Snake Bite


Snake  Bite

 

Edited By :

Dr.Salim Al Mamun

MBBS(Raj);CCD(BIRDEM);

CMU(DU);DMUD(Course)

 

About snake

There are about 2500 species of snake in the world, among them 250 are poisonous. In Bangladesh among the 82 species of snake 28 are venomous, 12 species of them are sea snake.1 Venomous snakes of the world belong to the families Viperidae (sub family Viperinae: Old world vipers; sub family Crotalinae: new world and Asian pit vipers), Elapidae (including cobras, kraits, coral snakes and all Australian venomous snakes), Hydrophiidae (sea snakes), Atractaspididae (burrowing asps), and Colubridae (a large family, of which most species are non venomous and only a few are dangerously toxic to humans).2 There are 5 medically important groups of snake in our country, these are- cobra, krait, russel viper, green pit viper and sea snake. Among this majority of venomous bites in our country are cobras and kraits. They are mainly neurotoxic, and respiratory failure is the main cause of death following envenomation1. Snakes are docile in nature3. They bite defensively or when agitated. All the snake bites do not produce symptoms, only the bites by poisonous snake produces specific sign symptoms. Even 50% of the bite inflicted by poisonous snake does not produce any sign of envenomation. Bites rates are highest in temperate and tropical regions where the population subsists by manual agriculture. Estimates indicate >5 million bites annually by venomous snakes worldwide, with > 12,5000 deaths2. A World Health Organisation-funded study estimated about 8,000 cases of snakebite with over 20% mortality in BangladeshBangladesh are recorded between May and October (rainy season) with highest number in June. Lower and upper limbs are most common sites of snakebite, but it may happen in other sites as well. Delayed presentation to the hospital, lack of availability of antisnake venom and modern management facility are the main causes of death4.

Habitat of Snake

1. Paddy field

2. Lake

3. Hill

4. Root of tree

5. River

6. Ponds3

Foods and Feeding

Types of prey: all snakes are carnivorous3.

Snake venom

Snake venom is modified digestive juice. Main

function is digestion, to kill the prey. Composition:

complex-protein and non protein mixture5.

Venom injected by snake

• Cobra injects ~ 60 mg venom / bite (average)

•  Only 12mg is fatal.

The venom is 15-40 times more potent than Tubocurarine.

50% of the venomous snake bite does not

produce sign of envenomation

Venom action

 Venom action                  Clinical effect
 Vasodilators               Hypotension
 Coagulopathic           Consumption coagulopathy
 Hyalurodinase               Spread of venom
 Haemmolysin           Bleeding from fangs site
 Haemorrahagin               Bleeding from fangs site
 Myotoxin           Local tissue necrosis
Neurotoxin      Muscle paralysis, respiratory failure
Cardiotoxin        Coronary vasoconstriction, AV block5

Epidemiology of snake bite

  • World wide 3-5 million victims/ year
  • 50000 death annually
  • 400000 amputation/ year
  • Epidemiology of snake bite in Bangladesh
  • Incidence : about 8,000 per year
  • Mortality : 22%
  • Age: 11 – 20 years
  • Most of the incidents occur during May to October (Rainy season).
  • Because snakes are flushed out of their natural environment4.

Symptoms following  Snake bite

    Non specific symptoms– Headache, Vomiting, loss of

consciousness

    Neurological symptoms–  Muscle paralysis, Ptosis,

dysphagia

    Haematological symptoms– Sponteneous bleeding

e.g. gum bleeding, Haematuria

    Other symptoms– severe muscle pain, dark urine,

Progressive local swelling5

Laboratory investigation
(Depending C/F)

FBC

 Urea & Creatinine

 Urine analysis & naked eye exam. Of    urine

 CPK

 ECG

 ELISA

Blood grouping & Rh typing

20 min whole blood coagulation test

20 min whole blood coagulation test is a

Simple bed side test to detect venom induced

consumption coagulopathy.

 

 

References:

  1. Faiz MA, Hossain M, Amin R, Ghose A, Basher A, National guideline of management of snake bite, second edition, DGHS, 2008; 1-32.
  2. Paul S.Auerbach, Robert L. Norris, Disorders Caused by Reptile Bites and Marine Animal Exposure. In Fauci AS, Braunwald E, Kasper DL, et al. 17th edition. Harrison’s Principles of Internal Medicine. New York: The McGraw- Hill Companies, 2008:2741- 2748.
  3. Apobo nandy, animal irritants, Principle of Forensic Medicine, second edition. New central book agency, 2004: 506-516.
  4. http://www.banglapedia.org/httpdocs/HT/S_0439.HTM
  5. Thomas S.H.L, . White J, Poisoning  In:  Colledge NR,  Walker B R, Ralstone S H Davidson’s Principles & Practice of Medicine, 21th edition, Churchill Livingstone Elsevier, 2010; 203-207

Spittimg cobra

Medically important snakes of Bangladesh

1.Group I: Cobra

2.Group II: Krait

3.Group III: Russel viper

4.Group IV: Green pit Viper

5.Group V: Sea snake

Group I: Cobra

Monocellete cobra/ghokra

Distributed all administrative divisions in Bangladesh

Binocellate cobra

More co        Common in west of Jamuna.

King cobra

King cobra, Raj ghokra, Sankochur

Distributed in Shylet, Chittagong and Barisal

out krait

Group II: Krait

Bungarus caeruleus, common krait, kal kewtey, Malcha alad

Distributed all administrative divisions in Bangladesh.

Bangarus faciatus, Banded krait, Mama-bhagna

More in Chittagong and rare  in Rajshahi

Copy right Dr. Ratindra Nath Mondal

Bungarus niger (black krait), Bungarus wall

Recently found in  Chittagong and other

 Parts of the country

Group III Russel viper

Daboia (Daboia russeli, Russel viper

Distributed in Rajshahi & Khulna, may be found in Chittagong.

Group IV Green pit Viper

Ovophis Green snake, bash-bora, sabuj-bora

Distributed in Shylet, Chittagong, Barisal & Khulna

Group V Sea snake

Enhydrina schistosa, Hooknosed sea snake, Samudrik shap

Distributed in sea and coastal saline water of Bangladesh.

Copy right:Dr.Ratindra Nath Mondal

Fig: Non-poisonous snake

First aid in snake bite

Why the snake bite???

Snake are docile in nature

Snakes do not attack man.

They bite defensively or when agitated

!? What to do if you see a snake!?

  1. Don’t hello the snake
  2. Do not be afraid
  3. Do not get close to them
  4. Allow the snake to go away
  5. Do not kill the snake unnecessarily

What to do in case of snakebite ?

  1. If you are the victim: Do not panic
  2. Sit down, be calm, seek help
  3. Wipe the site of bite
  4. Cover it with dressing
  5. Assurance: Reassure the victim who may be very anxious.
  6. If the bite is in upper limb: do not move the limb.
  7. Ideal is – to provide pressure immobilization (cobra and krait bite).
  8.  Figure….
  9. This should not be used for viper bite & Green snake bite. Fig: Procedure of immobilization as first aid
  10. Fig: Ideal procedure of immobilization
  11. Immobilize the bitten limb with a splint or sling as practiced in fracture of long bone.
  12. If the bite is in lower limb: do not walk.
  13. If the snake is killed, bring the snake with the patient to hospital for identification
  14. Get the victim to the closest hospital or medical facility as soon as possible 

First Aid Methods – Not Recommended

1.       Multiple ligature with application of herbal medicines

2.       Incisions at the site of snake bite or any other place. 

3.       Local suction either by mouth or by application of chick. 

4.       Application of ice at the biting area

  1. Application of herbal medicines, stones, seeds, saliva, potassium permanganate solution. 
  2. Actively attempt to locate a venomous snake
  3. Unnecessary delayingn to take the pt. to hospital.

 

Fig: Tight arterial ligature not recommended

Fig: Suction at the bite mark not recommended

Fig: Incision around the bite mark not recommended

Fig: Wrong first aid by faith healers not recommended

Why these traditional methods are not practised?

Effect of  “Traditional tight tourniquets

Fig: Effect of tight ligature

Management of snake bite in Health care facility

20 min whole blood coagulation test

Simple bed side test to detect venom induced consumption coagulopathy.

Steps of 20 minutes whole blood coagulation test

Fig: Blood is drawn(3-5 ml), kept in test tube in vertical position & waite for 20 minutes

Fig: After 20 minutes look whether the blood in the test tube is cogulated or not.

The test is positive if blood is not cogulated after 20 minutes.

In perspective of Bangladesh, incoagulable blood is diagnostic

of Viper bite and rules out Elapid bite (Krait & Cobra).

