Uttara Adhunik Medical College

Department of Forensic Medicine

Name :

UM :

Roll :

Reg. No :

Session :
 Index

SL No Topic of the Assignment Page No

1 Concept of death and preventive measures

2 Electrocution lightening and burn

3 Poisoning

4 Substances Abuses
 Concept of death and
preventive measures

Department Involved

 Forensic Medicine
 Medicine
 Pathology
 Community Medicine
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
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Concept of death & life.
Philosophical, legal &
medical/scientific concept of death.
Oxford dictionary gives the meaning
of death as - The end of life".
Chamber's twentieth century
dictionary defines death as -
Extinction of life.
"Black “slaw dictionary defines
death as - The cessation of life; the
ceasing the exist"

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 Death
Law does not define death clearly. Definition of death (Medico
legal definition):
Death may be defined as permanent & irreversible cessation of
three interlinked vital systems of body, called tripod of life,
namely -the nervous, Circulatory & respiratory systems after
withdrawal of artificial maintenance.
In the United States, a person is dead by law if a Statement of
Death or Death certificate is approved by a licensed medical
practitioner. Various legal consequences follow death, including
the removal from the person of what in legal terminology is called
personhood.

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 Suspended Animation/Apparent
Death/Death Trance/Catalepsy:

Death trance is a condition in which all the signs of life or vitality

are seemed to be absent although the individual still remains
alive.
It is a condition, where in the vital functions of body (heart beat
and respiration) are maintained at a low pitch reduced to a
minimum for some time that they could not be detected by
routine methods of clinical examination.

Causes Of Suspended
Animation/Apparent Death/Death
Trance
Voluntary-Yoga practicing.
Involuntary-
1. Newborn infants 8. Shock
2. Drowning 9. Sun-stroke
3. Electrocution 10. Snake bite
4. Thunder injury 11. Epilepsy
5. Severe diarrhea/Cholera 12. Head injury
6. Poisoning 13. Sever narcosis
7. Anesthesia

MEDICO LEGAL IMPORTANCE OF

SOMATIC DEATH
 Resuscitation & organ transplantation.
 Disposal of the body.
 Presumption of death.
 Presumption of survivorship.
 Issuing death certificate.

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Criteria For Diagnosing Brain Death

(1) The patient must be in a deep coma, which is not due to

depressant drugs, metabolic or endocrine disorder.
(2) The patient must not be in hypothermia.
(3) The patient must be on a mechanical ventilator/heart-lung
Machine.
(4) Diagnostic test for brain death:-
(a) Absence of corneal reflex.
(b) Dilated and fixed pupil not reacting to light.
(c) Absence of vestibule-ocular reflex.
(d) Absence of cranial nerve response to painful stimuli. (e) Absence
of cough reflex.

Fig : Diagnosis Of Brain Death

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Death Certification
A doctor is the person who is legally authorized to declare a death &
issue a death certificate.
To issue a death certificate/Condition of certifying death:
1. Inspection of the dead body by the doctor himself.
2. Full satisfaction about the death
3. The doctor must sure of the cause of death
4. The doctor should free from least suspicion of foul play 5. The
doctor has seen/examined the person within 14 days before death
as alive.
6. The doctor registered as a qualified medical practitioner.

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 DEATH CERTIFICATE (WHO)
I do herby certify that I attended the deceased
(Name)...............aged................residing at ................................
.................... During his last illness and that to the best of my belief
the cause of his death (time) ............... on (date) was as stated below:

Cause of Death Approximate interval between onset and

death
1. Disease of condition or condition
Directly leading to death (a).....................Years Months
(due to or as consequence of) Days Hours
Antecedent cause (b) ...........................Years Months
(Due to or as consequence of) days hours
Morbid conditions, if any, (c) .......................Years Months
Giving rise to the above cause,
Days hours stating the underlying condition last
2. Other significant conditions. ........................years months
Contributing to the death but not.................... Day’s hours
Related to the disease or condition causing it.
Address or rubber stamp of the institution

Signature, designation, degree

and registration number.
·

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 PATHOLOGY
Death is said to be sudden or unexpected when a person not known
to have been suffering from any dangerous disease, injury or
poisoning is found dead or dies within 24 hours after the onset of
terminal illness.
Many diseases are known to have caused sudden death. A list is
provided below.

Fig: A Healthy Heart

I ist of causes of sudden death

1. Due to heart causes
- Myocardial infarct (MI), Arrhythmias, congestive cardiac failure
(CCF), rupture of the heart muscles.
- Toxic myocarditis (diphtheria)
- Congenital heart disease (in the new born)
- Prosthetic heart valves.
2. Due to lungs causes:
- Pulmonary embolism.
- Pulmonary edema, consolidation
- Collapse of lungs (pneumothorax, pleural effusion)

1
0
 - Inhalation impactions in the bronchi (mucous plugs in asthma,
foreign body) Malignancy.
Inhalation obstruction (Edema of glottis, e.g. diphtheric
membrane)
- Bleeding from lungs (hemoptysis) i
3. Due to abdominal causes:
- Acute appendicitis, acute cholecystitis, acute pancreatitis,
gastric/duodenal perforation. Bleeding from peptic ulcerations,
esophageal varies.
- Rupture of aorta, liver, spleen, kidneys
4. Causes in the brain:
Hemorrhage, (extradural, subdural, Sub arachnoid,-
intracranial)
- Cerebral infarcts (thrombo-embolism)
- Increased intracranial pressure (ICP).
Immediately after of blood, the muscles will stop contraction. ATP will
be gradually depleted and in 10 minutes 50% will be lost. In about
half an hour cardiac muscles will undergo irreversible damage,
subsequent changes noted are-
Time Macroscopic Microscopic
4-12 Hours Congestion at the neutrophilic
periphery of the infarct infiltration
18-24 hours Pale, firm appearance of Marked neutrophilic
the Marked neutrophil infiltration
infiltrations infarct area,
border hyperemic
24-72 hours Pale firm appearance Dense neutrophilic
border hyperemic infiltration
3-7 days Pale, soft appearance; Disintegration of
border Hyperemic myofibrils.
Hyperemic
Macrophages
invasions granulation
timon at the border.
10-12 days Area becomes soft, Total liquefication of
yellowish. the area.

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1
 Granulation, tissues
invade the
area.
2-4 weeks Area, pinkish or Liquified materials
yellowish or pale removed, Collagen
tissues laid down
4-6 weeks Are becomes firm, Fibrosis occurs
Pale (scarring)

Examination of the Coronaries:

Feeling:
Normally the coronaries feel soft collapsed. Knobby, irregularly hard-
atherosclerosis slicing through the course of the coronaries every
5mm in then made; first through t left anterior descending branch.
then through the left circumflex and finally through t right coronary.
Thrombo-embolism may be found, also atherosclerotic changes such
roughening, thickening of the intima. Calcifications may be noted
Note:
1. In 5-10% cases of MI. no coronary occlusion is found. In
these cases MI believed to be caused by spasms of the
coronaries.
2. No pathologic change may be demonstrated in the heart if
the patient dies with 2 hours of the attack. However in these
cases (patient dying within 2 hours. attack) depletions of
enzymes (glycogen, enzymes (glycogen, oxidases,
dehydrogenase phosphorylases) can be demonstrated by
putting heart muscle tissues into solution of triphenyl-
tetrazolium chloride. The affected tissues will remain pa but the
tissues not deprived of blood supply will stain red brown colour..
3. In death resulting from angina, arrhythmias, and pathologic
lesions may not be found in the heart.

