2. • Poisoning refers to the development of harmful
effects following exposure to chemicals.
• Over dosage is exposure to excessive amounts of
a substance normally intended for consumption
and does not necessarily imply poisoning.
• Poisoning can be acute, or less commonly,
symptoms may arise only after prolonged
exposure, as occurs with many heavy metals.
• Poisoning may be accidental or deliberate.
3. Common sources of poisoning
• Carbon monoxide
• Acetaminophen
• Analgesics
• Antidepressants
• Sedative-hypnotics
• Narcoleptics
• Stimulants
• Cardiovascular drugs
• Anticonvulsants
• Antihistamines
• Many other non pharmaceutical agents implicated in fatal
poisoning include alcohols and glycols, gases and fumes, chemicals,
cleaning substances, pesticides, and automotive products
4. Suspect poisoning even without history of exposure
to a poison if patient present with:
1. Coma
2. Seizure
3. Acute Renal failure
4. Acute Liver cell failure
5. Acute Bone marrow failure
5. DIAGNOSIS
• History
• Physical exam
• Routine laboratory evaluation
• Toxicologic laboratory evaluation.
• Assessment of prognosis
6. History
Exposure history
• When
• Route
• Dose
• Intention
Clinical picture
• Symptoms
• Onset
• Duration
• Severity
Past medical history
Psychiatric history
7. Toxidromes
According to assessment of
1. Vital signs
2. Pupillary diameter
3. Urinary retention
4. Bowel sound
5. Skin manifestations
5 common toxidromes:
• Sympathomimetics
• Cholinergic
• Anticholinergic
• Opioid
• Sedative hypnotics
21. Assessment of prognosis
• Dose ingested
• Time since ingestion
• Symptoms and signs of poisoning
• Preexisting: cardiac, renal, hepatic or
respiratory diseases.
• Serum level of drug used
27. Airway
The most common factor contributing to death from drug overdose or
poisoning is loss of airway-protective reflexes with subsequent airway
obstruction
Causes of compromised airway
1. the flaccid tongue
2. pulmonary aspiration of gastric contents
3. respiratory arrest
Assessment:
A. Patients who are awake and talking are likely to have intact airway reflexes
but should be monitored closely because worsening intoxication can result
in rapid loss of airway control.
B. In lethargic or obtunded patients, the gag or cough reflex may be an
indirect indication of the patient's ability to protect the airway. If there is
any doubt, it is best to perform endotracheal intubation
28. 1. Optimize the airway position to force the flaccid tongue forward and
maximize the airway opening. The following techniques are useful.
A. Place the neck and head in the "sniffing" position, with the neck flexed
forward and the head extended
B. Apply the "jaw thrust" maneuver to create forward movement of the tongue
without flexing or extending the neck. Pull the jaw forward by placing the
fingers of each hand on the angle of the mandible just below the ears.
C. Place the patient in a head-down, left-sided position that allows the tongue
to fall forward and secretions or vomitus to drain out of the mouth
2. If the airway is still not patent, examine the oropharynx and
remove any obstruction or secretions by suction, by a sweep
with the finger, or with Magill forceps.
3. The airway can also be maintained temporary with artificial
oropharyngeal or nasopharyngeal airway devices.
4. Perform endotracheal intubation if personnel trained in the procedure
are available. Intubation of the trachea provides the most reliable
protection of the airway, preventing aspiration and obstruction and
allowing for mechanically assisted ventilation. There are two routes for
endotracheal intubation: nasotracheal and orotracheal.
29. Breathing
Causes of impaired ventilation:
1. Respiratory depression
2. Pulmonary edema (cardiogenic, non cardiogenic)
3. Bronchospasm
4. Aspiration
5. Carboxyhemoglobin
6. Methemoglobin
Assessment:
1. ABG
2. Pulse oximetry : not useful in carboxy, met hemoglobinemias
Support:
1. Bag valve mask device
2. Mechanical ventilation
3. Later specific antidote
30. Circulation
1. Check blood pressure and pulse rate and rhythm
2. Begin continuous electrocardiographic (ECG) monitoring.
3. Secure venous access (2 cannula)
4. Draw blood for routine studies
5. Begin intravenous infusion
6. place a Foley catheter.
