice a day as ascending of necrosis may occur especially in cobra bite.
CNS complication and Intracranial bleeding
This usually occurs secondary to coagulation defects or due to cerebrovascular accidents. Depending on the site of involvement, the physical signs vary. However, monitoring the level of consciousness, looking for focal neurological signs and neck rigidity would detect problems early. CT scan of head is needed to define site and the nature of the pathology. Reversible coma could occur due to venom induced neuronal dysfunction.
include autonomic nervous system dysfunction, hepatic dysfunction, pancreatitis, endocrine insufficiency and deep venous thrombosis and the clinician should detect the relevant clinical manifestations accordingly. Hence, looking for icterus, abdominal pain and tender swollen calf is important.
Acute respiratory paralysis
These patients are usually calm and quiet despite hypoxaemia due to neuromuscular paralysis. The patient has shallow fast breathing. At this juncture, giving oxygen via face mask is necessary whilst continuing monitoring. If the facilities are available, the patient should be connected to a cardiac monitor and pulse oxymeter for recording pulse rate and percentage of oxygen saturation (Sa02 %) respectively. Falling tidal volume to 300 ml and hypoxaemia are indications for early intubation and assisted ventilation. At the time of intubation, the correct endotracheal tube should be selected and it should be anchored to the mouth to avoid slipping into right bronchus which would lead to collapse of left lung. Initially, assisted ventilation could be done with Ambu-bag and in children forceful Ambu-ventilation might lead to pneumothorax. The patient should thereafter be connected to a ventilator in the Intensive Care Unit (ICU). It is important however not to trust the machine and hence the patient should not be left unattended as mechanical problems in the machine could be fatal. Furthermore, it is dangerous to ventilate the patient in a busy medical ward where nursing staff are not geared to look after a ventilated patient. Ambu ventilation is safe and should be continued until the patient is transferred to an ICU.
Respiratory paralysis could occur whilst the patient is in a peripheral hospital with no ICU facilities. In this situation, the patient should be intubated at the earliest sign of respiratory paralysis and arrangements should be made to transfer the patient accompanied by a Medical Officer carrying an Ambu bag, additional endotracheal tubes, oxygen, facemasks and basic drugs for resuscitation. During the journey the endotracheal tube may slip into right bronchus leading to left lung collapse and right side pneumothorax may also occur. To prevent the tube being bitten, a mouth gag should be inserted. The tube may get obstructed due to secretions or kinking leading to cyanosis and resistance to Ambu-ventilation. Then the tube should be pulled out immediately and Ambu- ventilation could be continued with a face mask.
In the ICU, the standard protocol should be followed during assisted ventilation and the patient should be monitored for all parameters including level of consciousness. Drugs such as sedatives, morphine and neuromuscular blocking agents should be avoided. Some patients go into a deep coma state but recover completely. Hence, diagnosis of brain death should not be considered. Recovery of respiratory muscles is reflected by improvement of neck flexors where flexing the neck against gravity indicates timing to wean off ventilation. Prophylactic antibiotics are unnecessary.
Minor coagulopathy represented by positive WBCT20 is generally reversed with the standard dose of antivenom. In the case of acute severe coagulopathy, the initial dose of antivenom should be increased up to 30 vials. Persisting positive WBCT20 beyond 24h can be considered as subacute severe coagulopathy where repeated doses of antivenom would be beneficial. Furthermore, replacement of clotting factors with fresh frozen plasma may be useful. If prothrombin time is prolonged, vitamin K is indicated. Occasionally, clotting defects might persist without further deterioration and normalize with the clinical improvement.
Multiple organ failure (MOF)
Management is supportive, and prevention of organ damage in those at risk are therefore crucial. Aggressive early resuscitation, adequate antivenom therapy, excision of devitalized tissue and treatment of infection are important. Prompt recognition of organ dysfunction and immediate intervention may reverse organ impairment and improve the outcome.
Hyperkalaemia and acute renal failure
Definitive treatment for hyperkalaemia is either peritoneal or haemo dialysis to remove potassium from the body. However, emergency treatments for hyperkalaemia are as follows:
(1) 10 ml of 10% calcium gluconate bolus iv over 3 min would protect myocardium. This drug can be given repeatedly and it doesn’t alter the serum K+ level.
(2) Soluble insulin 10 units in 50ml, 50% dextrose iv over15-30 min. This will drive potassium into cells and the effect lasts up to 2hrs and repeat it as necessary Beware that patient may develop hypoglycaemia.
(3) Correction of severe acidosis with 1.26% NaHCO3 solution, 50 – 100ml intravenous infusion over 15 min. In acidosis, hyperkalaemic effects are severe.
