Lecture on some therapeutic poisons based on subject of Forensic Medicine. Aspirin , Salicylate, aconite and barbiturates poisoning is beutifully explaned with treatments

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2. The important therapeutic preparation of
salicylic acid include sodium salicylate, methyl
salicylate (oil of wintergreen), and
acetylsalicylic acid (aspirin). Salicin and
methyl salicylate are naturally occurring forms
of salicylates, forms in the leave and bark of a
numbers of plants, especially the willow tree
(salix alba vulgaris)

3. 1. Sodium salicylate: Odourless, white, scaly
crystals with unpleasant saline taste.
2. Acetyl salicylic acid: Odourless, white
crystalline powder tasting the same as
sodium salicylate
3. Methyl salicylate: colourless liquid with
aromatic odour and sweetish taste

4. Uses
1. Antipyretic
2. Analgesic
3. Antirheumatic
4. Keratolytic (Salicylic acid)
Signs and symptoms: It is perhaps a taxonomic error to
include salicylate under corrosives. They are
powerful irritants of the gastrointestinal tract, but
true corrosive action is lacking.

5. 1. Gastrointestinal: Epigastric pain, vomiting, GI-haemorrhage
, pylorospasm
2. Pulmonary (Salicylic dyspnoea): Tachyponea, pulmonary
odema and respiratory alkalosis(Co2 retention) at toxic
level respiratory center paralysis hene resp. acidosis.
3. CNS: Tinnitus, deafness, vertigo, hallucinations,
convulsions and salicylate jag, i.e. a form of delirium
with confusion, excitement and restlessness. Coma
occurs only in the terminal stages.
4. Renal: Proteinuria, sodium and water retention and
tubular necrosis.
5. Haemotologic: Hypovolaemia, hypoprothrombinaemia,
hypokalaemia and platelet dysfunction.
6. Metabolic: Hyperpyrexia, hyperventilation and
metabolic acidosis.

6. Usual fatal dose
Salicylic acid: 70 to 80 gm
Sodium salicylate and acetyl salicylic acid: 15 to 20 gm
Methyl salicylate: 10 to 20 ml
Toxicity rating 4.
Diagnosis
1. Lee-Jones test:
2. Ferric chloride test:
3. Plasma salicylate level
4. Prothrombin
5. Test for metabolic acidosis, hypokalaemia, etc.

7. 1. Decontamination: Stomach wash can be of benefit ,
even though the several hours may have elapsed since the
incident. When many tablets of salicylate are taken
together, they cake into a mass of concretion in the
stomach delaying gastric absorption and emptying. As a
result, blood level of aspirin may continue to rise several
hours after ingestion giving rise to the clinical maxim, “ it is
never to late to was out the stomach in salicylate
poisoning” gastric lavage must preferably be done with
sodium bicarbonate solution. Activated charcoal
suspension can be administered in the usual manner.

8. 2. Forced alkaline Diuresis: This can help in
eliminating aspirin or other salicylate from the
body. For this purpose sodium bicarbonate is
given intravenously initially in a dose of 1 to 2
mEq/Kg, with subsequent administrations as
required. Do not gives sodium bicarbonate orally as
it may enhanced salicylate absorption from the gut
by increasing dissolution. Also, do not administer
acetazolamide to alkalinize urine since it can
aggravate metabolic acidosis.

9. 3. IV Fluids and electrolytes
4. In severe cases, haemodialysis or haemoperfusion is of
benefit
5. Vit. K1 can be given if there is severe
hypoprothrombinaemia
6. Supportive measures.
Postmortem Appeareances
1. Haemorrhagic gastritis
2. Subpleural and subpericardial haemorrrhages
3. Pulmonary and cerebral oedma
4. Congestion of viscera

10. Medicolegal Importance
1. Accidental: Fatal accidental poisoning with aspirin in
children is reported from time to time. This has, however,
becomes relatively rare since th introduction of
paracetamol ( acetaminophen). In adults, accidental
fatalities are even more uncommon those cases involving
hypersensitivity reactions
2. Suicidal owing to easy availability of aspirin and related
products and also to their ubiquitous presence in the
average home, suicidal poisoning with this drug is not at
all uncommon
3. Homicidal These cases are extremly rare.