Hypotension:
Iv infusion 20 ml/kg normal saline (2 L guided by CVP)
Vasopressors e.g. Norepinephrine, dopamine
Intraaortic balloon pump
– For betablockers : glucagon 5- 10 mg iv, glucose insulin, intralipid
– Na Hco3 in Na channel blockers: TCA
– For CCBs calcium chloride iv 1-2 g iv, glucose insulin, intralipid
Hypertension
in amphetamine cocaine other sympathomimitics : use ca channel blockers not
beta blockers because closing β receptor cause hypertensive crisis with
unopposed α receptors,
give nitroprusside or nitroglycerine
BDZ for agitated hypertensive patients
31. Arrythmia
– Drug effect
– Hypoxia
– Metabolic acidosis
– Electrolyte imbalance
• Treat the cause, then specific management
– Trosade de points:
1. Magnesium (2 g iv over 2 minutes)
2. Lidocaine
3. Override pacing
– Ventricular arrythmia
1. Lidocaine
2. Amiodarone
3. Not use phenytoin
4. Digitalis Fab fragment
– Wide complex tachycardia with TCA give NaHCO3 (50-100 meq
Iv bolus)
– Tachyarrythmia caused by sympathomimetics (give
propranolol or esmolol)
32. Seizure
• Causes:
1. Drugs: amphetamine, TCA, venalfaxine, Antihistaminic, cocaine,
antipsychotics, INH, thyophylline.
2. Hypoxia
3. Hypoglycemia
4. Hypocalcemia
5. Hyponatremia
6. Alcohol withdrawal
• Prolonged seizure leads to hypoxia, acidosis, hyperthermia,
rhabdomyolysis.
• Management:
1. Benzodiazepine is first line
2. 2nd line is phenobarbitol preferred over phenytoin for drug induced
seizure
3. Propofol for resistant drug induced seizure
4. Specific measures see table
35. Coma
• Any coma: (Dextrose+ naloxone+ thiamine+
flumazenil)
• Dextrose: 50- 100 ml of D 50%
• Thiamine 100 mg intramuscular for alcoholics,
malnourished specifically
• Naloxone 0.4-2mg iv but has shorter duration of
action than opioid so repeated doses up to 5- 10
mg. newer nalmefene has longer duration of
action.
• Flumazenil 0.2- 0.5 mg iv repeated upto 3 mg (not
for pt with epilepsy, or chronic BDZ abuser to
avoid precipitating seizure) and (duration of
action 2-3 hours)
37. GI decontamination
Depends on:
1. The time since ingestion
2. The existing and predicted toxicity of the poison.
3. The availability, efficacy, and contraindications of the
procedure
4. The nature, severity, and risk of complications.
No benefit if presented> 1 hour after ingestion
38. Methods of GI decontamination
• Gastric lavage.
• Activated charcoal
• Whole-bowel irrigation
• Syrup of ipecac (emesis)
• Cathartics
• Endoscopic or surgical removal, or both
39. Gastric lavage
• performed using a 40F orogastric tube in adults. Saline or
tap water may be used in adults. Place pt in Trendelenburg
and left lateral decubitus position to minimize aspiration
(occurs in 10% of pts).
• Lavage is contraindicated with corrosives and petroleum
distillate hydrocarbons because of risk of aspiration-
induced pneumonia and gastroesophageal perforation.
• Lavage should not be performed with an unprotected
airway if the patient has lost airway protective reflexes. In
these cases, lavage should be performed only after
endotracheal intubation.
• Lavage with 200-mL boluses of warm saline, repeated until
the effluent is clear, and follow this by instillation of
activated charcoal
40. Activated charcoal
• AC has comparable or greater efficacy, fewer
contraindications and complications, and is less invasive than
gastric lavage and is the preferred method of GI
decontamination in most situations.
• AC is prepared as a suspension in water, either alone or with
a cathartic.
• The recommended dose is 1 g/kg body weight, using 8 mL of
diluents per gram of charcoal if a premixed formulation is not
available.
• Do not use activated charcoal when bowel obstruction or
perforation is present.
• Not used in comatose patient, seizure may induce vomiting
and risk of aspiration unless protect airway
• Has no role in poorly adsorbed substances include iron,
lithium, potassium, sodium, mineral acids, and alcohols.
41. Whole-bowel irrigation
With ingestions of:
1. foreign bodies
2. drug packets
3. slow-release medications.
polyethylene glycol is given orally or by gastric tube
up to a rate of 2 L/h total of 10 L.