(4) Calcium or sodium resonium given orally 15g three times daily with laxatives will deplete body potassium.
(A) Dialysis in acute renal failure
Dialysis is indicated in oliguria or anuria with rising blood urea or creatinine, fluid overload leading to pulmonary oedema, metabolic acidosis in addition to hyperkalaemia. Peritoneal dialysis is commonly used and haemodialysis is recommended in complicated situations such as continuous bleeding into peritoneum and peritonitis. Duration of peritoneal dialysis varies from 4 – 14 days.
Problems encountered during dialysis are as follows:
(1) Repeated obstruction due to the omentum: This problem is common if the dialysis catheter is placed close to umbilicus and if it is not placed in the pelvic cavity. The catheter should be inserted between the umbilicus and symphysis pubis and directed towards the pelvic cavity. Initial dialysis cycles should be done continuously without a dwelling time. Adding 100 units of heparin to each cycle could be done if there is no bleeding.
(2) Positive fluid balance: Adding 100ml of 50% dextrose to each liter of dialysis fluid would produce a negative balance. After achieving adequate dehydration and negative balance, dextrose should be tailed off by adding it to every other cycle.
(3) Hypokalaemia: Continuous peritoneal dialysis removes body potassium and may produce hypokalaemia usually after 48 hours of dialysis. It is detected by regular electrolyte measurement and an ECG which show U waves. Potassium level could be maintained with 2 ml of potassium chloride added to every other liter of dialysis fluid. Monitoring of serum potassium level should be done regularly and supplementation should be adjusted accordingly.
(4) Peritonitis: If the procedure of insertion of peritoneal catheter is not clean, contamination could occur. Repeated obstruction of the catheter, reinsertion, interruption to dialysis cycles, slow cycles with prolonged dwelling cycles also contribute to peritonitis. Development of abdominal pain, tenderness, turbid dialysis output, fever and poor well being are suggestive of peritonitis. In suspected cases, dialysis fluid should be sent for culture and antibiotic sensitivity test. However, cultures should be done periodically from 3 rd day of dialysis for early detection of peritonitis. Management includes continuation of rapid cycles, parenteral antibiotics and adding antibiotics to dialysis fluid. If the condition gets worse peritoneal dialysis should be terminated and arrangements made for haemodialysis.
(5) Infection around the catheter site: Insertion of dialysis catheter under strict asepsis with minimum handling thereafter, would minimize this problem. However, established infection should be treated with appropriate antibiotic pending culture report of the swab taken from the site.
(6) Continuously blood stained dialysis drainage: This is not an uncommon problem in snake bite due to persisting coagulopathy and oozing blood into peritoneal cavity. Coagulopathy should be managed accordingly and fresh blood transfusions may be given to correct anaemia and to replace clotting factors. However, it is not an indication to terminate the dialysis.
(7) Trauma to internal organs and tissues: In this situation blood clots are detected with haemorrhagic dialysis drainage. Surgical intervention may be required.
Polyuric phase: When the renal tubular function improves, the patient starts to produce more urine. However, ability to concentrate urine is diminished and the patient passes a large volume of urine. Dialysis should be terminated with the development of polyuric phase. Potassium supplements are needed as there is a risk of hypokalaemia. Oral KCL is recommended if tolerance is good. Simultaneously adequate hydration of the patient should be maintained with either intravenous fluids or oral fluids.
(B) Conservative management of acute renal failure
If there is no indication for dialysis, patient can be managed conservatively, anticipating an improvement in renal function. These include limiting fluid input to insensible loss and urine output, avoiding all potassium containing foods and liquids, limiting proteins and intermittent diuretic challenge. Diuretic challenge means infusion of 200ml of intravenous fluid either 5% dextrose or normal saline added with intravenous frusemide 40 – 60mg. The purpose of this is to shift the oliguric state into a polyuric acute renal failure which carries a better prognosis than oliguric acute renal failure. However, close monitoring is needed as patient may require dialysis at any time.
Acute respiratory distress syndrome (ARDS)
This needs mechanical ventilation with a high inspired concentration of oxygen. Very often 100% oxygen is needed despite potential oxygen toxicity. Additionally, positive end expiratory pressure (PEEP) 5 – 10mmHg would improve the hypoxaemia. Despite these measures, prognosis is not satisfactory in most of the cases. Patient should be dehydrated by giving a limited amounts of intravenous fluids as that would help to reduce the pulmonary oedema. However, fluid management is crucial and hypovolaemic hypotension should be avoided. Broad spectrum antibiotic may be given to prevent secondary pneumonia. With the improvement of oxygenation, inhaled oxygen concentration should be reduced to minimize lung damage.