Salient valvular pathology

Valvular disorders Cause/Causes Effect of valvular disorders

8. Mitral Stenosis Rheumatic fever, Left atrial dilatation,

rarely congenital pulmonary congestion,
passive venous congestion, 10
 8. Mitral incompetenceRheumatic fever, Left atrial dilatation,
rarely congenital pulmonary congestion,
passive venous congestion,

3. Mitral valve prolapse not known Mitral incompetence. passive

venous congestion

8. Aortic stenosis Congenital bicuspid Left atrial dilatation,

Valve, rheumatic fever pulmonary congestion,
passive venous congestion,

5. Aortic incompetence Rheumatic fever, hypertrophy, Left ventricular

rarely congenital failure, pulmonary congestion
passive venous congestion.
6. Tricuspid stenosis ,
Rheumatic fever Right heart failure passive
and incompetence. venous congestion of liver,
spleen
7. Pulmonary stenosis Congenital, rarely Right ventricular failure,
and Incompetence Rheumatic fever passive venous congestion
. of liver, spleen
8. Vegetations on Infective, thrombotic, Infective, thrombotic-
the cusps of rheumatic, Libmans embolisations
valves Sach's rheumatic. Libman
Sach's-stenosis,
incompetence.

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 Fig : Myocardial infarction

Examination of the brain:

on opening the skull, inspection is to be made for-
- presence of blood in the extradural space ( bleeding from middle
me artery)
- subdural hemorrhage blood present on the surface of brain
(bleeding. bridging veins)
- Normal pattern of gyri and sulci absent. brain appears swollen,
edematous gyri become flattened and sulci obliterated ( in
increased in cranial pressure due to intracerebral hemorrhage,
tumor, infections)
- brain appears small, gyri thin knife edge like, sulci widened
(cerebral atrophy seen in Alzheimer’s disease pick’s disease)
- spongyform brain (spongi form encephalopathy)
Note: for intracranial and subarachnoid lesions (including
hemorrhage) brain is to sliced at cm intervals. Better information
is obtained when slicing is done after fixing the brain in 10%
formaline (4% formaldehyde) for a week

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 Cerebral blood vessels are to be examined for atherosclerotic
changes thrombo embolism internal carotid, circle of Willis anterior
middle and posterior cerebral arteries.
Lung: Pulmonary embolism is an extremely common cause of
death
 More frequent in elderly
 Certain feature makes possible for diagnosis even over
telephone
 Often accompanied by cyanosis and breathlessness
 Usually occurs during defecation >20% in toilet & bed pan
 Classically occurs after trauma, Surgery, fracture, soft tissue
injury & range from 1day- few months but peak incidence
about 14days.
 Rule of thumb, death in middle-aged women is most frequent-
eg, complication of pregnancy, subarachnoid hemorrhage or
Pulmonary embolism
The lungs are first examined macroscopically. The pulmonary artery
and its branches are opened to look for presence of thromboemboli.
Apart from Pulmonary embolism lung may show other findings eg,
 Fluid in the pleural space: watery fluid
 Voluminous lungs with air bulla (emphysema).
 Foreign body, mucous plugs within bronchi, asthma .Diplitheric
membrane in the larynx. Glottis. trachea.
 Thromboemboli within the pulmonary artery - Pulmonary
embolism.
The lungs are first examined macroscopically & then microscopically.
The lungs are sliced I cm apart intra- pulmonary collections of blood,
cysts, abscess cavities, granulomas, tumours, may be noted.

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Fig: Normal Lungs

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 Fig: Pulmonary Edema

Gastrointestinal tract, abdomen & others

 Esophagus is opened along the, anterior wall and is looked for
varies at its lower end. Presence of foreign body/ mass/ tumor
may be noted.
 On opening the abdomen amount of peritoneal fluid is noted.
Normally it is only a few ml. (less than 15 ml). Peritoneal fluid

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 may increase in infarcts, ruptures of intestine, liver, ectopic
pregnancy, and ruptured uterus.

Macroscopic (Naked eye) examination is then made into the

abdominal organs for external abnormality.
 In acute appendicitis - the appendix will appear swollen
distended and necrotic.
 In acute cholecystitis - the gall bladder will be distended and
may show rupture.
 In acute pancreatitis - the pancreas will appear red,
hemorrhagic and will show calcifications and fat necrosis.
 Over distension of the intestine will suggest paralytic ileus
 Examination of supra renal glands may reveal evidences of
shock - hemorrhage into the medulla of adrenal gland.
 Peptic ulcer & ectopic pregnancy may cause death in a few
minutes.
Conclusion: A sudden death is not necessarily unexpected an
unexpected death is not necessarily sudden, but very often the
two are in combination.

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 Preventive Measures

Statistics
Statistics is the discipline that concerns with the collection, organization,
analysis, interpretation and presentation of data.

Death statistics

Death statistics expressed as termed Mortality rate.

A mortality rate is the number of deaths in a specified area in a given
year divided by total population.

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It expressed in per 1000 population.

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For example,
If there are 25 lung cancer deaths in one year in a population of 300,000,
then the mortality rate for that population is
Mortality rate = 25
× 1000
300000

= 0.083/1000 ppl

Types

• Crude Death Rate (CDR)

• Infant Mortality Rate (IMR)
• Maternal Mortality Ratio (MMR)
• Perinatal Mortality Rate (PNMR)
• Child Mortality Rate (per 1000 child 1 to 4 years)

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 • Under five mortality rate (per 1000
live birth)
• Age-specific Mortality Rate
• Cause specific Mortality Rate
• Case Fatality Rate (CFR)

In Bangladesh Mortality Rates

According to BBS 2023
1. CDR = 6.1/1000 population
2. IMR = 27/1000 live birth
3. MMR = 1.36/ 1000 live birth
4. PNMR = 20/1000 live birth
5. Under five Mortality Rate = 33/1000 live birth
6. Cause specific mortality rate
• Heart attack = 1.02/1000 ppl
• Stoke = 0.64/1000 ppl
• Respiratory disease = 0.57/1000 ppl
• Asthma = 0.27/ 1000 ppl etc.

Death Audit
In a mortality audit, data are collected on deaths, and a qualitative and
quantitative review is conducted.
Such audits are also called ―mortality reviews‖, ―death audits‖ or ―death
reviews‖.
It is a means of
• documenting the causes of a death and the factors that contributed
to it,

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 • identifying factors that could be modified and actions that could
prevent future deaths,
• putting the actions into place and reviewing the outcomes.

Importance
Mortality data are some of the best sources of information about the
health of living communities.
• It provide a snapshot of current health problems,
• Suggest persistent patterns of risk in specific communities,
• Show trends in specific causes of death over time,
• Lend a hand in distribution of health infrastructures,
• Helps in health policy making and development.

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Electrocution lightening
and burn

Department Involved
 Forensic Medicine
 Pathology
 Surgery
 Community Medicine

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 BURN

Burn is a dry heat injuries caused by application of flame

or heated solid substances to the body.
The minimum temperature for producing burn is about
44°C for an exposure of abuts 4-5 hours. At 65° C, two
seconds is sufficient to produce burn.