It is contraindicated:
1. bowel obstruction
2. Ileus
3. intestinal perforation
4. hemodynamic instability
5. compromised unprotected airway
42. Syrup of ipecac
Because there is no evidence to show that administration
of ipecac improves outcome and there is some
evidence to suggest an increase in complications, and
because of its many contraindications, routine use in
the emergency center has largely been abandoned.
Contraindications to ipecac use include:
1. decreased level of consciousness
2. absent gag reflex
3. caustic ingestion
4. convulsions or exposure to a substance that is likely to
cause convulsions
5. Do not give ipecac for ingestion of unknown toxins, as
aspiration may occur if coma or seizures develop.
43. cathartic
• The use of a cathartic is not supported by clinical
evidence and is therefore not routinely recommended.
• If used, give no more than a single dose.
– Acceptable forms:
• Magnesium citrate, 4 mL/kg (300 mL maximum)
• Sorbitol, 1-2 g/kg (150 g maximum)
• Magnesium or sodium sulfate, 25-30 g
Do not give magnesium salts to patients with renal failure.
Contraindicated in suspected intestinal obstruction.
Avoid sodium-based cathartics in patients with
hypertension, advanced kidney disease, and heart failure
Sorbitol (an osmotic cathartic) can cause hypotension and
dehydration due to third-spacing and also causes intestinal
cramping and vomiting.
45. DECONTAMINATION OF THE SKIN
1. Wash the affected areas with copious quantities of
warm water or saline.
2. For oily substances (eg, pesticides), wash the skin
at least twice with plain soap and shampoo the
hair.
3. Alcohol better avoided and in some cases
paradoxically enhance absorption.
4. For exposure to chemical warfare poisons such as
nerve agents use a dilute hypochlorite solution
(household bleach diluted 1:10 with water), but
not in the eyes
46. DECONTAMINATION OF THE EYES
1. Flush the eyes with copious amounts of saline or water.
2. Remove contact lenses if present.
3. Lift the tarsal conjunctiva to look for undissolved particles
and to facilitate irrigation. Continue irrigation for 15
minutes or until each eye has been irrigated with at least
1 L of solution.
4. If the toxin is an acid or a base, check the pH of the tears
after irrigation, and continue irrigation until the pH is
between 6 and 8.
5. After irrigation is complete, perform a careful examination
of the eye, using fluorescein and a slit lamp to identify
areas of corneal injury. Immediately refer to an
ophthalmologist.
48. Enhancement of Elimination
• Activated charcoal in repeated doses of 20-30 g q2–4h
• Forced urinary alkalinization 100 meq Nahco3 added to I
L of 5% dextrose or hypotonic saline(salicylate,
phenobarbitol)
• Acidification of urine(rarely used for amphetamine,
phencyclidine) contraindicated when rhabdomyolsis or
myoglobinuria)
• Peritoneal dialysis or hemodialysis
• Exchange transfusion removes poisons affecting red
blood cells.
• Antidote
50. Asymptomatic cases should be observed for
the appropriate duration
4-6 hours
Longer in:
1. Sustained release formula
2. Drugs that inhibit GIT motility
(opioid, salicylate, anticholinergics)
1. Drugs with delayed onset of action
(acetaminophen, colchicine)
54. Acetaminophen
• Toxicity:
1. acute acetaminophen overdose (greater than 150–200 mg/kg, r
8–10 g in an average adult)
2. Overdose occur when prescription exceeds the recommended
maximum dose of 4 g/day for several days.
Pathophysiology:
• Acetaminophen metabolised by glucuronidation and sulfation, only
small amount oxidized to toxic intermediate by the P450 mixed-
function oxidase system (2E1).
• This toxic intermediate normally detoxified by Glutathione.
• When glutathione depletion occur, cellular necrosis occurs
• Patients with enhanced P450 2E1 activity, such as those who
chronically abuse alcohol and patients taking INH or other P450
enzyme inducers(phenytoin, barbiturate, smoking), are at increased
risk for developing hepatotoxicity.
• Other risk factors for depleted glutathione: Fasting, malnutrition,
chronic illness, febrile illness, anorexia nervosa, alcoholism
55. Clinical picture
1. Asymptomatic phase:
– 24-48 hours: only nausea, vomiting or anorexia
– With massive toxicity 500-1000 mg/L rapid development of coma,
seizure, renal failure, hypotension, and acidosis without evident
hepatotoxicity.
2. Hepatotoxic stage (after 24 or 48 hours)
– ↑transaminases, bilirubin, PT, INR.
