Prep. By :
Dr.Alaa Eldeen Elmassry
Egyptian fellowship of internal medicine ( E.F.I.M.),
Palestinian board of internal med...
 Recognize the epidemiology of drug
overdose?
 What are the different toxidrome pattern
seen in clinical practice?
 Wha...
1-A 24-year-old male is brought to the
emergency department after taking cyanide in
a suicide attempt. He is unconscious o...
2-Which of the following findings suggests an
opiate overdose?
A. Anion gap metabolic acidosis with a
normal lactate
B. Hy...
3-A patient with metabolic acidosis, reduced
anion gap, and increased osmolal gap is most
likely to have which of the foll...
4-Which of the following is true regarding drug
effects after an overdose in comparison to a
reference dose?
A. Drug effec...
5-Which of the following statements
regarding gastric decontamination for toxin
ingestion is true?
A. Activated charcoal’s...
 6-Which one of the following statements
regarding paracetamol overdose is false?
1. Metabolic acidosis with pH of <7.3 a...
Analysis of 2001 data from US poisoning centers
revealed the following statistics:
95 % caused minor or no effects
92 % ...
Adolf Hitler
Cyanide and gunshot simultaneously before capture
 Socrate (d. 399 BC) , Greek philosopher —
According to Plato, sentenced to kill himself
by drinking poison hemlock
 Is a former pediatric nurse who killed
somewhere between 11 and 46 infants and
children in her care.
British doctor acquitted in 1957 but suspected
of killing 163 patients via morphine and
barbiturates
 The Bhopal disaster (commonly referred to as
Bhopal gas tragedy) was a gas leak incident in
India , considered one of th...
When to suspect the poisoning ?
1.Rapid onset of symptoms like vomiting,
abdominal pain or depressed
consciousness.
2.Mass...
 Is often unreliable when provided by a
patient following intentional ingestion
 Knowledge of drugs prescribed for the
p...
 The mental status, vital signs, and pupillary
examination are the most useful elements
and allow classification of the p...
 Physiologic depression, manifested by
a depressed mental status, blood
pressure, pulse, respiratory rate and
depth, and ...
 Characteristic odors
 Pupillary findings
 Neuromuscular abnormalities
 Mental status alterations
 Skin findings
 Te...
Odor Agent(s)
Acetone (fruity)
Ethanol, isopropyl alcohol,
chloroform, salicylates
Bitter almonds Cyanide
Garlic
Arsenic, ...
Mydriasis
Sympathomimetics
Cocaine
Caffeine
Ephedrine
Amphetamines
Methylphenidate
Anticholinergics
Atropine
Scopolamine
T...
Miosis
Opioids
Heroin
Morphine
Hydromorphone
Oxycodone
Hydrocodone
Codeine
Propoxyphene
Sedative-hypnotics
Barbiturates
Be...
Nystagmus
Barbiturates
Carbamazepine
Phencyclidine
Phenytoin
Lithium
Ethanol
Toxic alcohols
Organophosphates
Strychnine
MA...
Cyanotic
Cyanide
Methemoglobinemia
Sulfhemoglobinemia
Hypoxemia
 Carbon monoxide
 Mushrooms
 Ethanol
 Scombroid fish poisoning
 Anticholinergic agents  
 Antihistamines
 TCAs
 At...
Hypertension with tachycardia
Thyroid hormone
Anticholinergics 
Drug withdrawal states
Organophosphates
Sympathomimet...
 MAOIs (foods with tyramine)
 Disulfiram reaction (early)
 Cholinergic agents
 Organophosphates
 Alpha-adrenergic ago...
 TCAs
 Theophylline
 Albuterol
 Toxic alcohols
 Beta-adrenergic agonists
 Barbiturates
 Beta-blockers
 Calcium-channel blockers
 Digoxin
 Cyanide
 Opiates
A toxidrome, or toxic syndrome, is a
constellation of clinical examination findings
that assists in the diagnosis and trea...
There are five general toxidromes :
1.Sympathomimetic
2.Cholinergic
3.Anticholinergic
4.Opiate
5.Sedative hypnotic
 Hypertension
 Pyrexia .
 Pupillary dilatation,
 Diaphoresis
 Altered mental status.
Drugs that can cause this type o...
 Bradycardia
 Respiratory depression due to paralysis
 Bronchoconstriction and bronchorrhea.
 Pinpoint pupils
 SLUDGE...
 Tachycardia
 CNS effects include agitation, delirium, and
in severe cases, seizures.
 Mydriasis ,
 Dry , flushed skin...
 Respiratory depression and oxygen
desaturations
 Miosis
 Decreased GI motility, and
 Coma .
These agents include Morp...
 Sedation or coma in the setting of
NORMAL vital signs.
 A common misconception is that ingested
benzodiazepines cause r...
 Blood sugar : This test should be considered
one of the vital signs in the patient with
altered mental status.
 Chemist...
 Rarely contributes to the management of the patient
◦ Amphetamines: commonly cross-reacts with over-the-
counter cold me...
 Cardiac toxins tend to prolong the :
1. PR interval (reflecting nodal blockade)
2. The QRS (reflecting sodium channel
bl...
 May reveal radiodense material in the
stomach or gut in the following ingestions :
◦ Chloral hydrate
◦ Heavy metals
◦ Ir...
1- Prevention of absorption
Gastric lavage
Activated charcoal (AC)
Whole-bowel irrigation
Cathartics.
Ipecac syrup.
2- Inc...
Endoscopy
Surgery
Dilution
AC is an insoluble, nonabsorbable,
inert, fine carbon powder.
AC is often the only GI
decontamination measure needed
to ...
 The greatest benefit from AC is seen
when it is administered within one
hour of ingestion, and when used AC
should be ad...
AC administration is not recommended:
1. In patients who have ingested nonabsorbable
acidic or alkaline corrosives (hydroc...
Corrosives Arsenic
Acids Lead
Alkali Mercury
Hydrocarbons Iron
Alcohols Sodium
Acetone Calcium
Ethanol Potassium
Ethylene ...
 Common side effects include:
 Nausea , vomiting, abdominal cramps,
and diarrhea, particularly when the
drug is used wit...
 Dose — The recommended dose of
activated charcoal  (AC) is 1 g/kg
 The usual single adult dose is 25 to 100 g
mixed wit...
 Routine use of gastric lavage in the
management of poisoned patients is not
recommended by the American Academy of
Clini...
 Gastric lavage is less effective activated
charcoal (AC) in reducing the
absorption
 Gastric lavage in combination with...