Treatment in Health Facility

1.     Airway  -Rapid assessment and resuscitation

2.     Breathing

3.     Circulation

4.     Antibiotic

5.     Tetanus prophylaxis

6.     Polyvalent Antisnake venom

Poly valent Antivenom:

1.      Each vial 10 mg of antivenom. Work against Cobr, krait, Russel’s viper & saw scaled viper.

2.     Not used in bites by Green snake, Sea snakes and identified nonvenomous snake.

3.     One vial of polyvalent ASV neutralize 6 mg of the cobra venom.

4.     Neurotoxicity usually improves -30 minutes.

5.      Response is best within 4 hrs of bites.

Dose of Antivenom

Fig: Polyvallent antivenom

Each dose require 10 vial of antivenom. 10 such vials

(100 ml) are further diluted or mixed with 100 ml of

fluid (Dextrose water or saline).

Then it is administered with intravenous infusion

within 40-60 min (60-70 drops/min).

Children must therefore be given exactly the same

dose of antivenom as adult.

Criteria: using Polyvalent  ASV

1.     Neurotoxic signs

2.     Rapid extension of local swelling

3.     Acute renal failure

4.     Cardiovascular abnormalities

5.     Bleeding abnormalities

6.     Haemoglobinuria / myoglobinuria

Contraindication to antivenom

There is no absolute contraindication to antivenom treatment.

Additional treatment

1. If neurotoxicity

– inj. Neostigmine & Atropine (Inj. Atropine 15

µg/kg IV followed by Inj. Neostigmine50-100 µg/kg S/C

4 hourly until neurotoxic features improves)

2. If Haematological abnormalities

– Fresh frozen plasma/

– Fresh Blood transfusion

Criteria for repeating the initial dose of antivenom:

• If no improvement or deterioration after 1-2 hours

• Persistence or recurrence of blood incoagulability after 6 hours

Conservative treatment when no antivenom is available

1. Assisted ventilation in respiratory paralysis.

2. If Neurotoxicity

– Neostigmine &

– Atropine

3. In case of haemostatic abnormalities

– Strict bed rest

– Avoid I/M injection.

– Fresh blood transfusion.

– Avoid NSAID or Aspirin for pain

How we can avoid snake bite??

  • Avoid places where snakes may live.
  • Watch where you step and where you sit when outdoors.
  • When moving through tall grass or weeds, poke at the ground in front of you with a long stick to care away snakes

• Wear loose, long pants, thick leather or rubber boots.

• Shine a flashlight on your path when walking outside at night.

  • Look care fully before going to bed, wearing shirt
  • Switch on the light when entering room

Never handle a snake, even if you think it is dead. Recently killed snakes may still bite by reflex.

 

 

 

Introduction of poisoning management

 

What is a poison?

A poison is any substance that causes harm if it gets into the body.
Harm can be mild(for example, headache or nausea) or severefor example,
fits or very high fever),and severely poisoned people may die.

The amount of a chemical substance that gets into the body at one
time is called the dose. A dose that causes poisoning is a poisonous
dose or toxic dose. The smallest amount that causes harm is the threshold
dose. If the amount of a chemical substance that gets into the body is
less than the threshold dose, the chemical will not cause poisoning and
may even have good effects. For example, medicines have good effects
if people take the right doses, but some can be poisonous if people
take too much.

Exposure to a poison

When people are in contact with a poison they are said to be exposed
to it. The effect of exposure depends partly on how long the contact
lasts and how much poison gets into the body, and partly on how much
poison the body canget rid of during this time. Exposure may happen
only once or many times. Acute exposure is a single contact that
lasts for seconds, minutes or hours, or several exposures over about
a day or less.

Chronic exposure is contact that lasts for many days, months or years.
It may be continuous or broken by periods when there is no contact.
Exposure that happens only at work, for example, is not continuous.

Chronic exposure to small amounts of poison may not cause any signs
or symptoms of  poisoning at first. It may be many days or months
before there is enough chemical inside the body to cause poisoning.
For example, a person may use pesticide every day. Each day the person
is exposed to only a small amount of pesticide, but the amount of
pesticide in the body gradually builds up, until eventually, after many
days, it adds up to a poisonous dose. Only then does the person
begin to feel unwell.

How poison gets into the body:

The way poison gets into the body is called the route of exposure or
the route of a bsorption. The amount of poison that gets into the
blood during a given time depends on the route.

1) Through the mouth by swallowing (ingestion)

Most poisoning happens this way. Small children often swallow poison
accidentally, and adults who want to poison themselves may swallow
poison. If people eat, drink or smoke after they have been handling
poisons, without first washing their hands, they may accidentally
swallow some of the poison. This is a common cause of pesticide
poisoning.

When poisons are swallowed they go to the stomach. Some poisons can
pass through the gut walls and into the blood vessels. The longer
a poison stays in the gut the more will get into the blood and the
worse the poisoning will be.

If a person vomits soon after swallowing a poison, it may be expelled
from the body before a poisonous dose gets into the blood. So, if
the person does not vomit straight away, it is sometimes useful to
make the person vomit. There are two other ways to stop poisons
passing from the gut into the blood: (1) give activated charcoal
because this binds some poisons so that they cannot pass through
the gut walls; or (2) give laxatives to make the poison move through
the gut and out of the body more quickly. Poisons that do not pass
through the gut walls do not get into the blood and so cannot affect
other parts of the body. They move along the gut and leave the body
in the faeces.

2) Through the lungs by breathing into the mouth or nose  (inhalation)

Poisons in the form of gas, vapour, dust, fumes, smoke or fine spray droplets may be
breathed into the mouth and nose and go down the air passages into the lungs. Only
particles that are too small to be seen can pass into the lungs. Larger particles are
trapped in the mouth, throat and nose and may be swallowed. A person may breathe in
poison when working with a poisonous substance inside a building without fresh air,
or when spraying pesticide without wearing adequate protection. Oil or gas heaters,
cookers, and fires give off poisonous fumes which may reach dangerous concentrations
if the smoke cannot get outside or if the room does not have a good supply of fresh
air. Poison that gets into the lungs passes into the blood vessels very quickly
because the air passages in the lungs have thin walls and a good blood supply.

3) Through the skin by contact with liquids, sprays or mists

People working with chemicals such as pesticides may be poisoned

if the chemical is sprayed or splashed onto the skin, or if they wear clothes soaked
with chemical. The skin is a barrier that protects the body from poisons. However,
some poisons can pass through the skin. They pass through warm, wet, sweaty skin more
quickly than through cold, dry    skin, and they pass through skin damaged by
scratches or burns more quickly than through undamaged skin. A poison that damages
the skin will pass through more quickly than one that does not damage the skin. It
may be possible to wash poison off the skin before a poisonous dose gets into the
body.

4) By injection through the skin

Poisons can be injected through the skin from a syringe, or a pressure gun, or during
tattooing, or by the bite or sting of a poisonous animal, insect, fish or snake. The
injection may go directly into the blood vessels or under the skin into muscle or fatty
tissues. Poison injected into the blood has a very quick effect. Poison injected
under the skin or into muscle has to pass through several layers of tissue before
reaching the blood vessels, so it acts more slowly.

How poison is carried round the body

Once a poison gets into the blood it is carried to the whole body as the blood is
pumped round the body by the heart.

How poison is broken down by the body

Some poisons are changed by the body into other chemicals. These are called metabolites,
and may be less poisonous or more poisonous than the original substance. The
metabolites are more easily passed out of the body than the original chemicals. These
changes take place mostly in the liver.

How poison leaves the body

Unchanged poisons or their metabolites usually leave the body in the urine, faeces or
sweat, or in the air that a person breathes out. The movement of poison from the blood
into urine takes place in the kidneys, and the movement of poison from blood into
breathed-out air takes place in the lungs. Poison in the faeces may have passed down
the gut without being absorbed into the blood or it may have been absorbed into the
blood and then passed out into the gut again. Some poisons, like DDT, pass into body
tissues and organs where they may stay for a long time.

Effects of poison

The effects of a chemical substance on the body may be described as either local or
systemic.

A local effect is limited to the part of the body in contact with the chemical: the
skin, the eyes, the air passages or the gut. Examples of local effects are skin rashes,
skin burns, watery eyes, and irritation of the throat causing coughing. Many poisons
cause local effects, but there are also many poisons that do not.

A systemic effect is a more general effect that occurs when a poison is absorbed into
the body.

Some poisons cause both local effects and systemic effects. If someone has local
effects from exposure to a chemical it is important to check whether they also have
signs or symptoms of systemic poisoning.

Local effects

1) On the skin

Chemicals that damage the skin cause reddening or a rash, pain, swelling, blisters or
serious burns. The burns are like the burns caused by fire.

An irritant chemical causes itching, a burning feeling, or pain when it first touches
the skin, but does not cause burns if washed off straight away. However, if it is in
contact with the skin for a long time, for example when people wear contaminated
clothes for several hours, it might cause burns.

