Thursday, July 30, 2009

Treatment for Snake Bites

Sorry for the delay. I kinda forgot that we have PCL until a few hours ago...Well..Better late than never.


HOW IS ANTIVENOM ADMINISTERED?
Snake antivenoms must be given by the intravenous route. In dire circumstances, if a vein cannot be cannulated, antivenom may be given intraosseously, particularly in young children. The intramuscular route is useless in emergencies as absorption is slow, and there is a large volume of fluid to be administered. If required for small children, the dilution may be less to prevent excessive fluid administration.
In emergencies the antivenom may be infused quickly in high concentration. A test dose of antivenom to determine allergy should not be given since it is unreliable and a waste of precious time.

Freeze-dried (lyophilised) antivenoms are reconstituted, usually with 10 ml of sterile water for injection per ampoule. The freeze-dried protein may be difficult to dissolve. Two methods of administration are recommended:
i) Intravenous "push" injection: reconstituted freeze-dried antivenom or neat liquid antivenom is given by slow intravenous injection (not more than 2 ml/minute). This method has the advantage that the doctor/nurse/dispenser giving the antivenom must remain with the patient during the time when some early reactions may develop. It is also economical, saving the use of intravenous fluids, giving sets, cannulae etc.
ii) Intravenous infusion: reconstituted freeze-dried or neat liquid antivenom is diluted in approximately 5-10 ml of isotonic fluid per kg body weight (ie 250-500 ml of isotonic saline or 5% dextrose in the case of an adult patient) and is infused at a constant rate over a period of about one hour.

Patients must be closely observed for at least one hour after starting intravenous antivenom administration, so that early anaphylactic antivenom reactions can be detected and treated early with epinephrine (adrenaline).

Local administration of antivenom at the site of the bite is not recommended!
Although this route may seem rational, it should not be used as it is extremely painful, may increase intracompartmental pressure and has not been shown to be effective.

Intramuscular injection of antivenom
Antivenoms are large molecules (F(ab0)2 fragments or sometimes whole IgG) which, after intramuscular injection, are absorbed slowly via lymphatics. Bioavailability is poor, especially after intragluteal injection and blood levels of antivenom never reach those achieved rapidly by intravenous administration. Other disadvantages are the pain of injection of large volumes of antivenom and the risk of haematoma formation in patients with haemostatic abnormalities.
Antivenom must never be given by the intramuscular route if it could be given intravenously.
Situations in which intramuscular administration might be considered :
-at a peripheral first aid station, before a patient with obvious envenoming is put in an ambulance for a journey to hospital that may last several hours;
-on an expedition exploring a remote area very far from medical care;
-when intravenous access has proved impossible.
Although the risk of antivenom reactions is less with intramuscular than intravenous administration, epinephrine (adrenaline) must be readily available.
Under these unusual circumstances, the dose of antivenom should be divided between a number of sites in the upper anterolateral region of both thighs. A maximum of 5-10 ml should be given at each site by deep intramuscular injection followed by massage to aid absorption. Local bleeding and haematoma formation is a problem in patients with incoagulable blood.
Finding enough muscle mass to contain such large volumes of antivenom is particularly difficult in children.

Antivenom should never be injected into the gluteal region (upper outer quadrant of the buttock) as absorption is exceptionally slow and unreliable and there is always the danger of sciatic nerve damage when the injection is given by an inexperienced operator.


Amount/dose
Test patient's sensitivity to antivenom by giving 0.2 ml subcutaneously first, then observe for 30 minutes. If no adverse reactions occur, administer the required amount of antivenom diluted in 200 ml of saline or 5%D by slow IV drip over 1 hour.
If anaphylaxis occur, adrenaline 0.5 ml of 1:1000 should be drawn up. Reaction may develop despite negative sensitivity but can be controlled by adrenaline subcutaneously with or without antihistamines and steroids. Routine anti-histamine, SC adrenaline and hydrocortisone may be given prior to infusion to prevent reaction to antivenom.
For a patient with a known allergic history, two lines should be set up. One for the antivenom; the other line for adrenaline and hydrocortisone. Adrenaline and hydrocortisone should not be mixed in the same bottle but the same line can be used for infusion (e.g via Y-connector).
For a patient with positive skin reaction, consultation with the nearest hospital with medical specialist as regards next course of action should be made.
For children, it is recommended that half to two- thirds of adult dose should be given.
If there is no improvement after the first dose of antivenom, a repeat treatment may be given an hour later. Antivenom is probably of less value after 12 hours; however, it can be effective, particularly for clotting defects, even after 24 hours.

Snakes inject the same dose of venom into children and adults. Children must therefore be given exactly the same dose of antivenom as adults.
Manufacturers’ recommendations are usually based on inappropriate animal tests in which venom and antivenom are incubated before being injected into the test animal. The recommended dose is often the amount of antivenom required to neutralise the average venom yield when captive snakes are milked of their venom. In practice, the choice of an initial dose of antivenom is usually empirical.
Antivenom manufacturers, health institutions and medical research organisations should encourage and promote the proper clinical testing of antivenoms as with other therapeutic agents. This is the only reliable guide to the initial dose (and safety) of an antivenom.
Since the neutralising power of antivenoms varies from batch to batch, the results of a particular clinical trial may soon become obsolete if the manufacturers change the strength of the antivenom.


SHOULD ADRENALINE BE ADMINISTERED FIRST?
Antivenom serum is the most effective, if not the only effective, treatment available for management of snake bite envenomation. Adverse effects of the serum are common, and anaphylaxis can be fatal. Increasing the safety of treatment with antivenom serum for snake bite victims is, therefore, a matter of high priority.

Adrenaline is the drug of choice in the treatment of anaphylaxis, and it is likely to be useful in the prevention of such acute reactions to serum. There is a general reluctance to use adrenaline because of potential side effects and lack of clear guidelines on use. The only available data on use of adrenaline before treatment with antivenom serum are from a few uncontrolled retrospective studies from Australia. These data suggest that adrenaline is safe and effective in reducing acute adverse reactions.

What WHO says:

At the earliest sign of a reaction:
i) Antivenom administration must be temporarily suspended
ii) Epinephrine (adrenaline) (0.1% solution, 1 in 1,000, 1 mg/ml) is the effective treatment for early anaphylactic and pyrogenic antivenom reactions

Epinephrine (adrenaline) is given intramuscularly (into the deltoid muscle or the upper lateral thigh) in an initial dose of 0.5 mg for adults, 0.01 mg/kg body weight for children. Severe, life-threatening anaphylaxis can evolve very rapidly and so epinephrine (adrenaline) should be given at the very first sign of a reaction, even when only a few spots of urticaria have appeared or at the start of itching, tachycardia or restlessness. The dose can be repeated every 5-10 minutes if the patient’s condition is deteriorating.