– Rt upper quadrant tenderness
3. Stage of fulminant liver failure (2-4 days)
– Jaundice, coagulopathy, hepatic encephalopathy, hypoglycemia,
hepatorenal with oliguria, cerebral edema, coma or death.
4. Stage of recovery: 4-14 days if patient survive stage 3
56. investigation
• FBG
• INR
• LFT
• Phosphate
• Serum acetaminophen level 4 h after ingestion
for nomogram
• ABG
• KFT
57. Nomogram for prediction of acetaminophen hepatotoxicity following acute overdosage.
Patients with serum levels above the line after acute overdose should receive antidotal
treatment.
58. Management
1. Supportive
2. Activated charcoal within 1 hour of ingestion
3. Antidote according to nomogram:
– N-acetylcysteine is indicated; it can be given orally
or intravenously.
– Oral treatment begins with a loading dose of 140
mg/kg, followed by 70 mg/kg every 4 hs for 72
hours(FDA approved 20-48 hrs).
– The FDA-approved 21-hour intravenous regimen of
acetylcysteine (Acetadote) : a loading dose of 150
mg/kg given intravenously over 60 minutes,
followed by a 4-h ur infusion of 50 mg/kg, and a 16-
hour infusion of 100 mg/kg.
60. Anticonvulsant
• Phenytoin, fosphenytoin: cerebellar ataxia,
hepatotoxic, agraulocytosis, iv pheytoin dt propylene
glycol lead to VD and myocardial suppression,
extravastion (purple glove syndrome)
• Carbamazepine: seizure, coma, QRS prolongation (TCA
like side effects), hypotension, SIADH
• Valproic acid: hepatotoxicity, hyponatremia,
pancytopenia
• gabapentin, levetiracetam, vigabatrin, and
zonisamide: sedation, dizziness, somnolence
• Felbamate: crystalluria, renal failure
• lamotrigine, topiramate, and tiagabine: seizure, coma
61. Important notes
• They can’t be used for drug induced or drug
withdrawal seizure: use BDZ, phenobarbital, or
propofol.
• Carbamazepine >60mg/L and valoproic acid>800
mg/L warrant hemodialysis.
• carbamazepine exhibit TCA like effects that
require NaHCO3 in its management.
• All of them cause seizure and coma with high
overdose
62. Phenytoin, fosphenytoin
Clinical picture:
• Cardiotoxicity: Im or Iv phenytoin due to propelene glycol or ethanol
solvent causes hypotension, bradycardia and suppressed cardiac
contractility (not fosphenytoin).
• Neurotoxicity: nystagmus, ataxia,confusion, seizure.
• Chronic exposure: gingival hyperplasia
• Extavasation: the purple glove syndrome require debridement
Lab
• Serum phenytoin level corrected to albumin
• CBC, LFT: agranulocytosis and hepatotoxicity may be seen
Management:
1. Multiple activated charcoal, whole bowel irrigation
2. Seizure managed by BDZ
3. Iv fluid and other supportive measures
63. Carbamazepine /oxacarbamazepine
• TCA like structurally
Clinically:
1. Neurological : ataxia, nystagmus, severe toxicity leads to seizure
and come
2. Dilated pupil
3. TCA like blocking Na channels:Tachycardia, hypotension
4. SIADH: Excess ADH
Management:
1. Support airway
2. BDZ for seizure
3. NaHCO3 for cardiotoxicity
4. Multiple activated charcoal
5. Hemodialysis if serum level> 60 mg/L
64. Valproate
Clinial picture:
1. Ataxia, nystagmus, seizure, coma
2. Pancytopenia
3. Metabolic acidosis and hyponatremia
4. Hypocalcemia, and hypoglycemia
5. Fatal hepatitis with chronic toxicity or acute: measure ammoia level
for ttt decision
6. Pancreatitis may occur
Management:
1. Airway support
2. BDz if seizure
3. Activated charcoal
4. If ammonia > 80 ug/dL use L carnitine 50-100 mg/kg/day divided
into 4 doses a day till ammonia below 80ug/dL
5. Hemodialysis if serum valproate > 800mg/L
66. opioid
Clinically:
1. Drowsiness, respiratory depression, constricted pupil.
2. Methadone ↑QT interval &torsades de pointes.
3. Tramadol, dextro-methorphan, and meperidine : seizures.
4. Propoxyphene:wide QRS, seizure
NB:
1. Usually negative in toxicological screening
2. Naloxone is specific antidote with short duration of action(2- 3
hours) compared to opioids e.g.methadone 72 hours. So repeated
doses are required (intially 0.04- 2 mg) then repeat the effective
dose every 2or 3 hours
3. Nalempfene is another antidote with longer duration of action
4. AC after secure airway, ventilation
67. Salicylate
Clinically
1. Mild cases: nausea, vomiting, gastritis, malaise
2. Moderate cases: tinnitus, hyper apnea
3. Severe cases: seizure, coma, metabolic acidosis, pulmonary
edema(acute toxicity >100mg/dL or chronic toxicity >60
mg/dL) need dialysis.
Management:
1. AC multiple dose due to delayed absorption and bezoar
formation.
2. Alkalanization of urine
3. Hemodialysis
4. NaHCO3 in metabolic acidosis
68. NSAIDs
1. Severe gastric upset(vomiting)
2. Renal dysfunction
3. Ibuprofen severe toxicity: seizure
Management:
1. AC and gastric lavage
2. Antacid and antiemetic
3. IV fluid if dehydration
4. BDZ if seizures
69. Colchicine
• Very narrow therapeutic index
• Serum level of 3ng/ml is associated with severe toxicity
• Phases :
– 1: nausea, vomiting, diarrhea
– 2: multiorgan failure: pancytopenia(early leukocytes), renal
failure, adrenal hemorrahge(electrolyte monitor needed), ARDS
(CXR needed), hepatotoxicity, cardiovascular collapse,
arrythmia, DIC.
– 3 if patient survive phase 2: alopecia, motor neuropathy.
• Management:
– supportive
– Lavage and AC can’t be used in vomiting
– Hemodialysis fails dt large volume of distribution but used in RF
71. TCA
• Multiple receptors.
• CP:
– Antimuscarinic: dilated pupil, tachycardia, dilated pupil, ileus, urine retention,
dry skin dry Mucus membrane., hyperthermia
– Antihistaminic: sedation
– Alpha blocker: hypotension, reflex tachcardia
– Na channel blocker: cardiotoxicity wide QRS arrythmia correlate with severity
more than serum level of drug (quinidine like action)
– GABA receptors: seizures
• Management:
– Airway management, GL, AC
– Seizure: BDZ
– Nahco3: narrow complex and elevate blood pressure (target PH 7.5- 7.55)
– Norepinephrine for hypotension
– Amiodarone for ventricular arrythmia also may use lidocaine (class Ia, Ic
should be avoided)
72. MAOI
• CP
– Poisoning is similar to serotonin syndrome but more delayed
onset (24 hours) or severe sympathomimitic toxidrome
– Diaphoresis, agitation, hypertension, dilated pupil, tachycadia,
rigidity, hyperthermia,seizure later on with depletion of
neurotransmitters, cardiovascular collapse which is refractory
– Multiorgan damage: RF, Rhabdomyolysis, DIC, MI
• Management:
• AC, GL after airway secured
• Rapid cooling
• Mange HTN with short acting tridil, niprid as soon
cardiovascular collapse will occur then NE is needed
• BDZ for seizure
• Cyproheptadine or neuromuscular blocker for rigidity
74. lithium
• Acute: GIT (nausea, vomiting, diarrhea,
abdominal pain)
• Chronic neurologic (ataxia nystagmus,
confusion, tremor, myoclonus, seizure)
• It doesn’t bind to AC
• Consider dialysis
75. antipsychotic
• Old typical antipsychotics(phenothiazines):
– cardiotoxic : Na channel blocker wide QRS, K channel
blocker: QT prolongation.
– Dopamine antagonists: extrapyramidal manifestation,
acute dystonia, Rigidity
– α blocker: hypotension
– Anticholinergic effects: agitation or delirium, which
may progress rapidly to coma. Pupils may be mydriatic
and deep tendon reflexes are depressed. Seizures and
disorders of thermoregulation, particularly
hyperthermia, may occur.
76. • Emesis is contraindicated.
• Consider gastric lavage, which may be effective hours later due to delayed
gastric emptying caused by the phenothiazines.
• Consider whole-bowel irrigation for ingestion of sustained-release
formulations.
• Monitor the cardiac rhythm.
• Treat ventricular arrhythmias with lidocaine and phenytoin; class Ia agents (e.g.,
procainamide, quinidine, disopyramide) are contraindicated; avoid sotalol.