 A corrosive agent (eg, strong alkali,
concentrated acids, such as hydrochloric or
sulfuric)
 Low viscosity hydrocarbons...
1. Aspiration
2. Laryngospasm
3. Hypoxia and hypercapnia,
4. Esophageal and gastric erosions ,
bleeding, perforation
5. In...
  Syrup of Ipecac (SOI), which is derived
from the dried rhizome and roots of the
ipecacuanha, induces emesis in more tha...
 Refers to the enteral administration of a
polyethylene glycol balanced electrolyte
solution (PEG-ELS) in order to rapidl...
  Isosmotic high molecular weight
polyethylene glycol (PEG-3350) electrolyte
lavage solution is administered by mouth or
...
 Cathartics are intended to decrease poison
absorption by enhancing rectal evacuation
of the poison-activated charcoal co...
Recommended adult doses of commonly used
agents are:
 1 g/kg (1 to 2 mL/kg) of 70 percent
sorbitol (0.9 g/mL)
 4 mL/kg o...
 Dilution is recommended following the
ingestion of acidic or alkaline corrosives
 Dilution must be performed within min...
Antidote administration is appropriate
when:
1. There is a poisoning for which an
antidote exists.
2.The actual or predict...
Poison/syndrome Antidote(s) Adult dose
Acetaminophen
N-acetylcysteine (Mucomyst 20
percent)
Initial oral dose: 140 mg/kg, ...
Carbon monoxide Oxygen ± hyperbaric chamber
100 percent oxygen by ventilator or
NRB; high-flow oxygen by tight-
fitting fa...
Poison/syndrome Antidote(s) Adult dose
Heparin Protamine sulfate
1 mg neutralizes 90-115 U heparin; Initial
dose: 1 mg/min...
Methemoglobinemia
Methylene blue (1
percent solution)
Initial dose: 1-2 mg/kg (0.1-0.2
mL/kg) IV over 5 min; repeat prn
Op...
◦ Patients who have taken an overdose as a
suicidal gesture should all receive a
psychiatric evaluation prior to discharge...
 N-acetyl-para-aminophenol (APAP) is the leading
cause of toxicologic fatalities per year in the
United States, and
 APA...
 Decreased glutathione stores (fasting,
malnutrition, anorexia nervosa, chronic
alcoholism, febrile illness, chronic
dise...
 First 24 hours—asymptomatic stage:
◦ Early symptoms are very nonspecific and
primarily related to the GI tract (nausea,
...
24 to 48 hours—hepatotoxic stage:
◦RUQ tenderness is the most
common symptom.
◦Transaminitis, bilirubinemia, and
elevated...
 2 to 4 days—fulminant hepatic failure stage:
Significant hepatic dysfunction develops
(i.e., a peak in hepatic enzyme el...
 Assess airway, breathing, and
circulation (ABCs) and mental status.
 Especially in patients who are
nauseated or vomiti...
 Obtain an APAP serum level at 4 hours or
later after ingestion.
 Plot the APAP concentration on the
Rumack-Matthew nomo...
◦ pH < 7.3 two days post ingestion Or ,
◦ All of the following: PT > 100, serum
creatinine > 3.3 mmol/L, severe hepatic
en...
 Gastric lavage is not useful in APAP
overdose; however, it may be indicated in
presence of certain other coingestants.
...
◦ Any patient after acute poisoning with a toxic
APAP level according to the nomogram.
◦ Patients who present more than 24...
◦ Oral dosing: Loading dose of 140 mg/kg PO,
then 70 mg/kg PO every 4 hours for a total of 17
doses (i.e., 1,330 mg/kg ove...
 Salicylate toxicity may result from acute or
chronic ingestion of acetylsalicylic acid.
 Toxicity is usually mild after...
 Nausea, vomiting, tinnitus, tachypnea,
hyperpnea, and malaise are common.
 Hyperthermia
 Severe intoxications may incl...
 Obtain electrolytes, BUN, creatinine,
glucose, and salicylate concentration.
 ABGs may reveal an early respiratory
alka...
 Administer 50 to 100 g AC if presentation is
within 1 hour of ingestion
 Alkaline diuresis is indicated for symptomatic...
 Treat altered mental status with IV dextrose,
despite normal blood glucose.
 Treat cerebral edema with hyperventilation...
 Organophosphates (OPs) are
commonly used as pesticides and
insecticides (e.g., parathion). Some of
them also have medica...
 Inhibition of ACh breakdown through blocked
AChE leads to accumulation of ACh at
nicotinic and muscarinic receptors resu...
 The cholinergic toxidrome is a result of overstimulation
of nicotinic and muscarinic receptors
 Muscarinic effects:
◦ S...
◦ Ganglionic: tachycardia, hypertension,
diaphoresis, mydriasis.
◦ Neuromuscular: neuromuscular
depolarization, fasciculat...
Cholinesterase levels
relatively useless in assessing the
severity of exposure in acute
intoxications because of its wide...
 Remove patient from potential source of
poisoning.
 All clothing, especially leather, should be
removed from the patien...
 Is an Antimuscarinic agent which competes with
ACh for receptor binding
 GOAL: Atropinization, that is, drying of bronc...
 forms a complex with OPs that are bound to
AChE. The pralidoxime-OP complex is then
released from the enzyme and thus re...
1- Intermediate syndrome (IMS):
◦ This syndrome is a post-acute paralysis from
persistent ACh excess after the acute choli...
Generally speaking,
benzodiazepines have a wide safety
margin so its overdose rarely
represent a medical problem.
 The typical presentation of a pure oral
benzodiazepine overdose is coma with
normal vital signs.
 Respiratory depressio...
 Supportive care with observation is the
mainstay of therapy.
 In patients with co-ingestions and
respiratory depression...
 Traditional recommendations include the use
of flumazenil; however, given the propensity to
precipitate seizures and acu...
 Multiple TCAs are on the market,
including Amitriptyline, Clomipramine,
Doxepin, Imipramine, Trimipramine,
Desipramine, ...
 TCAs interact with a wide variety of receptors
with many consequent effects
 It has a:
1. Anticholinergic effect : dry ...
 In one classic study, one-third patients
with a QRS of ≥100 milliseconds
developed seizures.
 Fifty percent of patients...
After the patient's airway is protected, a dose
of AC 1 g/kg is warranted .
Sodium bicarbonate has been demonstrated
to ...
 Norepinephrine is the pressor of choice in
hypotensive patients who do not respond to
alkalinization because of its dire...
