This document discusses drug overdoses, including definitions, common drugs involved, risk factors, evaluation and treatment. It notes that overdoses can be intentional or accidental and are a major cause of morbidity and mortality worldwide. The most common drugs involved in overdoses are opioid analgesics and benzodiazepines. Men ages 45-49 have the highest death rates. Evaluation involves assessing vital signs and mental status while treatment focuses on stabilization, supportive care, prevention of further exposure, and administration of antidotes if available.

1. S.R.SRUTHI MEENAXSHI

3. DRUG OVERDOSE
 Consumption of a therapeutic agent, drug, or narcotic, in excess of that required to produce the
desired effects.
 When a drug is eaten, inhaled ,injected or absorbed through the skin in excessive amounts and injures
the body
 Overdoses are either intentional or unintentional
 Accidental and intentional poisonings or drug overdoses constitute a significant source of aggregate
morbidity, mortality, and health care expenditure worldwide.

5.  In 2018, over two million calls were made to United States poison control centers regarding known
or suspected human toxicities
 The exact incidence of this problem in our country remains uncertain but it is estimated that about
10-15 million cases of drug overdose poisoning are reported every year ,of which ,more than
50,000 die

8. Most common drugs involved in overdoses
 Of the 22,767 deaths relating to pharmaceutical overdose ,16,235 (71.3%) involved opioid
analgesics (Prescription painkillers) an 6973 (30.6%) involved benzodiazepines
 Benzodiazepines are frequently found among people treated in ED s for misusing or abusing
drugs
 People who died of drug overdoses often had a combination of benzodiazepines and opioid
analgesics in their bodies

9. Risk Factors for drug overdose
 Men were 59 % more likely than women to die
 High death rates among people 45-49 years of age
 Lowest death rates were among children less than 15 years old

10. INITIAL EVALUATION AND TREATMENT
 A brief initial screening examination should be performed on all patients to identify immediate
measures required to stabilize and prevent deterioration of the patient.
 Assess the airway, vital signs, mental status, pupil size, and skin temperature and moisture.
 Immediate diagnostic studies to be performed include pulse oximetry, continuous cardiac
monitoring, an electrocardiogram (ECG), and a capillary glucose measurement (in altered
patients).
 Intravenous (IV) access should be obtained in all cases of serious ingestion.

11.  In patients with suspected occult trauma, maintain in-line cervical immobilization.
 In cases of suspected opioid toxicity, a brief trial of naloxone may be performed prior to
performing tracheal intubation, provided ventilation can be assisted using noninvasive measures.
 Provide advanced cardiac life support measures as required.

12.  In patients with altered consciousness, a capillary glucose should be performed.
 Patients who are hypoglycemic should immediately be given dextrose (25g in adults, 0.5g/kg in
children).
 Administer IV naloxone to patients with respiratory depression and signs, symptoms, or a
suggestive of opioid intoxication .

13.  The notion that thiamine must be given prior to dextrose to avoid precipitating Wernicke
encephalopathy is unsupported .
 Uptake of thiamine into cells is slower than that of dextrose , and withholding dextrose until
administration of thiamine is complete may prove detrimental to those with actual hypoglycemia.

14.  Search clothing, wallets, and pocketbooks for pills, pill bottles, or drug-related equipment, but
take care when doing so to avoid a needle stick.
 A medical alert bracelet or necklace may provide important history. A more detailed diagnostic
evaluation can then ensue.
 A thorough search of the exposure environment should be conducted for pill bottles or a suicide
note, which may provide clues to etiologic agent(s).
 Knowledge of drugs prescribed for the patient or the patient's family or friends and to which he
she could have had access may prove important.

15.  History — The history, although intuitively the source of the most helpful information for
identifying the etiology of poisoning, is often unreliable when provided by a patient following
intentional ingestion .