The routine mode of administration of adrenaline should be the subcutaneous route because it does not cause significant hypertension. However, in a moribund or critically ill patient when it is essential to administer antivenom as soon as possible, adrenaline may be given intramuscularly or even intravenously in smaller doses. In general, intramuscular and intravenous routes are not recommended since they may induce hypertension which in the presence of venom-induced coagulopathy could cause an intracerebral haemorrhage.

Next paragraph is from http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=27835
Based on a research published in British Medical Journal:

The prophylactic use of 1:1000 adrenaline in a dose of 0.25ml given subcutaneously immediately before infusion of antivenom serum significantly reduces the risk of acute adverse reactions.

There is no clear scientific evidence or uniform policy for the use of premedication to prevent acute adverse reactions to antivenom serum.

A major concern regarding the use of adrenaline as premedication is the potential risk of intracerebral haemorrhage; a result of the combination of the ability of certain snake venoms to cause coagulopathy and the risk of hypertension with use of adrenaline. This has led to a reluctance to use adrenaline.

Few studies have analysed the risk of cerebral haemorrhage after use of adrenaline. Of seven cases of fatal intracerebral haemorrhage after snake bite documented in Australia, only three patients had received adrenaline as premedication, making the evidence incriminating adrenaline as the cause of cerebral haemorrhage weak. Fears of development of hypertension after low dose adrenaline also seem unfounded.

From http://www.flyingdoctor.net/monographs/snakebite.pdf
by: Dr Struan Keith Sutherland & Dr James Tibballs
It is not prudent to forgo premedication and elect to treat anaphylaxis if it occurs. Iatrogenic anaphylaxis has a high mortality despite vigorous and expert resuscitation. If there is no adverse reaction to the first ampoule of antivenom, subsequent doses do not need to be preceded by adrenaline.


SERUM SICKNESS
What is serum sickness?
Serum sickness is a reaction similar to an allergy. Specifically, it is an immune system reaction to certain medications, injected proteins used to treat immune conditions, or antiserum, the liquid part of blood that contains antibodies that help protect against infectious or poisonous substances.

Serum sickness is a reaction by the immune system against large amounts of foreign protein that have entered the bloodstream. A common source of such foreign protein is horse serum, an ingredient present in many venom antidotes (antivenoms) that are used to treat poisonous snake and spider bites and scorpion stings.

Symptoms of serum sickness include fever, rash, joint pains and sometimes swollen lymph nodes. Rarely, kidney damage and death can occur.

Doctors treat serum sickness with antihistamines, such as diphenhydramine Some Trade Names BENADRYL, and corticosteroids. Antivenoms that do not contain horse serum are unlikely to result in serum sickness.

Corticosteroid creams or ointments or other soothing skin medications may relieve discomfort from itching and rash.
Antihistamines may shorten the length of illness and help ease rash and itching.
Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or naproxen, may relieve joint pain. Corticosteroids taken by mouth (such as prednisone) may be prescribed for severe cases.

Prevention of serum reaction: before injecting the antivenom
-Enquire whether patient has been given serum injections before (eg the old ATS but not ATT).
-Patient has personal or family history of allergy
-Test sensitivity of patient to serum by intradermal injection of 0.1 ml of serum diluted 1:10. Observe for 30 minutes for local and general reactions. If these occur, consider giving IV diphenhydramine, IV corticosteroids and/or IM adrenaline 1:1,000 or IV adrenaline 1:10,000.
-Inject antivenom in allergic or sensitive patients under cover of antihistamines and hydrocortisone given 15-30 minutes before administration of the antivenom.
-Give anticholinesterases for patient with severe neurotoxic symptoms, administer test dose of IV edrophonium chloride (Tensilon) 10 mg with IV atropine 0.6 mg. If response is convincing, administer IV neostigmine. Consultation with a neurologist is advised.


References:
http://74.125.153.132/search?q=cache:u0Zd8aFc5Q8J:www.moh.gov.my/MohPortal/DownloadServlet%3Fid%3D2100%26type%3D2+management+snakebite&cd=4&hl=en&ct=clnk&gl=my

http://www.flyingdoctor.net/monographs/snakebite.pdf

http://www.searo.who.int/EN/Section10/Section17/Section53/Section1024_3900.htm

http://www.merck.com/mmhe/sec24/ch298/ch298d.html

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=27835 (research paper by british medical journal. quite interesting.)

All about serum sickness:
http://www.nlm.nih.gov/medlineplus/ency/article/000820.htm#visualContent

http://emedicine.medscape.com/article/887954-overview








King Cobra(Ophiophagus hannah)
-longest venomous snake, can grow over 18 ft.
-light coloured bands that run across its body.
-large scale on its head and prominent eyes.
-When angered, it will flatten out its neck and raise 1/3 of its body.
-Emits a chilling sound to warn off predators.













Malayan Pit Viper(Agkistrodon rhodostoma)
-Average size: 5 ft
-Have a pit that sets pit vipers apart from others. (heat sensing organ between eyes and nostrils)
-Folds its fangs under and back into the roof of its mouth and extends when it strikes in stabbing motion.
-Head usually triangular and wider than its neck. Due to the large venom glands in the snake's jaw.

Prevalence Of Snake Bite in Malaysia from 1999-2003

A hospital based retrospective study of the prevalence of snakebite cases at Hospital Kuala Lumpur was carried out over a five-year period from 1999 to 2003. A total of 126 snakebite cases were recorded. The highest admission for snakebites was recorded in 2001 (29 cases). The majority of cases were admitted for three days or less (79%). Most of the snakebite cases were reported in the 11-30 years age group (52%). The male:female ratio was 3:1. The majority of cases were Malaysians (80%, 101 cases). Of the non-Malaysians, Indonesians constituted the most (56%, 14 cases). Bites occurred most commonly on the lower limbs (49%), followed by upper limbs (45%) and on other parts of the body (6%). No fatal cases were detected and complications were scarce. In 60% (70 cases) the snake could not be identified. Of the four species of snakes that were identified, cobra (both suspected and confirmed) constituted the largest group (25%), followed by viper (10%), python (4%) and sea snake (1%). The most common clinical presentations were pain and swelling, 92% (116 cases). All patients were put on snakebite charts and their vital signs were monitored. Of the snakebite cases, 48% (61 cases) were treated with cloxacillin and 25% (32 cases) were given polyvalent snake antivenom.