 The toxicity associated with an overdose of
β-blockers is largely due to the effects of
antagonism at catecholamine rece...
 Patients with a significant ingestion of an
immediate-release product will exhibit signs
of toxicity within 6 hours.
 T...
 Patients with significant ingestions present
with:
1. Bradycardia
2. CHF.
3. Patients with propranolol ingestions may
de...
 The ECG may reveal sinus bradycardia
or atrioventricular block.
 In propranolol ingestions, a wide QRS
manifesting sodi...
 Patient should have an IV placed, and
continuous cardiac monitoring should be
instituted.
 Hypoglycemia should be treat...
 Atropine 1 mg IV may be given up to 3 mg for
symptomatic bradycardia; however, this is usually
ineffective as the bradyc...
 Any patient with hypotension is a candidate
for high-dose insulin euglycemia therapy.
 This involves a bolus of 1 U/kg ...
 Catecholamines should be approached with
caution in these patients because α-
stimulation in conjunction with β-blockade...
QUESTIONS
??
 Most of poisoning events pass uneventfully without
significant harm.
 The most important clinical approach is to try to...
 ECG is important investigation in poisoned
pat.
 Paracetamol poisoning is a common cause
of drug overdoses and is the m...
 The goal of GOAL of Atropinization is
1. A heart rate > 80 bpm
2. A systolic BP > 80 mm Hg
but not dilated pupils.
 The...
Thank you
Approach to drug poisoning in adults by Dr Alaa Elmassry
Approach to drug poisoning in adults by Dr Alaa Elmassry
Approach to drug poisoning in adults by Dr Alaa Elmassry
Approach to drug poisoning in adults by Dr Alaa Elmassry
Approach to drug poisoning in adults by Dr Alaa Elmassry
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Approach to drug poisoning in adults by Dr Alaa Elmassry

  1. 1. Prep. By : Dr.Alaa Eldeen Elmassry Egyptian fellowship of internal medicine ( E.F.I.M.), Palestinian board of internal medicine ( P.B.I.M. ), Consultant internist Head of the medical dept., Naser hospital.
  2. 2.  Recognize the epidemiology of drug overdose?  What are the different toxidrome pattern seen in clinical practice?  What are the general lines of therapy of poisoned patient?  Different specific poisoning that might face in our practice.
  3. 3. 1-A 24-year-old male is brought to the emergency department after taking cyanide in a suicide attempt. He is unconscious on presentation. What drug should be used as an antidote? A.A. Atropine B.B. Methylene blue C.C. 2-Pralidoxime D.D. Sodium nitrite alone E.E. Sodium nitrite with sodium thiosulfate
  4. 4. 2-Which of the following findings suggests an opiate overdose? A. Anion gap metabolic acidosis with a normal lactate B. Hypotension and bradycardia in an alert patient C. Mydriasis D. Profuse sweating and drooling E. Therapeutic response to naloxone
  5. 5. 3-A patient with metabolic acidosis, reduced anion gap, and increased osmolal gap is most likely to have which of the following toxic ingestions? A. Lithium B. Methanol C. Oxycodone D. Propylene glycol E. Salicylate
  6. 6. 4-Which of the following is true regarding drug effects after an overdose in comparison to a reference dose? A. Drug effects begin earlier, peak earlier, and last longer B. Drug effects begin earlier, peak later, and last longer C. Drug effects begin earlier, peak later, and last shorter D. Drug effects begin later, peak earlier, and last shorter E. Drug effects begin later, peak later, and last longer
  7. 7. 5-Which of the following statements regarding gastric decontamination for toxin ingestion is true? A. Activated charcoal’s most common side effect is aspiration. B. Gastric lavage via NGT is preferred over the use of AC in situations where therapeutic endoscopy may also be warranted. C. Syrup of ipecac has no role in the hospital setting. D. There are insufficient data to support or exclude a benefit when gastric decontamination is used more than 1 h after a toxic ingestion. E. All of the above are true.
  8. 8.  6-Which one of the following statements regarding paracetamol overdose is false? 1. Metabolic acidosis with pH of <7.3 after fluid resuscitation is an indication for liver transplant 2. The first bag of NAC in treatment of paracetamol overdose contains NAC 100mg/kg. 3. NAC has anti-oxidant property 4. Prognostic accuracy of Rumack-Matthew nomogram decreases after 15hours 5. Paracetamol level is highest after 4 hours after ingestion
  9. 9. Analysis of 2001 data from US poisoning centers revealed the following statistics: 95 % caused minor or no effects 92 % were due to acute rather than chronic ingestions 92 % involved a single substance 85 % were unintentional 59 % fatalities occurred in individuals aged 20 to 49 52 % occurred in children younger than 6 years 47 % involved pharmaceuticals
  10. 10. Adolf Hitler Cyanide and gunshot simultaneously before capture
  11. 11.  Socrate (d. 399 BC) , Greek philosopher — According to Plato, sentenced to kill himself by drinking poison hemlock
  12. 12.  Is a former pediatric nurse who killed somewhere between 11 and 46 infants and children in her care.
  13. 13. British doctor acquitted in 1957 but suspected of killing 163 patients via morphine and barbiturates
  14. 14.  The Bhopal disaster (commonly referred to as Bhopal gas tragedy) was a gas leak incident in India , considered one of the world's worst industrial catastrophes .  The official immediate death toll was 2,259
  15. 15. When to suspect the poisoning ? 1.Rapid onset of symptoms like vomiting, abdominal pain or depressed consciousness. 2.Mass affection. 3.Psychiatric patients. 4.Specific toxic syndrome.
  16. 16.  Is often unreliable when provided by a patient following intentional ingestion  Knowledge of drugs prescribed for the patient or the patient's family or friends to which (s)he could have had access  A thorough search of the exposure environment should be conducted for pill bottles or a suicide note
  17. 17.  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  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, or by drug withdrawal states.