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Classification of Burn:

Three different types of classification are accepted they

are-
1. Dupuytren classification.
2. Wilson's classification
3. Modern classification

Management of a burn patient:

 General:
1. Removal of the patient from the source
2. Removal of clothing's.
3. Ensure adequate air ways.
4. Application of cold to burn.
5. Covering as quickly with sterile dressing.
6.Monitoring urinary output.
 Immediate general:
1. Anti tetanus toxoid should be given.
2. Emergency sedation-I/V opiates (morphine, Pethidine,
etc.)
2. I/V infusion of Dextrose saline

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3. treatment of shock:
-I/V infusion of Dextrose saline
- Infusion of plasma in six rations
- 3 rations in 1st 12 hours
- 2 rations in 2nd 12 hours
-Last ration in 3rd 12 hours.
(1 ration= 0.5 x Weight in Kg x %of burn)
In case of fluid replacement: 4 x Weight in Kg x % of burn
Half of the amount should be transfused in first 8 hours
and half of the amount should be transfused in last 16
hours4.
4. Blood transfusion if necessary.
5.Antibiotics if necessary.
 Local Treatment:
1. Open method: (superficial burn, burn in head and
face)
>Apply local antiseptic cream (Silver sulphadiazine
1%)
>Avoid dressing
>Maintain clean room
2. Close method: (deep. burn, infected superficial burn.): It
should be dressing in three layers-
>Inner most layer- apply acraflavin, chlorhexidine
or silver sulphadiazine.

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 >Middle layer- cotton gauze
>Outer layer- absorbent wool
3. Skin grafting.

Causes of death due to burn:

Immediate (death occurring within 48
hours): Victim may die due to-

1. Shock:
-Primary (Neurogenic) due to- fear, severe pain, injury to
vital organ etc.

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-Secondary (vascular) due to loss of serum from burnt
area , causing depletion of blood volume and hypovolumic
shock.

2. Coma: due to congestion of brain and serious effusion in

to the ventricles.

3. Asphyxia: suffocation due to inhalation of smoke or

gases of combustion. Asphyxia may be caused by
pressure on the chest due to falling roof, beams, walls
etc., when a house is on fire.

Delayed (death occurring after 48 hours):

Victim may die due to:
1. Toxemia: toxemia due to absorption of histamine
formed as a result of combustion of tissue.
2. Septic absorption: due to excessive suppuration.
3. Biochemical disturbance: hypokalemia.
inhalation of smoke containing carbon dioxide and carbon
monoxide.
4. Gangrene, tetanus, pyemia.
5. Pulmonary embolism due to thrombosis of leg vein
following immobility.

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6. Hepatorenal Syndrome: In every case of burn there is
absorption of altered protein occurs and this in turn leads
to cellular damage to liver and kidneys(acute tubular
necrosis).
7. Gastrointestinal disturbance: curling ulcer (acute
peptic ulcer) may occur.

SCALD
Scald is the moist heat injuries produced by the
application of liquid at or near its boiling point or in its
gaseous form such as steam to the body.

Medicolegal importance:
1) Accidental burning-

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 Large number of deaths are accidental. It may occur
inside the kitchen, in factories, house conflagration,
flaming of highly inflammable fuel, electrical short
circuits etc. Infant, children, epileptics, intoxicated
persons may fall into afire.

2) Suicidal burn-
it is relatively common among women, mostly on
account of domestic worries, cruelty by the husband
and in-laws or because of problem of dowry or some
disease. Women commit suicide by pouring kerosene
on their head and cloths before setting fire to
themselves (self emoliation) Sometimes suicidal
burning is resorted to as a mode of public protest.

3) Homicidal burning-
it is rare, commonly due to suspected infidelity of
women or inadequate dowry. Among adult female,
burns are produced usually on the pudenda as a
punishment for adultery

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ELECTROCAUTION AND LIGHTENING

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Electrocution
The passage of substantial electrical current through the
tissue can cause skin lesion organ damage and
death.This injury is commonly called electrocution.

General effects of electrocution:

>The moment of electrocution is painless.
>There may be tingling and numbness.
>The person may also get stunted for a moment and may
fall on the ground.
>In serious contact the victim may be unconscious for
time.
>Some problem may persist for some hours or days e.g.
mental confusion, lack of response, partial deafness,
defective vision, incontinence, vertigo, hemiplegia,
paraplegia etc.

Effects of lightening
A.Direct:
>Burning due to heat.
>Fusing and magnetization of metallic substances (rings
spectacles etc.)

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>The skin may be ruptured at the point of exit and shoes
may be torn·
>Development of intense edema of the skin.
B. Indirect:
>There may be cardiac failure.
> Epicardial and subendocardial hemorrhage may be
found.
>Subserosal and mucosal hemorrhages of gastro
intestinal and respiratory tract.
>Fracture of bones may be found.

Causes of death
ELECTROCUTION :-
Circuits from any of the limbs to the head involve the
brainstem and upper cervical cord. The cause's are-
>Ventricular fibrillation:
This occurs when entry of current through left upper
involve heart and causes ventricular fibrillation. It is
commonly occur due to low voltage current.
>Paralysis of the respiratory centre:

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It occurs when current passes through the brain and
involve upper cervical cord. It is commonly occur due to
high voltage current.
LIGHTENING:-
1. Involvement of the central nervous system.
2. Paralysis of the cardiac center.
3. Paralysis of the respiratory center.

Complication of electrocution:
 Cardiac arrest.
 Respiratory failure.
 Organ damage (including brain liver, kidney).
 Rhabdomyolysis.
 Dehydration associated with hypovolemia & hypotension.

Treatment of electrocution:
If the person is in contact with the source of electricity, he
should not be pulled with bare hands, but the current
should be switched off or the victim moved by a stick or
the hands should be wrapped in dry cloth or newspaper,
or rubber gloves worn. Artificial respiration and closed
chest cardiac massage are the principal forms of
treatment.

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34
Post mortem appearance
ELECTROCUTION:-

A. External:
>Singing of hair.
>Usually there are external marks of electric burning,
contusion and laceration.
>Characteristics appearance of puckering of the skin of
trunk.
>Evidence of blunt injury may present due to fall.
>Face pale, eye congested, pupil dilated.
>Rigor mortis early appear, post mortem lividity well
marked.
>Sometimes bloodstained froth comes out at mouth and
nostril.

B. Internal:
>Lungs-congested and edematous.
>Heart-right side full and left side empty.

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>Minute hemorrhage may found in brain and meninges.
>Extensive muscle damage may produce haemglobin.

LIGHTENING:-
A. External:
1. Bum may be present,the cloth also bum.
2. External injuries (bruise, laceration, fracture etc.) maybe
found.
3. Brown parchmentisation of the skin.
4.Arborescent mark may be present.
B. Internal:
1. Congested membranes -often with laceration.
2.Intracranial and intracerebral effusion of blood.
3.Patchy hemorrhages on the lungs and pleura.
Death due to electrocution occurs when a person is exposed
to a lethal amount of electrical energy.
Mechanisms Leading to Death:
 Cardiac Arrest: The most common cause of death from
electrocution is cardiac arrest due to disruption of the
heart's electrical activity.
 Respiratory Arrest: The electric current can paralyze the
respiratory muscles, leading to respiratory failure.

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  Severe Burns: High voltage can cause severe burns,
both internal and external, which can lead to
complications such as infection or multi-organ failure.
 Organ Damage: The passage of current can cause
significant damage to internal organs, leading to their
failure.

Death due to lightning, also known as a lightning strike,

occurs when a person is directly or indirectly hit by a bolt of
lightning.
Mechanisms Leading to Death:
1. Cardiac Arrest:
o Immediate Cardiac Arrest

o Asystole

2. Respiratory Arrest.
3. Neurological Damage.
4. Severe Burns.
5. Blunt Force Trauma.
6. Shockwave Impact.

Death due to burns can result from several

mechanisms, depending on the severity and extent of
the burns, as well as the time and quality of medical
intervention

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1. Shock (Hypovolemic Shock)
2. Infection (Sepsis)
3. Cardiac Arrest
4. Respiratory Complications
5. Multi-Organ Failure
6. Complications from Treatments.

