Toxology Source: FOMSCU Lectures & Osama R. El-Ghamry's Book .

Vital Functions GIT Decontamination

Bradycardia • Stimulate C.T.Z of medulla oblongata Contraindicated with :
- Central stimulation: Apomorphine
(PACED) • 5mg S.C. / ac=on: 3-5 min. 1- Organophosphate
• Propanolol (β-blockers), Action: 2- Phenol
phenylpropanolamine (α-agonists) • Early vomi=ng (within 30 minutes):
• Anticholinesterase drugs(OPC) 3- Iron
- Central & peripheral: Syrup of ipecac. due to the direct local irritant action of on gastric mucosa,
• Clonidine, CCBs Emesis • Late vomi=ng (aGer another 30 minutes) :
4- Corrosives
• Ethanol / alcohols Plant
lant alkaloid consists of:
of due to central stimulation of the (C.T.Z)
• Digoxin, Darvon (opiates) • Emetine & Dose :
Tachycardia • Cephaline • 30 ml for adults
adults, 15 ml for children & 5- 10 ml for infants (6 months & 2 y.)
(FAST) • If vomi ng does not occur a er 30 minutes, the dose is repeated.
• Free base (cocaine/stimulants) • If still no vomiting, gastric lavage should be carried out to remove
• Anticholinergics, antihistamines ipecac from the stomach (emetine is cardiotoxic component).
• Sympathomimetics Amount & composition of fluid: 1- Organophosphate
• Theophylline (methylxanthines) Gastric lavage Insertion of tube into stomach and • 10 ml/kg/lavage of 0.9% saline- up to 400ml in adults.
2- Corrosives
Hypotension waching it with water & saline. • Con=nue lavage =ll clear (3000ml).
N.B. Tape water lavage might produce hyponatremia.
(CRASH)
Action:
• Clonidine
Is combustion of organic material & • It works by adsorption of toxins from the gut before absorption 1- Iron
• Reserpine (antihypertensives)
treated to increase surface area (1000-
(1000 • It interrupt the enterohepatic & circulation of toxic metabolites.
• Antidepressants
Activated charcoal 2- Lithium
• Sedative hypnotics 2000 cm2) Dose :
• 1g / kg Then 0.5g/kg at 4-6 hr intervals 3- Corrosives
• Heroin (opiates)
• Freshly repared by adding powder to 250 ml water and shaken to form
Hypertension slurry then taken orally or via nasogastric tube.
(CT-SCAN) 1- Interruption of enterohepatic ,
Cocaine Dose: 0.25 – 0.5 gm/kg/1-4hr (oral)
• MDAC enteroentric circulation
0.25 – 0.5 gm/kg/hr (NGT)
• Theophylline, thyroid supplements 2- GIT dialysis .
• Sympathomimetics • Saline cathartics : Action : 1- Iron
• Caffeine Mg sulphate , Mg citrate , Na sulphate • Catharsis is produced by osmotic retention of fluid in GIT with increases
• Anticholinergics, amphetamines 2- Corrosives
intrluminal bulk of fluids, activates GIT motility leading to propulsion of
• Nicotine Cathartics • Saccharides: sorbitol GIT contents
Hypothermia (purgation) Dose:
(COOLS) • Mg sulphate: adult 15 – 20 gm
• Carbon monoxide • Sorbitol : adult 1ml/kg (70% soul=on)
• Opiates
Consists of using surgical bowel-
bowel • Consists of using surgical bowel
bowel-cleansing
cleansing solution polyethylene
• Oral hypoglycemics/insulin
• Liquor (EtOH) cleansing solution polyethylene glycol (PEG),60
60 gram in a balanced isotonic electrolyte salt solution.
• Sedative hypnotics Procedure: GIT decontamination
glycol (PEG), 60 gram in a balanced
Hyperthermia Whole bowel isotonic electrolyte salt solution. • It is administered by nasogastric tube or orally. not indicated in Ethanol
because it's absorbed
(NASA) irrigation • The solution is administered at a rate of :
rapidly
• Neuroleptic malignant syndrome Available as : • 0.5 L/h in children < 5 years &
• Antihistamines • Golytely • 2 L/h for adults.
• Salicylates, sympathomimetics, • Colyte • End point when the stools are clear
serotonin syndrome Enhancement of elemination
• Anticholinergics, antidepressants
1) GUT Substances poorly adsorbed : ( CHACLICE
CHACLIC )
Seizures Caustics
austics & corrosives
(OTS SCAMPBELL) Indication : Dose: 0.25 – 0.5 gm/kg/1-4hr (oral) Hydrocarbons
• Organophosphates 1. Drug remaining in the gut for long time: 0.25 – 0.5 gm/kg/hr (NGT) Acids
cids & Alkalies & Alcohols
MDAC • Sustained release preparation: Theophylline.
heophylline.
• Tricyclic antidepressants Chlorine, Iodine
• INH, insulin ( Gut dialysis ) • Concretions: Salicylates , Phenobarbitol Lithium
• Sympathomimetics • Slowing GIT motility: Anticholinergic. Iron
• Camphor, cocaine Cyanide
• Amphetamines, anticholinergics 2. Substances with EHC: Digitalis , TCA , Salicylates
Ethylene glycol
• Methylxanthines 2) KIDNEY Objective is to alter PH making the toxin in polar or PH alteration by alkalinization or acidification of urine.
• Phencyclidine ionic form which is unable to cross cell membranes
• Benzodiazepine withdrawal, resulting in reabsorption & enhanced excretion in
botanicals renal tubules
• Ethanol withdrawal Alkalinization of the urine
• Lithium, lidocaine Indications : (PSMC) • NaHCO3 (1-2mEq/kg)
2mEq/kg) is mixed in 5 % dextrose/0.5
PH alteration & forced
• Lead, lindane • Phenobarbital, saline (15ml/Kg) infuse i.v. over 3 to 4 h
diuresis •
Toxic Causes of Coma Salicylates, • to maintain urine volume at 3-6
6 ml/Kg/h & urine PH at
• Methotrexate 7.5 to 8
1- Volatiles :
• Chlorpropamide,
• Methanol , Ethanol , cyanide
3) BLOOD Drugs with delayed toxicity Dialyzable drugs (LET
LET ME SAV P)
, CO Indications:
Dialysis • Patients unstable despite maximum • Paracetamol • Lithium
2- Non- volatiles :
supportive therapy • Ethanol • Ethylene
thylene glycol
• Atropine , TCA , Cocaine ,
A) Hemodialysis • Renal compromise WHEN • Organophosphate • Theophylline
CNS sympathomimetics , Toxins metabolized or excreted by kidneys • MEthanol
amphetamines , nicotine , B) Peritoneal dialysis, If : • Hepatic compromise WHEN
Drugs metabolized to more toxic drugs • Salicylates
organophosphates , • Renal failure Toxic substance metabolized by liver
• Bleeding disorders • Methanol • Atenolol
carbamate , salicylates. • Blood Level of toxin is lethal
• Vascular access problems • Toxicity of agent of delayed toxicity • Ethylene glycol • Valproic acid
3- Sedatives & hypnotics :
• HD & HP not available or • Toxicity agent metabolized to more toxic form • Paraquat • Potassium, Paraquat
araquat
• Barbiturates & Benzodiazpine
contraindicated • Dialyzable drugs .
4- Narcotics :
Indication
• Opium , codeine , morphine ,
Hemoperfusion • The same as hemodialysis but because the charcoal can ad adsorb
sorb the toxin , hemperfusion can
ca be performed in toxins characterized by:
methadone , heroin
1- Hight M.W. - High protein binding - Poor water solubility
5- Metals :
Plasma Exchange & • Replacement of plasma with protein solution Plasma exchange / Replacement of plasma with crystalloid solution plasmaphoresis.
• Lead, iron encephalopathy
Plasmaphoresis • Effective for toxins that : - have high protein binding & - poorly dialyzed or filtered as phenytoin
6- Secondary to toxins effect :
• Hypoglycemia m hypoxia , • Compounds
ompounds which unite with absorbed poisons ( Metallic poisons ) to form Chelates which are non toxic & rapidly excreted in urine.
Chelators
hepato & nephro-toxicity 1 Iron toxicity
1- Deferoxamine (desferal) : has high affinity to ferric iron & hemosiderin (doesn't affect trasferrin , cytochrome & heme )
Antidotes Coma Cocktail
Poison Antidote Dose 1- Dextrose
Atropine nitial atropine dose (IV or IM) 1-2mg (adult) 0.05mg/kg
Initial 0.05mg/kg(child) • Rationale: Hypoglycemia common cause of ↓LOC
Organophosphate Dose can repeated every 10 min. till Clear chest or ATROPINISATION.. • D50W ( 50 -100cc
100cc IV ) or D25W 2-4cc/kg
2 in peds
Pralidoxime 1-2g (adult) 25-50 mg/kg (children)
• DDx – hypoglycemia :
N-acetyl cystenine loading dose of 140 mg/kg followed by 70 mg/kg q4h for 17 - Tox insulin, oral hypoglycemic, EtOH, salicylates
Acetaminophen addi=onal doses, giving a total of 72 hrs of therapy
- Non-tox sepsis, hyperthermia, hepatic failure, myxedema
Digoxin specific If dose ingested in known :
Digoxin • Cautions : diabetic or hyperosmolar pts, cerebral infarct
FAB fragments No. of vials=(Ingested X 0.8) / 0.6
2- Thiamine
Naloxone 0.4- 2 mg (max 10mgin adults) / 0.01/kg (child) IV, IM, SC
Opioids • factor for pyruvate dehydrogenase, and α-ketoglutarate
Co-factor ketoglutarate
dehydrogenase.(Vit B1)
Ethanol Thiamine 100 mg IV • Decreased levels in:
Alcohol -PO
PO 1ml/kg loading dose then 0.5ml/kg/4hrs to maintain level at 100mg/dl
- Ethanol 100% - chronic liver ds, folate deficiency, malabsorption,
Methanol malnutrition, EtOH intake
- Fomepizole -15
15 mg/kg initial dose then repeated
- adults: 2 mg in 100 ml normal saline slow iv infusion over 10 min.