  18. 18.  Physiologic depression, manifested by a depressed mental status, blood pressure, pulse, respiratory rate and depth, and temperature, is most commonly precipitated by cholinergic (parasympathomimetic), sympatholytic, opiate, or sedative- hypnotic agents, or alcohols
  19. 19.  Characteristic odors  Pupillary findings  Neuromuscular abnormalities  Mental status alterations  Skin findings  Temperature alterations  BP and heart rate alterations  Respiratory disturbances
  20. 20. Odor Agent(s) Acetone (fruity) Ethanol, isopropyl alcohol, chloroform, salicylates Bitter almonds Cyanide Garlic Arsenic, organophosphates, phosphorus, thallium, selenium Mothballs Naphthalene, paradichlorobenzene Kerosene Organophosphates, parathion Freshly mown hay Phosgene Rotten eggs Hydrogen sulfide Wintergreen Methyl salicylate
  21. 21. Mydriasis Sympathomimetics Cocaine Caffeine Ephedrine Amphetamines Methylphenidate Anticholinergics Atropine Scopolamine TCAs Antihistamines Antiparkinson agents Muscle relaxants Antispasmodics Phenothiazines (some) Plants (with belladonna alkaloids) Hallucinogens
  22. 22. Miosis Opioids Heroin Morphine Hydromorphone Oxycodone Hydrocodone Codeine Propoxyphene Sedative-hypnotics Barbiturates Benzodiazepines Organophosphate insecticides Carbamate insecticides Pilocarpine Edrophonium Physostigmine Sympatholytics Clonidine Oxymetazoline Tetrahydrazoline Antipsychotics Miscellaneous
  23. 23. Nystagmus Barbiturates Carbamazepine Phencyclidine Phenytoin Lithium Ethanol Toxic alcohols Organophosphates Strychnine MAOIs Serotonin syndrome
  24. 24. Cyanotic Cyanide Methemoglobinemia Sulfhemoglobinemia Hypoxemia
  25. 25.  Carbon monoxide  Mushrooms  Ethanol  Scombroid fish poisoning  Anticholinergic agents    Antihistamines  TCAs  Atropine
  26. 26. Hypertension with tachycardia Thyroid hormone Anticholinergics  Drug withdrawal states Organophosphates Sympathomimetics
  27. 27.  MAOIs (foods with tyramine)  Disulfiram reaction (early)  Cholinergic agents  Organophosphates  Alpha-adrenergic agonists
  28. 28.  TCAs  Theophylline  Albuterol  Toxic alcohols  Beta-adrenergic agonists
  29. 29.  Barbiturates  Beta-blockers  Calcium-channel blockers  Digoxin  Cyanide  Opiates
  30. 30. A toxidrome, or toxic syndrome, is a constellation of clinical examination findings that assists in the diagnosis and treatment of the patient who presents with an exposure to an unknown agent. The toxicologic physical examination should include documentation of vital signs, pupillary diameter, skin findings (dry, flushed, or diaphoretic), as well as the presence or absence of bowel sounds and urinary retention.
  31. 31. There are five general toxidromes : 1.Sympathomimetic 2.Cholinergic 3.Anticholinergic 4.Opiate 5.Sedative hypnotic
  32. 32.  Hypertension  Pyrexia .  Pupillary dilatation,  Diaphoresis  Altered mental status. Drugs that can cause this type of toxidrome include : cocaine and the amphetamines. vasopressors and β- adrenergic agonists
  33. 33.  Bradycardia  Respiratory depression due to paralysis  Bronchoconstriction and bronchorrhea.  Pinpoint pupils  SLUDGE syndrome of salivation, lacrimation, urination, defecation, gastrointestinal (GI) distress, and emesis.  Fasciculations and paralysis.  Seizures and coma. These agents include organophosphate insecticides and nerve gases, as well as carbamate pesticides.
  34. 34.  Tachycardia  CNS effects include agitation, delirium, and in severe cases, seizures.  Mydriasis ,  Dry , flushed skin  Urinary retention  Decreased intestinal motility. Therapeutic agents that cause this toxidrome include atropine, scopolamine, and antihistamines.
  35. 35.  Respiratory depression and oxygen desaturations  Miosis  Decreased GI motility, and  Coma . These agents include Morphine , Pethedin , Tramadol Other agents that produce a similar toxidrome include the imidazolines, including clonidine, tetrahydrozoline, and oxymetazoline.
  36. 36.  Sedation or coma in the setting of NORMAL vital signs.  A common misconception is that ingested benzodiazepines cause respiratory depression.  While this may be true in the setting of intravenously administered benzodiazepines, patients with a benzodiazepine ingestion generally do not develop respiratory compromise.
  37. 37.  Blood sugar : This test should be considered one of the vital signs in the patient with altered mental status.  Chemistry (bicarbonate and the creatinine)  Blood gases.  Serum drug screen: In general, the studies included on this panel include acetaminophen, salicylate, and ethanol concentrations. Some laboratories include a tricyclic antidepressant (TCA) screen as well.
  38. 38.  Rarely contributes to the management of the patient ◦ Amphetamines: commonly cross-reacts with over-the- counter cold medications. ◦ Opioids: This assay frequently misses the presence of the synthetic opioids such as fentanyl and meperidine ◦ Cocaine: This assay is not directed at the parent compound which is very short lived ◦ Cannabinoids: its presence does not have any bearing upon the diagnosis of intoxication. ◦ Benzodiazepines: detection of oxazepam; however, some commonly used benzodiazepines (such as lorazepam) don’t produce it and therefore often missed by this screening
  39. 39.  Cardiac toxins tend to prolong the : 1. PR interval (reflecting nodal blockade) 2. The QRS (reflecting sodium channel blockade) 3. The QT interval (potassium channel blockade).
  40. 40.  May reveal radiodense material in the stomach or gut in the following ingestions : ◦ Chloral hydrate ◦ Heavy metals ◦ Iron ◦ Phenothiazines ◦ Enteric-coated preparations ◦ Sustained-release preparations (Goldfrank's Toxicologic Emergencies. 8th Ed. 2006:62)
  41. 41. 1- Prevention of absorption Gastric lavage Activated charcoal (AC) Whole-bowel irrigation Cathartics. Ipecac syrup. 2- Increased elimination: Forced diuresis Urinary alkalinization Hemodialysis and hemoperfusion 3- Antidote
  42. 42. Endoscopy Surgery Dilution
  43. 43. AC is an insoluble, nonabsorbable, inert, fine carbon powder. AC is often the only GI decontamination measure needed to treat an overdose.
  44. 44.  The greatest benefit from AC is seen when it is administered within one hour of ingestion, and when used AC should be administered as soon as possible after patient presentation.  The decision to use AC is not algorithmic and depends upon the toxin ( BLAST ), the clinical status of the patient, and the time since ingestion.
  45. 45. AC administration is not recommended: 1. In patients who have ingested nonabsorbable acidic or alkaline corrosives (hydrochloric or sulfuric acid) 2. Pt who require endoscopy because charcoal will obstruct the view of the endoscopist. 3. In patients who have ingested low-viscosity hydrocarbons (eg, gasoline, kerosene, liquid furniture polish) and who are at high risk for aspiration. 4. If the agent ingested is not bound by charcoal.