SEPTICEMIA
Septicemia, also known as sepsis, is a life-threatening
condition that arises when the body's response to an
infection causes widespread inflammation and organ
dysfunction.
Multi-organ failure, can occurs due to septicemia, trauma,
or other critical illnesses.
1. Initial Infection:-

>Localized Infection: Septicemia usually begins with a

localized infection, which could be bacterial, viral, fungal,
or parasitic.
>Entry into the Bloodstream: Pathogens, or their toxins,
can enter the bloodstream directly from the infection site
through injured tissues, medical procedures, or due to a
weakened immune system.
2. Systemic Inflammatory Response

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 >Immune Activation: Once pathogens or their toxins are
in the bloodstream, the body's immune system is
activated. White blood cells (leukocytes) recognize the
invaders and release cytokines (small proteins), which
signal other immune cells to mount a defense.
>Inflammatory Cascade: The release of cytokines
triggers a systemic inflammatory response known as the
systemic inflammatory response syndrome (SIRS). This
response is characterized by widespread inflammation
throughout the body, not just at the site of the initial
infection
3. Vasodilation and Increased Capillary Permeability
>Vasodilation: Cytokines cause blood vessels to
dilate (widen) to allow more immune cells to reach the
infection. This vasodilation leads to a drop in blood
pressure, which can cause shock.
>Increased Capillary Permeability: The blood
vessels also become more permeable (leaky),
allowing fluids, proteins, and immune cells to escape
into surrounding tissues. This can lead to edema
(swelling) and reduced blood volume, further lowering
blood pressure and impairing organ function.
4. Tissue Hypoperfusion
>Impaired Blood Flow: The combination of
vasodilation, increased capillary permeability, and
decreased blood pressure leads to inadequate blood
flow (hypoperfusion) to vital organs.

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5. Cellular and Metabolic Dysfunction
>Mitochondrial Dysfunction: Sepsis can impair the
function of mitochondria (the energy-producing parts
of cells), leading to a lack of energy (ATP) in cells and
contributing to organ failure.
>Lactic Acidosis: As cells switch to anaerobic
metabolism due to lack of oxygen, they produce lactic
acid, leading to lactic acidosis. This further impairs
cellular functions and exacerbates organ failure.
>Acid-Base Imbalance: The accumulation of acid in
the blood disrupts the body's normal acid-base
balance, leading to metabolic acidosis, which affects
multiple organ systems.

6. Immunosuppression
>Immunosuppression: In the later stages of sepsis,
the immune system can become suppressed, making
the body vulnerable to secondary infections. This
immunosuppression can result from the depletion of
immune cells and the overproduction of anti-
inflammatory cytokines.
7. Coagulation Abnormalities

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Disseminated Intravascular Coagulation (DIC): Sepsis
can trigger abnormal blood clotting throughout the body.
Small blood clots form in the vessels, using up clotting
factors and platelets, which can lead to excessive bleeding
elsewhere in the body. DIC is a severe complication that
can cause multiple organ failure
8. Death
If the septic process is not quickly controlled, the
persistent low blood pressure, widespread clotting, and
lack of oxygen can lead to irreversible organ failure and
death.
 Lung (ARDS): Inflammatory damage to the lungs can
lead to Acute Respiratory Distress Syndrome (ARDS),
characterized by fluid accumulation in the alveoli,
impaired gas exchange, and severe hypoxemia.
 Kidney (AKI): Reduced blood flow and microvascular
damage in the kidneys can cause Acute Kidney Injury
(AKI), characterized by a rapid loss of kidney function,
fluid retention, and electrolyte imbalances.
 Heart (Cardiovascular Collapse): Myocardial
depression and impaired perfusion can lead to
cardiovascular collapse, characterized by reduced
cardiac output, hypotension, and circulatory failure.
 Liver (Hepatic Dysfunction): Hypoxia and
inflammation can impair liver function, leading to

41
 hepatic dysfunction, reduced detoxification, and
impaired synthesis of essential proteins.

 Brain (Encephalopathy): Hypoperfusion and

inflammation can cause encephalopathy, leading to
altered mental status, confusion, and coma.

Complications
Complications from electrocution, lightning, and burns can
vary widely depending on the severity of the injury. Here
are some common complications associated with each:
Complications of Electrocution, Lightning Strikes and
Burn:
 Cardiac Complications:
o Arrhythmias
o Cardiac Arrest
o Myocardial Damage
 Neurological Complications:
o Nerve Damage
o Seizures
o Cognitive Impairment
 Respiratory Complications due to lightning
o Respiratory Arrest
o Pulmonary Edema

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 Musculoskeletal Complications:
o Rhabdomyolysis
o Bone Fractures.
 Burns.
 Infection:
o Sepsis
o Chronic Wound Infections
 Metabolic Complications
o Hypermetabolism
o Nutritional Deficiencies
o Organ Damage
o Kidney Failure
o Respiratory Complications
 Psychological Complications:
o PTSD
o Depression and Anxiety
o Body Image Issues

PREVENTIVE MEASURE OF
ELECTROCUTION AND LIGHTENING
� Lightning is a natural electrical discharge causedby
imbalances between storm clouds and the ground

43
 that creates heat and magnetic forces of great
magnitude.
� Lightning destroys crop fields and trees, causes rock
disintegration and shift boulders.
� It can cause temporary blindness and severe hearing
problem.
� Death due to lightening and electrocution and burn is
increasing globally.
� Poor technological support and agriculture based
countries of tropical and subtropical areas like
Bangladesh is at risk.
� Lack of awareness is a challenge in prevention.

Statistical facts

44
� Bangladesh experiences more than 5,600 deaths due
to burn and electrical injuries every year.
� Considering the incidence rate of 3.97 per 100,000
populations per year.
� The government declared lightning a natural disasterin
2016

Electrocution Occur due to illegal connections and use

of substandard equipment.
� Lack of awareness and negligence by authorities is a
challenge.
� The deaths due to electrocution were 1.7 and 4.3 per
1000000 population in 2003 and 2016 survey
respectively

Burn: According to the health care cost and utilization

project, national admission due to burn is 29,165
admission per year
� Overall mortality due to burn was 2.2 per 1000000
populations per year
� Most of burn deaths are in rural area, among females
and are accident.

45
Who are affected?
� In Bangladesh From 2015 to 2022, due to lightning
2,142 people died and 538 were injured.
� The at risk population are
� Agricultural workers
� Construction workers
� Children playing outdoor

46
 � Outdoor recreationers

Lightning prevention
� Installing lightning warning system at vulnerable
places
� Proper structural and surge protection systemsto
the buildings should be applied
� Low cost outdoor shelters like abandoned cargo
container should be grounded at open places
� Displaying warning signs at out door locations
like play ground, swimming pool e.t.c
� Repairing of power and communication lines
according to weather forecast.

Outdoor lightning safety

� Tall trees need to be planted to absorb the
impact of the strikes.
� Lightning sheds in fields should be build, so
farmers can take safe shelter
� Early warning systems to alert people about
possible thunderstorms.