• Deficiency - Wernicke’s encephalopathy :
Anticholinergics Physostigmine - Ophthalmoplegia,Nystagmus, Ataxia, Altered mental status
- children: 0.02 mg/kg.
• Dose: 100 mg IV
TCA , Cocaine , Salicylates Na bicarbonate 1 – 2 mEq/kg bolus
3- Naloxone
Benzodiazepines Flumazenil 0.2 mg IV/3-55 min. (max. dose: 5mg)
• Pure opioid antagonist, used for reversal of acute intoxication
Iron Deferoxamine 15 mg/kg/hr slow IV infusion (max. 6 gm) or disappearance of • Diagnostic and therapeutic
vin
in rise color
co of urine. • Dose: 0.4- 2 mg (max
(m 10mgin adults) / 0.01/kg (child) IV, IM, SC
Arsenic, mercury, lead Dimercaprol (BAL) Deep
eep IM oily
o solu=on, 2-5 mg/kg/dose/4-6h h for 2 d
days , 4- Oxygen
then/12h
hen/12h for 7 days.
General Toxology Scheme
Toxidromes

Muscarinic "Cholinergic" actions Adrenargic actions

(DUMBELSS)
1- Diarrhea 1- Hypertension , Tachycardia
2- Urination 2- Hyperthermia , Tachypnea
3- Miosis 3- Mydriasis
4- 3B 4- Diaphoresis
- Bradycardia Hypotension 5- Excessive motor activity
- Bronchospasm Wheezes 6- Excessive Speech
- Bronchorrhea Pulm. edema 7- Tremors
5- Emesis 8- Hyperactive bowel sounds. Withdrawal Symptoms of Opioids
6- Lacrimation
7- Salivation
8- Skin sweating&subnormal temp.
Examples: Examples:
1- Organophosphate 1- Amphetamine
2- Carbamate 2- Cocaine
3- Theophylline
Anti
Anti-Cholinergics
1- Peripheral manifestations: 2- Central manifestations:
• Dry mucous membranes • Delirium
• Hot, dry, flushed skin • Disorientation
• Hyperthermia • Agitation
• Sinus tachycardia (early & most • Impairment of short-term
term
reliable sign of muscarinic receptor memory
block). • Incoherent speech
• Markedly dilated pupils & blurred • Meaningless motor activity
vision. • Visual hallucinations
• Urinary retention (palpable urinary • Seizures (not common)
bladder).
• Bowel sounds are hypoactive or
absent.
Anticholinergic Agents :
Belladonna alkaloids:
• Atropine
• Scopolamine
Antipsychotics:
• Chlorpromazine
Cyclic antidepressants:
• Amitriptaline CNS manifestation of cannabis
Antihistamines
• Chlorpheniramine
Local mydriatics:
• Cyclopentolate
Antispasmodics:
• Clidinium bromide
Antiparkinsonian medications:
• Biperiden
Plants & mushrooms:
• Atropa belladonna
• Datura stramonium
• Amanita muscaria

Nicotinic actions Opioids

(MMATCH)
1- Mydriasis 1- Mental status depression
2- Muscle weakness & paralysis 2- Miosis (PPP)
3- Adrenal
drenal medulla activity is 3- Respiratory depression
increased, leading to : T&H (slow rate & shallow resp.)
4- Tachycardia 4- Decrease bowel sound
5- Cramps
ramps of skeletal muscles 5- Bradycardia
6- Hypertension 6- Hypothermia
1- Muscle weakness :
• Fasiculations
• Clonus
• Tremors
Examples: Examples:
1- Organophosphate 1- Opium
2- Morphine
3- Heroin
Sedative hypnotics
1- Mental status depression
2- Delirium , confusion , Hallucination & coma
3- Slurred speech , Blurred vision & diplopia
4- Ataxia , Nystagmus
5- Hypotension
6- Bradycardia
 Toxic agent Treatment (don’t forget antidotes)

Supportive & Symptomatic treatment GIT decontamination Enhancement of elemination

• Prevention of further exposure
Organophosphate 1. General management: 1- Activated charcoal.
1. General management: • ABC & ComaCocktail if coma.
2. Decontamination • Monitoring of cardiac functions. - Emesis &
3. Antidote 2. Antidote: " Atropine" - Gastric lavage
4. Symptomatic TTT
3. Symptomatic : TTT of seizures are contraindicated
1. General management:
• ABC & ComaCocktail if coma. 1- Activated charcoal &
2. Antidote: “Physostigmine” repeated doses of AC to
3. Symptomatic TTT: prevent further absorption.
Anticholinergics • Seizures:
2- Gastric emptying procedures
- benzodiazepines or barbiturates.
are useful even
en up to 12 hrs
• Rhabdomyolysis:
after ingestion.
- Creat.
reat. Phosphokinase & urine myoglobin level. (due to slowed GIT absorption).
- IV fluids, alkalization of urine & mannitol to avoid acute tubular necrosis.
• Sinus tachycardia: rarely needs intervention.
• Hyperthermia: cold compresses
• Urine retention: catheterization
• Constipation: enema
Alcohol 11- ABCD & ComaCocktail if coma. Hemodialysis. Indication :
22- Folic acid: Folinic acid (1mg/kg i.v. up to 50 mg/dose)
mg/d followed by folic acid are Preventing further absorption by:
• Blood methanol level is 25 mg/dl
needed for conversion of formic acid to co2 and water. 1- Emetics or severe acidosis.
Methanol 33- Methylpyrazole (4-MP) : is a strong inhibitor of alcohol dehydrogenase (15mg/kg).
2- Gastric lavage • Persistent fluid and electrolyte
44- Fluid replacement:: for dehydration. disturbances despite treatment.
55- Bicarbonate : should be used to correct acidosis. (1 to 2 mEq/kg) • Visual symptoms, or renal failure.
66- Diazepam and phenytoin. There is no role for peritoneal dialysis or
If seizure occur diazepam 5 to 10 mg i.v. over 2 to 3 min repeated every 10 to 15 min hemoperfusion in the management of
as needed to a maximum of 30 mg. methanol poisoning.
11- ABCD & ComaCocktail if coma. Gastric decontamination
Ethanol 22- Metabolic derangement. NOT INDICATED Hemodialysis.
Correction of alcoholic ketoacidosis
ketoacidos by dextrose . Hypokalemia or hypomagnesemia should be corrected. because ethanol absorbed rapidly .
3- Withdrawal. N.B.
1- Diazepam 5 to 20 mg i.v. every 4 h in mild symptoms. It is poorly absorbed to activated charcoal
2- Diazepam 10 to 20 mg i.v. every 20 min un=l moderate symptoms resolve. BUT If ethanol intoxication is associated
3- Diazepam 10 to 40 mg i.v. every 20 min un=l severe symptoms resolve up to 200mg total dose. with another toxic agent decontamination
4- Psychiatric evaluation. and activated charcoal are indicated.
General measures: 1- Gastric lavage : - Treat acid-base
base disorders
Ventilatory support - Cardiovascular support - Control seizures
Phenol Toxin-specific measures :
Repeated lavage if there is no
- Treat methemoglobinemia:
esophageal injury followed by
For dermal exposure: administrated of olive oil or If > 30% → ingest methylene blue
wash with undiluted polyethylene glycol or copious amount of water vegetable oil and can followed If > 70% → exchange transfusion
For inhalational exposure: by 2- Cathartic
remove from contaminated area & given 100% humidified oxygen NO Emetics
Iron poisoning 1. General:
- ABCs , resuscitation and removal of the offending agent. 1- Gastric lavage :
- Obtain empty bottles and calculate amount of elemental Fe ingested preferred method Dialysis
TTT: 2. Anti-dote : Chelation Therapy: Deferoxamine
1- Decontamination Mechanism of action : 2- Whole Bowel Irrigation
2- Anti-dote
• Limits Fe entry into the cell with Poly ethylene glycol (GoLytely)
3- Sympt. TTT :
- IV fluids • Also chelates : to remove iron tablets from gut
- Liver support - Intracellular Fe outside mitochondria. - Adults 1.5-2.0 2.0 liters per hr.
- Dialysis - Intra-mitochondrial
mitochondrial free iron and further
further preventing lipid peroxidation - children 25 ml/kg/hr
Dose & Rote : - Con=nue for 5 hours
End point of therapy : • Must be given IM or IV (poorly absorbed from GIT), IV is the preferred. Gastric lavage with Bicarbonate ,
• 24- hours after patient • Dose: 15 mg/kg/ hour IV ( max. 6 gm ) un=l urine returns to normal color or Phosphate or Deferoxamine not
urine has turned clear recommended (why ?? )
toxicity disappears
• Serum iron falls < 100 μg/dl
- Fe +Deferoxamine = Ferrioxamine
• Patient becomes asymptom.