11.  The mechanism of paracetamol toxicity has now been
elucidated. In therapeutic doses it is metabolized in the
liver, largely to inactive sulphate and glucuronide
conjugates. However, about 8 percent is converted into a
highly toxic intermediate metabolite which is normally
immediately inactivated by conjugation with hepatic educed
glutathione and eventually excreted in the urine as cysteine
and mercapturic acid conjugates. After over dosage,
however, increased amounts of this metabolite are formed
and rapidly deplete the limited hepatic stores of
glutathione. It is then free to bind irreversibly with
macromolecules in the hepatocytes producing necrosis.
Children, however, seem less susceptible to paracetamol
hepatotoxicity and this may reflect differences in metabolic
pathways.

12.  Features:
 Nausea and vomiting are frequent within a few hours of the
overdose and there may be generalized abdominal pain
secondary to the effort of retching and liver tenderness.
 It is unusual for paracetamol hepatotoxicity to be clinically
apparent before 12 – 36 hours. The usual warning
signs comprise continuation of vomiting,
localization of abdominal pain to the right sub
costal area and the presence of liver tenderness .
Early renal tubular necrosis may also cause renal angle pain
at this stage. Jaundice dose not usually become obvious
before the third or fourth day. If hepatocellular necrosis is
extensive, hepatic failure ensues on about the fourth or fifth
day ( though occasionally sooner ) with impaired
consciousness, confusion, hyperventilation, hypoglycaemia
and bleeding secondary to coagulation abnormalities.

13.  Fatal cases often develop respiratory or Gram-negative
infections, cerebral oedema and
disseminated intravascular coagulation.
Acute renal failure occurs in a small proportion of
patients, usually, but not always, those with severe
liver damage and hepatic failure. Paracetamol
causes renal tubular necrosis in the same
way as it produces hepatic necrosis. In
addition renal failure is common in hepatic
encephalopathy from any cause.

14.  If the patient presents at about the critical ingestion-treatment
interval of 8 hours or at any interval from 8-15
hours after ingestion of >7.5 g paracetamol N-acetylcysteine
should be started immediately without
waiting for the result of the plasma paracetamol
concentration. If the latter subsequently suggests that the
likelihood of liver damage is low, treatment can be
stopped. This policy will inevitably result in the
unnecessary treatment of some patients but is justified
by the apparent lack of serious toxicity of N-acetylcysteine
and the need to minimize hepatic damage (with a
possible fatal outcome) in those at risk.

15.  The serum alanine and aspartate aminotransferase (ALT
and AST ) levels may begin to rise as early as 12 hours but
peak values are not usually attained until 72 - 96 hours
after the overdose. Aminotransferase activity of up to
10000 units/L is common but elevation of the alkaline
phosphates is usually minimal. Plasma biluribin
concentration rise more slowly than the enzymes and
seldom exceed 190 u mol/1 (10mg/dl) in survivors. The
prothrombin time ratio is often abnormal within 24 – 36
hours (maximum 48 – 72 hours). Hyperglycaemia is
occasionally found in some jaundiced patients but with
hepatic failure severe hypoglycaemia may occur. Plasma
creatinine concentrations rise more rapidly than the urea
when renal failure develops.

16.  TREATMENT:
 It has been shown clinically and experimentally that paracetamol
induced liver damage, renal failure and death can be prevented by
the administration of Sulphydryl donors such as Cysteamine,
methionine and N- acetylcysteine although their mode of
action is uncertain. Cysteamine ( intravenously) was the first of
these to be tried in clinical practice and though it was highly
effective if given within 10 hours, it had distressing adverse effects
and has been superseded by n-acetylcysteine. The latter provides
virtually complete protection against liver damage when given to
those at risk within 8 hours of the overdose but its efficacy
declines thereafter. However, there is still considerable protection
up to 10 hours and even from 10 to 12 hours but, like other
Sulphydryl donors, N-acetylcysteine seems completely ineffective if
given later than 15 hours after ingestion. Intravenous N-acetylcysteine
rarely cause any significant adverse effect and it
should be regarded as the treatment of choice for severe
paracetamol poisoning. Parenteral methionine is less effective.