47
 � Installation of lightning
arresters in the open fields
with little tree coverage.
� Installation of lightning
detection sensors in
lightning-prone districts for
early warnings
Lightning prediction system
� It detects atmospheric conditions likely to
produce lightning strikes and sounds an alarm,
warning those nearby that lightning is imminent
and giving them the chance to find safety before
the storm arrives in the area.
� Installed in outdoor areas like agricultural fields,
parks, college campuses, swimming pool or play
ground

Indoor lightning safety

� Stay away from windows, doors and porches
� Switch off corded phones, computers and other
electrical equipment that put you in direct
contact with electricity

48
 � Avoid washing, shower or any other contact with
water during thunderstorm as lightning can
travel through building’ s plumbing

Electrocution prevention
� Electrical safety should be an integral part of the
safety plan of the workplaces
� Proper maintenance of industries, power
sectors, building construction sites should be
ensured
� Annual Employee training proggrame on
workplace safety should be arranged
� Training on first aid is also needed
� Take care about overhead and underground
electrical wires when working outside
� Avoid storing flammable liquids near a fire
source
� Keep the hot items in kitchen, iron out of reach
of children
� Do not remove radiator cap from a hot engines
� Do not smoke in bed or fall asleep while
smoking

49
50
 Poisoning

Department Involved
 Forensic Medicine
 Pharmacology
 Medicine

51
Description of Poison:
Poison:
Poison is a substance (solid, liquid or gaseous). which if introduced in the living
body, or brought into contact with any part thereof, will produce ill-health or
death, by its -constitutional or local effects or both.

Medico legal classification:

Suicidal poison
 Organophosphorus compound.
 Barbiturate
 Endrin.
 Opium.
 Potassium cyanide.
Homicidal poison: Arsenic, Antimony, Aconite.

52
Accidental poison:
 Household poison = disinfectant, insecticide spray, nail polish
remover, dish washing compound, rat paste.
 Arsenic.
 Snake bite.
 Lead.
 Sulphuric acid.

Stupefying poison:
 Dhatura,
 Cannabis indica.
 Infanticide
 Opium,
 Nacl solution,
 Madar.
Abortifacient :
Calotropis, Ergot, Arsenic, Lead.

Cattle poison:
Abrus precatorius, Calotropis, Oleander.

Arrow poisons:
Abrus precatorius, Calotropis , aconite, strychnine, curare.

Aphrodisiacs:
Cocaine ,Cannabis , Opium, Strychnine , Arsenic.
Rare- Bacteria , Insulin.

53
Principles of management of poisoning: Ethical &
legal issues related:

A doctor when dealing with emergency cases like suspected poisoning case needs
to be fulfilled legal as well as ethical duties. He is bound to fulfill all legal and
ethical duties concerning a poisoning case otherwise he is liable for punishment
as per the current law.

Legal issues:

To assist the police to determine the manner of death.

1) Note preliminary particulars of the patient, e.g., sex, address, date and
time, identification marks, etc.

2) In case of suspected poisoning, the doctor must confirm his suspicion

before expressing an opinion.

a) Collect vomit and urine, and submit for analysis.

(b) Carefully observe and record the symptoms.

(c) Consult in strict confidence with senior practitioner and keep him
informed about the case.

(3) Remove the patient to hospital.

4) Any suspected articles of food, excreta, and stomach wash samples ,vomit and
urine full or empty bottles, capsules, paper packets, or liquids should be collected
and preserved.
Any recent stains on bedclothes, furniture, etc., should be preserved if possible.
 Non-compliance is punishable under S. 201, B.P.C. if it is proved that the
doctor did it with the intention of protection the accused.
5) Doctor should inform the police officer.

54
  In Government hospital it is mandatory to inform police/authorities
regarding a poisoning case. He is bound to inform legal authorities of all
the cases of poisoning regardless of their manner either suicidal /
homicidal accidental.

 A private medical practitioner on the other hand, is not legally bound to

inform the legal authorities of all the cases of poisoning. He is only having
a legal obligation to inform in homicidal cases{i.e murder/attempt to
murder) of poisoning as per section 39 Cr.P.C.

 If he is sure that the case is suicidal /accidental in nature, he needs not to

inform any authority. However, a doctor can never be sure about the
manner of poisoning, to be on the safe side, he should always inform the
legal authority about any case of poisoning.

6) If the practitioner is summoned by the investigation police officer, he is

bound to give alt information regarding the case that has come to notice.

If the doctor do not provide the same, the doctor can be penalized under Sec.193
BPC.

If the doctor do not provide the same, the doctor can be penalized under Sec.
193 BPC.
If the doctor intentionally gives false evidence shall be with imprisonment for a
term which may extend 7 yrs and also liable fine.

Section 202 BPC makes legally bound to a doctor to give information if he has
reason to believe that the case belong to case of homicidal & in case omission in
such legal obligation, he shall be punished with imprisonment for a term which
may extend to 6 months or with fine, or with both.

55
Section 177- if he furnish false information shall be punished with simple
imprisonment for a term which may extend to 6 months or with fine(1000), or
with both.
7) If the condition of the patient is serious. He must arrange to record the dying
declaration.
8) If the patient dies, doctor should not issue a death certificate, but he should
inform the police.
9) At autopsy he should preserve viscera for chemical analysis.
10) In case of food poisoning, public health authorities must be notified.

Discussing the mechanism of Action of Organophosphorus

compound poisoning.

Organophosphorus compound poisoning

Organophosphorus compounds bind covalently to acetylcholinesterase (AChE)
||
Long lasting increase in AChE at all sites where it is released.

Atropine and pralidoxime

 Atropine prevents muscarinic side effects of these agents.

56
  Diazepam is administered to control convulsion.
 Pralidoxime can reactivate inhibited AChE

Preventive therapy for chemical warfare

 Auto injection containing pyridostigmine and atropine.
 Prior binding of pyridostigmine with AChE impedes binding of
organophosphates with the enzyme.
 Prevents prolonged inhibition of cholinesterase.

Atropine poisoning
 Occurs mainly in children, results in hyperactivity and rise in body
temperature.
 These central effects are the result of blocking mAChRs in the brain and
opposed by anticholinesterase drugs such as physostigmine.

Paracetamol poisoning
 N-acetylcystein (NAC) is the antidote for paracetamol poisoning.
 NAC works to replenish body stores of the glutathione.
 Glutathione reacts with the toxic N-acetyl-p-benzo-quinone
imine (NAPQIJ) metabolite so that it does not damage cells and can be
safely excreted.
Glucoronide conjugation(non toxic) Acetaminophen sulfate conjugation (non toxic)

P450
N-acetyl-p-benzo-quinone imine (NAPQI) ( (toxic)
glutathione N-acetylcystein
Cystein and mercapturic acid conjugates (non toxic)

Morphine poisoning
 Breathing is usually impaired in patients with a morphine poisoning.

57
  Naloxone is a mu receptor antagonist and reverses respiratory depression.
 Naloxone rapidly displaces all receptor-bound opioid molecules and
minimizes the effect of a morphine poisoning within 30 seconds.
Benzodiazepines poisoning
 Flumazenil is a GABA receptor antagonist, rapidly counteract the effects
of benzodiazepines.
 Half life is about 1 hour, frequent administration may be necessary to
maintain reversal of long acting benzodiazepine.
 Flumazenil may precipitate seizures if the benzodiazepine is used to
control seizure.

Iron poisoning
 Desferrioxamine is used to treat acute and chronic iron poisoning.
 Desferrioxamine forms a complex with ferric iron, which is excreted in
the urine.
 In chronic poisoning it must be given by slow subcutaneous infusion
several times a week.
 In acute cases it is given intramuscularly or intravenously Deferiprone
and deferasirox
 Oral iron chelator, alternative treatment for iron poisoning in patients
who are unable to take desferrioxamine.
 Agranulocytosis is the serious adverse effect of deferiprone and
deferasirox can cause gastrointestinal bleeding.