Source:
http://www.ncbi.nlm.nih.gov/pubmed/16771235?dopt=AbstractPlus
http://www.tm.mahidol.ac.th/seameo/2004/35_4/33-3302.pdf

First Aid

First Aid

1. Keep the person calm, reassuring them that bites can be effectively treated in an emergency room. Restrict movement, and keep the affected area below heart level to reduce the flow of venom.

2. If you have a pump suction device (such as that made by Sawyer), follow the manufacturer's directions.

3. Remove any rings or constricting items because the affected area may swell. Create a loose splint to help restrict movement of the area.

4. If the area of the bite begins to swell and change color, the snake was probably poisonous.

5. Monitor the person's vital signs -- temperature, pulse, rate of breathing, and blood pressure -- if possible. If there are signs of shock (such as paleness), lay the person flat, raise the feet about a foot, and cover the person with a blanket.

6. Get medical help right away.

7. Bring in the dead snake only if this can be done safely. Do not waste time hunting for the snake, and do not risk another bite if it is not easy to kill the snake. Be careful of the head when transporting it -- a snake can actually bite for up to an hour after it's dead (from a reflex).

8.Immobilise the bitten limb with a splint or a sling (any movement or muscular contraction increases absorption of venom into the bloodstream and lynphatics.

9.Avoid any interference with the bite wound as this may introduce infection, increase absorption of venom and increase bleeding.

DO NOT

* DO NOT allow the person to become over-exerted. If necessary, carry the person to safety.
* DO NOT apply a tourniquet.
* DO NOT apply cold compresses to a snake bite.
* DO NOT cut into a snake bite with a knife or razor.
* DO NOT try to suck out the venom by mouth.
* DO NOT give the person stimulants or pain medications unless a doctor tells you to do so.
* DO NOT give the person anything by mouth.
* DO NOT raise the site of the bite above the level of the person's heart.
* DO NOT make local incisions or punctures at the site of the bite or in the bitten limb.
* DO NOT use (black) snake stones.
* DO NOT give electric shock, topical instillation or application of chemicals, herbs and ice packs.

Aims of first aid

attempt to retard systemic absorption of venom

preserve life and prevent complications before the patient can receive medical care (at a dispensary or hospital)

control distressing or dangerous early symptoms of envenoming

arrange the transport of the patient to a place where they can receive medical care (5.2)

ABOVE ALL, DO NO HARM!


The special danger of rapidly developing paralytic envenoming after bites by some elapid snakes: use of pressure-immobilisation

Bites by cobras, king cobras, kraits or sea snakes may lead, on rare occasions, to the rapid development of life-threatening respiratory paralysis. This paralysis might be delayed by slowing down the absorption of venom from the site of the bite. The following technique is currently recommended:

Pressure immobilisation method Ideally, an elasticated, stretchy, crepe bandage, approximately 10 cm wide and at least 4.5 metres long should be used. If that it not available, any long strips of material can be used. The bandage is bound firmly around the entire bitten limb, starting distally around the fingers or toes and moving proximally, to include a rigid splint. The bandage is bound as tightly as for a sprained ankle, but not so tightly that the peripheral pulse (radial, posterior tibial, dorsalis pedis) is occluded or that a finger cannot easily be slipped between its layers.

* Pressure immobilization is recommended for bites by neurotoxic elapid snakes including sea snakes but should not be used for viper and cobra bites because of the danger of increasing the local effects of the necrotic venom.

*Ideally, compression bandages should not be released until the patient is under medical care in hospital, resuscitation facilities are available and antivenom treatment has been started.

*The use of a local compression pad applied over the wound, without pressure bandaging of the entire bitten limb, has produced promising results in Myanmar and deserves further study.

Transport to hospital

The patient must be transported to a place where they can receive medical care (dispensary or hospital) as quickly, but as safely and comfortably as possible. Any movement, but especially movement of the bitten limb, must be reduced to an absolute minimum to avoid increasing the systemic absorption of venom. Any muscular contraction will increase this spread of venom from the site of the bite. A stretcher, bicycle, cart, horse, motor vehicle, train or boat should be used, or the patient should be carried.

Investigation and Diagnosis

5.4 Detailed clinical assessment and species diagnosis

5.4.1 History

A precise history of the circumstances of the bite and the progression of local and systemic symptoms and signs is very important. Three useful initial questions are:

"In what part of your body have you been bitten?" The doctor can see immediately evidence that the patient has been bitten by a snake (eg fang marks) and the nature and extent of signs of local envenoming.

"When were you bitten?" Assessment of the severity of envenoming depends on how long ago the patient was bitten. If the patient has arrived at the hospital soon after the bite, there may be few symptoms and signs even though a large amount of venom may have been injected.

"Where is the snake that bit you?" If the snake has been killed and brought, its correct identification can be very helpful. If it is obviously a harmless species (or not a snake at all!), the patient can be quickly reassured and discharged from hospital.

Early clues that a patient has severe envenoming:

* Snake identified as a very dangerous one

* Rapid early extension of local swelling from the site of the bite

* Early tender enlargement of local lymph nodes, indicating spread of venom in the lymphatic system

* Early systemic symptoms: collapse (hypotension, shock), nausea, vomiting, diarrhoea, severe headache, "heaviness" of the eyelids, inappropriate (pathological) drowsiness or early ptosis/ophthalmoplegia

* Early spontaneous systemic bleeding

* Passage of dark brown urine

Patients who become defibrinogenated or thrombocytopenic may begin to bleed from old, partially-healed wounds as well as bleeding persistently from the fang marks.

The patient should be asked how much urine has been passed since the bite and whether it was a normal colour.

An important early symptom of sea snake envenoming that may develop as soon as 30 minutes after the bite is generalised pain, tenderness and stiffness of muscles and trismus.

5.4.2 Physical examination

This should start with careful assessment of the site of the bite and signs of local envenoming.

5.4.2.1 Examination of the bitten part

The extent of swelling, which is usually also the extent of tenderness to palpation, should be recorded. Lymph nodes draining the limb should be palpated and overlying ecchymoses and lymphangitic lines noted.

A bitten limb may be tensely oedematous, cold, immobile and with impalpable arterial pulses. These appearances may suggest intravascular thrombosis, which is exceptionally rare after snake bite, or a compartmental syndrome, which is uncommon. If possible, intracompartmental pressure should be measured (see Annex 5) and the blood flow and patency of arteries and veins assessed (eg by doppler ultrasound).

Early signs of necrosis may include blistering, demarcated darkening (easily confused with bruising) or paleness of the skin, loss of sensation and a smell of putrefaction (rotting flesh).