17.  Oral methionine is advocated in some centers (2.5
g 4 hourly to a total of 10 g, provided the first dose
can be given within 10 hours of ingestion) but in
one study 10 percent of patients treated in this
way subsequently had AST levels above 1000
units/1. Oral NN-acetylcysteine has also been tried
but the high incidence of vomiting in patients
requiring treatment must necessarily raise doubts
about the reliability of oral therapy

18.  The patient presenting with paracetamol poisoning within
15 hours of ingestion should be managed as follows:
 Blood should be taken immediately ( or at 4 after ingestion
if the patient presents earlier than this ) for urgent
estimation of the plasma paracetamol concentration.
 The stomach should be emptied while waiting for the
laboratory result if more than 7.5 g have been taken within
4 hours.
 The plasma paracetamol concentrations should be
related to the time from ingestion and
seriousness of the condition, intravenous N-acetylcysteine
(Parvolex) should be started
immediately. The dose is 150 mg/kg in 200 ml of
5% dextrose over 15 minutes followed by 50
mg/kg in 0.5 liter 5% dextrose over 4 hours and
the same dose given over each of the subsequent
two 8 hour periods.

19.  These agents depress mental and respiratory
function when taken in overdose. Fatalities are
rare, ut mixed overdoses are common.
Flunitrazepam intoxication has emerged as
increasing problem. Ten times as potent as
diazepam. It is mixed with low-quality heroin and
used to soften the effects of cocaine. It is also
mixed with alcohol as date rape drug. Effects are
similar to those of other benzodiazepines. It may
cause hallucination, and mixing with alcohol
increases respiratory depression. It often is not
detected on standard toxicology screens.

20.  Symptoms.
 Include drowsiness dysarthria ataxia. Slurred speech, and confusion.
 Treatment.
 Do not induce emesis. Consider gastric lavage if presentation
is within 1 hour of ingestion . administer activated charcoal.
Provide general supportive measures for hypotension and
bradycardia. Rarely, respiratory depression may require
intubation. Flumazenil, a benzodiazepine antagonist, reverses
toxicity without causing respiratory depression. Administer
0.2 mg ( 2 ml) IV over 30 seconds, followed by 0.3 mg at 1
minute intervals to a total dose of 3 mg. if no response is
observed after such treatment, benzodiazepines are unlikely
to be the causes of the patients sedation. If a partial
response has occurred, give additional 0.5 mg increments to
a total of 5 mg. rarely, as much as a 10 mg total dose may be
necessary for full reversal. If no IV access is available, the
drug can be administered by endotracheal tube. Treat
recurrence of sedation or respiratory depression by repeating
the preceding regimen or by continuous infusion of 0.1 - 0.5
mg/hour. If mixed overdose with cyclic antidepressants is
suspected or the patient has a known history of seizure
disorder, Flumazenil should not be used. Forced diuresis and
hemodialysis are ineffective.

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22.  Aconite, also known as MONK’S HOOD, WOLF
BANE, BLUE ROCKET, is one of the most fast
acting and dangerous Poisons.
 As it is sweet in taste it is also known as Metha
Zehr

 In Indo. Pak it is found in temperate Himaliyan
regions and usually known by the name of
ACONITUM NAPELLUS.


23.  The different species of Aconite are:

 ACONITUM FEROX
 ACONITUM CHASMANTUM
 ACONITUM SPICATUM

 Of all these, Aconitum Ferox is the most toxic
and contains and alkaloid known as PSEUDO
ACONITINE.

24.  The whole plant is Poisonous but he root is
most Poisonous. Chiefly dry root is used as a
Poison. The dry root is more or less concial or
tappering in shape with longitudiual wrinkles.
Externally it is dark brown and white and
starchy internally, when freshly cut, but
becomes Pink on exposure to air. It has no
odour.

25.  MODE OF ACTION:

 It first stimulates and then paralyses the
peripheral terminations of sensory and
secretory cells. It also produces same effect on
motor nerves and centres in Medulla and
spinal cord, but does not effect higher centres
in the brain.