Some irritant chemicals have no effect the first few times they touch the skin, but
with continued contact they cause reddening or a rash. This might happen with repeated
use of a household cleaner.

Sometimes people become sensitive to a chemical after they have used it many times.
They may have no effects at first but after a few weeks or months they get a rash every time they use it.

A corrosive or caustic chemical very quickly causes painful burns and destroys the
skin. There may be blisters and the skin may turn grey-white or brown.

2) On the eyes

Irritant or corrosive chemicals can cause severe pain if they get into the eyes.
They may very quickly burn the surface of the eye and cause scars or even blindness.
The eyes will look red and watery. The person may not want to open the eyes and bright
light will hurt.

3) Inside the gut

Irritant or corrosive chemicals may damage the mouth and throat or the inside of the
gut. The person will have belly pain, vomiting and diarrhoea, and the vomit and faeces
may contain blood. If the throat is burnt it may swell very quickly, so that the person
cannot breathe.

4) Inside the air passages and lungs

Some gases and vapours can irritate the nose, throat and upper air passages and cause
coughing and choking. Some gases and vapours damage the lungs in a way that causes
them to fill with water. This may happen very soon after a person breathe in the
substance, or it may happen up to 48 hours afterwards. A person with water in the
lungs cannot breathe properly and may drown. He or she must be taken to a hospital as
quickly as possible. Water in the lungs is called
lung oedema. Some of the gases that cause lung oedema also irritate the nose, throat
and upper air passages, and make people cough and choke.

Some poisonous gases, such as carbon monoxide, have no effect on the nose and throat.
Poisonous gases that do not cause coughing and choking are very dangerous because
people may not know they are breathing poison.  Petroleum distillate liquids, such as
kerosene, may cause lung oedema when swallowed.

5) At injection sites

Irritant poisons that are injected into the skin, such as poisons from insect stings
and snake bites, may cause pain and swelling where they are injected. People who
accidentally inject themselves with veterinary products, when giving injections to
animals or birds, may get local effects.

6) Systemic effects

There are many ways in which poisons can cause harm:

*    By damaging organs such as the brain, nerves, heart, liver,

lungs, kidneys, or skin. Most poisons have a greater effect on

one or two organs than on other parts of the body. The organs

that are most affected are called the target organs.

*    By blocking messages between nerves.

*    By stopping the body working properly, for example, by blocking

energy supply or oxygen supply.

Effects on unborn babies

Some poisons can harm a baby inside the womb. This is most likely during the first
three months of pregnancy when the nervous system and all the major organs begin to
form. The parts of the baby usually affected are the bones, eyes, ears, mouth and
brain. If the damage is very bad the baby will stop growing and die. Some poisonous
chemicals may harm a baby in the womb without harming the mother. This is serious
because there is nothing to warn the mother that her baby is in danger. If a mother
drinks alcohol or smokes during pregnancy it may harm her baby. Medicines may also
harm a baby in the womb. Pregnant women should never take medicines unless they are
prescribed by a doctor.

When systemic effects happen

Systemic effects only happen when the amount of poison in the body is greater than
the amount the body can get rid of, and the poison builds up and reaches the threshold
level.

Some poisonings happen by accident but some happen when people try deliberately to
harm themselves (self-poisoning) or others. There are other circumstances that may
result in poisoning:

–       eating food containing poison;

–       taking, or being given, the wrong kind of medicine or the wrong dose;

–       taking drugs because they change mood or behaviour, or using

–       plants or chemical products for this purpose.

Accidental poisoning

Accidental poisoning may happen when:

–       young children or old people handle poisons not knowing what they are;

–       people mistake poison for food or drink because it is not in its original
container;

–       people misuse chemical products or medicines;

–       people use or misuse pesticides;

–       people work with chemicals;

–       people are exposed to carbon monoxide, usually at home.

Poisoning in childhood

Many poisoning accidents in the home happen to small children aged between 1 and 4
years. At this age children want to explore. They like to put things in their mouths
but they are not old enough to understand that some things might be harmful.

The chemical products most often swallowed by children are:

–       household cleaners such as bleach, detergent and disinfectant;

–       paraffin and kerosene used as household fuels;

–       cosmetics;

–       medicines;

–       paint and products for household repairs;

–       household pesticides.

Poisoning in old age

Old people may poison themselves accidentally. If they cannot see very well, they may
pick up the wrong bottle and swallow a household cleaner, for example, instead of a
drink or a medicine.

Taking products out of their own containers

Accidents can happen when someone takes a chemical product out of its container and
puts it in another one. The new container does not have the right label so nobody
else will know what is inside. Even the person who did it may forget.

Pesticide poisoning

Most pesticides are also poisonous or harmful to humans if they get on the skin, or
if they are breathed into the lungs in the form of gases, fumes, dust or fine spray
droplets, or if they are swallowed.

Poisoning at work

Many chemicals that are made, used, or stored in workplaces are poisonous. People who
work with these chemicals need to know how to handle them safely to avoid being
poisoned. Sometimes workers may not know that they are handling a poisonous chemical,
or they may know that the chemical is poisonous but not have been told or shown how
to handle it safely. They may not have read the label or the safety information.
Sometimes they may know the dangers but be too lazy or careless to use safe methods.         Accidents, fires or explosions at work may result in chemicals spilling or leaking out of their containers onto roads or into rivers, or vapours and gases being released into the air. Sometimes chemicals spread over a large area and poison many people. Chemical waste and empty chemical containers may be serious safety hazards if they are not dealt with in the right way.

Self-poisoning

People may try to harm themselves by deliberately taking poison -this is called
self-poisoning. In some countries people take medicines to poison themselves, but
people living in rural communities are more likely to take pesticides. People
suffering from depression, serious illness, or alcohol dependence may try to kill
themselves by taking poison. They may swallow large amounts of medicine, pesticide
or other poisons. If they recover they might try to poison themselves again unless
they receive appropriate treatment.

Poison in food or drink

Food or drink can be contaminated by poison from microscopic organisms such as
bacteria, viruses, or mould, or by chemical poisons. Some plants, mushrooms, animals
or sea-creatures contain poisonous chemicals. Poisons made by plants, animals or
microorganisms are called toxins.

Chemical poisons

There are many ways chemical poisons can get into food and drink, for example:

–       when people working with chemicals eat in the workplace or do not wash
their hands before eating;

–       when chemicals spill onto food as it is being moved from place to place,
or when it is in a storeroom;

–       when food or drink is stored or cooked in containers that are contaminated
with chemicals;

–       when people make flour from grain that has been treated with pesticide
because it was meant to be used for seed or bait, not for food;

–       when people brew their own alcoholic drinks and produce poisonous alcohols,
such as methanol;

–       when water supplies are polluted by accidental spills of chemicals, or by
chemical waste from factories or waste dumps near watercourses.

Medical poisoning

Sometimes people are poisoned by medicines given to them by a doctor or another health
care worker. They may be given the wrong medicine or be given the wrong dose of the
right medicine.

Abuse of drugs, chemicals or plants

People may take drugs to change their mood or behaviour, to feel relaxed, or to get
more energy. This is called drug abuse because it is not a medical use of the drug.
Some people abuse drugs such as heroin, cocaine or barbiturates. Drinking too much
alcohol is an important kind of drug abuse.

Common Poisoning Symptoms and signs                                                                                                                                 

Poisons

Symptoms and signs

Atropine, Amitriptyline, Antihistamines, Datura stramonium Atropa belladonna, some kinds of  Mushrooms dry, hot skin, fever, thirst, dry mouth, large pupils, fast pulse, difficulty in passing urine, hallucinations, fits, shallow breathing unconsciousness
Organophosphorus and  Carbamate insecticides, some kinds of Mushrooms small pupils, wet mouth, sweating, wet eyes vomiting, slow pulse, diarrhoea, fits, unconsciousness
Opiates small pupils, slow breathing, unconsciousness,  weak pulse                                    low temperature, , vomiting
Amfetamines, cocaine, Theophylline large pupils, fever, fast pulse, hallucinations, fits, anxiety, sweating, flushed skin, over-                                              activity, confusion
Barbiturates, Diazepam and similar drugs, Meprobamate,  Drug withdrawal, barbiturates, diazepam and similar  medicines, opiates

              

unconsciousness, low blood pressure, shallow breathing, low temperature

diarrhoea, gooseflesh, fast pulse, watering eyes, yawning, cramps, hallucinations, restlessness, shaking

Dr. Ratin’s Personal Site

Principle of poisoning management

Assessment: Airway, Breathing, Circulation and Consciousness, should be assessed in all patients with poisoning.

Level of consciousness:

  • The Glasgow Coma Scale (GCS) is commonly used though it is not validated. A GCS score of less than 8 (not obeying commands, not speaking, not eye opening) is unarousable unconsciousness.
  • Are laryngeal (gag) reflexes present? If it is lost, prompt assessment of respiration is essential.