5.4.2.2 General examination

Measure the blood pressure (sitting up and lying to detect a postural drop indicative of hypovolaemia) and heart rate. Examine the skin and mucous membranes for evidence of petechiae, purpura, ecchymoses and, in the conjunctivae, chemosis. Thoroughly examine the gingival sulci, using a torch and tongue depressor, as these may show the earliest evidence of spontaneous systemic bleeding. Examine the nose for epistaxis. Abdominal tenderness may suggest gastrointestinal or retroperitoneal bleeding. Loin (low back) pain and tenderness suggests acute renal ischaemia (Russell’s viper bites). Intracranial haemorrhage is suggested by lateralising neurological signs, asymmetrical pupils, convulsions or impaired consciousness (in the absence of respiratory or circulatory failure).

5.4.2.6 Examination of pregnant women

There will be concern about fetal distress (revealed by fetal bradycardia), vaginal bleeding and threatened abortion. Monitoring of uterine contractions and fetal heart rate is useful. Lactating women who have been bitten by snakes should be encouraged to continue breast feeding.

5.4.3 Species diagnosis

If the dead snake has been brought, it can be identified. Otherwise, the species responsible can be inferred indirectly form the patient’s description of the snake and the clinical syndrome of symptoms and signs (see above and Annex 1 & 2). This is specially important in Thailand where only monospecific antivenoms are available.

5.5 Investigations/laboratory tests

5.5.1 20 minute whole blood clotting test (20WBCT)

This very useful and informative bedside test requires very little skill and only one piece of apparatus - a new, clean, dry, glass vessel (tube or bottle).

20 minute whole blood clotting test (20WBCT)

* Place a few mls of freshly sampled venous blood in a small glass vessel

* Leave undisturbed for 20 minutes at ambient temperature

* Tip the vessel once

* If the blood is still liquid (unclotted) and runs out, the patient has hypofibrinogenaemia ("incoagulable blood") as a result of venom-induced consumption coagulopathy

* In the South East Asian region, incoagulable blood is diagnostic of a viper bite and rules out an elapid bite

* Warning! If the vessel used for the test is not made of ordinary glass, or if it has been used before and cleaned with detergent, its wall may not stimulate clotting of the blood sample in the usual way and test will be invalid

* If there is any doubt, repeat the test in duplicate, including a "control" (blood from a healthy person)

5.5.2 Other tests

Haemoglobin concentration/haematocrit: a transient increase indicates haemoconcentration resulting from a generalised increase in capillary permeability (eg in Russell’s viper bite). More often, there is a decrease reflecting blood loss or, in the case of Indian and Sri Lankan Russell’s viper bite, intravascular haemolysis.

Platelet count:this may be decreased in victims of viper bites.

White blood cell count: an early neutrophil leucocytosis is evidence of systemic envenoming from any species.

Blood film: fragmented red cells ("helmet cell", schistocytes) are seen when there is micro-angiopathic haemolysis.

Plasma/serum may be pinkish or brownish if there is gross haemoglobinaemia or myo-globinaemia.

Biochemical abnormalities: aminotransferases and muscle enzymes (creatine kinase, aldolase etc) will be elevated if there is severe local damage or, particularly, if there is generalised muscle damage (Sri Lankan and South Indian Russell’s viper bites, sea snake bites). Mild hepatic dysfunction is reflected in slight increases in other serum enzymes. Bilirubin is elevated following massive extravasation of blood.Creatinine, urea or blood urea nitrogen levels are raised in the renal failure of Russell’s viper and saw-scaled viper bites and sea snake bites.Early hyperkalaemia may be seen following extensive rhabdomyolysis in sea snake bites. Bicarbonate will be low in metabolic acidosis (eg renal failure).

Arterial blood gases and pH may show evidence of respiratory failure (neurotoxic envenoming) and acidaemia (respiratory or metabolic acidosis).

Warning : arterial puncture is contraindicated in patients with haemostatic abnormalities (Viperidae)

Desaturation: arterial oxygen desaturation can be assessed non-invasively in patients with respiratory failure or shock using a finger oximeter.

Urine examination: the urine should be tested by dipsticks for blood/haemoglobin/myoglobin. Standard dipsticks do not distinguish blood, haemoglobin and myoglobin.Haemoglobin and myoglobin can be separated by immunoassays but there is no easy or reliable test. Microscopy will confirm whether there are erythrocytes in the urine. Red cell casts indicate glomerular bleeding. Massive proteinuria is an early sign of the generalised increase in capillary permeability in Russell’s viper envenoming.

Taken From :
http://www.searo.who.int/EN/Section10/Section17/Section53/Section1024_3900.htm

Wednesday, July 29, 2009

TYPES OF NEUROTOXINS + CLINICAL EFFECT OF NEUROTOXINS

Presynaptic neurotoxins (β-bungarotoxins)

  • Modified phospholipase A2 toxins
  • Found in selected Elapid and Viperid venoms.
  • slow onset
  • specifically target the terminal axon of the neuromuscular junction, causing first release of neurotransmitter, then extensive damage to the axonal structure, completely disrupting transmitter synaptic vesicle production and thus cessation of transmitter release
  • Clinically this causes a progressive flaccid paralysis, with onset of first signs usually 1+ hours post bite, with progressive paralysis thereafter
  • Full respiratory paralysis, including the diaphragm, may take 3-24 hours
  • irreversible
  • only respond to antivenom if given early
  • recovery rate is determined by axonal repair and is not influenced by antivenom therapy


Postsynaptic neurotoxins
(α-bungarotoxins)

  • polypeptides of varying size
  • present in many Elapid and a few Viperid venoms
  • target the neuromuscular junction
  • Usually rapid onset
  • act extracellularly
  • binding to the acetylcholine receptor on the muscle end-plate, blocking neurotransmitter binding, thus causing paralysis
  • The cell is not specifically damaged, therefore this type of flaccid paralysis is often reversible with antivenom therapy, even if very extensive
  • Respond to antivenom and anticholinesterases


Dendrotoxins and Fasciculins

  • synergistic neurotoxins
  • found in some African mamba venoms
  • target the neuromuscular junction
  • causing paralysis and muscle spasms or fasciculation
  • dendrotoxins
    • target certain voltage-gated potassium channels in the terminal axon membrane, ultimately resulting in over-release of neurotransmitter molecules, which swamp and overstimulate the adjacent muscle end-plate receptors
  • fasciculins
    • Inhibit or interfere with the cholinesterases in the junctional space, significantly reducing the normal removal of synaptic acetylcholine.
    • enhances the effect of the dendrotoxins
  • resulting in gross overstimulation of the muscle, causing spasm or fasciculation, effectively paralysing the victim
  • In doing so they also stimulate many types of nerves, resulting in a diversity of effects, which can include pain, sweating, salivation, tearing, piloerection (body hair standing on end), muscle fasciculation, high blood pressure, tingling sensation, particularly around the lips, and flooding of the lungs with fluid (pulmonary oedema)
  • exert their effect rapidly, thus the clinical effects may manifest in less than an hour post-bite