 ROUTE OF EXCRETION:
 KIDNEYS
 SALIVA (ONLY TRACES)

26. SYMPTOMS:
 Symptoms supervene immediately or with in a few
minutes after swallowing a poisonous dose of aconite.
Symptoms are:
 Sweet Taste.
 Severe burning and tingling of lips. Tongue, mouth and
throat, followed by numbness and anesthesia of these
parts.
 Sensation of swelling of Pharyngeal fauces.
 Nausea and vomiting.
 Salivation.
 Dysphagia.
 Pain in the abdomen.

27. Later there is :
Tingling and formication spread over the whole
body, causing gret uneasiness.
 The pupils contract and dilate alternately, but
finally dilate.
 Diplopia and impaired vision.
 Vertigo.
 Restlessness.
 Difficulty in speech.
 Great prostration.
 Pain and weakness of muscles with twitching
and Spasm.

28.  Pulse is slow, feeble and irregular.
 B.P. decreases.
 Respiration is rapid first but soon becomes
slow, laboured and shallow.
 The skin is cold and clammy.
 Temperature is subnormal.
 In most cases the consciousness is retained till
the end.
 Death occurs from Syncope, or from asphyxia.

29. F.D.20-30 GRAINS OF Aconite root. F.D. of
Extract 4 grains within an hour
F.D. of liniment 20 minims F.D. of Tincture
Aconite 5 ml.
F.P. 1 – 5 hours.

30.  Stomach Wash with Iodide or Potassium Iodide
solution with a solution containing Animal
Charcoal and Tannic acid.
 Digitalis may be used to counter-act cardiac
depression .
 Atropine is used to prevent vagal slowing of
heart.
 Maintain reccumbent position and administer
Amyl nitrite Inhalation.

31.  Keep the body Warm by blankets etc.
 Give artificial respiration or 02 inhalation.
 Dextrose saline drips.
 Coramine 25% sol. 10-15 ml I/V immediately
and when even necessary

32.  Pallor of mucus membrane of mouth,
congestion or engorgement of brain and lungs.
 Inflammation of mucus membrane of Stomach,
Congestion of Liver and Kidneys.

33.  It is an ideal Homicidal Poison.
 Can be used for abortion.
 In Himaliyan tribes the arrows are Poisoned by
aconitine.
 Used rarely as a Suicidal Poison.
 Occasionally cattle Poison.

35.  Digitoxin
 Digoxin
 Plants:
Foxglove
Lily of the valley
Oleander
Strophantus
 And others

36.  Interference with the Sodium-Potassium
pump mechanism mediated by ATP- ase
 Decrease in intracellular potassium leads to
disturbances of conductivity
 Reduction in resting membrane potential
 Loss of pacemaker function in sinusknot
and AV- knot
 Hyperkalemia and loss of excitability of
cardiac tissue

37.  Neurological symptoms:
 Fatigue
 Headache
 Confusion
 Dizziness
 Lethargy

38.  Cardial symptoms:
Harmless: Sinus-bradycardia and ST-scoop
AV-block I
 Less harmless: AV Block II,
Bigeminus, PAT
 Dangerous: Polytope ventricular
extrasystolia, Ventricular tachycardia
 Near death: Ventricular fibrillation
and asystolia

39.  Hypokalemia : harmless
 Hyperkalemia: most dangerous
 Eu-therapeutic range for digoxin:
1-2 ng/ml
 Eu-therapeutic range for digitoxin:
10-35 ng/ml
 Toxic levels can only be decided on 12 hours
after ingestion

40.  Forget all about:
Charcoal
Cholestyramin
Phenytoin
Lidocain
Hemoperfusion
Potassium
Pacemaker
Or what ever you have heard

41.  The only thing that helps is Immuno-therapy
with Digitalis antibodies
 This is a 100% therapy
 But it is expensive
 And you should store the stuff
 If you do not have it get it or start praying
and call for the priest
 Funerals are as expensive as antibodies but
only for the patient`s relatives
 Not to have the antibodies is neglect

42.  Man is more like sheep as like horse
 It was developed in Germany by Böhringer
Mannheim, a firm,that does not exit any
more
 Roche took it over and than off the market
so we have no longer 80 mg vials
 Only Digibind® with 40 mg per vial is
available

43.  Side effect don`t matter if the patient goes
on to life
 There may be allergy
 We used it again in the same patient after
tree week and saw no allergy
 You can do intra-conjunctival or intra-dermal
testing but it does not save you from
possible allergic reactions
 Be aware of hypokalemia!!