• Treat hypotension with IV fluid administration and α adrenergic vasopressors
(nor- epinephrine). Dopamine is an acceptable alternative. Paradoxic
vasodilation may occur in response to epinephrine administration because of
unopposed β-adrenergic response in the setting of strong α adrenergic
antagonism.
• Recurrent torsades de pointes may require magnesium, isoproterenol, or
overdrive pacing
• Treat seizures with diazepam and propofol.
• Treat dystonic reactions with benztropine or diphenhydramine.
• Treat hyperthermia with cooling
• . Forced diuresis, hemodialysis, and hemoperfusion are not useful.
• Frank neuroleptic malignant syndrome may complicate use of these agents
• Admit those patients who have ingested a significant overdose for cardiac
monitoring for at least 48 hours.
77. New antipsychotics
– Anticholinergic effects occur, including blurred vision, dry
mouth, and tachycardia, somnolence and coma, hypotension,
tachycardia, fasciculations, tremor, and myoclonus
– Clozapine: agranulocytosis
– Olanzapine: DKA
– Risperidone, ziprasidone, and quetiapine: TDp
• Management:
– Induction of emesis is contraindicated.
– Consider gastric lavage if presentation is within 1 hour of
ingestion.
– Give activated charcoal.
– Treat hypotension with fluids and, if ineffective,
norepinephrine or dopamine.
– Give benzodiazepines and phenobarbital for seizures.
– Provide ventilatory support for respiratory failure, which occurs
uncommonly.
78. Sedative hypnotics
BDZ
• CNS suppression with normal vital data except
for hypothermia
• Respiratory depression not very common
• Management:
– Flumazenil except for epilepsy and abuser of BDZ
79. Barbiturates
• Mild intoxication resembles alcohol intoxication.
• Moderate intoxication is characterized by coma,
decreased deep tendon reflexes, and slow respirations.
• Severe intoxication causes coma and a loss of all
reflexes (except the pupillary light reflex).
• Plantar reflexes are extensor.
• Characteristic bullae may be seen over pressure points
and on the dorsum of the fingers.
• Hypothermia and hypotension may occur.
• In severe cases, no electrical activity is seen on an EEG.
80. • Maintain a patent airway and adequate ventilation.
• Do not induce emesis.
• Perform gastric lavage if presentation occurs within 1
hour of ingestion.
• Administer multidose activated charcoal
• Forced alkaline diuresis
• Hemoperfusion may be effective for excretion of
phenobarbital and short-acting barbiturates.
• Treat hypotension with crystalloid administration. If
this fails, administer norepinephrine or dopamine.
82. Ethanol
• Acute intoxication:
– With mild to moderate intoxication: euphoria, mild incoordination,
ataxia, nystagmus, and impaired judgment and reflexes. Social
inhibitions are loosened, aggressive behavior. Hypoglycemia may
occur.
– deep intoxication, coma, respiratory depression, the temperature,
blood pressure, and pulse rate are often decreased
• Chronic ethanol abuse is associated with numerous complications
– Hepatic toxicity
– GIT toxicity
– Carditoxicity
– Neurotoxic
– Alcohol ketoacidosis
• Acute intoxication. Treatment is mainly supportive.
– Airway
– Give glucose and thiamine. Glucagon is not effective for alcohol-
induced hypoglycemia.
– Correct hypothermia with gradual rewarming
• AC not effective for alcohols
83. Ethylene glycol
• metabolized by alcohol dehydrogenase to glycolic and oxalic acids
– CNS suppression directly by EG before metabolism(ataxia, nystagmus,
slurred speech, Coma, Respiratory suppression)
– Oxalic acid bind to Ca: hypocalcemia and oxalate stone with tubular
obstruction Acute renal failure.
– Glycolic acid: Anion Gap acidosis, Cardiotoxicity ( hypotension, tachycardia,
heart failure)
• Management:
– airway and assist ventilation
– Treat coma (delay thiamine pyridoxine till correct acidosis)
– Seizures
– cardiac arrhythmias (Ventricular arrhythmias),
– metabolic acidosis
– Treat hypocalcemia
– Administer fomepizole or ethanol (Ethanol) to saturate the enzyme alcohol
dehydrogenase
– hemodialysis
84. Methanol
• Metabolized by alcohol dehydrogenase to formic
acid leading to anion gap acidosis
• CP:
– Gastritis, pancreatitis
– Blurred vision, field defects
– Ataxia, nystagmus, slurred speech, confusion, coma,
respiratory suppression
– Hypothermia
• Management: as EG
86. General notes
• α&β stimulation: tachycardia, hypertension(
amphetamine, cocaine, vasopressors)
• Only βstimulation (tachycardia, hypotension)
Methylxanthine(theophilline, caffeine) B2 agonists.