- Ferrioxamine excreted in urine (also dialyzable) N.B.
Deferoxamine Challange Test • Ipecac is less favored agent.
• Give 50 mg/kg IM up to 1 gram • No activated charcoal (Poor Fe
• Ferrioxamine gives “vinrose”color to urine binding)
• Compare color of urine pre and post Deferoxamine • No emetics
- If test Positive, start chelation • No cathartics
- If test Nega=ve &no symptoms for 6hrs, pta=ent may be discharged
Negative Deferoxamine test by itself does not rule out Fe toxicity
3. General:
• ABC’s (early elective tracheostomy & mechanical ventilation) 1- Gastric lavage
• Nasogastric suction (ileus)
Botulism • Foley catheterization (urine retention) 2- Emetics
2. Toxin-specific measures:
• Trivalent ABE antiserum : Dose: 1 vial IM & 1 vial IV (AA dose/ 4hrs if serum toxin persists
persists)
Snake Bite Scorpion Sting
A- First aid measures A- First aid measures
• Immobilization of the affected limb B- At hospital
• Light tourniquet may be applied proximal to site of the bite I- Stabilization of the patient
B- At hospital Best given in the first 4 h but can s=ll be given as late as 24 hours) :
II- Antidote (Best
I- Stabilization of the patient Indications: All children, and senile patients Adults presenting with any of the systemic manifest.
II- Antidote : ( Polyvalent Antivenom ) Patients with previous cardiovascular disease, hypertension or diabetes
Dose :
Animal • It neutralizes the venom but don't reverse local injury
sensi=vity test to be repeated every 30
Adult : 3 - 5 amp slow IV or IM aGer nega=ve skin sensi=vity
• It should be given within the first 4 hours to prevent local injury
Poisoning • Skin sensitivity test must be done before administration.
minutes if signs still progress or do not regress
Pediatric: The same dose as adults (Dose is not related to body weight but to neutralizing
• Initial dose is 3 - 5 vials to be repeated according to the severity
power of the circulating venom)
• It is given in normal saline up to 1: 1 dilu=on .
III- Supportive treatment
III- Supportive treatment
- Pain killers : NSAIDs & Local anesthesia.
• IV Fluids for hypotension
- Corticosteroids:
• Blood for bleeding and hemolysis Indications : Stridor , Myocarditis , Non cardiogenic pulmonary edema,, Cranial palsy
• Platelets concentrates - IV vasodilators (Na Na nitroprusside, hydralazine or prazocin):
prazocin To control hypertension.
• Fresh frozen plasma to replenish coagulation factors - Mechanical ventilation :
• Artificial ventilation for the paralytic
paralytic syndrome of Cobra or the pulmonary Indications : Respiratory failure, Non cardiogenic pulmonary edema in which PEEP mode is used.
edema of vipers - Dehydration, hypotension and shock
• Antibiotics and antitetanic serum - IV fluids
Care of the wound - Dobutamine if cardiogenic
genic sho
shock 2ry to myocardi=s complicates the picture
• Cleansing, debridementment of necrosed
n tissues and fasciotomy if peripheral
ipheral - Anticonvulsants e.g. diazepam
vascular impairment nt follow limb edema and compartment syndrome. - Malignant hyperthermia : Cooling measuresmeas and chlorpromazine
 Therapeutic Drugs
• Assessment of the case
• Electrolyte disturbance
Digitalis never use Calcium)
- Hyperkalemia (never Calcium 1- Gastric Lavage (with care)
care NOOOOOOOOOOOOOOOOOO
- Hypokalemia Hemodialysis or hemoperfusion
- Hypomagnesaemia: MgSo4 .
2- RDAC
are, of limited utility in removal
• Manage dysrhythmia : of digoxin , why? because of its :
- Lidocaine and phenytoin are antiarrhythmic drugs of first choice
- Severe bradyarrhythmias are treated with atropine, electrical pacing - Extensive
xtensive tissue binding
is used in unresponsive patients - Very
ery large volume of
- Verapamil is useful for SVT’s distribu=on (5.6 L/kg)
- MgSo4
- Cardioversion should be limited to patients with life-threatening
life threatening
arrhythmias and used at the lowest effective energy level
• Digoxin-specific
specific antibody Fab fragments (Digibind®) :
purified from sheep IgG, rapidly bind to circulating digoxin and are indicated in:
( see lecture )
Salicylates ABCS: Pulmonary edema (Intubate), tends to improve as serum salicylate level 1- Gastric lavage : 1- Alkanization of urine :
Symptomatic & Supportive Care : Within
hin 1 to 2h following Sodium bicarbonate : 1-2
1 mEq/kg,
• Fluid/electrolyte management : ingestion , up to 12 hours followed by an IV infusion of 3
1- ABCS ampules in 1 L of D5%
- Rehydrate with 0.9% saline ( due to presence of concretions )
2- GIT decontamination • Maintain urine pH at 7.5- 8.0 &
3- Elimination from blood
- Urinary output : 2-32 mL/kg/hr
2- Activated Charcoal & RDAC : correct hypokalemia.
hypokalemia
- Be careful with elderly/renal/cardiac patients
4- Symptomatic & 1g AC absorb 550 mg of ASA. • Why Hypokalemia???
supportive TTT. • Coma: care of coma ( due to intacellular shift of potassium
Effec=ve in 10:1 AC to salicylate
• Convulsions: give succinylcholine with artificial respiration & oxygen in exchange for hydrogen ions to
( avoid the use of a CNS depressant) compensate for the alkalemia).
3- Whole
hole bowel irrigation 2- Hemodialysis : (indications*)
(indications
• Hypoprothrombinemia : vitamin K , Fresh blood or platelet transfusion.
shown to be more effective for These are indicated due to the ability
• Hypoglycemia: glucose 50%
enteric coated or sustained to remove salicylates, correct fluid,
• Hyperthermia: Sponge bath, fans, cold water submersion electrolyte, and acid-base
base disorders
release forms
• Pulmonary edema: Oxygenation , Intubation (tends tends to improve as serum salicylate level ) 3- Hemoperfusion.
Acetaminophen AGer 4 hrs : Antidote : N-Acetylcysteine
Acetylcysteine (NAC) Within first 6 hrs of ingestion give:
Mechanism ofaction : 1- Activated charcoal : - Dialysis :
- It acts by increasing glutathione concentration to bind the toxic metabolite 2- Cathartic : if renal failure persists more
1- GIT decontamination - It serves as a source of slupher , so it increases conversion of paracetamol to its
2- Antidote (saline sulfate cathartic): than 48 hrs .
sulphate metabolite decrease formation of other toxic metabolite.
enhances activity of the sulfate
Oral NAC dose: loading dose of 140 mg/kg followed by 70 mg/kg q4h for 3 days. metabolic pathway → hepa=c
I.V. NAC dose : Given if oral NAC failed (Increased risk of anaphylactic response.) protection.
- 150mg/kg in 20 min. then 50 mg/kg in 4 hr. then 100mg/kg in 16 hr.
- Dura=on of I.V regime is 48 h.. h.
Psychotropic drugs A) General measures :
1- ABC & ComaCocktail if coma ( Intubation if severe R.D. / Assisted ventilation with PEEP )
2- ABG , Cardiac monitoring , Serum electrolytes
electrolytes & toxicology screen.
3- Venous access with a large bore IV line : to give IV fluid in hypotension.
B) Management if complication :
1- CNS depression & coma Supportive care - Seizures Diazepam
1- Anti-psychotics 2- Hypotension: Respond to Ringer's lactate or normal saline
If failed : a adrenergic agonist ( Phenylephrine ).
3- Cardiotoxicity :
• Direct current cardioversion used in : SVT , VT , Torsade de points
• Defibrillation followed by lidocaine used in : ventricular fibrillation.
• Lidocaine is the 1 line agent , if fail we use phenytoin. 1- Gastric lavage:
st
No hemodialysis &
4- Acute dystonia: Diphenylhydramine (Benadryl) - Benzatropine (Cogentil) Should started as soon as possible , hemoperfusion
5- Parkinsonism: anti-parkinsonism
parkinsonism drugs and may after several hours (GIT
mo=lity decreased due to a1 blockage)
6- NMS : Dantrolene - Bromocriptine – Diazepam - Cool the patient. as they bind to plasma protein
A) General measures : As above 2- Activated charcoal (1g/kg) in anti-psychitucs
B) Specific TTT : followed by And ineffective in TCA.
a- Alkalinization is the first line treatment for TCA induced conduction defects ,
arrhythmias & hypotension. 3- Cathartic
A bolus of NaHCO3 mEq/kg is given over several minutes.Serum . (targeted pH 7.45 - 7.55 )
b- Management of complicating factors :
2- Antidepressants 1- CNS depression & coma Supportive care - Seizures Diazepam
2- Hypotension: Respond to Ringer's lactate or normal saline AND alkalinization
If failed : a adrenergic agonist ( Phenylephrine ). In Tricyclic Anti-depressants
depressants :
3- Cardiotoxicity : Alkalinization of urine
• Alkalinization is the most effective TTT for cardiac arrhythmias and for
• Dose: Repeated 3-5 3 minutes
sinus tachycardia with widened QRS > 0.10 second.