58
Poisonous substances and their specific antidote
Drug/Agent Antidote
Organophosphorus Compound Atropine
Atropine Physostigmine
Paracetamol N-Acetylcysteine
Morphine Naloxone
Iron Desferrioxamine, Deferiprone,
Deferasirox

Sign-symptoms/clinical features of OPC poisoning:

[OPC increases all secretions]
Muscarinic manifestations: Muscarinic effects are more intense than nicotinic
effects.
a. Bronchial tree: Bronchoconstriction (results in wheeze), increased bronchial
secretion, dyspnea. cyanosis, pulmonary edema.
b. GIT: Anorexia, nausea, vomiting, cramp, diarrhea, fecal incontinence,
tenesmus.
c. CNS: Bradycardia and hypotension. _
d. Sweat gland: Increased Sweating. ‗
e. Salivary gland: Increased salivation.
f. Lacrimal gland: Increased lacrimation. _
g. Pupil: Myosis, occasionally unequal or dilated.
h. Ciliary body: Blurred vision.

I. Bladder: Urinary incontinence.

B. Nicotinic manifestations: Seen in only 10-20% cases.
a. Striated muscle: Initial constriction followed paralysis.
Muscular weakness, twitching, fasciculations and cramps.
b. Sympathetic ganglia: Tachycardia, hypertension, pallor and
mydriasis.

59
C. CNS manifestations: Restlessness, emotional lability, headache, tremors,
drowsiness, confusion slurred speech, ataxia, generalized weakness, coma,
convulsions, depression of respiratory circulatory centers.

Treatment/management of OPC poisoning:

A. Decontamination:
1. Remove patient from source of expose
2. Remove his clothes
3. Wash exposed areas with soap and water.
4. Gastric lavage: With 1:5000 KMnO4, if poison is ingested.
o Activated charcoal should be administrated in doses of 1 g/Kg.

B. Antidotes:
Atropine: Start with 2-4 mg IV (0.05 mg/kg in children) and repeated
after every 5-10 min till
atropinization. [Note: Each ampule of atropine contains 0.6 mL atropine
i/v, and in clinical

60
 practice initially 5 amp is used which is doubled at every 5 min till
atropinization occur. |
2. Pralidoxime: Specific choline-esterase re-activator. [Note: adult dose is
1-2 g IV either as a 5% solution given over 5 min, or in 150 mL of saline
and infused over half-an-hour.}
C. Supportive care:
a. Absolute rest (if necessary by giving sedative).
6. Maintain patency of airway.
c. Suction to remove respiratory secretions.
d. Oxygen inhalation.
e. Respiratory support if necessary.
f. Diazepam to control convulsion.
g. Antibiotics to prevent pulmonary infection.
h. Diuretics to prevent pulmonary edema.

Postmortem findings of insecticides

Organophosphorus poisoning:
External Findings:
Signs of asphyxia-

61
  Face congested.
 Cyanosis.
 Blood stained froth is seen at the mouth and nose.
Internal Findings:
 The stomach content may of smell kerosene oil.
 The mucosa of the stomach is congested, sub mucus petechial
hemorrhage.
 Organophosphorus compounds resist putrefaction and poisoning can be
detected in exhumed bodies.
Endrine
 Signs of asphyxia.
External
 Kerosene like smell from the mouth and nostrils, even in decomposed
bodies.
 Fine white froth, occasionally blood stained.
 The face and finger nails are cyanosed.
 The conjunctiva congested.
 The pupil dilated.

Internal:
 The respiratory passages contain frothy mucous, mucous membrane
congested.
 Petechial hemorrhages over the lungs and heart.
 The lungs is large and bulky and pulmonary edema is a constant feature.
 The blood is dark and fluid.
 The mucous membrane of the esophagus, stomach, and intestine is
congested & emits a kerosene-like smell.

62
Carbamates:
 Violet discoloration of the esophagus and stomach mucosa.
Chlorinated hydrocarbons:
 Fatty degeneration of liver and kidneys.

63
 APPROACH TO A PATIENT OF
POISONING

CASE SCENERIO-1
A 21 years old student, came to emergency with sleepiness.

On query parents give history of found her in bed and empty drug strip.

As they arranged marriage against her will.

ON EXAMINATION
Patient sleepiness, confused

Heart rate/ respiration rate/ bp ---low

SEDATIVE -HYPNOTIC
Benzodiazepines
Barbiturates

Case Scenario-2
38 years farmers wife came to emergency with urination, frothy and bad smells
discharge from mouth with respiratory distress.

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On Examination

Spo2--88%

Pulse—60 b/m

R/r--. 12 breath / min

Blood pressure -. 80/60 mm hg
Pupil–pin point

Organophosphorus Poisoning
 Malathion
 Fenthion
 Diazinon

Opc Management

What do you do about it?

 Antagonize muscarinic symptoms
Atropine
 Stop aging of enzyme blockade
2-PAM
 Prevent and terminate seizures
Diazepam
 Supportive care

What goes wrong?

 D-Diarrhea
 U-Urination

65
  M-Miosis
 BBB-Bradycardia,Bronchorrhea, Bronchospasm
 E-Emesis
 L-Lacrimation
 S-Salivation

Case scenerio-3
A 23 years helper works in public transport came to emergency with agitation,
violence, accompanying give history of convulsion.

On examination
Agitation / violent
Pulse-120 b/ m
Blood pressure -220/90 ( ^pp)
Temp-raised/ normal
Skin -wet

Sympathomimetic

Yaba (methamphetamine + caffeine)

Cocain

Case scenario -4
A 44 years businessman, brought by police in a drawsycondition.

On examination
Temp-104
Pulse -120

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 Blood pressure –180/100
Retention of urine
Pupil-dilated

Anticholinergic
Dhatura
Tca

Case scenerio-5
Sedative
Coma
P/rr/bp-low
Pupil constricted
Needle mark

Opioid
Heroin
Fentanyl

Management
A supportive care
Airway, breathingand circulation (abc)
Complication :
Hypotension–iv fluid rarely vasopressor.
Seizure :: iv benzodiazepine
Arrhythmia ---correction of electrolyte and
acid-base disorder and hypoxia

67
B. Gastrointestinal decontamination
1. Activated charcoal ( upto1 hr)
2. Gastric aspiration and lavage(within 1 hour)
3. Whole bowel irrigation ( iron, li,)

C. Urinary Alkalinisation
Salicylates, methotrexate enhance urinary excretion by urinary
Ph>7.5 by iv sodium bicarbonate.

D. haemodialysisand Haemoperfusion
Methanol
Salicylates
Theophylline
Carbamazepine

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E. lipidemulsuontherapy
Local anaesthetic
Beta blocker
Ccb

F. antidote
Benzodiazepine—flumazenil
Opc-atropine, pralidoxim
Paracetamol-n acetylcystein
Warfarin-vitaminek
Methanol–ethanol

Psychiatric evaluation

69
Substances Abuses

Department Involved
 Forensic Medicine
 Pharmacology
 Psychiatry
 Community Medicine

70
 SUBSTANCE ABUSE IN FORENSIC MEDICINE & TOXICOLOGY

Definition
Substance abuse is the excessive use of a drug in a manner that is harmful to
oneself, society, or both. This definition encompasses both physical and
psychological dependence on a substance.

Sources of Various Poisons

 Dhatura :
Dhatura is derived from Dhatura plants which are of 2 varieties.
Dhatura Alba - White flowered plants.
Dhatura Nigra - Purple flowered plants.

All parts of Dhatura are poisonous. But seeds and fruits are the most noxious.
Active principles :
(i) Hyoscine
(ii) Hyoscymine
(iii) Traces of Atropine.

 Cannabis indica :
It is derived from a plant called Cannabis Sativa or Indian Hemp in India.
Dagga in south & Central Africa.
Hashish in Egypt.
Marijuana in America.