44.  Give as much as necessary
 But not to much
 Give it at the right time
 Timing is saving money
 Don’t believe always what is written in the
instruction
 To give the whole dose in one go is wasting
antibodies

45. 40 mg Fab bind 0,6 mg Digoxin
40 mg Fab bind 0,6 mg Digitoxin
Vials in Germany contained 80 mg but
are no longer available now
Vials in US and GB contain 40 mg

46. 1. Affinity of Fab to Digoxin und Digitoxin is nearly the same
(clinically no difference)
2. Affinity of Digitalis to Fab is larger than to Na +-K+-ATPase
3. Dissociation- half-live of digitalis from Na+-K+ ATPase 50
min.
4. Starting up time 1 hour
5. Half-live of the digitalis–antibody-complex 10-20 hours
6. Volume of distribution of Fab: 0,5 -1 l/kg
7. No dissociation of Digoxin from antibody
8. If to much Fab is given in the beginning it is wasted

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48. Source
Tobacco is usually prepared from curved leaves
of Nicotiana tabacum belonging to family
Solanaceae. Turkish tobacco is prepared from the
leaves of Nicotiana rustica, and is more potent.
Indian tobacco refers to Lobelia inflata.

49. Nicotiana tabacum and N.rustica contain the
following alkaloids:
 Nicotine
 Nornicotine
 Anabasine
 Anabatine

50. Lobelia inflata contains lobeline. It is cometimes used as
a nicotine substitute. Nicotine is a tertiary amine, and is
a colourless, bitter, volatile liquid that is weakly alkaline.
Uses
Nicotine is a stimulant of the central nervous system,
and is abused widely all over the world in the form of
inhalation (cigarette, cigar, pipe,), nasal insufflations
(snuff), or chewing.
Nicotine is also used as an insecticide.

51. By far the commonest source of nicotine poisoning
(acute or chronic) results from smoking tobacco in
the form of cigarettes. When a cigarette is lit and
inhaled, the smoker is exposed to both gaseous
and particulate matter. The usual nicotine content
of a “regular” cigarette varies between 13 and
20mg, while certain European and Turkish
cigarette can contain higher amounts. “Low
nicotine” cigarette contain 7 to 10 mg of the
alkaloid.

52. Cigars contain 15 to 40 mg of nicotine. When
a cigarette is smoked, more than half the
nicotine escapes in the sidestream smoke,
while a large fraction remains in the butt and
filter, and it is only 0.5 to 02 mg (average 1
mg) of nicotine that finally is delivered to the
smoker. Smoke from no-filtered
cigarettes contains slightly higher
amounts of nicotine.

53. There are several aspects to the mode of action of
nicotine:
1. Nicotine binds stereo-specifically to select
acetycholine receptors (nicotine receptors). These
receptors are present throughout the body,
particularly in the autonomic ganglia, adrenal
medulla, central nervous system, spinal
cord, neuromuscular junctions, and
chemoreceptors of carotid and aor tic bodies .
in the CNS, the highest concentration of nicotine
receptors are found in the limbic system, midbrain,
and brainstem.

54. 2. At moderate doses, nicotine stimulates the
reticular activating system producing an
altering pattern on the EEG, with resultant
favourable effects on memory and attention.
But higher doses cause tremor and
convulsions due to a CNS disinhibition
mechanism.

55. 3. Nicotine stimulation of vagal centres in the
medulla induces nausea and vomiting, while
the gastro-oesophagal reflux is provoked due
to a lowering of sphincter pressure and
increased acid secretion. Larger doses cause
diarrhoea due to both central and
parasympathetic excitation.

56. Acute poisoning
Early Effects (15 min- 1 hour)-
GIT: NAusa, salivation, vomiting, abdominal pain
CVS: Tachycardia, hypertension
RS: Tachypnoea, bronchorrhoea
CNS: Agitation, anxiety, sweating, headache, blurred
vision, confusion, vertigo, tremor, ataxia, muscle
fasciculations, convulsions. Pupils are at first
constricted, but may dilate later.