Airway:

Most common factor contributing to death from poisoning and drug overdose is loss of airway protective reflex.

  • Assessment:

o      Patient who are awake and talking- Likely to have intact airway, but should be monitored closely.

o      In lethargic and obtunded patient- Check gag reflex. If lost: Airway reflex is likely to be lost.

Breathing:

Along with the airway problem, breathing difficulties are the major cause of morbidity and mortality in poisoning. These are: ventilatory failure, hypoxia and bronchospasm.

Assessment:

Be done by observing efforts of ventilation, respiratory rate, cyanosis, use of accessory muscle of respiration and SP02 by pulse oximetry. Ineffective respiration and cyanosis are two important clinical parameters for assessing the ventilation. If these parameters are present, the patient may need ventilator support.

Pulse oximetry to measure oxygen saturation (Displayed reading is inaccurate if 02 saturation is below 70%, poor perfusion, presence of carboxyhaemoglobin and methaemoglobin).

  • SP02 <90% demands immediate 02 inhalation.
  • SP02 91-95% states 02 inhalation necessary.
  • SP02 >95% is normal.

Circulation:

Maintenance of adequate circulation is a must for every case of poisoning and drug overdose.

Assessment:

Check BP, pulse rate and rhythm, capillary refill time (CRT).

If SBP <90mm Hg and pulse >100/min; patient is in shock.

In Children: SBP <80mm Hg.

In shock CRT >2sec

ECG monitoring may be needed in case of TCA, yellow oleander, Digitalis glycoside and beta blocker poisoning.

History taking:

Medical, psychiatric, toxicological and socioeconomic history should be taken in every case of poisoning.

In Adult: 80% of patients who arrived at the hospital are conscious and diagnosis of self poisoning is made from history. In the rests who are unconscious, history from relatives, friends or attendants is helpful and diagnosis is often inferred from brought specimen (e.g. tablet bottles or a suicide note) or made by exclusion of other causes.

It is pertinent to try to establish the nature of the substance taken, the amount involved, the route and the time of exposure to anticipate the clinical course and to assess risks. In children (<13 yrs) history is very unreliable in regard to amount.

Assessment of psychiatric problems:

1     Events that preceded the act

2.     Degree of suicidal intent

3.     Current problems faced by the patient

4.     H/O psychiatric disorder

5.     Personality traits and disorder

6.     Family and personal history

7.     H/O previous self injury

8.     Risk of further overdose and subsequent suicide

Circumstantial evidences:

  • Suicide note is a reliable indicator of drug overdose in absence of evidence of physical violence as a cause of coma.
  • Circumstances in which the patient was found: Children may be found eating potential toxins or with tab around clothing, or having smell of the ingested substances from body and oral cavity. Similar thing may be seen in unconscious adults or may be with empty drug containers, tablets or capsules nearby.

Physical examination:

Initial assessment of vital signs and managed accordingly.

Subsequent examination depends upon type, amount, nature and time of poisoning. Some common clustering features may point towards a particular poisoning, and are described below.

 

 

 

 

 

 

Common clusters of features that may be diagnostic:

Feature cluster

Likely Poison

Coma, hypotonia, hypo-reflexia, plantar responses: flexor or non-elicitable, hypotension.

hypotension.

Barbiturates, benzodiazepines and alcohol combinations, severe TCA poisoning

TCA poisoning.

Smell of OPC, bronchorrhea, incontinence of urine & stool, miosis and hyper salivation Organophosphorus and carbamate insecticides, nerve agents
Coma, miosis, reduced respiratory rate Opioids.
Nausea, vomiting, tinnitus, deafness, sweating, hyperventilation, vasodilatation, metabolic acidosis. Salicylates
Restlessness, agitation, mydriasis, anxiety, tremor, tachycardia, convulsion, arrhythmias

arrhythmias.

Sympathomimetic drugs (Bronchodilator, theophylline)
Blindness (usually with other features) Quinine, methanol
Smell of OPC, bronchorrhea, incontinence of urine & stool, miosis and hyper salivation Organophosphorus and carbamate insecticides, nerve agents

NB: All the features of a particular poison may not be present in a particular case.

Diagnostic trial of antidotes:

Administration of I.V naloxone and flumazenil has been used to make rapid clinical diagnoses of opioid and benzodiazepine poisoning respectively; this approach depends on noticeable improvement in the patient’s clinical condition within 1-2 minutes.

 

Toxicological investigations:

Toxicological screening of blood or urine can be used to establish a diagnosis of poisoning. The concentration is measured in the plasma or serum rather than whole blood except Carboxyhaemoglobin.

Emergency measurement of plasma concentration of known toxins is necessary for the following toxins:

  • Carboxyhaemoglobin
  • Ethanol
  • Ethylene glycol
  • Iron
  • Lithium
  • Methanol
  • Paracetamol
  • Salicylate
  • Theophylline
  • Benzodiazepine

Screening for unknown toxins:

In multiple drug overdoses benzodiazepine and paracetamol measured routinely. Laboratory screening for poisons in an unconscious patient usuaIly concentration are requested when the cause of coma is unknown.

Urine (20ml) is usually a more appropriate fluid for detecting unknown poison. Once identified their concentration in blood or plasma can be determined by specific method if necessary.

Non-toxicological investigations:

Inspection of brought specimen – Generic name, amount left in bottle smell color etc.

Inspection of blood:

  • Chocolate-coloured blood indicates methaemoglobin caused by drugs e.g. Dapsone, nitrites or nitrates.
  • Pink plasma suggests hemolytic poisons e.g. sodium chlorate
  • Brown plasma suggests the presence of circulating myoglobin secondary to rhabdomyolysis

Inspection of urine:

  • Brown discolouration of the urine by the presence of heamoglobin (intravascular haemolysis), myoglobin secondary to rhabdomyolysis or metabolites of paracetamol.
  • Crystals in primidone overdose or ethylene glycol.

Haematology:

Is of little value except prolongation of prothrombin time in anticoagulants or paracetamol overdoses and also in snake bite.

Biochemical indicator of various poisoning:

  • Serum sodium: e.g. hyponatraemia in Ecstasy poisoning.
    • Serum potassium: e.g. hypokalaemia in theophylline, hyperkalaemia in digoxin poisoning, rhabdomyolysis and haemolysis.
    • Plasma creatinine e.g. renal failure in ethylene glycol poisoning.
    • Blood sugar e.g. hypo or hyperglycaemia in salicylate poisoning.
    • Serum calcium e.g. hypocalcaemia in ethylene glycol poisoning.
    • Serum ALT/AST e.g. increased in paracetamol poisoning.
    • Serum phosphate e.g. hypophosphataemia in severe paracetamol induced renal tubular damage
    • RBC cholinesterase activity e.g. organophosphorus and nerve agents poisoning.
    • Whole blood methaemoglobin concentration e.g. in nitrite poisoning.

Radiology and ECG are of little value but sometimes important for complication of poisoning. Radiology can be used to confirm ingestion of metallic objects (coins, button, batteries or ingestion of globules of metallic mercury) and iron tablet.

In ECG sinus tachycardia with prolongation of PR & QRS interval should prompt consideration of tricyclic antidepressant poisoning. ECG is also important in yellow oleander poisoning and phenothiazines overdose.

 

 

Clinical Features and Complications of Poisoning:

The toxicity of a substance and therefore the features of poisoning can generally be predicted from:

  • Its physiochemical properties
  • Its pharmacological / toxicological actions
  • Its route of exposure
  • Its dose

These features are classified as either direct or systemic

Principles of Management of Poisoned Patient:

Most patients with self-poisoning require only general care and support of the vital systems. However, for a few drugs additional therapy is required. The challenge for clinicians managing poisoned patients is to identify at an early stage, those who are at risk of developing serious complications and who might potentially benefit from an antidote or treatment to increase elimination of the poison.

 

Strategy:

  • Provide immediate supportive treatment (ABC).
  • Is the use of an antidote appropriate?
  • Is it appropriate to attempt to reduce poison absorption?
  • Is it appropriate to perform toxicological investigations?
  • Will non-toxicological investigations assist?
  • Should urine alkalinization, multiple-dose activated charcoal, and haemodialysis be employed to increase poison elimination?

 Airway, Breathing and Circulation (ABC) (See Chapter-17)

Respiratory support:

Food, vomit, secretion and dentures should be removed from the patient’s mouth and the pharynx and the tongue prevented from falling back. The patient should be nursed in left lateral position to minimise the risk of aspiration of gastric contents into the lungs.

If respiratory depression is present, as determined by clinical features and pulse oximetry or preferably by arterial blood gas analysis. Supplemental oxygen should be administered in needed. Pulse oximetry alone will detect hypoxia but not hypercapnia.