• For any drug causing hyperthermia look for end organ
damage (MI, Rhabdomyolysis, RF, DIC)
• Anxiety agitation, tremor, seizure, late coma
• Hypertensin or hypotension, tachcardia (SVT, VT) late
cardiovascular collapse
• Dilated pupil, diaphoresis, hyperthermia
• Cocaine normally present with MI
87. management
• Agitation with BDZ, barbiturates
• HTN: CCBs Not BBs leave α unopposed Better
short acting Nitrate, nitroprusside to withhold
in case of collapse
• Arrhythmia: esmolol or propranolol
• Hyperthermia: cooling, NM blockers
• Heamoperfusion, hemodialysis eliminate
theophylline
89. • Common drugs that have anticholinergic activity
include antihistamines, antipsychotics,
antispasmodics, skeletal muscle relaxants and
tricyclic antidepressants, atropine,
antiparkinsonian
– The anticholinergic syndrome is characterized by
warm, dry, flushed skin; dry mouth; mydriasis;
delirium; tachycardia; ileus; and urinary retention.
– Jerky myoclonic movements and choreoathetosis are
common and may lead to rhabdomyolysis.
– Hyperthermia, coma, and respiratory arrest may
occur.
– Seizures are rare with pure antimuscarinic agents,
although they may result from other pharmacologic
properties of the drug (eg, tricyclic antidepressants
and antihistamines).
90. Treatment
A. Emergency and supportive measures
– Maintain an open airway and assist ventilation if needed
– Treat hyperthermia
– coma
– Rhabdomyolysis
– seizures
B. Specific drugs and antidotes
– 1. A small dose of physostigmine given to patients with severe toxicity (eg,
hyperthermia, severe delirium, or tachycardia). Caution: Physostigmine can cause
AV block, asystole, and seizures, especially in patients with tricyclic antidepressant
overdose.
– 2. Neostigmine, a peripherally acting cholinesterase inhibitor, may be useful in
treating anticholinergic-induced ileus.
– C. Decontamination Administer activated charcoal orally if conditions are
appropriate. Gastric lavage is not necessary after small to moderate ingestions if
activated charcoal can be given promptly. Because of slowed gastrointestinal
motility, gut decontamination procedures may be helpful even in late-presenting
patients.
– D. Enhanced elimination. Hemodialysis, hemoperfusion, peritoneal dialysis, and
repeat-dose charcoal are not effective in removing anticholinergic agents.
92. Organophosphorus and Carbamate Insecticides
• Most OPs and carbamates can be absorbed by any
route: inhalation, ingestion, and absorption through
the skin. Highly lipophilic organophosphates
(disulfoton, fenthion) are stored in fat tissue, and this
may lead to persistent toxicity lasting several days after
exposure.
A. Muscarinic manifestations include vomiting, diarrhea,
abdominal cramping, bronchospasm, miosis, bradycardia,
and excessive salivation and sweating. Fluid losses can
lead to systemic hypovolemia, resulting in shock.
B. Nicotinic effects include muscle fasciculations, tremor, and
weakness. Respiratory muscle weakness complicated by
bronchorrhea may lead to respiratory arrest and death.
C. Central nervous system poisoning may cause agitation,
seizures, and coma.
93. • Intermediate syndrome:
• Patients may develop proximal muscle weakness 2–
4 days after the resolution of the acute cholinergic
crisis. This is often first noted as neck weakness,
progressing to proximal limb weakness and cranial
nerve palsies.
• Respiratory muscle weakness and respiratory arrest
may occur abruptly.
• The intermediate syndrome is thought to be caused
by a redistribution of lipophilic pesticides or result
from inadequate oxime therapy.
• Symptoms may last 1–2 weeks and do not usually
respond to additional treatment with oximes or
atropine
94. B. Specific drugs and antidotes. Specific treatment includes the
antimuscarinic agent atropine and the enzyme reactivator
pralidoxime.
1. Give atropine every 5 minutes until signs of atropinization are
present (decreased secretions and wheezing, increased heart
rate).