57. Delayed Effects (After 1 hour)-
GIT: Diarrhoea
CVS: Bradycardia, arrhythmias, hypotension, shock
RS: Hypoventilation, apnoea
CNS: Lethargy, weakness, hyporeflexia, hypotonia,
paralysis, coma.

58. Death may occur, especially in the case
of ingestion of cigarettes (inadver tently)
by children, or exposure to insecticidal
nicotine.
Occupational dermal exposure to wet, uncured
tobacco may produce “green tobacco sickness”
among workers, characterized by nausea,
vomiting, headache, vertigo, pallor, and sweating.

59. Chronic Poisoning (Addiction)
Nicotine dependence is the most widely prevalent and
deadly of all substance dependencies. The dependence-producing
effects of nicotine appear to be modulated by
dopamine which is increased in smokers. Nicotine also
increases noradrenaline, adrenaline, and serotonin
levels. Like most substance use, nicotine use begins
because of social reinforcement.

60. With repeated exposure, many youngsters find
the physiological effects of nicotine well suited to
help them with the difficult periods during
adolescence. In addition, physical dependence
begins so that cessation of nicotine use becomes
uncomfortable.

61.  Lung cancer
 Non-pulmonar y cancers: Mouth, Lar ynx,
Oesophagus, Stomach, Liver, Pancreas,
Bladder, Uterine cervix, Breast, Brain.
 Respirator y disease: Emphysema,
Bronchitis, Asthma, Pneumonia.
 Cardiovascular diseases: Coronar y
hear t disease, hyper tension, ar terial
thrombosis, stroke.

62. Obstetric and neonatal conditions: Abortion,
abruptio placenta, placenta praevia, preterm
labour, pre-eclampsia, growth retardation,
congenital malformations, sudden infant death
syndrome, foetal or neonatal death.
Other conditrions: Peptic ulcer,
osteoporosis, Alzheimer’s disease.

63. Manifestations of nicotine withdrawal can occur
within 4 to 8 hours of the last cigarette. In fact, most
chronic smokers experience some withdrawal
symptoms on waking up each morning.
Manifestations include changes in mood, insomnia,
difficulty in concentrating, restlessness, decreased
heart rate (average decline is 8 beats per minute),
and weight gain (average is 2 to 3 kg). Craving is
common, and increased coughing, poor performance
on vigilance tasks, etc. can occur.

64. Nicotine is highly toxic; 2 to 5 mg can cause
nausea, and 40 to 60 mg can cause death.
However, survival has occurred with ingestions of
1 to 4 gm.

65. Acute Poisoning
Mild overdose (with spontaneous vomiting)
requires only observation for 4 to 6 hours, after
which the patient can be discharged.

66. 1. Decontamination by stomach wash or (less
preferably) by induction of emesis. Activated
charcoal is effective and must be
administered in the usual manner. In cases of
dermal exposure (e.g. wet tobacco leaves,
spillage of nicotine liquid), clothing should be
removed, and skin thoroughly washed.

67. 2. Since nicotine is weakly alkaline, excretion can
be enhanced by acidification of urine. But it is
not recommended by most investigators since it
can aggravate the condition of a convulsing
patient in whom there is rhabdomyolysis.
3. Animal experiments indicate that drugs such as
pempidine and mecamylamine may have
antidotal effects against nicotine.
Hexamethonium (a ganglionic blocking agent)
has prevented nicotine-induced convulsions in
animals.

68. 4. Symptomatic and supportive measures-
• Benzodiazepines for convulsions.
• Atropine for bradycardia.
• IV fluids and vasopressors for hypotension
Respirator y compromise is managed by
oxygen, intubation, and positive pressure
ventilation

69. Nicotine withdrawal must be treated by a
combination of therapies including psychosocial,
psychopharmacological, and nicotine
replacement. A psychiatrist's help is crucial 0
effective management of withdrawal and
prevention of relapse.

70. The rationale behind nicotine replacement is to
prevent or relieve nicotine withdrawal symptoms
while stopping smoking behavior by replacing it
with another behavior. Pharmacological nicotine
is of various forms and dosages.

71. 1. Nicotine gum (polacrilex)
2. Nicotine transdermal patch
3. Nicotine spray

72. 1. Clonidine
2. Antidepressants
3. Nicotine agonists and antagonists