Loss of the cough or gag reflex is the prime indication for intubation. The gag reflex can be assessed by positioning the patient on one side and making him or her gag using a suction tube. In many severely poisoned patients the reflexes are depressed sufficiently to allow intubation without the use of sedatives or relaxants.

If ventilation remains inadequate after intubation, as shown by hypoxaemia and hypercapnia, intermittent positive-pressure ventilation (IPPV) should be instituted.

Cardiovascular support:

Although hypotension (systolic blood pressure below 90 mmHg) is a recognized feature of acute poisoning, the classic features of shock – tachycardia and pale cold skin – are observed only rarely. As a first step the patient should be placed head down position (the foot end should be elevated by 15 cm). If there is no improvement, infusion of crystalloid solution should be started. In patients with marked hypotension, volume expansion with gelatins or etherified starches (e.g. heta- starch, hexa-starch) should be used, guided by monitoring of central venous pressure (CVP). Urine output (aiming for 35-50 mL/h) is also a useful guide to the adequacy of the circulation.

If a patient fails to respond to the above measures, more intensive therapy is required. Dobutamine 2.5-10 microgram/kg/min or epinephrine 0.5-2 microgram/kg/min is indicated in such case. Dopamine 10-20 microgram/kg/min is an alternative (see flow chart).

Arrhythmias are observed occasionally in poisoned patients, for example after the ingestion of a tricyclic antidepressant or theophylline. All patients with shock should have ECG monitoring. Known arrhythmogenic factors such as hypoxia, acidosis and hypokalaemia should be corrected.

Care of unconscious patient:

In all cases the patient should be nursed in the lateral position with the lower leg straight and the upper leg flexed; in this position the risk of aspiration is reduced (see fig. chapter 17). A clear airway passage should be ensured by removal of any obstructing object, vomit or dentures, and by backward pressure on the mandible. Nursing care of the mouth and pressure areas should be instituted.

Immediate catheterization of the bladder in unconscious patients is usually unnecessary as it can be emptied by gentle suprapubic pressure.

Insertion of a venous cannula is usual, but administration of intravenous fluids is unnecessary unless the patient has been unconscious for more than 12 hours or is hypotensive.

On admission, or at an appropriate time post-overdose, a timed blood sample should be taken. The determination of the concentrations of the drugs will be valuable in management. Drug screens on blood and urine are occasionally indicated in severely poisoned patients in whom the cause of coma is unknown.

Some routine investigations are of value in the differential diagnosis of coma or the detection of poison-induced hypo or hyperkalaemia, hypo or hyperglycaemia, hepatic and renal failure or of acid-base disturbances. Measurement of carboxyhaemoglobin, methaemoglobin and cholinesterase activities are of assistance in the diagnosis and management of cases of poisoning due to carbon monoxide, methaernoglobin-inducing agents such as nitrites, and organophosphorus insecticides respectively.

 

Other Problems:

Body temperature:

Hypothermia -a rectal temperature below 35°C is a recognized complication of poisoning, especially in older patients or those who are comatose. The patient should be covered with a ‘space blanket’ and, if necessary, given intravenous and intragastric fluids at normal body temperature. Inspired gases should also be warmed to 37°C.

Hyperthermia may develop with CNS stimulant ingestion. Removal of clothing and sponging with tepid water will promote evaporation.

Rhabdomyolysis:

Rhabdomyolysis can occur from pressure necrosis in drug-induced coma, or as a complication of sea snake bite or MDMA (Ecstasy) abuse in the absence of coma. Patients with rhabdomyolysis are at risk of developing firstly, renal failure from myoglobinaemia, particularly if they are hypovolaemic and have an acidosis, and. secondly, wrist or ankle drop from the development of a compartment syndrome.


Convulsions:

These may occur in poisoning due to tricyclic antidepressants, mefenamic acid or opioids. Usually the fits are short-lived but, if they are prolonged, diazepam 10-20 mg i.v. should be administered. Persistent fits must be controlled rapidly to prevent severe hypoxia, brain damage and laryngeal trauma. If diazepam in repeated doses is ineffective, the patient should also receive a loading dose of phenytoin (15 mg/kg) administered intravenously at a rate of not more than 50 mg per minute, with blood pressure and ECG monitoring.

Stress ulceration and bleeding:

Medication to prevent stress ulceration of the stomach should be started on admission in all patients who are unconscious and require intensive care. An H2-receptor antagonist or a proton pump inhibitor should be administered intravenously.

Specific Management: Antidotes:

Specific antidotes are available for only a small number of poisons.

Poison

Antidote

Aluminium Desferrioxmine
Arsenic Dimercaprol (BAL), DMSA
Benzodiazepines Flumazenil
ß-adrenoceptor blocking drugs Atropine, glucagon
Copper Dimercaprol, D-penicillamine, DMPS
Cyanide Oxygen,dicobaltedetate,hydroxocobalamin, Sodium thiosulphate
Digoxin and digitoxin Digoxin-specific antibody fragments
Ethylene glycol Fomepizole, Ethanol
Iron salts Desferrioxamine
Lead (inorganic) Sodium calcium edetate, DMSA
Methaemoglobinaemia Methylthioninium chloride (Methylene blue)
Methanol Fomepizole, Ethanol
Mercury (inorganic) DMPS
Opioids Naloxone
Organophosphorus compounds Atropine, pralidoxime
Paracetamol N-acetylcysteine,Methionine
Thallium Prussian (Berlin) blue
Warfarin and other anticoagulants Vitamin K1

Dose of antidotes—annexure 3

Antidotes may exert a beneficial effect by:

  • Forming an inert complex with the poison (e.g. desferrioxamine, dicobalt edetate, dimercaprol, DMSA, DMPS, digoxin-specific antibody fragments, hydroxocobalamin, penicillamine, pralidoxime, protamine, Berlin (Prussian) blue, sodium calcium edetate)
  • Accelerating the detoxification of the poison (e.g. methionine, N-acetylcysteine, sodium thiosulphate)
  • Reducing the rate of conversion of the poison to a more toxic compound (e.g. ethanol, fomepizole)
  • Competing with toxic substances for essential receptor sites (e.g. oxygen, naloxone, vitamin K1)
  • Blocking essential receptors through which the toxic effects are mediated (e.g. atropine)
  • Bypassing the effect of the poison (e.g. oxygen).

Reduction of Poison Absorption:

Inhaled:

To reduce poison absorption through the lungs, the casualty should be removed from the toxic atmosphere, without the rescuers themselves being put at risk.

 

Skin:

If clothing is contaminated this should be removed to reduce dermal absorption. In addition, contaminated skin should be washed thoroughly with soap and water.

 

Gut decontamination:

The efficacy of current methods to remove unabsorbed drug from the gastrointestinal tract remains unproven. The two major international societies of clinical toxicology (American Academy of Clinical Toxicology (AACT) and the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT)) have produced Position Statements on each method and are quoted below.

 

Gastric lavage:

Gastric lavage involves the insertion of a large-bore orogastric tube into the stomach. Small amounts (200-300 mL in an adult) of warm (38°C) fluid (water or 0.9% saline) are introduced and removed by suction. Lavage is continued until the recovered solution is clear of particulate matter. Gastric lavage should not be employed routinely in the management of poisoned patients. The amount of marker removed by gastric lavage is highly variable and diminishes with time. There is no certain evidence that its use improves clinical outcome and it may cause significant morbidity. Gastric lavage should only be considered, therefore, if a patient has ingested a potentially life-threatening amount of a poison and the procedure can be undertaken within 1 hour of ingestion.

Gastric lavage can be given upto 4 hours in poisoning with salicylates, anticholinergic and iron. Gastric lavage is contraindicated if airway-protective reflexes are lost (unless the patient is intubated) and also if a hydrocarbon with high aspiration potential (e.g. Kerosine) or a corrosive substance has been ingested.

 

Syrup ipecacuanha:

Syrup of ipecacuanha contains two alkaloids, emetine and cephaeline, which induce vomiting by a central action and by a local action (emetine). Syrup of ipecacuanha should not be administered in the management of poisoned patients. There is no evidence that it improves the clinical outcome and therefore its administration, even in children, should be abandoned.

 

Single dose activated charcoal:

Activated charcoal has a highly developed internal pore structure which is able to adsorb a wide variety of compounds and drugs, e.g. aspirin, carbamazepine, aminophylline, digoxin, barbiturates, phenytoin, paracetamol. It does not absorb strong acids and alkalis, ethanol, ethylene glycol, iron, lithium, mercury and methanol.

Single-dose activated charcoal should not be administered routinely in the management of poisoned patients. Based on volunteer studies, the effectiveness of activated charcoal decreases with time; the greatest benefit is within 1 hour of ingestion. The administration of activated charcoal should only be considered if a patient (with an intact or protected airway) has ingested a potentially toxic amount of a poison (which is known to be adsorbed to charcoal) up to 1 hour previously. Again, there is no evidence that this improves the clinical outcome.