  46. 46. Corrosives Arsenic Acids Lead Alkali Mercury Hydrocarbons Iron Alcohols Sodium Acetone Calcium Ethanol Potassium Ethylene glycol Magnesium Isopropanol Fluoride Methanol Iodide Essential oils Drugs not absorbed by AC
  47. 47.  Common side effects include:  Nausea , vomiting, abdominal cramps, and diarrhea, particularly when the drug is used with sorbitol .  Aspiration  Constipation  Mechanical bowel obstruction
  48. 48.  Dose — The recommended dose of activated charcoal  (AC) is 1 g/kg  The usual single adult dose is 25 to 100 g mixed with water and administered as a slurry by mouth or nasogastric tube.  Doses larger than 100 g are not recommended in obtunded patients due to the increased risk of vomiting and aspiration.
  49. 49.  Routine use of gastric lavage in the management of poisoned patients is not recommended by the American Academy of Clinical Toxicology or the European Association of Poison Centres and Clinical Toxicologists  Controlled studies in animals and human volunteers show that gastric lavage decreases the absorption of ingested poison by an average of 26 percent when performed 30 minutes after ingestion and 12 percent when performed at 60 minutes
  50. 50.  Gastric lavage is less effective activated charcoal (AC) in reducing the absorption  Gastric lavage in combination with AC (administered either following lavage or both before and after) is more effective in reducing drug absorption than AC given alone
  51. 51.  A corrosive agent (eg, strong alkali, concentrated acids, such as hydrochloric or sulfuric)  Low viscosity hydrocarbons (eg, gasoline, kerosene, liquid furniture polish)  The patient has a depressed mental status and tracheal intubation has not been performed  There is a risk of hemorrhage or perforation due to esophageal or gastric pathology or recent surgery  The patient is unable to cooperate with the procedure
  52. 52. 1. Aspiration 2. Laryngospasm 3. Hypoxia and hypercapnia, 4. Esophageal and gastric erosions , bleeding, perforation 5. Inadvertent tracheal insertion and pulmonary lavage, 6. Cardiac arrhythmias, cardiac ischemia, 7. Pneumothorax, 8. Fluid and electrolyte imbalances, and 9. Hypothermia
  53. 53.   Syrup of Ipecac (SOI), which is derived from the dried rhizome and roots of the ipecacuanha, induces emesis in more than 90 percent of overdose patients with a mean time of onset of 20 minutes  Ipecac should NOT be administered routinely in the management of poisoned patients since there is no evidence from clinical studies that it improves important outcomes
  54. 54.  Refers to the enteral administration of a polyethylene glycol balanced electrolyte solution (PEG-ELS) in order to rapidly cleanse the gastrointestinal (GI) tract of its contents and prevent intoxicant absorption.  An effective means of GI decontamination following ingestion of drug packets, sustained-release or enteric-coated preparations, or agents not well adsorbed by activated charcoal (AC).
  55. 55.   Isosmotic high molecular weight polyethylene glycol (PEG-3350) electrolyte lavage solution is administered by mouth or nasogastric tube at a rate of 2 L per hour in adults until the rectal effluent is clear; volumes required to accomplish this vary from 5 to 50 L  Complications — Abdominal cramps, bloating, nausea, vomiting, and aspiration pneumonitis
  56. 56.  Cathartics are intended to decrease poison absorption by enhancing rectal evacuation of the poison-activated charcoal complex.  Two types of osmotic cathartics are used to treat poisoned patients: 1. Saline cathartics (eg, magnesium citrate, magnesium sulfate, sodium sulfate). 2. Saccharide cathartics (eg, sorbitol, mannitol).
  57. 57. Recommended adult doses of commonly used agents are:  1 g/kg (1 to 2 mL/kg) of 70 percent sorbitol (0.9 g/mL)  4 mL/kg or 250 mL of magnesium citrate  250 mg/kg or 15 to 20 g of magnesium sulfate
  58. 58.  Dilution is recommended following the ingestion of acidic or alkaline corrosives  Dilution must be performed within minutes of exposure to be effective and does not prevent the absorption of poison.  The recommended volume for adults is up to 5 mL/kg or 250 mL of water or milk.
  59. 59. Antidote administration is appropriate when: 1. There is a poisoning for which an antidote exists. 2.The actual or predicted severity of poisoning warrants its use. 3.Expected benefits of therapy outweigh its associated risk. 4.there are no contraindications.
  60. 60. Poison/syndrome Antidote(s) Adult dose Acetaminophen N-acetylcysteine (Mucomyst 20 percent) Initial oral dose: 140 mg/kg, then 70 mg/kg q 4 h x 17 doses Anticholinergic agents Physostigmine (Antilirium) Initial dose: 0.5-2.0 mg slow IV over 3-5 min Benzodiazepines Flumazenil (Romazicon) Initial dose: 0.1-0.2 mg IV over 30-60 sec, repeat 0.1-0.2 mg IV every minute prn up to 1.0 mg Beta-blockers 1) Glucagon 1) Initial dose: 5-10 mg IV bolus, then 2-10 mg/hr IV infusion 2) Calcium 2) Calcium chloride 10 percent: 1 gm (10 cc) IV; repeat as necessary 3) Insulin + dextrose 3) Insulin load: 0.5 units/kg IV bolus, then 0.5-1.0 U/kg/h IV Dextrose 10 percent IV infusion (with KCl) - titrate to euglycemia Calcium-channel blockers 1) Calcium 1) Calcium chloride 10 percent: 1-4 gm (10-40 cc) IV; repeat as necessary 2) Glucagon 2) Initial dose: 5-10 mg IV bolus, then 2-10 mg/hr IV infusion 3) Insulin + dextrose 3) Insulin load: 0.5 units/kg IV bolus, then 0.5-1.0 U/kg/h IV
  61. 61. Carbon monoxide Oxygen ± hyperbaric chamber 100 percent oxygen by ventilator or NRB; high-flow oxygen by tight- fitting facemask Crotalid snakebite Wyeth polyvalent crotalidae antivenin (equine) Mild: 3-5 vials; moderate: 6-10 vials; severe: 10-20 vials Mix reconstituted antivenin in 1000 mL NS over 4-6 hours Cyanide 1) Amyl nitrate pearls 1) One ampule by inhalation for 15 sec every 3 min until IV access 2) Sodium nitrite (3 percent solution) 2) 10 mL (300 mg) IV over 3 min 3) Sodium thiosulfate (25 percent) 3) 50 mL (12.5 g) IV over 10 min Digitalis Digoxin immune Fab (Digibind) 1) (# mg ingested x 0.8) ÷ 0.6 = #vials needed 2) (Dig concentration [in ng/mL] x 5.6 x kg [weight]) ÷ 600 = #vials 3) Empiric dose: 10 vials (acute poisoning); 1-3 vials (chronic) 4) Reconstitute Digibind in NS and administer IV over 5-30 min Ethylene glycol Methanol 1) Ethanol 10 percent in D5W ± hemodialysis 1) Initial load: 10 mL/kg IV of 10 percent ethanol over 30 min, then 1.5 mL/kg IV infusion (titrate drip to serum ethanol 100 mg/dL); double to triple infusion during hemodialysis 2) Fomepizole [4-MP] (Antizol) ± hemodialysis 2) Initial load: 15 mg/kg IV over 30 min, then 10 mg/kg every 12 hours IV over 30