- 1-3 meq/kg bolus (if not in shock)
• Alkalinization + Pacemaker for third degree heart block. - 3-6
6 meq bolus (if in shock)
• Drugs to be avoided Physostigmine , Propranolol , Verapamil.
4- Acidosis : treated by alkalization of urine
5- Hyperthermia : cooling the patient.
A) General measures : As above ( + Serial estimation of lithium level ) 1- Gastric lavage. IF :
3- Lithium B) Specific treatment : main line of treatment is : 1- Kidney function is impaired
- Sodium polystyrene sulfonate 2- Emetics. or
- Furosamide Usually not recommended because the 2- In Severe toxicity :
C) Symptomatic treatment : patient is comatosed , but used if Serum lithium level > 4meq/Li
4
1- In mild to moderate cases with serum level < 4 meq/L securing airway.
• Good hydration with IV infusion of normal saline. Hemodialysis
After the patient is rehydrated fluid administration should be Activated Charcoal is
continued with half normal saline until toxicity is resolved. NOT effective
• Maintenance of electrolyte & fluid balance .
2- Severe toxicity : TTT of Coma - Convulsions - Arrhythmias
For BOTH Barbiturate & Benzo. For Barbiturates only
4- Sedative & A) General measures : As above 1- Gastric lavage : 1- Forced Alkaline Diuresis :
• With protected airway by cuffed - Help elimination of long-acting
long
hypnotics B) Specific TTT : barbiturate.
Endotracheal tube.
• CNS depression. • Used as soon as possible in first 6 - Help ttt of Rhabdomyolysis
- Barbiturates • Flumazenil (anexate) .2 – 5 mg IV Benzodiazepine antidote hours of greatest benefit . - Not useful in short or Intermediate acting.
• but also delay used is possible (GIT 2- Hemodialysis (HD) :
- Benzodiazepines • Treating withdrawal - 4-6
6 =me effec=ve than FAD
motility decrease )
- Used in associated ARF or
2- Activated Charcoal : compromised MI
• 1 gm / kg / BW - Not useful in short-acting
acting
3- Hemoperfusion
sion (HP
(HP).
 Drug dependence & drug abuse
Stabilization : If ingested : They are eliminated by the
- ABC , Oxygen , ECG monitoring , artificial ventilation . kidney & the rate of elimination
Amphetamine Symptomatic ttt : 1- Activated charcoal depends on urine PH (the more
1- Stabilization : • Agitation Benzodiazepine (high
high therapeutic index & good anticonvulsant activity
activity) acidic, the more ionized, the
2- GIT decontamination • Seizures Benzodiazepines 2- Gastric Lavage more eliminated), but not
3- Symptomatic ttt • Hypertension & tachycardia Alpha blocker or Na nitroprusside. recommended????
Never use beta blockers as they exaggerate alpha stimulation & worsen hypertension.
• Arrhythmia antiarrythmia measures.
Rhabdomyolysis
• Hyperthermia cold compresses
• Rhabdomyolysis Na bicarbonate & hydration & maintain urine output of at least
3ml/kg/h.
• Treat psychosis later with phenothiazines
Stabilization :
- ABC , Oxygen , ECG monitoring , artificial ventilation . • Body stuffing or body packing :
Symptomatic ttt : (intense decontamination)
• Agitation Benzodiazepine (highhigh therapeutic index & good anticonvulsant activity
activity) 1- Activated charcoal
• Seizures Benzodiazepines
• Hyperthermia immediate rapid cooling with ice water immersion
2- Whole bowel irrigation,
Cocaine • Hypertension & tachycardia Alpha blocker (phentolamine) or Na nitroprusside
nitroprusside. 3- surgical removal in case of
• Dysrhythmias : intestinal obstruction
- Resolves
esolves following sedation, cooling, rehydration, and time to metabolize drug.
- Additional pharmacological therapy for : • If the nares contain residual
• Supraventricular tachycardia: white powder presumed to be
in stable patient (benzodiazepines & Ca channel antagonists) & cocaine:
in thermodynamically unstable patients (cardioversion). gentle irrigaMon with 0.9%
• Ventricular arrhythmia (lidocaine & Na bicarb,), unstable patients should be defibrillated.
sodium chloride solution will
• Rhabdomyolysis Na bicarbonate & hydration & maintain urine output of at least help remove adherent material.
3ml/kg/h.
Acute Coronary Syndrome Read the lecture.
A) General measure :
1- ABC : 1- Gastric lavage
- If mild respiratory depression Oxygen supplementation with a large-bore
bore orogastric tube
- If severe CNS depression and apnea Endotracheal tube with
2- with altered consciousness endotracheal intubation to
- I.V. thiamine (100 gm) protect against aspiration
- Glucose : Adult: 25g of 50% solu=on / Pediatric: 1 g/kg of 10-25%
25% solution
B) Opioid antagonists (Naloxone: both diagnostic and therapeutic ) 2- Activated charcoal (1 g/kg)
Opioids - It's short acting pure competitive opioid antagonists 3- Cathartic :
- Mechanism of action : Sorbitol 0.5-1g/kg or
competes with opioids for their receptors sites & rapidly reverses opioids actions. Magnesium sulfate 250mg/kg up to 30 g
- Routes of administration: I.V., S.C., I.M., Intralingual, Endotracheal (rapid onset) 4- Body packers or body stuffers:
- Dose : - Multiple dose activated charcoal
• With CNS depression or mild respiratory depression : - Whole bowel irrigation
- Initial dose should be low 0.1 mg i.v.
• With sever respiratory depression
- Initial dose 2 mg i.v.
- with no response aGer 2-32 3 minute , this dose can be doubled
un=l there is a response or a total dose of 10 mg.
The Planned withdrawal of opioids (detoxification): methadone (in lecture)
1- ABC
Cannabis 2- Clinical assessment for evidence of co-ingestions.
co Decontamination.
3- Decontamination - Rarely toxicity is serious so,
4- Patients with acute paranoia or toxic psychosis : not indicated
The drug should be stopped - Can be used with securing airway.
No specific antidotes for The progress of symptoms observed
cannabis Support & gentle sedation with a benzodiazepine
Heavy user may need antidepressant medication
5- Addiction TTT : behavioral & group therapy.
Others
A) Stabilization :- - Emesis
1- Secure the patient’s airway .ageal
. and gastric tissue. - Gastric lavage
2- Establish an i.v. line. - Cathartics
3- Monitor vital signs closely. - Charcoal
4- Perforation . Preparation of the patient for surgery Are all Contraindicated
ontraindicated
5- Serologic testing.
6- Monitor fluid & electrolyte status and pH. - Demulcents :
7- Patient is to keep fasting until endoscopy is performed. It minimizes damage to oral,
8- Serial evaluation is performed . eosphageal and gastric tissue.
B) Supportive care :- One to two glassfuls of milk
maybe administrated within 30
Corrosives - Pain killers as morphine
minute.
- Anti-Shock
Shock measures: IV fluids , Blood transfusion and crystalloids.
- Anti-biotics
biotics , to guard against infection
- H2 blockers or proton pump inhibitors to minimize acid secre=on
- Steroids to prevent fibrosis.
- Total Parenteral Nutrition (TPN) for at least three
thre weeks.

C) Surgical :-
1- Emergency surgery in severe hemorrhage & in perforation
2- Elective surgery :
- Esophageal bypass surgery
- Dilatation of esophageal strictures
- Repair of bronchoesophageal fistula
- Gastrotomy for feeding purposes.
• In ocular corrosive burn Irrigate with running tap water for 2 min.
• In corrosive inhalation Oxygen, aerosol thrapy with B2 s=mulant &
steroids.
 Toxic agent & Doses Clinical Features
Iron poisoning Stage I / 0-6
6 hour Stage II / 2-48 hours Stage III / 12-48 hours Stage IV / 2-6
2 weeks
Toxicity by Peak Serum Iron Level : Direct corrosive insult to the intestinal mucosa Quiescent phase: Worsening of hemorrhage, sever Healing of GI insult :
50-175 μg/dl Normal • GIT upsets : Apparent ( false ) improvement of lethargy and coma • LIVER :
<350 μg/dl None to mild toxicity most of victims …
Nausea, vomiting, diarrhea (Multiple organ dysfunctions)
dysfunctions Hepatic damage &
350-500 μg/dl Moderately toxic
> 500 μg/dl Severely toxic to • GIT bleeding : • Coma : CNS depression cirrhosis
Initial correction of hypovolemia
lethal upper or lower GI bleeding • Cardiovascular
ardiovascular collapse : • INTESTINE :
and stabilizing measures no
• If severe , GIT perforation : overt clinical signs
- Direct massive post-
post Intestinal scarring
Dose Related Toxicity : Abdominal pain, perforation, peritonitis arteriolar vasodilatation . ( cicatricial fibrosis) :
< 20mg/kg Non toxic • Apparent recovery
• Hypotension, shock, tachycardia - Hypovolemia in hemorrhage - strictures
20-60mg/kg Moderately toxic • GI symptoms subside
> 60 mg/kg Severely toxic - Vasodilatation • Cerebral
erebral edema - with or withour
• Little changes in mental
180-300 mg/kg Lethal - Hypovolemia in bleeding. • Pulmonary edema obstruction.
status.