Clinical effect: Paralysis

  • Flaccid paralysis caused by neurotoxins affects skeletal muscles and respiration
  • In most cases, clinically detectable paralysis will not be apparent until at least one hour post-bite and may be delayed up to 24 hours.
  • The cranial nerves are usually affected first, with ptosis often the first sign. Other common presenting signs are dysphonia, dysphagia, drooling and diplopia, the latter due to partial ophthalmoplegia. As paralysis progresses drooling may increase, ophthalmoplegia may become total, with fixed forward gaze, often associated with fixed dilated pupils. Limb weakness becomes apparent, the victim usually first noticing ataxic gait, then inability to walk, then stand or even sit up. The neck may become floppy ("broken neck" sign). Deep tendon reflexes will become reduced, then disappear. Respiratory distress develops and breathing may become shallow, rapid and cyanosis may be apparent. Complete respiratory failure will ensue, unless respiratory support is offered. Time from bite to respiratory failure is highly variable, from as little as 30 minutes (rare) to more than 24 hours, but commonly within 6-12 hours. Without antivenom therapy or anticholinesterases, the period of respiratory failure may vary from less than 24 hours, to several days, or even several weeks.

References

  1. Menez, A 2003, The Subtle beast: snake, from myth to medicine, Taylor & Francis, London
  2. http://www.venomdoc.com/index.html
  3. http://www.venomdoc.com/snake_neurotoxins.html
  4. http://www.toxinology.com/fusebox.cfm?staticaction=snakes/ns-venmed02.htm#

Signs and symptoms or cobra and viper bites

Signs and symptoms or a cobra and viper bite

Difference between a sign and a symptom
-sign: what the doctor sees on the patient with his/her own eyes.
-symptoms: what the doctor cannot see but has to dig out the information by history taking.
OR the information that the patient tells the doctor.

Symptoms of a viper bite.
Symptoms of a pit viper snakebite usually appear within a few minutes to a few hours after a bite and may include:
• Severe, immediate pain with rapid swelling.
• Bruising of the skin.
• Trouble breathing.
• Changes in heart rate or rhythm.
• A metallic, rubbery, or minty taste in the mouth.
• Numbness or tingling around the mouth, tongue, scalp, feet, or the bite area.
• Swelling in lymph nodes near the bite.
• Signs of shock.
Other symptoms may be caused by the bite itself or from fear or worry after being bitten. You may:
• Feel very worried or confused.
• Faint or feel like you might faint.
• Sweat and have chills.
• Be sick to your stomach or vomit.
• Feel weak or dizzy.
If you do not have symptoms within 8 to 12 hours, the snake might not have injected any venom; this is called a dry bite. At least 25%, perhaps up to 50%, of bites are dry.
• Dry bites or bites where only a very small amount of venom is injected may cause slight bleeding, pain, and swelling at the bite injury.
• If a moderate amount of venom was injected, you are more likely to have severe pain, swelling of the whole limb, and general ill feelings, such as nausea, vomiting, and weakness. Swelling of the whole limb is an effect of the venom and can cause to compartment syndrome. This is rare.
• Large amounts of venom usually cause severe pain and severe swelling. You may have trouble breathing, moderate to severe bleeding, and signs of shock after this type of bite.

Conclusion: viper bites cause bleeding disorders-haemotoxic...

Signs and symptoms of cobra bite(venomous or dry)

• Immediate, local pain (almost always present)
• Soft tissue swelling (may be progressive)
• Neurologic findings, which may begin early and be rapidly progressive (in anecdotal cases, victims have suffered respiratory arrest in a matter of minutes) or may be delayed in onset as long as 24 hours
• Alteration of mental status (eg, drowsiness, occasionally with euphoria)
• Complaints related to cranial nerve dysfunction, such as ptosis (often one of the earliest neurotoxic findings), ophthalmoparesis, dysphagia, and dysphasia
• Profuse salivation, nausea, vomiting, and abdominal pain
• Paresis of neck and jaw muscles and generalized muscular weakness followed by flaccid paralysis
• Shortness of breath, respiratory failure (muscular paresis and accumulated secretions)
• Chest pain or tightness
• Eye pain, tearing, blurred vision (with eye exposure to venom from spitting cobras)
Physical
• Impending respiratory failure
o Respiratory distress or weakness
o Cyanosis
• Neurologic dysfunction
o Altered mental status
o Ptosis (may be the earliest sign of systemic toxicity)
o Generalized weakness or paralysis
• Cardiovascular collapse
o Hypotension
o Tachycardia or bradycardia
• Soft tissue edema
• Signs of necrosis usually appear within 48 hours of the bite.
o The area around the fang punctures darkens.
o Blistering may follow.
o Necrosis is usually confined to the skin and subcutaneous tissue but may be quite extensive.
o A putrid smell is characteristic.
• Acute inflammation of the eye follows venom-spitting exposure and is characterized by ocular congestion, edema of the conjunctiva and cornea, and a whitish discharge.

Conclusion: cobra bites cause neurotoxicity. King cobra-myolitic effects.

http://www.revolutionhealth.com/articles/symptoms-of-a-pit-viper-snakebite/th1427
http://www.google.com.my/search?hl=en&safe=off&q=ophthalmoplegia&btnG=Search&meta=

Snake bites

Heyy ppl, this link is pretty useful.
http://www.flyingdoctor.net/monographs/snakebite.pdf

Snake Venom Detection Kit

http://www.toxinology.com/generic_static_files/cslavh_svdk.html

Diagnosis and Investigation

Diagnosis
• Identification of the snake
• Grading severity of envenomation
Definitive diagnosis requires positive identification of the snake and clinical manifestations of envenomation. History should include the time of bite, description of the snake, type of field therapy, underlying medical conditions, allergy to horse or sheep products, and history of previous venomous snakebites and therapy. A complete physical examination, including baseline measurements of limb circumference proximal and distal to the bite site, should be done.
Snake bites should be assumed to be venomous until proved otherwise by clear identification of the species or by a period of observation.
Snake identification: Patients often cannot recall details of the snake's appearance; however, pit vipers differ from nonvenomous snakes (see Fig. 1: Bites and Stings: Identifying pit vipers ). Consultation with a zoo, an aquarium, or a poison control center can help in the identification of snake species.