Cathartics:

Whole bowel irrigation (WBI) requires the insertion of a nasogastric tube into the stomach and the introduction of polyethylene glycol electrolyte solution 1500-2000 mL/h in an adult. WBI is continued until the rectal effluent is clear.

WBI should not be used routinely in the management of the poisoned patient. Although some volunteer studies have shown substantial decreases in the bioavailability of ingested drugs, no controlled clinical trials have been performed and there is no conclusive evidence that WBI improves the outcome of the poisoned patient.

Based on volunteer studies, WBI should be considered for potentially toxic ingestions of sustained-release or enteric-coated drugs. There are insufficient data to support or exclude the use of WBI for potentially toxic ingestions of iron, lead, zinc, or packets of illicit drugs; WBI remains a theoretical option for these ingestions.

WBI is contraindicated in patients with bowel obstruction, perforation, ileus, and in patients with haemodynamic instability or compromised unprotected airways. WBI should be used cautiously in debilitated patients or in patients with medical conditions that may be further compromised by its use.

 

Increasing Poison Elimination:

Treatments that might speed poison elimination are forced diuresis, urine alkalinization, acid diuresis, multiple-dose activated charcoal, dialysis and haemoperfusion.

Forced diuresis:

The efficacy of forced diuresis depends on the poison being excreted unchanged by the kidney or as an active metabolite. Most drugs are either degraded by the liver to non-toxic metabolites or have such large volumes of distribution that there is insufficient active drug elimination in urine for forced diuresis to be of any clinical value. The amount removed in this way is insignificant compared to that removed by hepatic metabolism and forced diuresis should not be used.

 

Urine alkalinization:

Most drugs, particularly unionized, lipid-soluble molecules, are largely reabsorbed by the renal tubules. Increasing the concentration of ionized drug in the urine should reduce reabsorption and further enhance elimination. This is achieved by manipulating urine pH which enhances ionization and hence elimination of weakly acidic compounds such as salicylates, phenobarbital, and chlorophenoxy herbicides. In practice, urine alkalinization is only employed commonly in salicylate intoxication.

 


Urine acidification:

Although, theoretically, induction of urine acidification increases the elimination of basic drugs such as amphetamines, there is no evidence that it is of clinical value in cases of poisoning.

 

Multiple dose activated charcoal:

Multiple doses of activated charcoal aid the elimination of some drugs from the circulation by interrupting their enterohepatic circulation and also by adsorbing the drug that has diffused into the intestinal juices. The rate of transfer of the latter is dependent upon the blood supply to the gut, the area of mucosa available for transfer, and the concentration gradient of the drug across the mucosa. The adsorptive capacity of charcoal is such that as zero concentrations of free drug are present in luminal fluid, the diffusion gradient still remains as high as possible. The process has been termed ‘gut dialysis’ since, in effect, the intestinal mucosa is being used as a semipermeable membrane.

Although many studies have demonstrated that multiple-dose activated charcoal increases drug elimination significantly, this therapy has not yet been shown to reduce morbidity and mortality. Multiple-dose activated charcoal should be considered only if a patient has ingested a life-threatening amount of carbamazepine, dapsone, phenobarbital, quinine or theophylline. In all of these cases there are data to confirm enhanced elimination, though no controlled studies have demonstrated clinical benefit. Adults should receive 50-100 g initially, followed by 50 g 4-hourly or 25 g 2-hourly until charcoal appears in the faeces or recovery occurs.

 

Dialysis:

Haemodialysis in acute poisoning is most commonly indicated for the treatment of acute renal failure and only infrequently to increase the elimination of poisons. The rate of elimination across the dialysis membrane depends upon a number of variables including the molecular weight of the poison, the extent to which it is protein-bound, the concentration gradient, and pH of blood and dialysate. Haemodialysis is of little value in patients who ingest poisons with large volumes of distribution, e.g. tricyclic antidepressants, because the plasma contains only a small proportion of the total amount of drug in the body. Haemodialysis is indicated in patients with severe clinical features and high plasma concentrations of ethanol, ethylene glycol, isopropanol, lithium, methanol or salicylate.

Peritoneal dialysis increases the elimination of poisons such as ethylene glycol and methanol but is much less efficient than haemodialysis.

 

Haemoperfusion:

This technique is not available routinely. It involves the passage of blood through an adsorbent material, e.g. activated charcoal, but is no better than oral multidose activated charcoal for the removal of phenobarbital, carbamazepine and theophylline. Other barbiturate and non-barbiturate hypnotics can be removed effectively but are now only rarely prescribed.


 

Research works  

Types of snake and pattern of envenomation in Rangpur

  Dr. Ratindra Nath Mondal1, Dr. Moni Rani2, Dr. Md. Sarawarul Islam3,  Dr. Md. Ashraful Haque4, Dr.  Md. Zakir   Hossain5, Dr. Amaresh Chandra Saha6,  Dr. M.A. Faiz7.

1,2Honarary Medical officer, 3MD thesis part student, 4Assistant Professor, 5, 6 Professor of Medicine, RpMC , 7Professor of Medicine, SSMC.

Abstract:

Background: Snakebite is the second leading cause of unnatural death in Bangladesh. Incidence of snake bite is common in rural areas. Objectives: To see the types of snake, incidence of envenomation and mortality rate of snake bite in Rangpur, a northern district of Bangladesh. Methods: It was a cross sectional study carried out in department of Medicine, Rangpur Medical College Hospital, Rangpur from 01/06/2010 – 28/02/11. A total number of 111 snake bite patient with age ranged from 18 years to above of both sexes were studied. Patient admitted in inpatient department with history of snake bite were enrolled. Result: A total 111 patient, 18 years of age and above were admitted. Among them male were 69 (62.16%) and female were 42 (37.84%). Among the study population most were farmer 35 (31.53%) and house wife 35 (31.53%), and least are snake charmer 01 (0.90%). The study showed that most of the snake bite did not show signs of envenomation 90.09% ( n=100) and envenomation occurred in 9.91% ( n=11) and most of the venomous bite were by krait (77.78%%) and cobra (22.23 %). Among the study population mortality were found 5.71%. Conclusion: In our study envenomation occurred in 9.91%, most of the venomous bite was by krait (77.78%) and mortality rate among envenomated patient was 54.55%.

Introduction:

There are about 2500 species of snake in the world, among them 250 are poisonous. In Bangladesh among the 82 species of snake 28 are venomous, 12 species of them are sea snake.1 Venomous snakes of the world belong to the families Viperidae(sub family Viperinae: Old world vipers; sub family Crotalinae: new world and Asian pit vipers), Elapidae (including cobras, kraits, coral snakes and all Australian venomous snakes), Hydrophiidae (sea snakes), Atractaspididae (burrowing asps), and Colubridae (a large family, of which most species are non venomous and only a few are dangerously toxic to humans).2 There are 5 medically important groups of snake in our country, these are- cobra, krait, russel viper, green pit viper and sea snake. Among this majority of venomous bites in our country are cobras and kraits. They are mainly neurotoxic, and respiratory failure is the main cause of death following envenomation1. Snake usually lives in the paddy field, river, hills, roots of the tree, rat hole etc. Snakes are docile in nature, they are carnivorous they eat frog, rats etc3. They bite defensively or when agitated. All the snake bites do not produce sign, symptoms, only the bites by poisonous snake produces specific sign symptoms. Even 50% of the bite inflicted by poisonous snake does not produce any sign of envenomation. Bites rates are highest in temperate and tropical regions where the population subsists by manual agriculture. Estimates indicate >5 million bites annually by venomous snakes worldwide, with > 12,5000 deaths2 A World Health Organisation-funded study estimated about 8,000 cases of snakebite with over 20% mortality in Bangladesh annually. Incidence of snakebite is usually recorded in young people (11-20 years) engaged in active physical work in rural areas. Most bites in Bangladesh are recorded between May and October (rainy season) with highest number in June. Lower and upper limbs are most common sites of snakebite, but it may happen in other sites as well. Delayed presentation to the hospital, lack of availability of antisnake venom and modern management facility are the main causes of death4.

Methods:

It was a cross sectional study carried out in department of Medicine, Rangpur Medical College Hospital, Rangpur from 01/06/2010 – 28/02/11. A total number of 111 snake bite patient with age ranged from 18 years to above of both sexes was studied. Patient admitted in inpatient department of medicine with history of snake bite were enrolled. The statistical analysis was done by using windows SPSS version 12.

Ethical Consideration

All patients will be given an explanation of the study, and informed consent will be taken. The study will not involve any additional investigation procedures and significant risk as well as economic burden to the patients.