  62. 62. Poison/syndrome Antidote(s) Adult dose Heparin Protamine sulfate 1 mg neutralizes 90-115 U heparin; Initial dose: 1 mg/min to total dose 200 mg in 2 h Iron Deferoxamine (Desferol) 15 mg/kg/h IV infusion until urine color clears or patient clinically well (not to exceed 6 gm/24 h) Isoniazid Pyridoxine (Vitamin B6) Initial dose: 1 gm pyridoxine for every gm INH ingested or empiric 5 gm IV over 10 min if amount ingested unknown Lead 2,3-dimercaptosuccinic acid [DMSA] (Succimer); 100 mg cpsl 30 mg/kg po in three divided doses x 5 days, then 20 mg/kg in twice daily doses x 14 days; repeat therapy prn after 2 week rebound Mercury Arsenic Gold British antilewisite, dimercaprol (BAL); in peanut oil Initial dose: 4-6 mg/kg IM every 4-6 h x 2 days
  63. 63. Methemoglobinemia Methylene blue (1 percent solution) Initial dose: 1-2 mg/kg (0.1-0.2 mL/kg) IV over 5 min; repeat prn Opiates Naloxone (Narcan) Nalmefene, naltrexone Initial dose: 0.1-2.0 mg IV push (opioid dependent patients should receive 0.1 mg IV every 30-60 sec until clinical response); synthetic opiates may need up to 10 mg for initial reversal dose Organophosphates Carbamates Nerve agents 1) Atropine 1) Initial dose: 0.5-2.0 mg IV; repeat q 3-5 min until sweat and secretions clear 2) Pralidoxime [2- PAM] (Protopam) 2) Initial dose: 1 gm IV over 15 min, then IV infusion of 3-4 mg/kg/h for 24-72 hrs or until clinical toxicity resolves Sulfonylurea Octreotide (Sandostatin) + dextrose Initial dose: 50-100 mcg SQ or IV, then 50 mcg q 12 h until euglycemia maintained without supplemental dextrose Tricyclic antidepressants Sodium bicarbonate (NaHCO3) Initial dose: 1-2 ampules (50-100 mEq) IV push, then IV infusion to maintain blood pH 7.45-7.55 and PCO2 30 mmHg (Usual drip: 3≅ amps NaHCO3 in 1 L D5W infused at 200-250 mL/h)
  64. 64. ◦ Patients who have taken an overdose as a suicidal gesture should all receive a psychiatric evaluation prior to discharge. ◦ In cases where the patient is stable and asymptomatic, a brief period of observation may be all that is necessary. ◦ In cases where potentially toxic agents have been ingested, patients should be monitored for 4 to 6 hours before discharge.
  65. 65.  N-acetyl-para-aminophenol (APAP) is the leading cause of toxicologic fatalities per year in the United States, and  APAP-induced hepatotoxicity is the most frequent cause of acute liver failure  APAP is often sold in combination preparations together with nonsteroidal anti-inflammatory drugs (NSAIDs), opiate analgesics, or sedatives  In general, a dose of 150 mg APAP per kilogram is the potentially toxic limit that requires therapeutic intervention.
  66. 66.  Decreased glutathione stores (fasting, malnutrition, anorexia nervosa, chronic alcoholism, febrile illness, chronic disease).  P450 enzyme inducers (ethanol, INH, phenytoin and other anticonvulsants, barbiturates, smoking).
  67. 67.  First 24 hours—asymptomatic stage: ◦ Early symptoms are very nonspecific and primarily related to the GI tract (nausea, vomiting, anorexia). ◦ High-dose APAP can cause pallor or lethargy in some patients. ◦ This initial phase is rare in symptoms and patients appear pretty unremarkable. ◦ Always think of other coingestants if a patient exhibits extreme vital sign abnormalities or other significant symptoms during the first 24 hours.
  68. 68. 24 to 48 hours—hepatotoxic stage: ◦RUQ tenderness is the most common symptom. ◦Transaminitis, bilirubinemia, and elevated PT/INR are also common findings during the second phase.
  69. 69.  2 to 4 days—fulminant hepatic failure stage: Significant hepatic dysfunction develops (i.e., a peak in hepatic enzyme elevation along with jaundice, coagulopathy with high risk of spontaneous bleeding, hypoglycemia, anuria, and cerebral edema with coma or even death).  4 to 14 days—recovery stage: If stage 3 is survived, the hepatic dysfunction usually resolves over the following days/weeks.
  70. 70.  Assess airway, breathing, and circulation (ABCs) and mental status.  Especially in patients who are nauseated or vomiting, the assessment of mental status is crucial to intervene with airway protection in time.
  71. 71.  Obtain an APAP serum level at 4 hours or later after ingestion.  Plot the APAP concentration on the Rumack-Matthew nomogram.  LFT—AST is a relatively sensitive nonprognostic marker for hepatic injury.  PT/INR, serum bicarbonate, blood pH, serum lactate, renal function panel, and serum phosphate level are the prognostic markers for hepatic injury.
  72. 72. ◦ pH < 7.3 two days post ingestion Or , ◦ All of the following: PT > 100, serum creatinine > 3.3 mmol/L, severe hepatic encephalopathy (grade III or IV). Additional criterion  Elevated serum phosphate levels > 1.2 mmol/L on days 2 to 4  Arterial serum lactate > 3.0 mmol/L after fluid resuscitation
  73. 73.  Gastric lavage is not useful in APAP overdose; however, it may be indicated in presence of certain other coingestants.  Activated charcoal  N-acetylcysteine (NAC) NAC replenishes depleted GSH glutathione stores. It should be administered early (i.e., within 8 hours after ingestion) to prevent any liver damage
  74. 74. ◦ Any patient after acute poisoning with a toxic APAP level according to the nomogram. ◦ Patients who present more than 24 hours after acute ingestion and still have a detectable serum APAP level or elevated AST. ◦ Patients with chronic APAP exposure (i.e., >4 g/d in adults, > 120 mg/kg/d in children) who present with elevated transaminases. ◦ Patients with signs of fulminant hepatic failure.