Doesn’t need specific treatment but the patient should be well hydrated to achieve a good diuresis. Complications should be treated accordingly.
Cardiac dysfunction and cardiogenic shock
Uncomplicated myocardial dysfunction and ischaemia need supportive management (oxygen) and monitoring to detect complications. Patients in cardiogenic shock must be managed in an ICU and inotropic agents are given to maintain cardiac output and perfusion of vital organs. Commonly used inotropic drugs are dopamine and dobutamine. Dopamine is a natural precursor of noradrenaline which acts on “b” and “a” receptors and dopaminergic (DA) receptors. At low doses of dopamine, dopaminergic effect is predominant which increases the hepatic and renal blood flow producing good urine output. Dobutamine has predominantly “b1“activity and no effect on DA receptors. Infusion of low doses of dopamine alone is adequate in a case of mild cardiogenic shock. However, in severe cases dobutamine is added to maintain blood pressure and cardiac performances.
Severe local necrosis
Management depends on the degree of local effects and the species of snake responsible for bite. Cobra bite produces severe necrosis early. Surgical intervention is mandatory and all necrotic tissues should be excised including subcutaneous fat. Margins of excision should be kept at healthy tissues and at depth tendons and muscles might get exposed. Inadequate debridement leads to persistent spreading of necrosis. Compartment syndrome needs a fasciotomy once haemostatic abnormalities have been corrected. Excised tissues should be sent for bacteriological studies. Systemic antibiotics with anaerobic cover may be beneficial. Hump nosed viper bite produces haemorrhagic blisters which need aspiration. Russell’s viper seldom produces necrosis. Finally, surgical wound may need skin grafting.
CNS complication and Intracranial bleeding
Should be managed according to the standard practice. Neurosurgical opinion may be requested according to intracranial pathology. However, haemostatic abnormalities must be corrected.
Coma, autonomic dysfunctions
Patient in deep coma recovers fully provided there is no hypoxic brain damage. Autonomic dysfunctions are transient and don’t need treatment. Sometimes treatment might be harmful e.g. treating with antihypertensive drugs to lower the increased blood pressure due to sympathetic hyperactivity.
Hepatic dysfunction, pancreatitis, endocrine insufficiency and deep venous thrombosis should be managed according to the standard practice.
Rehabilitation is needed for complicated patients who have recovered after a long hospital stay. These late complications occur due to the following reasons:>
1. Direct venom toxicity
2. Treatment procedures and interventions.
3. Prolonged bed ridden state
Direct effects of venom toxicity could lead to mononeuritis, peripheral neuropathy and ataxia. These are seen in common krait bite envenoming and reversible with time. Large scars at the bittten site with contractures due to deeper damage could occur following cobra bite. However, chronic organ failure such as chronic renal failure doesn’t generally occur. Hump nosed viper bite could produce tapering of bitten digits and severe neuralgic pain lasting many months.
Stridor due to subglotic or tracheal stenosis could happen due to prolonged intubation and ventilation. This is preventable by using correct sized endotracheal tube and intermittent release of the cuff. However, steroids may be helpful to reduce mucosal oedema during the acute stage and early referral to an ENT surgeon is mandatory. Due to prolonged bed stay, bedsores could develop and pressure on contact parts could produce nerve palsies. To prevent these, physiotherapy, and optimum nursing care are needed and a nutritionally balanced diet must be given. Parenteral nutrition or nasogastric feeding may be given during the acute stage.
Common krait and Ceylon krait
There is acute respiratory muscles paralysis (ventilatory support may be needed as early as 10 min from the time of bite or as late as 30 hours), deep coma, autonomic disturbances and metabolic disturbances such as hypokalaemia. Furthermore, ARDS is related to nasal insufflation and aspiration pneumonia and rarely myoglobinuria may also manifest.
Rapid onset neurotoxicity within a few minutes after bite may leads to acute respiratory muscles paralysis which requires artificial ventilation. Extensive local necrosis may occur at the bitten site.
Acute disseminated intravascular coagulation (DIC), hyperkalaemia, acute renal failure, cardiogenic shock, ARDS and rarely respiratory muscles paralysis requiring mechanical ventilation, rhabdomyolysis, myoglobinuria, bleeding to internal organs and organ dysfunction.
Acute renal failure due to renal cortical necrosis and reversible prolonged coagulation defect.
Green pit viper
Gross swelling and pain in the bitten limb and painful lymphadenopathy.