2. Pralidoxime is a specific antidote that acts to regenerate the
enzyme activity at all affected sites prior to aging
a. Pralidoxime should be given immediately to reverse
muscular weakness and fasciculations: 1–2 g initial bolus dose
IV over 5–10 minutes, followed by a continuous infusion It is
most effective if started early, before irreversible
phosphorylation of the enzyme, but may still be effective if
given later, particularly after exposure to highly lipid-soluble
compounds
b. Pralidoxime generally is not recommended for carbamate
intoxication
96. Beta blockers
• Most toxic agent is propranolol: lipophylic widely distributed(CNS
seizure, Coma), direct membrane depression effect.(Na channel blocker
QRS wide)
• Sotalol: arythmia QT prologation, TDP
• CP:
– Bradycardia, hyptension, CHF
– Seizure, Coma, hypoglycemia
• Management:
– Atropine, isoprotrenol, transient pacemaker for bradycardia
– NaHCO3 antagonise Na channel blockage for hypotension
– Dopamine, but not NE unopposed alpha receptor after iv fluid
– Glucagon 5mg then 1- 5mg/hr iv (inotropic effect)
– High Insulin euglycemia therapy for severe hypotension( unknown
mechanism)
– Intralipid 20%:1.5 ml/kg for propranolol poisoning hypotension
– Intraaortic balloon pump for persistent hypotension
97. CALCIUM CHANNEL BLOCKERS
• Patients may present with bradycardia, atrio ventricular
(AV) nodal block, hypotension. Hyperglycemia is common
due to blockade of insulin release. With severe poisoning,
cardiac arrest may occur.
• Management:
– activated charcoal, whole bowel irrigation.
– Treat bradycardia with atropine (up to 3mg), isoproterenol or
transcutaneous cardiac pacemaker
– hypotension, give calcium chloride 10%, 10 mL or calcium
gluconate 10%, 20 mL(raise the ionized serum calcium level
twice the normal level.
– High doses insulin (0.5–1 units/kg iv bolus, Then 0.5–1
units/kg/h with sufficient dextrose t maintain euglycemia
– Intralipid
98. Digoxin toxicity
– Acute: nausea, vomiting, hyperkalemia, AV block
bradycardia
– Chronic: hypokalemia, Ventricular arrythmia
– Digoxin levels may be only slightly elevated in patients
with intoxication
• Management:
– After acute ingestion, administer activated charcoal.
– Monitor potassium levels and cardiac rhythm
– Symptomatic: bradycardia: atropine or pacing
– For significant intoxication, administer digoxin-specific
antibodies
100. HYPOGLYCEMIC DRUGS
– insulin and the insulin secretagogues cause
hypoglycemia.
– Metformin can cause lactic acidosis, especially in
patients with impaired kidney function.
• Management:
– Give sugar and carbohydrate by mouth, or intravenous
dextrose if the patient is unable to swallow safely.
– maintain a blood glucose greater than 70–80 mg/dL.
– For hypoglycemia caused by sulfonylurea give
octreotide, blocks pancreatic insulin release. A dose f
50–100 mcg SC/ 6- 12 hr
– Admit all patients with symptomatic hypoglycemia
101. Cyanide
• binding to cellular cytochrome oxidase, it blocks the
aerobic utilization of oxygen.
• Symptoms include headache, nausea, dyspnea, and
confusion. Syncope, seizures, coma, agonal
respirations, and cardiovascular collapse, no cyanosis.
• Specific drugs and antidotes
– The cyanide antidote (consists of amyl and sodium
nitrites), which produce methemoglobinemia, and sodium
thiosulfate which accelerates the conversion of cyanide to
thiocyanate.
–The most promising alternative antidote
hydroxocobalamin
102. Carbon Monoxide
• CO binds to hemoglobin with an affinity 250 times that of
oxygen.
cp:
– headache, dizziness, and nausea.
– Patients with coronary disease may experience angina or
myocardial infarction.
– impaired thinking, syncope, coma, convulsions, cardiac
arrhythmias, hypotension, and death may occur.
– Although blood carboxyhemoglobin levels may not correlate
reliably with the severity of intoxication
– Delayed neurologic sequelae: parkinsonism and a persistent
vegetative state to subtler personality and memory disorders in
47% of cases.
• Antidote: Administer oxygen in the highest possible
concentration (100%). hyperbaric oxygen in severe cases