  75. 75. ◦ Oral dosing: Loading dose of 140 mg/kg PO, then 70 mg/kg PO every 4 hours for a total of 17 doses (i.e., 1,330 mg/kg over 72 hours). ◦ IV dosing ( 20 h protocol ) : Load with a dose of 150 mg/kg NAC IV over 1 hour. Then 50mg/kg over 4hours then 100 mg / kg over 16 h ◦ IV dosing : as oral dosing ( 72 h protocol ) Treatment can be stopped when the serum acetaminophen concentration is undetectable, the ALT is clearly decreasing or in the normal range, and the INR is less than two.
  76. 76.  Salicylate toxicity may result from acute or chronic ingestion of acetylsalicylic acid.  Toxicity is usually mild after acute ingestions of <150 mg/kg, moderate after ingestions of 150 to 300 mg/kg, and generally severe with overdoses of 300 to 500 mg/kg.  Toxicity from chronic ingestion is typically due to intake of >100 mg/kg/d over a period of several days
  77. 77.  Nausea, vomiting, tinnitus, tachypnea, hyperpnea, and malaise are common.  Hyperthermia  Severe intoxications may include lethargy, convulsions, and coma  Noncardiogenic pulmonary edema may occur and is more common with chronic ingestion
  78. 78.  Obtain electrolytes, BUN, creatinine, glucose, and salicylate concentration.  ABGs may reveal an early respiratory alkalosis, followed by metabolic acidosis.  Serum salicylate concentrations ◦ Salicylate concentrations > 70 mg/dL at any time represent moderate to severe intoxication. ◦ Salicylate concentrations > 100 mg/dL are very serious and often fatal.  Imaging : may shows Salicylate concretions
  79. 79.  Administer 50 to 100 g AC if presentation is within 1 hour of ingestion  Alkaline diuresis is indicated for symptomatic patients with salicylate blood concentrations > 40 mg/dL. Administer 150 mEq (three ampules) sodium bicarbonate in 1,000 mL D5W at a rate of 10 to 15 mL/kg/hr (target urine pH, 7 to 8) Give 40 mEq potassium chloride IVPB over 4 to 5 hours to maintain serum potassium concentration above 4 mEq/L.
  80. 80.  Treat altered mental status with IV dextrose, despite normal blood glucose.  Treat cerebral edema with hyperventilation and osmotic diuresis.  Treat seizures with a benzodiazepine (diazepam, 5 to 10 mg IV q15min up to 50 mg) followed by phenobarbital, 15 mg/kg IV.  Hemodialysis if : persistent acidosis, severe CNS symptoms, progressive clinical deterioration, pulmonary edema, or renal failure.
  81. 81.  Organophosphates (OPs) are commonly used as pesticides and insecticides (e.g., parathion). Some of them also have medical indications (e.g., malathion in lice shampoo).  In the developing world, OP and other pesticide poisonings represent the most common causes of death from intoxications
  82. 82.  Inhibition of ACh breakdown through blocked AChE leads to accumulation of ACh at nicotinic and muscarinic receptors resulting in excessive cholinergic stimulation  Most OPs bind AChE initially in a reversible way. Some OPs, however, become permanently bound over time, a phenomenon known as “aging.” If aging occurs, the only way to overcome the inhibitory effect is for the body to synthesize new enzyme.  OPs are hepatically metabolized.
  83. 83.  The cholinergic toxidrome is a result of overstimulation of nicotinic and muscarinic receptors  Muscarinic effects: ◦ SLUDGE syndrome: Salivation, Lacrimation, Urination, Diarrhea, GI cramping, Emesis. ◦ Bradycardia, bronchorrhea, bronchoconstriction ◦ Other effects: miosis, diaphoresis. ◦ NOTE: intoxicated patients may present with tachycardia instead of bradycardia due to hypoxia (bronchoconstriction,
  84. 84. ◦ Ganglionic: tachycardia, hypertension, diaphoresis, mydriasis. ◦ Neuromuscular: neuromuscular depolarization, fasciculations, motor weakness, paralysis with respiratory failure (analogous to succinylcholine, which is related to ACh). ◦ Central: confusion, agitation, lethargy, seizures, coma.
  85. 85. Cholinesterase levels relatively useless in assessing the severity of exposure in acute intoxications because of its wide range of normal values.
  86. 86.  Remove patient from potential source of poisoning.  All clothing, especially leather, should be removed from the patient and discarded in a ventilated area  Skin and hair decontamination requires thorough irrigation with water and might be enhanced through use of alcohol-based soaps.  Ocular decontamination should be irrigated with water only.  Gastric lavage might be indicated in stable patients who ingested contaminated fluids
  87. 87.  Is an Antimuscarinic agent which competes with ACh for receptor binding  GOAL: Atropinization, that is, drying of bronchial secretions with normalized oxygen saturation (which may require 10 to 100 times of usually common atropine doses): 1. A heart rate > 80 bpm 2. A systolic BP > 80 mm Hg The initial adult dose is 1 to 3 mg IV as a bolus. Then titrate according to persistence of bronchorrhea by giving the double of the previously used dose every 5 minutes until atropinization achieved
  88. 88.  forms a complex with OPs that are bound to AChE. The pralidoxime-OP complex is then released from the enzyme and thus regenerates AChE function.  Once the AChE bound OPs start aging, pralidoxime is rendered ineffective. Therefore it is crucial to start pralidoxime therapy early.  Dose : 1 to 2 g of pralidoxime in 100 mL NS IV over 20 minutes, then infusion of 500 mg/hr  Cardiac and respiratory failure have been reported after administration of pralidoxime
  89. 89. 1- Intermediate syndrome (IMS): ◦ This syndrome is a post-acute paralysis from persistent ACh excess after the acute cholinergic phase has been controlled. ◦ occurs hours to days after treatment of acute OP. 2- OP-induced delayed neurotoxicity (OPIDN): ◦ OPs also inhibit other neurotoxic esterases, resulting in polyneuropathy or spinal cord damage due to demyelination of the long nerve fibers. ◦ OPIDN usually occurs several days to weeks after acute OP poisoning leading to temporary, chronic or recurrent motor or sensory dysfunctions
  90. 90. Generally speaking, benzodiazepines have a wide safety margin so its overdose rarely represent a medical problem.