Results:

A total 111 patient were studied, among them male were 69(62.16%)and female were 42 (37.84%), in between 18-80 years of age. 35 (31.53%) were farmer, 35 (31.53%) were house wife, 32 (28.82%) were student, 04 (3.60%) were school teacher, 04 (3.60%) were shoop keeper, 01 (0.90%) was snake charmer. Among the victims (n-111) envenomation occurred in 11 (9.91%) and envenomation did not occur in 100 (90.09%). Among the envenomated patient 9 were bitten by krait & 2 were bitten by cobra (as detected by syndrome approach) and among the studied sample (n-111) day time bite was 64 (57.66%) and night time bite is 47 (42.34%) but in envenomated patient night time bite was 06 (54.55%)& day time was 05 (45.45%). 47 (42.34%)  bite was during working in the field, 43 (38.74%) bite was during house hold activities and 09 (8.10%)  bite was during sleeping, 12 (10.81%) while walking along road. Among the envenomous patient 6 (54.55%) were died & 5 (45.45%) survived completely.

Table I: Distribution of the patient by sex

N= 111

             Male          Female
        69(62.16%)      42 (37.84%)

Table II: Distribution of the patient by residence

N= 111

Rural Urban
89 (80.18)% 22 (19.81%)

Table III: Distribution of the patient by occupation

N= 111

              Occupation   Number/ percentage
           Farmer         35 (31.53%)
           House wife         35 (31.53%)
           Student         32 (28.82%)
           Teacher         04 (3.60%)
           Shop keeper         04 (3.60%)
           Snake charmer         01 (0.90%)

Table IV: Incidence of envenomation

N=111

     Envenomation         11 (9.91%)
     Not envenomation         100 (90.09%)

Table V: Time of biting in all patients

N=111

          Time of biting Number/ percentage
          Day time       64 (57.66%)
          Night time       47 (42.34%)

Table VI: Time of biting in envenomated patient

N=11

          Time of biting Number/ percentage
          Night time       06 (54.55%)
          Day time       05 (45.45%)

Table VII: Distribution of victim’s activities during biting

N=111

Activities during biting Number/ percentage
Working in the field   47 (42.34%)
House hold activities  43 (38.74%)
Sleeping  09 (8.10%)
Walking along road  12 (10.81%)

Table VIII: Distribution of patient by site of bite

N=70

      Site of biting Number/ percentage
      Lower limb            74 (66.67%)
     Upper limb            37 (33.33%)

Table XI: Distribution of first aid taken by victims

N=111

         Form of first aid      Number/ percentage
        Tight ligature            104 (93.69%)
        Both ligature & incision            03 (2.70%)
        Only multiple incision            03 (2.70%)
        None            01 (0.90%)

Table X: Type of snake among envenomous patient

(Detected by seeing snake & syndrome approach)

N=11

Krait  09 (77.78%)
Cobra  02 (22.23%)

Table XI: Mortality rate among envenomous patient

N=11

Survived 5 (45.45%)
Death 6 (54.55%)

Table XII: Distribution of mortality rate

  Mortality rate
        In all patient               6 (5.40%)
    In envenomated patient               6 (54.55%)

Discussion:

In our study venomous snake bite was found 9.91% and in other study 39.59 %5. Majority of the bite in lower limb was 66.67% but 65.95% % in other study6. Ligatures had been applied in 93.69%  but in other study 95% 5. Maximum reported cases from rural areas 80.18% in other study it was 99 %6. Mortality rate among venomous snake bite was 54.55% in other study mortality was 44%7.

Conclusion:

In our study envenomation of snake bites occurred in 9.91%  & majority of the victims were from rural areas. Most of the venomous snake bite was by Krait (77.78%).  Among the envenomous patient mortality rate was 54.55%. Delayed presentation to the hospital, lack of availability of antisnake venom & modern management facility is the main causes of death.

Recommendations:

Snake bite patients should be managed in ICU or well facilitated ward and by trained persons.  Improvement of mass awareness about snake bite in rural people and health workers will improve mortality.

Acknowledgement:

The authors of this study acknowledge to the professors, doctors and stuff of department of Medicine who were heartedly helped to do the study.

References:

  1. Faiz MA, Hossain M, Amin R, Ghose A, Basher A, National guideline of management of snake bite, second edition, DGHS, 2008; 1-32.
  2. Paul S.Auerbach, Robert L. Norris, Disorders Caused by Reptile Bites and Marine Animal Exposure. In Fauci AS, Braunwald E, Kasper DL, et al. 17th edition. Harrison’s Principles of Internal Medicine. New York: The McGraw- Hill Companies, 2008:2741- 2748.
  3. Apobo nandy, animal irritants, Principle of Forensic Medicine, second edition. New central book agency, 2004: 506-516.
  4. http://www.banglapedia.org/httpdocs/HT/S_0439.HTM
  5. John B. H., Md. Abul Faiz, M. Ridwanur Rahmanc, Md. M.A. Jalil, Md. Farid Ahsan, R. David G. Theakston, David A. Warrell, Ulrich Kuch; a study of bitten patients who developed no signs of systemic envenoming, in Chittagong Division, Bangladesh Volume 104Issue 5, Pages 320-327 (May 2010),
  6. Abu Bakar, Nazmul Ahasan, Manwar Ahsan, Snake bite in Bangladesh, Pak Armed Forces Med J Mar 2006;56(1):68-72.
  7. Md Titu Miah, AKM Aminul Hoque, Binoy Krishna Tarafder, Md Kamal Hossain Patwary, Raihan Rotap Khan, Shah Mohd Eftar Jahan Kabir, Epidemiology, Clinical Profile and Outcome of Patients of Snake Bite in Mymensingh Medical College Hospital, Journal of Bangladesh College of Physicians and Surgeons, volume 27, no2 (2009).
Study of incidence of acute poisoning in department of Medicine, Rangpur Medical College Hospital, Rangpur.

Dr.Ratindra Nath Mondal1, Dr.Nurmohammod2, Dr.Md.Zakir Hossain3, Dr.A.C.Shaha 4, Dr. Md. Rakibul Islam5, Dr.Ashraful Haque6, Dr.KamruzzamanSarkar7, Dr.Robed Amin8, Dr. Moni Rani9, Dr.M.A.Faiz10.

 

 1Honarary Medical officer, RpMC; 2Registrar of Medicine,RpMC; 3, 4 Professor of Medicine, RpMC 5 Associate Professor of Medicine,  RpMC; 6,7, Asst. Prof. of Medicine, RpMC;8 Asst. Prof. of Medicine,DMC;9 Honarary Medical officer, RpMC; 10Prof. of Medicine, SSMC.

Abstract:

Background: Acute poisoning is one of the most common reasons for acute admission to a medical ward.Poisoning is a common method of suicide, especially in the developing world. Objectives: To see the incidence, outcome and etiological aspect of different acute poisoning. Methods: It was a descriptive and cross sectional study carried out in department of Medicine, Rangpur Medical College Hospital, Rangpur from 01/12/2010 – 25/02/11. A total number of 188acute poisoning patient with age ranged from 18 years to above of both sexes were studied. Patient admitted in inpatient department with history of acute poisoning were enrolled. Result:  A total 188 patient were studied, majority of them female were 52.66%, maximum  92.55% in the age range  between 18 -40 years, 56.38% were married, farmer were 17.55%, 29.79% were house wife, 36.17% were student, 2.13% were serviceman, and others were 14.36%, 71.27% ingested poison due to familial disharmony, 6.91% Stupefied while travelling, 4.78% due to fail to pass in examination, 3.72% due to economic loss, 3.73% due to psychiatric illness, 1.60% due to chronic illness and accidental poison occurs in 7.44%. 81.92% ingested poison to committed suicide, 6.91% cases accidental exposure to poison occured, during travelling 6.91% stupefied, 3.19% ingested poison due to homicidal motive and recreational drug used by 1.06%. Majority 68.62% took OPC, 11.17% ingested sedative drugs, 11.17% by unknown poison, 5.85% corrosive, 2.12% rodenticide, 1.06% paracetamol, 1.06% TCA, 0.53% and other poison 1.06%. 84.04% patients survived, 7.98% died and abscondened 7.98%.

Conclusion: In our study 68.62% ingested OPC, suicidal motive were in 81.92%, 71.27% ingested poison due to familial disharmony, 6.91% stupefied by robbers during travel. Mortality rate was 7.98%.