It's accidental poisoning especially in • Hyperglycemia, - V.D. and permeability. • Gastric scarring
• Hyperglycemia,
children : Impaired glucose tolerance • Liver cell failure :
Fatalities have occurred after pediatric leucocytosis, acidosis
inges on of 1.200 to 4.500 mg of • metabolic acidosis, persist
- jaundice,
elemental iron . - hydrogen is released in the conversion of - hypoglycemia
ferrous iron to ferric iron:
iron - coagulation defect .
Careful observation is
Risk of Coma by Peak Serum Iron Level : -- in blood acidosis or
necessary. • Renal failure : due to
<500 μg/dl 10% -- interfere with Krebs Cycle disruption of - deposition of excess iron
500-1000 μg/dl 25%
>1000 μg/dl 75%
mitochondria forcing anaerobic respire. exceeding TIBC in soft tissues
• leucocytosis : - poor renal perfusion.
Due to invasion of damaged mucosa by bacteria • Severe metabolic acidosis,
acido
sis, elevated PT
leucocytosis
Psychotropic drugs Antipsychotics Tricyclic Anti-Depressants
Anti (TCA)
Mechanism of action : 2- Cardiovascular manifestations
ifestations Mechanism of action : 2- Cardiovascular manifestations :
1. Neuroleptics or antipsychotics e.g. Receptor blockade • Postural Hypotension : 1- Inhibition of neurotransmitter reuptake : Tachycardia :
(Phenothiazines) • Inhibit pre-synaptic
1) Dopamine receptors in the CNS . Low - Periph. V.D. (N1 & a1 blockage) synaptic neuronal reuptake • Good indicator of TCA ingestion
2. Anxiolytic e.g. (Benzodiazepines) affection To Dopamine sedation, - Direct myocardial depression of NA & 5HT . • Caused by cholinergic blockade
3. Mood stabilizing drugs (Lithium) High affection Extrapyramidal manifestation
• Sinus tachycardia : • Long use for more than 2-3 3 weeks • Catecholamine
4. Antidepressants ( e.g. TCA, MAOI). Neuroendocrine incr. prolactin, amenorrhea
- Reflux due to hypotension gives rise to: • Anxiety
2) Alpha adrenergic receptors - M blockage - Down-regulation
regulation of postsynaptic beta and Bradycardia :
3) Muscarinic receptors serotonin receptors plus presynap=c alpha2 • generally associated major
• Conduction abnormalities & receptors .
4) Histamine (H1) receptors conduction block
Arrhythmias : - Up-regula=on
regula=on of postsynap=c alpha1
Inhibition of C.T.Z antiemetic effect. • severe toxicity
- At therapeutic level : receptors (due to alpha 1 blocking effects).
Hypotension :
1- Neurological manifestations Qunidine like effect : 2- Receptor blockade • Vasodilation, hypovolaemia,
• CNS depression : altered mental ECG shows prolongation of 1) Alpha 1 adrenergic receptors alpha receptor blockade
status ataxia , stupor , coma PR interval & QT interval
2) Muscarinic receptors • Serious myocardial depression
• Sedation,, weight gain (H1 blockage) - At Toxic level : (normally wide QRS)
3) Histamine (H1 & H2)) receptors
Widening of QRS complex ,
• Extrapyramidal manifestations (D) 4) Seratonin receptors
AV block & arrhythmias.
a- Acute dystonia 5) GABA receptors Myocardial membrane depressant effect :
b- Parkinsonism 3- Eye manifestations : • Delayed depolarization and impaired
c- Akathisia • Miosis ( a1 blockage in iris dilator muscle ) 1- Neurological manifestations cardiac conduction
ction (quinidine like
d- Tardive dyskinesia 4- Anticholinergic effects : • Depressed
epressed mental status & coma effect) due to inhibition of fast inward
• Convulsions • Delirium Na+ channels delayed phase O of
(mydriasis + Hyperthermia + other mani.)
action potential receptors
( due to Lowered seizure threshold ) 5- Impaired thermoregulation : • Seizure
manipulation of extracellular PH and
• Gait problems • Hypothermia : • Myoclonus Na+ concentration
• Insomnia - Central anterior hypothalamus • Nonspecific Cerebellar &
• Anxiety • Ca+ channels inhibition. Decrease
- Peripheral
eripheral vasodilatation extrapyramidal signs
myocardium contractility.
contractility
• Low libido • Hyperthermia : anticholinergic effect.
• Anti-cholinergic
cholinergic manifestation : • Delayed Phase 3 and 4 Spontaneous
6- Respiratory effects : depolarization.
Pulmonary odema dry skin and mucosa, ileus, urinary
7- Neuroleptic malignant retention, hyperthermia and
syndrome(NMS) mydriasis

ILethality : ILethality :
cardiac arrhythmias, severe hypotension cardiac toxicity
Lithium Sedative & hypnotics
Lithium toxicity Symptoms with Acute toxicity:
toxicity Barbiturate Benzodiazpines
Acute Chronic I- CNS Mechanism of action :
GI 42% 20% 1. Mild toxicity: mental They bind to specific sites on GABA
GABA-sensitive ion channels in CNS enhance the GABA-mediated
GABA mediated chloride currents inhibit
CNS delayed Common > confusion, ataxia, tremors neuronal depolarization by potentiating and prolonging the actions of GABA (GABA is inhibitory neurotransmitter in CAN).
2.mmol/L
and exaggerated reflexes Effect : Indications/uses include :
Renal Usually Universal
non 2. Severe toxicity: convulsions CNS sedation & hypnosis . anxiety , panic , mania, seizure , phobias,
significant and coma Pulm. depression of medullary respiratory center
center. insomnia, alcohol withdrawal, muscle
ECG normal QT prolongation spasm, agitation, catatonia, akathisia
usual II- Renal CVS cardiovascular depression may occur follow
following
ing depression
- Polyuria, polydepsia, DI and of the medullary vasomotor centers. • Sedation
Thyroid none Hypothyroidism renal failure • Drowsiness
20%
Recovery Usual, Disability 10%
III- CVS • Ataxia
- Arrhythmias , if severe cardiac Toxicity :
rapid delayed
1- Coma : characterized by : 3- Hypotension : • Cognitive impairment,
arrest.
Level poor Good - Dilated reactive pupil It's due to vasoplegic mechanism • Anterograde amnesia
correlation IV- GIT • Lack of concentration , hallucination ,
- Skeletal muscle relaxation ( especially with short acting)
- Nausea, vomiting and diarrhea excitability
- Cyanosis - Shock may occur due to
- Signs of shock vasoplegic & cardiogenic • Coma
Serum lithium level: Symptoms with chronic toxicity
( rapid weak pulse , low BP , mechanisms.
Therapeutic level ( 0.4-1.3 meq/L ) cold skin & hypothermia) • Respiratory depression
4- Hypothermia:
Mmol/L effects
In mild to moderate toxicity : It's frequent with appearance of
Serum lithium level < 4 meq/L 2- Respiratory depression : • Dysarthria
J wave in ECG if temp. falls
Severe toxicity : 0.5 None resulting in hypoventilation & beyond 35 C. • Partial ptosis
Serum lithium level > 4 meq/LI apnea (short acting) • Diplopia
1.0 Mild tremor It's of rapid onset ( half hour )
5- Skin : • Nystagmus
Bullous skin eruption
1.5 Coarse tremor (barbiturate burn), in 7% of case • Hypothermia
between toes & fingers. • Hypotension
2.0 Hyperreflexia, ILethality : • Hypotonia & hyporeflexia.
dysarthria Asphyxia due to respiratory failure, circulatory failure , renal failure ,
pulmonary edema , Brain edema
edema. • Dependence & abuse
2.5 Myoclonia, • Tolerance
ataxia,confusion • Withdrawal symptoms
Fatal Dose:
- Long acting 6 – 10 gm
> 3.0 Delirium, coma,
- Short acting 2--3 gm
seizures
Fatal Period:
- 1-4 days, some=me
me=mes more prolonged.
 Amphetamines
sympathomimetic & CNS stimulants. 2 release :
Chemical Name :
Alpha-methyl phenyl ethylamine
thylamine 2 inhibiMon :
Amphetamine-type stimulants
(ATS), consists of :
General manifestations :
1- Amphetamines
methamphetamine). 1- Increased muscle activity Hyperthermia
(amphetamine,methamphetamine).
2- “Ecstasy”
(methylenedioxymethamphetamine
ethamphetamine
(MDMA) ) related substances
such as :
methylenedioxyamphetamine
mphetamine
(MDA)
3- Number of other synthetic
stimulants such as :
- methcathinone,
- phentermine
- fenetylline
Cocaine
Sympathomimetic, CNS stimulants &
local anesthetic
A natural alkaloid contained in the
leaves of Erythroxylum coca
Cocaine Vs Amphetamine
• The clinical manifestations &
complications are similar to those
from amphetamine use and may
be indistinguishable
Except for the duration of effect of
amphetamines, which tends to be
longer (up to 24 hours).
• Amphetamines are less likely than
cocaine to cause: seizures,
myocardial ischemia. Eyes, Nose, and Throat :
dysrhythmias,&myocardial
This may be related to :
- sodium channel-blocking
blocking effects - Vasospasm of the retinal vessels
- thrombogenic effect of cocaine.
• Amphetamines more likely to
causes psychosis
sychosis than cocaine,
This related to the more prominent
dopaminergic effects of amphetamines.