Coral snakes in the US have round pupils and black snouts but lack facial pits. They have blunt- or cigar-shaped heads and alternating bands of red, yellow (cream), and black, often causing them to be mistaken for the common nonvenomous scarlet king snake, which has alternating bands of red, black, and yellow. The distinguishing feature in the coral snake is that the red bands are adjacent to only yellow bands, not black bands. (“red on yellow, kill a fellow; red on black, venom lack”). Coral snakes have short, fixed fangs and inject venom through successive chewing movements.
Fang marks are suggestive but not conclusive; rattlesnakes may leave single or double fang marks or other teeth marks, whereas bites by nonvenomous snakes usually leave multiple superficial teeth marks. However, the number of teeth marks and bite sites may vary because snakes may strike and bite multiple times.
A dry pit viper bite is diagnosed when no symptoms or signs of envenomation appear over 8 h.
Severity of envenomation: Severity of envenomation depends on the following:
• Size and species of the snake (rattlesnakes > cottonmouths > copperheads)
• Amount of venom injected per bite (cannot be determined by history)
• Number of bites
• Location and depth of the bite (eg, envenomation in bites to the head and trunk tends to be more severe than in bites to the extremities)
• Age, size, and health of the patient
• Time elapsed before treatment
• Patient's susceptibility (response) to the venom
Severity of envenomation can be graded as minimal, moderate, or severe, based on local findings, systemic symptoms and signs, coagulation parameters, and laboratory results (see Table 2: Bites and Stings: Severity of Pit Viper Envenomation ). Grading should be determined by the most severe symptom, sign, or laboratory finding.
Envenomation may progress rapidly from minimal to severe and must be continually reassessed.
If systemic symptoms begin immediately, anaphylaxis should be assumed.
Table 2

Severity of Pit Viper Envenomation
Grade Description
Minimal Changes at bite site only
No systemic symptoms or signs or abnormal laboratory findings
Moderate Changes extend beyond the bite site
Non–life-threatening systemic symptoms and signs (eg, nausea, vomiting, paresthesias)
Mildly abnormal coagulation or laboratory changes without clinically significant bleeding
Severe Changes involving the entire extremity
Severe systemic symptoms and signs (eg, hypotension, dyspnea, shock)
Markedly abnormal coagulation and laboratory changes with or without clinically significant bleeding


Investigations
Basic investigations'-' in snakebite include; hll blood
counts, blood grouping and cross-matching,
prothrombin time, ECG, serum electrolytes, urea,
creatinine and where available venom detection from
the snakebite wounds, using venom detection kits2.
Unknown Snake
In cases of snakebite, effective treatment often depends heavliy on identifying, to an adequate degree, what type of snake was responsible. While the exact species is not always important, some knowledge of the identity can be valuable in prognosis and in selection of the most appropriate antivenom.
Snakes are notoriously variable in their appearance, and visual identification can usually be considered unreliable. Consequently, the health professional must weigh the information from a number of sources judiciously.
1. If a swab can be made of the bite site, or there is a urine, blood or serum sample available, then identification of immunotype may be made through use of the Snake Venom Detection Kit.
2. In some cases, the field can be narrowed by reference to the clinical signs and symptoms.
3. Depending on the locality where the envenomation took place, species distribution may aid in confirming putative identification. This , of course, does not apply in cases where the snake is non-endemic, such as in private collections or zoos.
4. If identification of an endemic snake cannot be made, antivenom - when indicated - should be administered according to the table below. The table does not apply in Victoria or Tasmania in the case of non-endemic snakes, for which the Snake Venom Detection Kit should be used.
5. If no animal was seen, but snakebite suspected, the presence of two puncture wounds close together should suggest either spiderbite or snakebite (some small snakes' fangs are closer together than those of large spiders). In the absence of evident fang marks, differential diagnoses may be considered:
• Insect or other arthropod sting or bite (ant, bee, wasp, fly, beetle, bug, caterpillar, centipede)
• Puncture wound from an inanimate object (e.g., thorn, needle), with or without the introduction of antigens or toxins

Tuesday, July 28, 2009

Histology of the Skin


Hello all, I've tried to come up with some slides and pictures which can help you with tommorow's practical session. Here are a few compilations of slides which I compiled from some websites across the internet. Most of the explanation are of my own so forgive me if it's not really accurate. Enjoy!

CLICK ON THE PICTURES TO ENLARGE AND TO GET A BETTER VIEW.
(Sorry, the pictures look a little off coz its too big)



THICK SKIN The following picture shows the histology slide for thick skin. Things to note for is the thickened keratinized layer or the stratum corneum.

Here is a close up of that layer ( thick purple layer as shown below)


Here shows another view of the whole layer of thick skin.

thick3.jpg picture by whizz35mb



THIN SKIN


Here is a picture of the thin skin: (Notice the much thinner stratum corneum layer as compared to the thick skin)




COMPARISON OF THICK AND THIN SKIN

Here is a side by side comparison of the thick and thin skin:


This plate shows the structural variation of the epidermis in different parts of the body.

The epidermis in all three areas is keratinized stratified squamous epithelium. The thickness varies from one site to the other. Note the marked thickness of the epidermis in C (palm). The epidermis of palms of the hands and soles of the feet is the thickest in the body. In these regions only four layers of the epidermis are well delineated.




SKIN APPENDAGES

Here are the labelled diagrams you can use for the pratical.





MELANOCYTES AND MELANOMA

Here is what melanocytes would look like:
(Notice the brown area? Those are the due to the production of melanin)


As you can see in this picture, the epidermal layer is much much more thicker in melanoma as compared to the normal skin. (Epidermal layer is the one in darker purple)


A closer view at 20x shows disorganisation of the cells. Not sure how else to describe it.


PSORIASIS

Four distinct pathological alterations characterise this disorder:

Inflammation.
Hyperproliferation of the epidermis
Altered maturation of the epidermis (resulting in scaling)
Vascular alterations (which add to redness).


Histology of psoriasis

  1. Marked hyperkeratosis with parakeratosis (abnormal maturation)

  2. Loss of granular layer

  3. Epidermal acathosis and elongation of rete ridges (reflecting hyperproliferative state)

  4. Vascular dilatation (these vessels are abnormal as well). Generalised inflammation can also be seen, with T-lymphocytes in the dermis and epidermis.

    For more info on this : Visit these websites!
    http://www.dermamed.com/tech_docs/psoriasis/psoriasis_lit.asp http://www.dermnet.com/thumbnailIndex.cfm?moduleID=15&moduleGroupID=462&groupIndex=0&numcols=0


Monday, July 27, 2009

Resource Website

http://www.avru.org/index.html

Just posting to share this resource website by the Australian Venom Research Unit. The 'First Aid', 'Clinical' and 'General' sections especially provide some decent amount of information.