16.  It is critical to inquire specifically about the use of over-the-counter medications, traditional or
herbal remedies, and dietary supplements
 Lastly, drugs of abuse may only be identified by colloquial or slang terms (eg, "ecstasy" for 3,4-
methylenedioxymethamphetamine [MDMA], or "bath salts" for synthetic cathinones)

17.  Physical examination — The physical examination of symptomatic poisoned patients may provide
invaluable clues to the agent involved.
 The mental status, vital signs, and pupillary examination are the most useful elements and allow
classification of the patient into either a state of physiologic excitation or depression

18. Physiologic excitation
 Physiologic excitation (manifested by central nervous system stimulation and increased pulse,
blood pressure, respiratory rate and depth, and temperature) is most commonly caused by
 anticholinergic,
 sympathomimetic, or
 central hallucinogenic agents;
 by drug withdrawal states.

19. Physiologic depression
 Physiologic depression (manifested by a depressed mental status, blood pressure, pulse,
respiratory rate and depth, and temperature)
 is most commonly precipitated by ethanol,
 other sedative-hypnotic agents,
 opioids,
 cholinergic (parasympathomimetic) agents,
 sympatholytics, or
 toxic alcohols (methanol or ethylene glycol)

20. Mixed physiologic effects
 Mixed physiologic effects may occur in polydrug overdoses or following exposure to certain
 metabolic poisons (eg, hypoglycemic agents, salicylates, cyanide),
 membrane-active agents (eg, volatile inhalants, antiarrhythmic drugs, local anesthetic agents)
 heavy metals (eg, iron, arsenic, mercury, lead), or
 agents with multiple mechanisms of action (eg, tricyclic antidepressants)

21.  Following the initial diagnostic evaluation and stabilization, other physical findings should be
sought to further define a particular toxic syndrome (toxidrome) and to narrow the potential
etiologies of poisoning.

22. Toxidromes
 Toxidromes are constellation of symptoms commonly encoutered with certain drug classes
,including anticholinergics ,cholinergics , opioids and sympathomimetics
 Evaluation of possible medication poisonings should include basic laboratory studies ,such as a
complete metabolic profile ,to be determine electrolyte imbalances and liver and renal function

25. Toxicokinetics and Toxicodynamics
 Toxicokinetics ( Determines the number of molecules that can reach the receptors)
 Uptake
 Transport
 Metabolism and transformation
 Sequestration
 Excretion

26. Toxicodynamics
 Determines the number of receptors that can interact with toxicants
 Binding
 Interaction
 Induction of toxic effects

28. Important Principles of Toxicokinetics
 The effect which a drug produces is dependent on
1) The dose
2) The concentration in the target organ
The kinetics of the drug may differ from therapeutic dose to its toxic dose
Toxicokinetics is important in predicting the plasma concentration of the drug

29. Toxicokinetics and Toxicity
 Toxicity depends on
 Duration and concentration of drug at the portal of entry
 The rate and amount (extent) of drug absorbed ,toxicity will be low at slow absorption rates
 The distribution of the drug within the body , where most drugs are distributed in highly perfused
organs like brain, liver and kidneys
 In some cases,the organ in which the drug is concentrated may not necessarily suffer the
damage
 An example is organochlorine compounds concentrated in adipose tissue while the target organ
is brain

30.  The efficiency of biotransformation and nature of metabolites ,where in some cases a drug maybe
transformed to more toxic metabolites or a more lipid or water soluble metabolite which affects the
absorption and distribution of the drug .
 Eg) paracetamol ,(INH ,dapsone ,hydralazine
 The ability of the drug to pass through cell membranes and interaction with cell constituents
Example , some organochlorine affect the DNA

31.  The amount and Storage duration of the drug or its metabolites in the tissue .
example Lead in bones is an example
 The rate and site of excretion , where the more rapid the excretion less toxicity it will produce

32. Cummulative Toxicity
 The state at which repeated administration of a drug may produce effects that are more pronounced
than those produced by the first dose is known as cumulative effectand resultsbinto cumulative toxicity
 Anticancer drugs induced cardiotoxicity
 Non cardiac pulmonary Edema – methotrexate,cocaine, hhydrochlorothiazide ,iodinated contrast
agents ,opiates , hydrocodone,morphine etc)
 Bronchiolitis obliternans organising pneumonia – Acebutolol, Amiodarone , Amphotericin B ,Bleomycin
, carbamazepine
 Bronchospasm – Amp B ,Asprin ,Amiodarone ,ACEI , beta blockers
 Iron , lead ,mercury ,aluminium ,arsenic – developmental disorders ,degenerative disorders
,haematological disorders