Read from lecture :
- Mechanism of pulmonary mani.
- msculoskeletal manifestations
- Obstetric manifestations
- Cocaine Dependency
Opioids
Opioids : Are a broad class of alkaloid
compounds that have opium or
morphine-like activity and they are
divided into :
• Naturally: Morphine & Codeine
• Semi-synthetic:
Heroin, Hydro-morphene ,
Oxy-morphene
• Synthetic:
Meperdine, Methadone & Fentanyl
ntanyl
• Mixed agonist & antagonist :
Pentazocine
Opium:
Naturally occurring substances with 20
constituents, derived from juice of opium
poppy (Papaver -somniferum)
Opiate:
Drugs derived from opium include
(naturally opium & semi-synthetic)
synthetic)
Cannabis
• Cannabis is a collective term
referring to the bioactive
substances from Cannabis sativa
sativa.
C. sativa plant contains a group of
more than 60 chemicals called
cannabinoids .
The major cannabinoids are :
cannabinol, cannabidiol, &
tetrahydrocannabinol.
The principal psychoactive cannabinoid 8- slurred speech
tetrahydocannabinol (THC) 9- Slow reaction time
1- delta 9-tetrahydocannabinol
The common form of cannabis
• Marijuana:(dried parts of plant)
1-5 % of THC.
• Hashish:(from
(from flowering tops of plant) 2- Agitation
5-15 % of THC.
• Hash Oil : 30 - 60 % of THC
A pharmaceutical grade form of THC :
• Dronabinol , Marinol
Mechanism of action : CNS , potent : (usually cause of emergency ) CVS :
1- Anxious,
nxious, hypertension, tachycardia,
tachycardia vasospasm lead to:
- Catecholamines ( Norepinephrine,
Norepinephrine dopamine ) 2- Aggressive,
ggressive,
Brain
- At higher dose Serotonin
3- Agitation.
gitation. 1 cerebral infarction,
1-
4- Seizures (Direct CNS effects) 2 Intraparenchymal & subarachnoid hemorrhage.
2-
- Catecholamines reuptake inhibition
- MAO inhibition decrease catecho.
cate Degradation. 5- Psychotic manifestations :
- Visual & tactile hallucinations Heart
- Acute psychosis , resembling paranoid 3-
3 myocardial ischemia or infarction angina
schizophrenia contributed to 4 Dysrhythmias
4-
2- Tachypnea suicide & Homscide. 5 aortic dissection
5-
3- Mydriasis
Lung
4- diaphoresis (sweating) Compulsive repetitive behavior patterns 6 Noncardiogenic pulmonary edema might
6-
Agitation, increased muscular activity, and Individuals may constantly pick at their skin, grind occur due to pulmonary vessels severe
their teeth , or perform repetitive tasks, such as
hyperthermia can result in: vasospasm, acidosis , hypoxia.
- metabolic acidosis, constantly cleaning their house or car.
- rhabdomyolysis , Intestine
- acute tubular necrosis (acute renal failure). Choreoathetoid movements (uncommon ) 7 ischemic colitis..
7-
with acute & chronic aamphetamine usage.
Death from amphetamine toxicity results from :
related to increased dopaminergic activity at If the drug is wrongly administered in the artery it will
- hyperthermia,
the striatal area . produce severe vasospasm & limb ischemia.
- dysrhythmias,
- intracerebral hemorrhage
Withdrawal symptoms: Anxiety , Abdominal cramps, Appetite
ppetite stimulation, Headache, Lethargy , Depression .
Mechanism of action : Neuropsychiatric (CNS) : CVS :
CNS : • Low-dose : Atherogenesis, Coagulation, and Heart
Enhances the release of euphoria,
uphoria, alertness, hypersexuality Ischemic
ic Cardiac Events : • Chest pain or discomfort
norepinephrine & excitatory amino acids The increased activation of dopaminergic • myocardial infarction is a common
blocks of reuptake : reward pathway leads to the feelings Mechanisms : concern, Many will have an ischemic
dopamine & serotonin of euphoria and the ‘high’ . hypertension and tachycardia increase cardiac event,
Sympathetic stimulation by : • As the cocaine dose increases, : myocardial oxygen demand. • Congestive heart failure..
Inhibition of reuptake of both (catecho.) - Anxious, • Dilated cardiomyopathy,, with chronic
- Aggressive, • Cocaine-induced
induced vasoconstriction : cocaine use is associated with
epinephrine & norepinephrine
- Agitation. 1- stimulation of the α-adrenergic
adrenergic repeated subclinical ischemic events.
Sympathomimetic findings : - Seizures (Direct CNS effects) receptors in smooth muscle cells • Infective endocarditis might occur
1- Hypertension, in the coronary arteries
- Psychotic (Hallucinations
Hallucinations) : due to I.V. drug abuse.
2- Tachycardia, 2- endothelin-1,1, which is a
3- Tachypnea, Chronic effect give rise to • Dysrhythmias
Magnan's syndrome. powerful vasoconstrictor locks neuronal Na channels
- Cocaine blocks
4- Hyperthermia occur (is the most critical)
- Movement disorders (depletion 3- nitric oxide, which is vasodilator. - Cocaine also blocks
ks cardiac potassium
5- Mydriasis,
or dysregulation of dopamine): channels QTc prolongation .
6- Diaphoresis, Thus,, cocaine decreases oxygen supply
7- Neuropsychiatric next column. • acute dystonias or
Pulmonary :
• choreoathetoid movements
Enhanced coagulation and impaired
-Enhanced • Smoked cocaine bronchospasm
- Mydriasis - Cerebrovascular accidents, due to thrombolysis . mediated by : • Pneumothorax,
hypertension, vasospasm,coagulopathies 1- in plasminogen-activator
activator pneumomediastinum, and
unilateral & bilateral loss of vision. inhibitor thereby impairing clot lysis. pneumopericardium
- Headache, due to :
- Corneal anesthesia, highly toxic to 2- in platelet count, • Noncardiogenic pulmonary edema
hypertension, vasospasm, dysregulated
the corneal epithelium platelet activation, and • exacerbates reversible airway disease
neurotransmitters .
- Perforation
erforation of the nasal septum : aggregability.
platelet hyper-aggregability. • hemorrhagic alveolitis
- A cocaine washed-out syndrome :
• Continuous V.C of nasal blood 3- reactive protein, von
levels of C-reactive • pulmonary infarction
vessels devitalization & slough. aGer usage for up to 24 hrs (dopamine Willebrand factor, and fibrinogen
• Irritation by adulterants depletion) : Abdomen :
• Cocaine anesthesia no pain of lethargy, want to sleep, trouble • local ischemia of the gastrointestinal tract
cocaine use is associated with premature
necrosis more sniffing initiating and sustaining movement. later may perforated ulcer
cer.
coronary atherosclerosis and thrombosis.
- Angioedema & oropharyngeal burns • Ischemic colitis
are associated with smoking crack.
crack • Intestinal infarction
• Bowel obstruction such as vomiting or
distension might suggest body packing
Mechanism of action : Cardiovascular GIT Endocrinology
• Opioids Exert their effects by interacting with
- Orthostatic hypotension, - Reduced motility - Reduced ADH,
specific upload receptors in the CNS (Mu, Kappa
- sinus bradycardia - Reduced bowel sound - Abnormal hypothalamic-
hypothalamic
& Delta) resulting in inhibition ofo synaptic
neurotransmission in central & peripheral nervous - ventricular arrhythmias Anorexia , malnutrition & pituitary adrenal axis
system. weight loss - Abnormal hypothalamic-pituitary
hypothalamic
The classical triad of opioid include : Dermatology Hypothermia gonadal axis
- Flushing & urticaria. (decreased libido, irregular menses)
CNS depression + Respiratory depression + Miosis
CNS - Skin boils, cellulitis &
• Range from euphoria to dysphoria & needle tracks are in I.V
• from sedation to coma. users.
• Amnesia , mental powers. Complications Withdrawal symptoms
• Noncardiogenic pulmonary edema.
Respiratory • Cellulitis & abscesses. See the picturein the general
• Respiratory depression • Pulmonary emboli & peripheral emboli. scheme.
• non-cardiogenic
cardiogenic pulmonary edema • Endocarditis and aspiration pneumonia.
Ophthalmology • Prolonged or unusual seizures.
Miosis , except in : • Rhabdomylosis with or without compartmental syndrome.
Overdose
verdose of meperdine & morphine, Hypoxia, • Active metabolites of meperdine has convulsant activity.
After use of naloxone, Presence of congestants. • Metabolites of propoxyphene has cardiotoxic activity
In Acute toxicity: In chronic toxicity
Low-
Low Moderate Doses On Respiratory system:
CNS Heart Smoking marijuana delivers more particulates to the lower respiratory tract than
1- Relaxation 11- Increased heart rate does smoking tobacco,, causing :
2- Drowsiness 12- Palpitations, 1- Asthma & bronchitis
3- Euphoria, results from stimulation of 13- Postural hypotension 2- cancers of the respiratory tract (mouth, larynx, sinuses, lung)
mesolimbic dopaminergic neurons 14- Chest tightness On Heart:
4- Disorientation
isorientation of time & space Pulmonary 1- ↑ heart rate & blood pressure (++sympathetic)
5- Balance impaired 15- Dry mouth. 2- ↑ risk of a heart a[ack
6- Coordination,
oordination, muscle strength, 16- Decrease
ecrease airway resistance & On Immune system:
hand steadiness. increase airway conductance Immunosuppressive
7- Inability to concentrate Ocular On Reproductive system:
17- Conjunctival injection & IOP Reduced fertility in chronic users is a result of :
(Ac=ng on CB1 receptors in the ciliary body) Oligospermia, Abnormal menstruation, and Decreased
Decreased ovulation
10- Transient psychotic episodes - Males: ↓ testosterone levels & sperm count
Higher Doses - Females: ↓ FSH & LH, and affect the menstrual cycle.