Anatomy of the Skin (Integumentary System)

Hey guys...this is what i have found. I used Saladin, Wheater's and a website for this...i wont label the images nor post them up coz they cannot be uploaded here..so i will post the link for you guys to refer to the images aites?...the images cl..early show both thick and thin skin enjoy your night ppl

1. Draw and label a diagram showing histological features of thick skin
2. Draw and label a diagram showing histological features of thin skin for
comparison.
Answer: refer to website-
connectiondev.lww.com/Products/eroschenko/documents/.../Ch10.pdf



3. List the 4 major cell types in epidermis and state their function. What are the key changes seen in disorders involving melanocytes such as vitiligo & malignant melanoma.
Answer:
Keratinocytes-synthesize keratin by a process known as keratinisation or cornification.Keratinocytes of the stratum basale undergo mitosis and produce new epidermal cells to replace the dead ones that exfoliate (flake off) from the surface.

Melanocytes-synthesize the pigment melanin. They have long branching processes that spread among the basal keratinocytes and continually shed melanin-containing fragments from their tips. The keratinocytes phagocytize these fragments and accumulate melanin granules on the “sunny side” of the nucleus. Like a little parasol, the pigment shields the DNA from ultraviolet radiation. People of all skin colors have about equal numbers of melanocytes. Differences in color result from differences in the rate of melanin synthesis and how clumped or spread out the melanin is in the keratinocytes. In light skin, the melanin is less abundant and is relatively clumped near the nucleus, imparting less colour to the cells.

Merkel cells-relatively few in number, are receptors for the sense of touch. The tactile cell and its dermal nerve fiber are collectively called a tactile (Merkel) disc.

Langerhan’s cell-antigen presenting cells(APC),express a large number of lymphocyte and macrophage surface markers.

Vitiligo-common disease in which symmetrical areas of depigmentation of the skin occur,often on the hands,fingers and face. The disease destroys all the melanocytes in the affected skin and skin becomes glaringly white, the keratinocytes are not affected. It is an autoimmune disease and destroys the melanocytes.

Malignant melanoma-malignant tumour of melanocytes, particularly affecting pale-skinned people who are exposed to excessive UV light.


4. With the help of a diagram, highlight the microscopic features of the major skin appendages.
Answer:
Refer to Saladin 4th Ed integumentary System


5. What is psoriasis? Briefly describe the main histopathological features associated with this disease.
Answer:
The transition of keratinocytes from replicating basal cell,through the keratinocytes of the prickle cell layer(stratum spinosum), to the flattening and degenerating granular layer cells(stratum granulosum) packed with tonofibrils and keratinohyaline granules can be regarded as an efficient sequence culminating in the production of a tough resistant keratin layer on the surface of skin. The normal transit time is 50-60 days but psoriasis causes the transition to only take about 7 days. It isa common skin condition with unknown aetiology but with an element of multifactorial inheritance. The maturation process is so rushed that there is insufficient time for full development of tonofibrils and keratohyaline in the stratum spinosum and the granular layer does not form. Instead of normal keratin, there is a surface opaque white scale composed of a mixture of keratin and nuclear and cytoplasmic debris of keratinocytes. The rapidly proliferating epidermis is thickened to produce raised red patches under the white scale.


Hope it helps...XD....

Antivenom Treatment

Guys, the antivenom treatment is in PDF file so I will give you the link to it. It is about Clinical Protocol Guildelines of Snake Bite in Malaysia and provides a guildline to all GP of how to manage a patient with snake bite. It is quite informative and easy to understand. Thanks! =)


HAPPPPPYYY BIRTHDAYY EWEJIN!!!! :P

Treatment of Snake Bites

HOW ARE SNAKE BITES TREATED?
• Wash the bite with soap and water.
• Restrict movement. Immobilize the bitten area and keep it lower than the heart.
• Remove any rings or constricting items because the affected area may swell. Create a loose splint to help restrict movement of the area
• Cover the area with a clean, cool compress or a moist dressing to minimize swelling and discomfort
• Monitor vital signs. temperature, pulse, rate of breathing, and blood pressure
• Apply a bandage, wrapped two to four inches above the bite, to help slow the venom. This should not cut off the flow of blood from a vein or artery - the band should be loose enough to slip a finger under it.
• A suction device can be placed over the bite to help draw venom out of the wound without making cuts. These devices are often included in commercial snake bite kits.
• DO NOT apply a tourniquet as it can block arterial blood flow to the affected area and worsen tissue damage
• DO NOT apply cold compresses to a snake bite.
• DO NOT try to suck out the venom by mouth.
• Do not slash the wound with a knife.
• Do not apply ice or immerse the wound in water.
• Do not drink alcohol as a pain killer.
• Do not drink caffeinated beverages.
• Bring in the dead snake only if this can be done safely. Do not waste time hunting for the snake, and do not risk another bite if it is not easy to kill the snake. Be careful of the head when transporting it -- a snake can actually bite for up to an hour after it's dead (from a reflex)

FIRST AID TREATMENT.
• General principles:
o Appropriate first aid has been shown to reduce mortality in patients who have been bitten by a venomous snake. Some traditionally recommended procedures may do more harm than good. For example incising the wound, sucking the wound, applying a tourniquet, ice or chemicals should be avoided.
o Follow basic emergency life support principles.
o Reassure the patient.
o Keep the patient still and immobilised.
o Arrange immediate transfer for definitive care.
• Non-venomous snake bites:
o The majority of snake bites in the UK will be non-venomous such as those from pythons and constrictors.
o These snake bites should be treated in the same way as any other animal bite.
o Clean and dress the wound
o Give anti-tetanus prophylaxis as required
o If the precise identity of the snake is unknown, keep under observation for several hours
If there are any systemic features (such as limb oedema, hypotension), assume that the bite is venomous and call the local poisons centre for further advice.
o Local blistering and transient dizziness and nausea are not suggestive of systemic involvement.
• Venomous snake bites:
o Venomous snake bites are very rare in the UK and are most commonly the result of an adder bite.
o Venomous snakes, even when they bite, do not always inject venom or not enough venom to cause envenomation.
o If the venom causes local damage and not neurotoxicity, like the adder bite, then pressure-immobilisation is not recommended. However an affected limb should be immobilised.
o In Australia most of the venomous snakes are systemically neurotoxic.16 Where a venomous snake other than an Adder is thought to have been involved (or snake not identified) the first aim is to prevent the snake venom from being systemically absorbed. In such cases a pressure immobilisation (PIM) bandage including a splint to reduce movement should be applied to the affected limb as soon as possible following the bite. The wound should not be cleaned prior to the application of the bandage, as traces of venom around the bite may help to identify appropriate anti venom if this is required.17 The following method is suggested for application of a PIM bandage:
 Identify the site of the bite from the patient's account (there may be no visible evidence of a bite mark).
 From the site of the bite, apply a compression bandage from the digits to the proximal end of the limb.
 The bandage should not be constricting (tension approximates to that applied for a sprained ankle).
 Mark the site of the bite on the outside of the bandage to allow a small window to be cut in the bandage for venom swabs to be taken.
 Apply a splint to immobilise the limb, and transport the patient to the nearest Accident and Emergency department. Keep movement to a minimum.
 For bites to the head neck and torso, local pressure should be applied

POTENTIAL FATALITY? MORBIDITY AND MORTALITY RATES.