  91. 91.  The typical presentation of a pure oral benzodiazepine overdose is coma with normal vital signs.  Respiratory depression is exceedingly unusual in oral overdose of benzodiazepines.  The differential diagnosis includes barbiturate overdose, hypoglycemia, ethanol intoxication, CNS, and other metabolic causes of coma.
  92. 92.  Supportive care with observation is the mainstay of therapy.  In patients with co-ingestions and respiratory depression, intubation and ventilation may be required.  Since this is a benign overdose, gastric lavage and AC are not necessary.  These interventions may cause aspiration in an otherwise stable patient.
  93. 93.  Traditional recommendations include the use of flumazenil; however, given the propensity to precipitate seizures and acute benzodiazepine withdrawal in patients on long-term benzodiazepine therapy, this therapy should be avoided.  In special cases such as reversal of iatrogenically induced respiratory depression, reversal of sedation, flumazenil may be given as a 0.1 mg/min dose intravenously.  Repeat injections may be given as resedation occasionally reoccurs.
  94. 94.  Multiple TCAs are on the market, including Amitriptyline, Clomipramine, Doxepin, Imipramine, Trimipramine, Desipramine, Nortriptyline, and Amoxapine.
  95. 95.  TCAs interact with a wide variety of receptors with many consequent effects  It has a: 1. Anticholinergic effect : dry mouth , urinary retention, and GI motility and mydriasis. 2. Antihistaminic effect : sedation 3. Central sympatholytic effect : hypotension and reflex tachycardia 4. Anti serotoninergic effect 5. Antagonism of CNS gamma-aminobutyric acid (GABA) A receptors
  96. 96.  In one classic study, one-third patients with a QRS of ≥100 milliseconds developed seizures.  Fifty percent of patients with a QRS of ≥ 160 milliseconds developed ventricular dysrhythmias  Prolongation of the QT interval.
  97. 97. After the patient's airway is protected, a dose of AC 1 g/kg is warranted . Sodium bicarbonate has been demonstrated to narrow the QRS, A bolus of 1 to 2 mEq/kg every 3 to 5 minutes ,continuous ECG monitoring until the QRS narrows or the BP improves. Serial VBGs should be obtained with a goal of maintaining the blood pH at 7.50 to 7.55.
  98. 98.  Norepinephrine is the pressor of choice in hypotensive patients who do not respond to alkalinization because of its direct effects on the vasculature.  Lidocaine may be considered in the presence of ventricular dysrhythmias precipitated by TCA toxicity. However, class Ia and Ic antidysrhythmics are contraindicated in the management of TCA-poisoned patients.  Benzodiazepines are the mainstay of treatment for seizures. Phenytoin should be avoided.
  99. 99.  The toxicity associated with an overdose of β-blockers is largely due to the effects of antagonism at catecholamine receptors.  In general, selectivity is lost in overdose, so bronchospasm may occur in the setting of β1-selective antagonists.
  100. 100.  Patients with a significant ingestion of an immediate-release product will exhibit signs of toxicity within 6 hours.  The exception to this rule is sotalol, which in overdose, can have delayed toxicity and prolonged effects  With the exception of propranolol and sotalol, β-blocker overdose in healthy people tends to be benign, with significant number of patients remaining asymptomatic after ingestion
  101. 101.  Patients with significant ingestions present with: 1. Bradycardia 2. CHF. 3. Patients with propranolol ingestions may develop coma, seizures, and hypotension. 4. Propranolol overdoses have a high mortality In patients with symptomatic bradycardia also consider overdose of CCB, clonidine, or digoxin.
  102. 102.  The ECG may reveal sinus bradycardia or atrioventricular block.  In propranolol ingestions, a wide QRS manifesting sodium channel blockade may be present.  With sotalol, QTc prolongation may appear as a delayed presentation and torsades de pointes may develop.
  103. 103.  Patient should have an IV placed, and continuous cardiac monitoring should be instituted.  Hypoglycemia should be treated with 50 mL of 50% dextrose.  Consider AC if patients present within 1 hour of ingestion.  Intubation and ventilation should be instituted in patients with altered mental status.
  104. 104.  Atropine 1 mg IV may be given up to 3 mg for symptomatic bradycardia; however, this is usually ineffective as the bradycardia is not vagally mediated.  A fluid bolus of 20 mL/kg should be given and may be repeated; monitor for the development of fluid overload.  Glucagon 2 to 4 mg IV may be given over 1 to 2 minutes. Then start infusion of 2 to 5 mg/hr—not to exceed 10 mg/hr.  Calcium gluconate 3 to 9 g IV may be given through a peripheral line in patients with hypotension.
  105. 105.  Any patient with hypotension is a candidate for high-dose insulin euglycemia therapy.  This involves a bolus of 1 U/kg of regular insulin, followed by an infusion of 0.5 to 1 U/kg/hr of regular insulin. This should be accompanied by a dose of 50 mL of 50% dextrose and a dextrose drip at 1 g/kg/hr of dextrose.  Glucose should be obtained every 30 minutes, and potassium levels should be followed every 2 hours
  106. 106.  Catecholamines should be approached with caution in these patients because α- stimulation in conjunction with β-blockade may precipitate acute heart failure.  Therefore, hemodynamic monitoring should be instituted with careful titration of epinephrine at 0.02 mcg/kg/min or norepinephrine at 0.1 mcg/kg/min.  Isoproterenol at 0.1 mcg/kg/min may be useful as well
  107. 107. QUESTIONS ??
  108. 108.  Most of poisoning events pass uneventfully without significant harm.  The most important clinical approach is to try to classify the patients toxidromes  ABCDE approach is the first priority in management of poisoned pt.  Gastric lavage is ineffective if done after one hour of exposure.  AC is an effective mode of decontamination but not in all overdoses 
  109. 109.  ECG is important investigation in poisoned pat.  Paracetamol poisoning is a common cause of drug overdoses and is the most common cause of acute hepatic failure in western countries.  The use of paracetamol nomogram is the best mode to determine the need for NAC use
  110. 110.  The goal of GOAL of Atropinization is 1. A heart rate > 80 bpm 2. A systolic BP > 80 mm Hg but not dilated pupils.  The classic presentation of Benzodiazepine overdoses is sedation with normal vital signs 
  111. 111. Thank you
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