1- Pseudo hallucinations - Crosses placental barrier : causing :
Lower birth weight.
3- Disorganized thoughts childhood cancer. Read withdrawal
4- Confusion symptoms
Neurobehavioral Effects
5- Poor cognitive performance (after 48 hr.. of cessation )
1- underachievement from the lectu
lecture.
6- Complex motor functionss & the ability
a to track objects are impaired . cognition and learning
2- deficits in cogniti
energy
3- and lack of energ
 Salicylates Pathophysiology : Renal
Metabolic acidosis : 3 criteria can rapidly indicate salicylate
• Renal tubular damage proteinuria poisoning are :
Toxic Dose : 1- Metabolic degradation of aspirin ( salicylic acid ). with Na & water retention.
retention
2- Renal dysfunction retention of acidic metabolites • Inappropriate secretion of ADH – Positive urine ketones
• Higher than 30 mg/dL symptomatic. 3- Stimulate lipid metabolism ketones & organic acids (B-hydroxybutyric
hydroxybutyric acid, Na & water retention. • Increase in fatty acid metabolism
• Acute single ingestion : aceto-acetic acid & acetone).
> 150 mg/kg mild toxicity. nhibition of prostaglandins necessary – Whole blood glucose and electrolyte
• Inhibition
4- Inhibit aminotransferases circulating
ng amino acids & aminoaciduria. to maintain renal blood flow
150-300 mg/kg moderate determination
>300-500 mg/kg severe 5- Uncouple le oxidative phosphorylation accumulation of pyruvic & lactic acids. reversible acute renal failure.
failure • Shows decreased bicarbonate and
>500 mg/kg poten=ally lethal Respiratory acidosis : other electrolyte and glucose
• Chronic ingestion : 1- Due to respiratory depression following respiratory stimulation. abnormalities
100 mg/kg/day for 2days Respiratory Alkalosis GIT effects
• Direct irritative effects nausea & – Whole blood ABG
- Aspirin stimulate the respiratory center hyperventilation respiratory alkalosis
vomiting • Shows characteristic acid-base
acid
- Increased excretion of HCO O3 (to compensate respiratory alkalosis) renal K losses. disturbance of salicylate
ate toxicity
• GI motility and pyloro-spasm
pyloro .
N.B.(The
The respiratory center is stimulated because it reads the resulting loss of ATP as hypoxemia ). • GI bleeding 2ry to gastri=s &
ENT (Salicylism) CNS Salicylate level :
exacerbation of ulcer.
• Tinnitus First stimulate and then depress the CNS. • Mild liver necrosis , may occurs. • Ferric chloride test to the urine.
• Confusion, (Qualitative test) ,purple color change
• Vertigo Blood
indicates presence of salicylates (false
• Moderate reversible hearing loss • Dizziness, It affects both platelets & prothrombin. negative is rare).
• psychosis,
th
due to 8 cranial n. affection • Small doses bleeding time.
• Monitoring serum salicylate level,
• Convulsions & coma in severe cases. inhibit thromboxane A2 forma=on
every 2 hrs for the first 4-8
4 hrs, to
Respiration & acid-base
base balance Hyperglycemia essential for platelet aggregation reach peak level. Then every 4-6
4 h
• Hyperventilation Stimulate tissue glycolysis & • Large doses hypoprothrombinemia un=l it is less than 30 mg/dL .
• Salicylate Acute lung injury gluconeogenesis hyperglycemia Aspirin change to dicumarol like
• Arterial blood pH.
Hyperthermia substance in the intestine interfere
- Metabolic acidosis. Due to uncoupling of oxidative with Vit. K synthesis decreases
- Respiratory Alkalosis. (see above) phosphorylation prothrombin synthesis in the liver
increases PT.
Skin Hypotension
So, the
he net result of aspirin toxicity is :
- Flushing & sweating Due to sweating & vasodilatation. - Purpuric rashes
Allergy - Bleeding from nose , gastric ulcer.
• Rhinitis, Edema , Urticaria
• Bronchial edema , shock

Alcohol Ethyl Alcohol ( Ethanol )

• Ethanol is CNS depressant from
• Concentration of ethyl alcohol in:
Beer: nearly 4-5%
Wine: 10-14%
Whisky & Vodka: 30-50%
50%
Route of admin.
- Oral (drinking).
- Ethanol can also be admin. I.V
when used as an antidote for
methanol or ethelene glycol
intoxication.
In chronic alcoholics,
This pathway increases the NADH /
NAD+ ratio, changes the redox
potential of the hepatocyte and
contributes to the development of:
- lactic acidosis
- alcoholic ketoacidosis.
. In chronic intoxication,
Ethanol is the alcohol constituent of “alcoholic” beverages (beer, wines & spirits) D- Alcoholic ketoacidosis
and is a solvent commonly used in medicinal preparation.
Mechanism of action : (Ethanol has toxic effects on almost every organ system
system).
E- Other clinical effects of chronic alcoholism:-
alcoholism:
• This toxicity is related to the effect of metabolite acetaldehyde. • Liver : Fatty liver Liver fibrosis Cirrhosis
• Cardiovascular: Cardiomyopathy, arrhythmias
• At very high concentration : • Hematologic: Bone marrow depression, anemia,
Ethanol interact with and became integrated into the lipid
lipid bilayer of cell thrombocytopenia, leucopenia.
membrane increased membrane fluidity, and thereby interfered with normal
• Infectious: Cellulitis, meningitis, peritonitis, sepsis.
cellular function where ethanol act as an anesthetic
• At lower intoxicating concantration : • Metabolic : Hyperuricemia, hypoalbuminemia,
hypoalbumi
Although almost every neurotransmitter system is affected by ethanol, there do hypocalcemia, hypoglycemima, hypothermia
not appear to be specific
ific receptors for ethanol. • Nutritional: Pellagra, beriberi.
- GABA is an inhibitory neurotransmitter ethanol potentiate its activity • Psychiatric: Depression, personality disorder , suicide .
- Glycine, another inhibitory neurotransmitter also influenced by ethanol .
- Glutamate iss an excitatory neurotransmitter
neurotransmitte ethanol inhibit it’s function, C- Alcohol withdrawal :--
- Ethanol influences the activity of adenylate cyclase which regulates synthesis
of (c-AMP)
AMP) which regulates many intracellular functions . 1- Minor:-
GIT - Symptoms begin 6 to 8 h after reduced alcohol intake may last for
In acute intoxication: several days.
Nausea, vomiting and abdominal pain . - Minimal sympathetic symptoms ( tremor, anxiety, nausea, vomiting,
flushed skin, sweating, tachycardia or hypertension) .
Abdominal pain is related to esophagitis, gastritis, pancreatitis, hepatitis or cirrhosis. 2- Moderate:-
CNS - 24-36 h after reduced ethanol intake .
1- Acute intoxication/ altered mental status (AMS). (AMS) It act as sedative hypnotic
hypnotic. - Increased sympathetic symptoms , with +
- Low BACs are associated with euphoric feelings - Hallucination (visual, auditory, tactile, olfactory) .
- At higher serum levels there is increasing CNS depression with : 3- Severe:-
Slurred speech - Altered perception of the environment - Ataxia – Nystagm
ystagm - Increased sympathetic symptoms,
symptoms with +
- At very higher serum levels : coma & respiratory depression . - Fever, Altered
ltered mental status or convulsion .
Hypoglycemia is another manifestation of acute intoxication, and may be associated a- Seizures
with malnutrition in the chronic alcoholic. • Tonic-clonic
Tonic convulsions
• 7-48
48 h after cessation of alcohol intake.
2- Wernicke-Korsakoff
Korsakoff syndrome :-
:
b- Delerium tremens (DTs)
- Ethanol interferes with thiamine (vitamin B1) absorpMon , ethanol induce hepatic
disease leads to: • Autonomic hyperactivity with fever, tachycardia
• decreased thiamin
iamin storage & tachypnea, hypertension
• decreased activation to coenzyme
coenzyme thiamine pyrophosphate.
- Manifested by : (respond to thiamin therapy )
• Ocular disturbance (diplopia, blurred vision, bidirectional nystagmus),
• Ataxic
taxic gait and confusion.
- Also, Thiamine deficiency may leads to wet beriberi cardiomyopathy.

3- Korsakoff psychosis : (not respond to thiamin)

• Poisoning is usually characterized
by a latent period (40min to 72 h),
during which no symptoms are
observed .
• This phase is followed by the
development of :
- acidosis &
- visual symptoms.
- Permanent state of cognitive dysfunction characterized by the inability to
remember recent events or learn new information ( retrograde / anterograde amnesia).