In India, the annual mortality incidence is 5.6-12.6 per 100,000 population. At one time, Burma listed snakebite as its fifth leading cause of death. More recently, the annual mortality incidence was 3.3 per 100,000 population. Data from Thailand and Malaysia in the 1980s demonstrate an annual mortality incidence of 0.1 per 100,000 population.
• Determining the exact contribution of cobras to overall snakebite morbidity and mortality is difficult. In most cases, bitten individuals are unable to identify the snake. In India, the tendency is to ascribe all fatal or serious bites to cobras. Physicians are also likely to attribute all bites with neurotoxic symptoms to cobras.
• In a Thai survey, cobras made up 17% of the 1145 snakes identified in bites and were responsible for 25% of the fatalities associated with those bites. In northern Malaysia, cobras accounted for 23 of 854 bites in which the snake was identified. In a survey in Taiwan, cobras were blamed for 100 of 851 bites in which the snake was identified; none was fatal. Cobras accounted for 2 of 95 bites on a Liberian rubber plantation. The ringhals was responsible for 18 of 314 envenomations in Natal. Based on patients' symptoms alone, 18 other bites in this series were ascribed to cobras.
• King cobra bites are considered more serious than bites from other cobra species because of the greater volumes of injected venom and the more rapid onset of neurotoxic symptoms. Mortality is also higher. In a series of 35 cases, 10 deaths occurred. Ringhals bites are similar to other cobra bites but are less serious both locally and systemically. Deaths are rare. A medical report of 4 bites by the desert black snake described relatively mild symptoms and reported recovery without specific treatment. Anecdotal reports of fatal bites exist. No medical accounts of bites by water cobras or tree cobras exist. Anecdotal evidence suggests both are dangerous.

Symptoms of Snake Bite

SIGNS AND SYMPTOMS OF SNAKE BITES.

There are two different types of snake bite:

  • venomous bites - where the snake releases venom, and
  • dry bites - where the snake releases no venom; this often occurs because the snake does not want to waste its venom on a prey that it considers to be too big to eat.

Symptoms of dry bites.

The symptoms of a dry bite are usually limited to the part of the body that has been bitten. The symptoms include:

  • pain,
  • swelling, and
  • redness.

Dry bites should not require specialist medical treatment. However, if you are bitten by a snake, you should still visit your local accident and emergency (A&E) department because there is a risk that the bite could become infected, and you may require antibiotics to prevent infection occurring.

Symptoms of poisonous bites.

While each individual may experience symptoms differently, the following are the most common symptoms of poisonous snake bites:

  • bloody wound discharge
  • fang marks in the skin and swelling at the site of the bite
  • severe localized pain
  • diarrhea
  • burning
  • convulsions
  • fainting
  • dizziness
  • weakness
  • blurred vision
  • excessive sweating
  • fever
  • increased thirst
  • loss of muscle coordination
  • nausea and vomiting
  • numbness and tingling

· tissue necrosis

· skin discoloration

  • rapid pulse
  • severe pain

Snake venoms can be classified as hemotoxic (attacking tissue and blood) and neurotoxic (damaging or destroying nerve tissue). Pit viper snake venoms are hemotoxic.

Terminology: drooping of the eyelid (ptosis),difficulty swallowing (dysphagia),double vision (diplopia)

SPECIFIC SYMPTOMS FOR COBRA BITE.

The onset of symptoms and signs following a cobra bite can be extremely variable.

  • Immediate, local pain (almost always present)
  • Soft tissue swelling (may be progressive)
  • Neurologic findings, which may begin early and be rapidly progressive (in anecdotal cases, victims have suffered respiratory arrest in a matter of minutes) or may be delayed in onset as long as 24 hours
  • Alteration of mental status (eg, drowsiness, occasionally with euphoria)
  • Complaints related to cranial nerve dysfunction, such as ptosis (often one of the earliest neurotoxic findings), ophthalmoplegia, dysphagia, and dysphasia
  • Profuse salivation, nausea, vomiting, and abdominal pain
  • Paresis of neck and jaw muscles and generalized muscular weakness followed by flaccid paralysis
  • Shortness of breath, respiratory failure (muscular paresis and accumulated secretions)
  • Chest pain or tightness
  • Eye pain, tearing, blurred vision (with eye exposure to venom from spitting cobras)

Physical

  • Impending respiratory failure
    • Respiratory distress or weakness
    • Cyanosis
  • Neurologic dysfunction
    • Altered mental status
    • Ptosis (may be the earliest sign of systemic toxicity)
    • Generalized weakness or paralysis
  • Cardiovascular collapse
    • Hypotension
    • Tachycardia or bradycardia
  • Soft tissue edema
  • Signs of necrosis usually appear within 48 hours of the bite.
    • The area around the fang punctures darkens.
    • Blistering may follow.
    • Necrosis is usually confined to the skin and subcutaneous tissue but may be quite extensive.
    • A putrid smell is characteristic.
  • Acute inflammation of the eye follows venom-spitting exposure and is characterized by ocular congestion, edema of the conjunctiva and cornea, and a whitish discharge.

Anaphylaxis (severe allergic shock)

In a small number of people, snakes bites (both dry and venomous) can trigger a severe allergic reaction, known as anaphylaxis or anaphylactic shock.

Symptoms of anaphylaxis include:

  • swollen face, lips, tongue, and throat,
  • swelling in the throat that can cause breathing difficulties,
  • rapid heartbeat, and
  • itchy skin.

Anaphylaxis can also cause a drop in blood pressure, which can lead to shock and cause symptoms of:

  • dizziness,
  • cold and clammy skin,
  • mental confusion, and in some cases
  • loss of consciousness.