Active Principles: (i) Cannabinol

(ii) Cannabidol
(iii) Tetrahydro Cannabinol

 Strychnine
It is derived from the seeds of strychonus nux vomica tree found in different
jungles of Bangladesh
Active principles : (i) Strychnine (Kuchila)
(ii) Brucine

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 Alcohol
It is derived by fermentation of carbohydrates like sugar or starches by yeast.
(i) Absolute Alcohol - 99.95%
(ii) Rectified spirit - 90%
(iii) Methylated Spirit - 95%

 Opium
It is derived from the plant Papaverum. Somriferum by giving multiple,
longitudinal incisons oven the surface at the unriped poppy capsule & white latex
juice comes out which is then dried in the air. And then a brown mass like
substance is obtained which is Crudopium.

Causes of Death

 Deliriants & Stupefying Agents: Death is rare but can occur.

 Somniferous & Hypnotics: Mainly lead to respiratory failure.
 Inebriants:
o Respiratory depression
o Circulatory failure
o Depression of the cardio-respiratory center
o Dehydration
o Acute renal failure

Ethical and Social Issues

1. Health and Public Safety:

o Addiction and Health: Substance abuse can lead to a range of health
issues, from overdose to chronic diseases, putting a strain on
healthcare systems.
o Spread of Diseases: Sharing needles increases the risk of diseases
such as HIV and hepatitis.
o Public Safety: Drug abuse is associated with crime, accidents (e.g.,
driving under the influence), and unsafe behaviors, endangering the
public.

72
 2. Family and Social Impact:
o Family Breakdown: Addiction can lead to emotional, financial, and
physical strain on families, often resulting in broken relationships,
neglect, or abuse.
3. Criminal Justice System:
o Incarceration: Many individuals are imprisoned for drug-related
offenses, leading to prison overcrowding. This raises ethical questions
regarding whether addiction should be approached as a criminal issue
or a medical condition.
4. Economic Impact:
o Cost to Society: Drug abuse imposes a significant economic burden,
with costs related to healthcare, lost productivity, and law
enforcement.
5. Ethical Issues in Treatment:
o Access to Treatment: Limited access to affordable and effective
rehabilitation programs raises concerns about health inequality.

Legal Issues
Individuals involved in illegal drug-related activities face various legal
consequences, which may include imprisonment and heavy fines.

73
 Pharmacology
Substance Abuse
Substance abuse is a growing global issue, with over 190 million users worldwide.
The problem is particularly alarming among young adults under the age of 30.

Drugs Commonly Used in Substance Abuse

 Abusive Substances:
o Ethyl alcohol
o Tobacco
 Psycho Dysleptics:
o LSD
o Cannabis
 Psycho Stimulants:
o Cocaine
o Amphetamine (Yaba)

Ethyl Alcohol (Ethanol)

 Overview:
Alcohol is widely consumed, but misuse poses a significant social problem.
In the United States, 8–10% of the population suffers from alcohol-use
disorder.

74
  Pharmacokinetics:
Ethanol is rapidly absorbed and widely distributed in the body due to its
water solubility. Approximately 90% of absorbed alcohol is metabolized by
alcohol dehydrogenase, with the remainder excreted in breath, urine, and
sweat.
 Pharmacodynamics:
Ethanol acts as a CNS depressant by enhancing the action of GABA (an
inhibitory neurotransmitter) and inhibiting the action of glutamate (an
excitatory neurotransmitter).
 Effects on the Body:
o Liver damage
o Vomiting
o Increased heart rate and blood pressure
o Blurred vision, slurred speech, and impaired coordination
o Rapid heat loss and dehydration

Cannabis
 Overview:
Derived from Cannabis indica, Cannabis sativa, and Cannabis americana,
cannabis is known by many names, including weed, pot, and ganja. The
resin from the plant is known as hashish, while smoked preparations are
called marijuana.

75
  Pharmacokinetics:
The main psychoactive ingredient, tetrahydrocannabinol (THC), undergoes
extensive metabolism, with its metabolites also having psychoactive effects.
 Pharmacodynamics:
THC binds to CB1 receptors in the brain (primarily in the hippocampus and
amygdala) and CB2 receptors in immune cells. These receptors regulate
memory, fear, emotion, and immune responses.
 Therapeutic Uses of THC:
THC is used to alleviate chronic pain, muscle spasticity in multiple sclerosis,
stimulate appetite in AIDS patients, and reduce chemotherapy-induced
nausea.
 Effects on the Brain:
o Increased appetite
o Altered mood and perception
o Paranoia, hallucinations, and memory impairment

Lysergide (LSD)
 Overview:
LSD, derived from ergot alkaloids, acts as an agonist on presynaptic 5-HT
receptors in the CNS. It is usually taken orally, inhaled, or injected.

 Serious Side Effects:

LSD can lead to severe psychotic reactions, sometimes resulting in suicidal
behavior.

76
Cocaine

 Overview:
Cocaine hydrochloride, a fine white powder, is extracted from coca leaves. It
is often snorted, smoked, or injected and can be mixed with heroin (known
as a "speedball").

 Mechanism of Action:
Cocaine blocks dopamine reuptake, causing dopamine to accumulate in the
synaptic cleft, leading to euphoria and psychological dependence.
 Side Effects:
Cocaine can cause euphoria, acute tolerance, and intense drug-seeking
behavior. Chronic abuse leads to paranoia, hallucinations, and violent
behavior.

Heroin
 Overview:
An opioid derived from morphine, heroin binds to mu-opioid receptors in
the brain, altering pain perception and creating feelings of euphoria.

77
  Side Effects:
o Respiratory depression
o Nausea and constipation
o Severe physical dependence
 Long-Term Effects:
o Lung infections
o Depression
o Nasal tissue damage (from snorting)

Amphetamine and Methamphetamine (Yaba)

 Overview:
Amphetamines are stimulants that release dopamine in the brain and act as
indirectly acting sympathomimetics, binding to alpha and beta-
adrenoreceptors.

 Side Effects:
o Insomnia and dehydration
o Paranoid thoughts and aggression
o Chronic use can lead to psychosis, hypertension, and violent behavior.

Volatile Substance Abuse

 Commonly Abused Substances:
Adhesives, aerosol sprays, nail polish remover, and butane gas. These
substances are often inhaled, especially by younger adolescents who may not
have access to alcohol or other drugs.

78
  CNS Effects:
o Confusion and hallucinations
o Ataxia, dysarthria, and coma
o Damage to the liver, kidneys, lungs, and heart

Substance abuse remains a critical issue, affecting both individual health and
broader societal structures. Each substance carries unique risks and mechanisms of
action, highlighting the importance of awareness and preventive measures.

Psychiatry
What Are Drugs?
Drugs are natural or synthetic chemical substances that can affect:

 Your Body: Impacting its processes, functionality, and overall health

 Your Mind: Influencing behavior, emotions, and mental health

Many drugs are illegal and highly dangerous, yet even legal drugs, such as
prescription medications and over-the-counter drugs, can become hazardous if
misused.

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Substance Categories
1. Drugs
These include substances like alcohol, tobacco, and various psychoactive
compounds.
2. Non-Drug Substances
Inhalants and solvents are not technically classified as drugs but are often
abused for their psychoactive effects.

The Challenge of Drug Abuse and Addiction

Drug abuse and addiction are critical public health concerns, often coexisting with
other physical and mental health disorders.