33. Digoxin
Cardiac adverse effects
o VT
o Nodal or ventricular extrasystole
o Pulsus bigeminus
o VF
o AFL,AF ,sever bradycardia

34. Bidirectional ventricular Tachycardia with Digoxin
Toxicity

35. Anti arrhythmic drugs
 Quinidine ,procainamide –
Torsades de pontes
 Sotalol – Intraventricular
conduction defect results into
VT and VF
 Adenosine - bronchospasm

36. Substance abuse and overdose
 Addiction
 Habituation
 Physiological dependence
 Psychological dependence
 Tolerance
 Withdrawal
 Drug overdose

37. Common drug for Abuse

40. Drug overdose General survey
 Directed cardiovascular . Respiratory , abdominal and neurological examination
 Vital signs ,pupils etc
 Temperature – hypothermia (phenothiazines ,barbiturate or TCA ) or Hyperthermia (
amphetamine , ecstasy ,MAOIs, cocaine, antimuscarnics, theophylline , serotonin syndrome )
 Muscle rigidity (ecstasy , amphetamines)

41.  Skin – cyanosis (methhemoglobinemia) very pink (carboxymethhemoglobinemia ,cyanide
,hydrogensulphide ), blisters ( barbiturates ,tricyclic antidepressants , benzodiazepine)needle tracks
 Hot flushed (anticholinergics)
 Breath –Ketones (diabetic/ alcoholicketoacidosis), bitter almonds ( cyanide) , garlic like
(organophosphorous,arsenic) , rotten eggs (hydrogen sulphide ) organic solvents
 Mouth – Perioral acneform lesions(solvent abuse, drug mouthanticholinergics , hyersalivation
(parasympathomimetics)

42. Investigations
 12 lead Electrocardiogram
 Blood glucose , Anion gap plus lactate and osmolal gap
 LFT and coagulation profile
 Arterial blood gas analysis
 Comprehensive Toxicology screen not normally indicated in emergency treatment unless
suspected cases
 Urinalysis - ?rhadomyolysis , save sample for toxicological analysis
 CXR if pulmonary edema/ aspiration suspected
 CT scan brain may be needed to exclude other causes of alterations in conscious level

43. Treatment
 Supportive care
 Prevention of further exposure
 Absorption
 Enchancement of toxin elimination
 Administration of antidotes
 Prevention of reexposure

44. Supportive care
 It include support of ABC and vital signs
 And also to prevent and treat secondary complications such as aspiration , cerebral and
pulmonary edema ,pneumonia , renal failure ,sepsis ,thromboembolic disease and generalised
organ dysfunction to hypoxemia or shock

45. DECONTAMINATION
 A. DECONTAMINATION OF THE SKIN
 cleansing with soap and water – used after dermal exposure to organophosphates
 Cleansing with acetic acid ( vinegar ) for nicotine
B . DECONTAMINATION OF THE STOMACH
 Emesis
 Gastric lavage
 Activated charcoal
 Endoscopic removal
C. DECONTAMINATON OF THE INTESTINES BY WHOLE BOWEL IRRIGATION (WBI)

46. ENHANCEMENT OF TOXICANT ELIMINATION
 A.INTRACORPORAL TECHNIQUES
 Forced diuresis and alkalization
 Repeated administration of charcoal
B.EXTRACORPOREAL TECHNIQUES
 Hemodialysis(Lithium)
 Hemoperfusion ( carbamazepine ,theophylline,digitoxin, phenobarbiturates , valproaic acid)
 Plasmapheresis ( Verpamil,thyroxine)

47. Antidotes

48. Differential diagnosis
 Head trauma( especially ,in the ethanol intoxicated patient)
 Stroke / subarachinoid hemoorhage (SAH)
 Meningitis
 Metabolic abnormalities ( such as hypoglycaemia , hyponatremia , hypoxemia)
 Liver disease
 Post ictal state

49. Poisoning reporting centres
 Toxbase :NHS intranet and internet based information from National poisons information centre
 Mims Colour index or TICTAC ( a computer aided tablet and capsule identification system
available to authorised users ,including regional Drug information Centres and Poisons
 Information centres to aid pill identification
 CMC Vellore Toxicology center

54. Thankyou