 

Introduction:

Acute poisoning is exposure to a poison on one occasion or during a short period of time1. In many hospitals all over the world, acute poisoning is one of the most common reasons for acute admission to a medical ward.2 Acute poisoning accounting for about 10% of hospital admissions in the UK. In developed countries, the most frequent cause is intentional drug overdose in the context of self harm and usually involves prescribed or ‘over the counter’ medicines.3 About 5million poisoning exposures occurs USA every year. Most are acute accidental, involve single agent, occurs in at home, result in minor or no toxicity and involve children less than 6 yrs of age. Pharmaceuticals are involved in 47% of exposure and 84% of serious or fatal poisoning.4

Poisoning is a common method of suicide, especially in the developing world.5  In many Indian reports, the rates of poisoning as suicidal method range from 20.6% (10.3% organophosphorus)6 to 56.3% (43.8% organophosphorus).7,8 Important substances involved in acute poisoning are organophosphorus and carbamate insecticides, snake venoms, anti depressants, sedatives, alcohol, stupefying agents and kerosene etc. In developing countries the frequency of self harm is more difficult to estimate because patient may be reticent in admitting to deliberate poisoning. Household and agricultural products such as pesticide and herbicides are more freely available, are common source of poisoning. In China and South-east Asia pesticides account for about 300 000 suicides each year.3

In adult, self poisoning is commonly a “cry for help.” Those involved are most often females under the age of 35 years who are in good physical health. In those older than 55years of age men predominant and the overdose is usually taken in the course of a depressive illness or because of poor physical health. A third of self poisoning patients state that they are unaware of the toxic effects of the substance involved. 2  Accidental exposures can result from the improper use of chemicals at work or play, product mislabeling, label misreading, mistaken identification of unlabeled chemicals, uninformed self medication and dosing errors by nurses, parents, pharmacist, physician and elderly.

Induced poisoning by robbers during travel and using public transport is an emerging social and public health emergency in Bangladesh, The trends of pattern of induced poisoning from dhutura to unidentified stupefying agent particularly during journey is a major concern of care facility.9

Background: Poisoning is an important health problem in Bangladesh leading around 16000 episodes and 1500 deaths per year (Bangladesh Health Bulletin 1976). Self harm is claimed as commonest mode of poisoning.9 Organophosphorus compounds are used as insecticide in agricultural sector by the farming community in Bangladesh for the control of pest.10 So it is easily available and people usually use it as a suicidal agent.

Aim and Objective:

  1. To see the incidence of different poisoning
  2. To see the outcome of different poisoning
  3. Study of aetiological aspect of acute poisoning

Materials and methods:

Study design: Descriptive and cross sectional study.

Place of study: Rangpur Medical College Hospital, Rangpur

Period of study: 1st December 2010 to 25th February, 2011

Study Population:

Acute poisoning patients admitted in medicine unit of Rangpur Medical College Hospital, Rangpur.

Inclusion Criteria:

Patients admitted with the history of acute poisoning in Medicine ward, Rangpur Medical College Hospital, Rangpur.

Exclusion criteria:

      1. Patient refuses to take part in the study.

      2. Patients below 18 years

Ethical Consideration

All patients will be given an explanation of the study, and informed consent will be taken. The study will not involve any additional investigation procedures and significant risk as well as economic burden to the patients.

   Data collection and sampling method

Data will be collected using a structured research instrument (data collection format) containing the variables of interest. Purposive sampling method will be followed as per inclusion and exclusion criteria. Evaluation of patient will be based on history, physical examinations.

Results:

A total 188 patient were studied, among them male were 47.34% and female were 52.66%, maximum  92.55% in the age range  between 18 -40 years, 56.38% were married and 43.62% are unmarried. 32.98% are from rural area and 67.02% from urban area. Farmer were 17.55%, 29.79% were house wife, 36.17% were student, 2.13% were serviceman, and others were 14.36%, 71.27% ingested poison due to familial disharmony, 6.91% Stupefied while travelling, 4.78% due to fail to pass in examination, 3.72% due to economic loss, 3.73% due to psychiatric illness, 1.60% due to chronic illness and accidental poison occurs in 7.44%. 81.92% ingested poison to committed suicide, 6.91% cases accidental exposure to poison occurs while giving pesticides in the paddy field, during travelling 6.91% stupefied, 3.19% ingested poison due to homicidal motive and recreational drug used by 1.06%. Majority 68.62% took OPC, 11.17% ingested sedative drugs, 11.17% by unknown poison, 5.85% corrosive, 2.12% rodenticide, 1.06% paracetamol, 1.06% TCA, 0.53% and other poison 1.06%. 84.04% patients survived, 7.98% died and abscondened 7.98%. Among the death cases maximum are OPC (66.67%).

Table I: Distribution of the patient by sex

N= 188

Male Female
47.34% 52.66%

Table II: Distribution of the patient by age

N= 188

Age 18-40 years Age 41-60 years Age >60 years
92.55% 5.85% 1.60%

Table III: Distribution of the patient by marital status

N= 188

Married Unmarried
56.38% 43.62%

Table IV: Distribution of the patient by occupation

N= 188

Farmer Student Housewife Service Others
17.55% 36.17% 29.79% 2.13% 14.36%

Table V: Distribution of the patient by residence

N= 188

Rural Urban
32.98% 67.02%

Table VI: Distribution of the patient by cause of poisoning

N= 188

Familial disharmony Failed to pass Economic loss Chronic illness Psychiatric illness Stupefying Accidental
71.27% 4.78% 3.72% 1.60% 3.73% 6.91% 7.44%

Table VII: Distribution of the patient by motive of poisoning

N= 188

Suicidal Homicidal Accidental Stupefying Recreational
81.92% 3.19% 6.91% 6.91% 1.06%

Table VIII: Distribution of the patient by types of poison ingested

N= 188

OPC Sedative Unknown Corrosive Paracetamol Rodenticide Alcohol TCA Other
68.62% 11.17% 8.51% 5.85% 1.06% 2.12% 0.53% 1.06% 1.06%

Table IX: Outcome of patent

N= 188

Survived Death Abscondened
84.04% 7.98% 7.98%

Table X: Sex distribution of death patient

N=15

                     Male               Female
8 (53.53%) 7 (46.67%)

Table XI: Age distribution of death patient

N= 15

18-40 years 41-60 years
10 (66.67%) 5 (33.33%)

Table XII: Types of poison ingested among death patient

N=15

OPC Unknown Herpic Nitric acid Methanol
10 (66.67%) 2 (13.33%) 1 (6.67%) 1 (6.67%) 1 (6.67%)

Conclusion: In our study 68.62% ingested OPC, suicidal motive were in 81.92%, 71.27% ingested poison due to familial disharmony, 6.91% stupefied by robbers during travel and using public transport is an emerging social and public health emergency in Bangladesh. There is an increasing tendency to ingest corrosive (5.85%) like detol, herpic, savlon etc. 84.04% patient survived and mortality rate was 7.98%. Among the death cases maximum are OPC (66.67%). Lack of ICU, well facilitied separate poisoning unit, trained stuff contributed to this high mortality rate.

Recommendations:

Acute poisoning  patients should be managed in ICU or well facilitated ward and by trained persons. Improving awareness, ensuring unavailability of OPC and sedative drugs without prescription of registered physician, will reduce the incidence of acute poisoning and mortality rate.

Acknowledgement:

The authors of this study acknowledge to the professors, doctors and stuff of department of Medicine who were heartedly helped to do the study.

 

References:

1. Complete diving manual by Jack Jackson

2. Rawlins M and Vale JA, Drug therapy and poisoning In:KUMAR P, CLARK M CLINICAL MEDICINE, 6TH EDITION, ELSEVIER SAUNDERS, Reprinted 2008; 1002

3. Thomas S.H.L, . White J, Poisoning

In:  Colledge NR,  Walker B R, Ralstone S H Davidson’s Principles & Practice of Medicine, 21th edition, Churchill Livingstone Elsevier, 2010; 203-207

4. Christopher H. Linden, Michael J. Burns Poisoning and Drug overdosage, In: Kasper, Braunwald, Fauci, Hauser, Longo, Jameson, et al., Harrison’s Principles of Internal Medicine. 16th edition. New York: The McGraw- Hill Companies, 2005:2580- 1562.

5. Vijayakumar L: Suicide prevention: the urgent need in developing countries. World Psychiatry 2004, 3(3):158-159.

6. Ponnudurai R, Heyakar J: Suicide in Madras. Indian Journal of Psychiatry 1980, 22:203-205.

7. Gururaj G, Isaac MK: Epidemiology of suicide in Bangalore. NIMHANS Publication No. 43, Bangalore; 2001.

8. Nandi DN, Mukherjee SP, Banerjee G, Ghosh A, Boral GC, Chowdhury A, Bose J: Is suicide preventable by restricting the availability of lethal agents? A rural survey of West Bengal. Indian Journal of Psychiatry 1979, 21:251-255.

9. Bangladesh Health Bulletin, UMIS, Director General of Health Services.(2001);vol17:121-122(s)

10.Faiz MA, Ahmed S, Amin M R, Ghose A, Hoque MM: Training Manual on Management of Poisoning  Guideline – 2007

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