Common Addictive Substances

CNS Depressants

 Alcohol (beer, wine, spirits)

 Opiates (morphine, heroin, methadone, codeine, opium)
 Benzodiazepines (e.g., Valium)
 Barbiturates
 General anesthetics
 Sedative antihistamines
 Volatile substances (solvents, glues, thinners, aerosols, gasoline)

CNS Stimulants

 Major Stimulants:
o Cocaine (coke, crack)
o Amphetamines (meth, speed, ice)
 Minor Stimulants:
o Nicotine (tobacco)
o Caffeine (coffee, tea, chocolate, cola drinks)

Hallucinogens

 Tryptamines: Psilocybin (magic mushrooms)

 Ergolines: LSD
 Phenethylamines: Mescaline

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Cannabis and Derivatives
 Marijuana (pot, grass)
 Hashish (hash)
 THC (tetrahydrocannabinol)

The Brain and Substance Abuse

 Dopamine Response: Drugs increase dopamine levels in the brain, creating a
feeling of reward. This repeated stimulation can alter the brain's reward system,
making natural rewards less pleasurable.
 Imaging Evidence: Positron emission tomography (PET) scans show that cocaine
abuse reduces the brain's ability to utilize glucose effectively, impacting brain
function.

Nicotine
Nicotine stimulates the reward circuit in the brain, particularly areas involved in
movement and attentiveness. This can explain why smokers report increased
vigilance and focus.

Marijuana and THC

Marijuana is derived from the cannabis plant, and its active ingredient, THC, is fat-
soluble. This means it remains in the body for extended periods, especially in fat-
rich areas like the brain, lungs, and reproductive system. Though the initial high
may wear off, THC can affect the user for days afterward.

Health and Social Impacts of Drug Abuse

 Health Risks: Drug abuse is linked to numerous injuries, illnesses, and even
death.
 Legal Consequences: Drug-related convictions can significantly disrupt lives,
leading to incarceration and criminal records.
 Financial Strain: Drug use can become financially burdensome, with some users
spending all their resources on substances.
 Social Difficulties: Drugs are often used as a coping mechanism, but this can lead
to worsened issues, creating new problems in the user’s life.

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Common Depressants ("Downers")
 Barbiturates ("barbs," "goofballs")
 Tranquilizers and Hypnotics ("roofies," "Valium")
 GHB ("G," "Georgia home boy")
 Alcohol

Yaba
A combination of methamphetamine and caffeine, Yaba is commonly abused and
has significant stimulant effects.

Gateway Drugs
Studies show that children aged 12-17 who smoke are 19 times more likely to use
cocaine. Additionally, two-thirds of drug abusers are regular tobacco users—
double the rate of the general population.

The Reward System in Addiction

Substance abuse disrupts the brain‘s ability to experience natural rewards, leading
to dependence and increased cravings.

Treatment Approaches

 Immediate:
o Detoxification
o Motivational interventions
 Long-Term:
o Relapse prevention strategies
o Social rehabilitation, addressing financial and social consequences

Substance abuse remains a pressing societal issue, affecting individual health,

family dynamics, public safety, and economic stability.

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 Community Medicine
Report on Substance Abuse in Bangladesh

Introduction: Substance abuse is a significant global issue, and it is increasing at

an alarming rate in Bangladesh. According to the World Health Organization
(WHO), approximately 275 million people worldwide use illicit drugs, with 31
million of them suffering from drug addiction. In Bangladesh, around 2.5 million
people are reported to be drug addicts. Notably, 80% of these addicts are
adolescents and young adults aged between 15 and 30.

Substance abuse involves the harmful or hazardous use of psychoactive substances,

including tobacco, alcohol, and illicit drugs. The adverse effects extend beyond
individual health to include mental health issues, economic burdens, and physical
health problems. The most commonly abused drugs in Bangladesh include opium,
cannabis, cocaine, amphetamine, heroin, Phensedyl, and glue. There are an
estimated 20,000-25,000 Injecting Drug Users (IDUs) in the country, with
buprenorphine being the most frequently injected drug.

Despite not being a drug-producing country, Bangladesh faces substantial risks of

drug abuse and trafficking due to its geographic location. The availability and
trafficking of various drugs pose a significant threat to the younger generation.

Preventive Strategies for Drug Abuse:

1. Policy and Legislation:

o Enforce legal control on drug distribution, including partial or
complete restriction to limit availability.
o Implement legislation regulating the manufacture, distribution,
prescription, sale, and consumption of drugs.
o Enforce laws prohibiting advertisements that promote the use of
drugs, tobacco, and alcohol.
o Strengthen laws and regulations to control drug trafficking and
enforce legal measures to address drug-related offenses.
o Bangladesh has implemented the Narcotics Control Act 1990, which
imposes strict penalties on drug abusers and dealers. This was further
amended in 2020 to enhance the legal framework.
2. Education and Awareness:
o Develop educational programs for youth, accompanied by public
information campaigns in electronic media.

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 o Integrate educational programs on substance abuse prevention in
schools, colleges, and communities to promote healthy lifestyles.
o Apply principles of effective communication to enhance the impact of
these educational approaches.
3. Anti-Smoking Measures:
o Prohibit the sale of tobacco products to minors.
o Ban smoking in public places such as schools, colleges, and other
public spaces.
o Restrict cigarette advertising on television, radio, and print media.
o Ensure public health education on the harmful consequences of
smoking.
o Make health warnings mandatory on cigarette packaging.
4. Alcohol Control Measures:
o Raise the legal age for alcohol consumption to reduce accessibility to
minors.
o Enforce legislation controlling the distribution of alcohol.
o Implement mandatory jail sentences for offenses like drunk driving.
5. Community Engagement:
o Engage local communities, religious organizations, and cultural
groups in drug prevention efforts.
o Encourage alternative activities for youth, such as sports, music, and
arts, to reduce the appeal of drug use.
o Establish groups or organizations to promote athletics and other
positive activities within the community.
o Support youth programs, including after-school activities and
vocational training, to provide alternatives to drug use.
6. Parental Guidance and Monitoring:
o Educate parents on drug addiction to empower them in guiding their
children.
o Encourage parents to set positive examples by avoiding tobacco,
alcohol, and drugs.
o Monitor children's internet use and observe any behavioral changes.
o Maintain open communication between parents and children about the
dangers of drugs.
7. Research and Data Collection:
o Conduct research to understand drug abuse trends and evaluate the
effectiveness of preventive strategies.
o Use data-driven policymaking to develop and improve intervention
programs.

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 o Cooperate internationally to tackle drug trafficking and share best
practices.

Treatment and Rehabilitation:

 Treatment: Addressing drug addiction starts with medical care, including:

o Identification and motivation of addicts for detoxification.
o Hospitalization for detoxification and post-detox counseling.
o Follow-up care and psychotherapy to support long-term recovery.
 Rehabilitation:
o The rehabilitation of former addicts is a lengthy and challenging
process, with a high relapse rate. There are 354 private treatment
centers in Bangladesh, along with government centers such as:
 Central Drug Addiction Treatment Center in Dhaka.
 Divisional Treatment Centers in Chittagong, Rajshahi, and
Khulna.
 Central Jail Treatment Centers in Jessore, Rajshahi, and
Comilla.
o Some notable private rehabilitation centers include Niramoy Hospital,
Golden Life BD, Phera BD, and Mukti Drug Helpline.

Conclusion: By approaching the issue of substance abuse from multiple angles—

legal, educational, social, and medical—Bangladesh can work towards reducing
both the demand and supply of illicit drugs. On June 26, 2024, the International
Day Against Drug Abuse and Illicit Trafficking was observed, with the theme,
"The Evidence is Clear: Invest in Prevention." Tackling drug abuse requires a
collaborative effort involving government bodies, non-government organizations,
and community volunteers to protect the youth from this growing menace.

END

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