Methyl Alcohol ( Methanol )
- Methanol is a colorless liquid, volatile at room temperature, methanol itself A. History.
is harmless, but its metabolites are toxic • Methanol is sometimes ingested as a substitute for ethanol, when
- Methanol is a common component of gasoline, antifreeze, photocopying ethanol is either too expensive or unavailable.
fluid, perfume, paint solvent and household cleaners. • Methanol poisoning has also occurred by cutaneous absorption and by
inhalation.
Mechanism of action :
- Methanol metabolism involves the formation of formaldehyde by an B. Physical examination.
oxida=on catalyzed by alcohol dehydrogenase. (formaldehyde is 33 1- Decreased visual acuity:
acuity
times more toxic than methanol) - peripapillary edema.
- Formaldehyde Is rapidly converted to formic acid , which is 6 times - Vertical & rotatory nystagmus, optic disc pallor & decreased
more toxic than methanol. pupillary response to light.
- may irreversible visual loss or blindness.
- Formic acid : 2- Breathlessness.
• is responsible for ocular toxicity . 3- Severe abdominal pain : Anorexia, nausea & vomiting .
It inhibits cytochrome oxidase in the optic nerve 4- Neurological symptoms : Seizures, coma & basal ganglia lia infarct.
disturbing the flow of axoplasm. 5- CNS depression : Coma, confusion, slurred speech .
6- Bradycardia : myocardial
ardial depression & hypotension
• Both formic acid & lactic acid are responsible for:
for
(signal of severe intoxication)
- metabolic acidosis &
7- Nuchal rigidity and
nd men
meningeal signs.
- decrease in plasma bicarbon
bicarbonate.
 Digitalis
- They are cardiac glycosides
- Most
ost come from the (foxglove) plant.
- The drugs have a low therapeutic index
Factors affecting distribution:
• Hypokalemia, (With
With thiazide or loop diuretics
diuretics)
• Hypomagnesemia, and
• Hypercalcemia :
digoxin binding to Na/k ATPase Results :
sensitivity to digoxin.
• Hyperkalemia inhibits binding
(K reverses toxicity in hypokalemic patient).
• Age & hypothyroidism :
digoxin binding sites ?
• Pregnancy & hyperthyroidism:
digoxin binding sites
• Hypoxia,
• Renal failure,
• Myocarditis
• Drug interactions :
Quinidine - Verapamil - Amiodarone
miodarone
Organophosphates
It's potent
otent cholinesterase inhibitors
High toxic agricultural
insecticides parathion
Intermediate animal insecticides
Low toxic household use malathion
Fatal oral dose:
Parathion 0.05 g/ 70 kg
Malathion 60 g/ 70 kg
Corrosives
Factor contributing to injury :
1- pH and concentration :
Esophagus begins to ulcerate at pH
12 . Acids with pH 2 or less cause
significant injury .
2- Volume of caustic ingested :
Large volume result in greater direct
injury and potential for perforation &
injury to other organ system. High
volumes enhance the risk of emesis,
causing further damage.
3- Contact time :
• Acid & alkalies with high viscosity
have prolonged tissue contact and
amplification of injury.
• The passage of caustic through
areas of normal anatomic narrowing
increase contact time in these areas.
• Crystal result in penetrating injury
that remain localized .
• Liquid formation increases the
contact time of the stomach
4- Preexisting state of the stomach :
• The presence of fluid in the stomach
affords immediate dilution effect on the B. Symptoms :-
ingested caustic .
•The presence of solid food in the
stomach induce buffering effect on
acid or alkalies and help to prevent
damage .
1) Ingestion of acid on an empty stomach
damage of the lower two-third of the
stomach, sparing only the fundus.
(2) Ingestion of acid on a full stomach
harm only the pylorus and lesser curvature.
Botulism
Gram +ve anaerobic bacillus that
release neurotoxin “Botulin”.
Toxin types:
• • Weakness,
A / B / C alpha / C beta
• D / E / F / G
• Food contaminated with C. botulinum
toxin types A and B often does not
look or smell normal and appears
putrefied because of the action of
proteolytic enzymes.
In contrast, because toxin type E
organisms are saccharolytic and not
proteolytic,
ytic, food contaminated with
toxin type E may look and taste normal.
Physical properties:
- Spores withstand 100 c for hours.
- Toxins are heat-labile and
destroyed
royed by boiling for 10 min. or
hea=ng at 80 c for 30 min.
Mainly not exposed to heat:
1. Salted fish “Fesikh”
2. Honey
3. Uncooked cold meat “Beef”
4. Home canned food
Mechanism of action Clinical manifestation of toxicity
1- Regulation of Ca concentration: Acute Chronic
+
- Inhibiting the ability of the myocyte to actively pump Na from the cell
+
• (Brady-dysrhythmias) • arrhythmia
(membrane-bound Na-K-ATPase
ATPase pump ) decrease the Na concentration • GIT manifestations • GIT manifestations
+ 2+
gradient consequently, the ability of the Na /Ca -exchanger
exchanger to move • lethargy, confusion, and • Visual (yellow vision)
calcium out of the cell.
weakness • Confusion, Delirium,
+
- Further, the higher cellular Na is exchanged by extracellular Ca by the
2+
• Hyperkalemia, why? hallucination
+ 2+
Na /Ca -exchanger increasing intracellular Ca .
2+
• Hypokalemia, why?
• Desited: + intropic effect (Increased
Increased contractility of the cardiac muscle)
• Side effect : Tachyarrhythmias
2- Decreased heart rate, by 2 mechanisms : • Cardiac effects:
- Increased myocardial contraction leads to a decrease in end-diastolic
diastolic volume, - The common cardiac side effect is arrhythmia,
thus increasing the efficiency of contraction (increased ejection fraction ) - Characterized by : slowing of atrioventricular conduction associated with
resulting improved circulation leading to reduced sympathetic activity, which atrial arrhythmias.
then reduces peripheral resistance Together, these effects cause a reduction in
heart rate. • Gastrointestinal effects:
- Vagal tone is also enhanced,
ed, so the heart rate decreases and myocardial oxygen Anorexia, nausea, and vomiting.
demand diminishes.
• Central nervous system effects:
Results :
• Desited: heart rate myocardial oxygen demand diminishes . Headache,
eadache, fatigue, confusion, blurred vision, alteration of color perception,
• Side effect : Bradyarrhythmias and halos
los on dark objects.
Mechanism of action : 1- Muscarinic Effects (DUMBELSS) see the scheme
2- Nicotinic Effects (MMATCH) see the scheme
• Organophosphorous compounds bind to and inhibits acetylcholinesterase
3- CNS effects (2C 2D D SHM) :
overabundance of acetylcholine in the synapse.
synapse
C onfusion C oma D isorientation
• By time the compound undergoes a conformational change (aging) renders the
D epression : Respiratory & circulatory centers
enzyme irreversibly resistant to reactivation.
S eizures
H eadache
• Carbamate compounds unlike organophosphates, are transient cholinesterase
M alaise
inhibitors.
Mechanism of action : Time course of injury
a. Alkaline agents : 1- Acute inflammatory stage :- :
- roduce tissue injury by liquefaction necrosis, which devastating and
Produce - During the first 4 to 7 days.
difficult to treat. - First, Edema and Erythema
rythema , followed by thrombosis & cellular necrosis .
- Fat & protein are saponified, resulting in deep tissue destruction. - Perforation & Acidosis
cidosis may occur .
- urther injury is caused by thrombosis of blood vessels.
Further Early endoscopy is recommended within 24 to 48h .
2- Granulation stage :-
b. Acids : - Starts at about day 4 and ends at 7 days aGer inges=on .
- Cause damage to the tissue by coagulation necrosis, resulting in - Fibroplasia results in the formation of granulation tissue with the lying
protective eschar. down of collagen over the denuded areas of mucosal sloughing.
• Coagulation of tissue impedes penetration of acid to deeper
layers. 3- Perforation :-
First, damage is superficial resulting in sloughing of extensive - between days 7 & 21 but may occur earlier.
areas of the stomach lining with resulting perforation . - The tissue is the weakest & the risk of perforation is highest .
• Despite the eschar,
eschar the acid can be absorbed resulting in 4- Cicatrization stage :
systemic acidosis & decreased cardiac output. - Starts at 3 weeks and may persist for years.
- Dense fibrous tissue formation occurs at variable rates .
• Hydrofluoric acid is unusual in that it cause liquefaction necrosis .
- Overproduction of scar tissue results in stricture formation .
Clinical picture Course of complication
A. History :-
1-Acute complications :-
• Trying to determine the following :
a. Type & concentration of caustic ingested a. Upper airway obstruction and injury .
b. GI hemorrhage .
b. Time of ingestion .
c. Quantity of agent ingested . c. Esophageal & gastric perforation .
d. If accidental versus intentional . d. Sepsis .
• Should determine if : a. Vomiting has occur Tracho
e. Tracho-bronchial necrosis, atelectasis.
b. A diluent has been administered .
2- Peri-esophageal
esophageal complications secondary to perforation
• Attempts should be made to obtain the product container .
a. Mediastinitis
b. percarditis
1- Pharyngeal pain .
c. pleuritis.
2- Dysphagia, sridor, drooling, and vomiting.
3- Chest & abdominal pain, respiratory distress and shock reflect severe tissue Tracheobronch
d. Tracheobronch-oesophageal fistula
damage . Esophago
e. Esophago-aortic fistula .
- A caustic ingestion in adults is usually intentional and severe .
3- chronic complications`:--
C. Physical examination :-
a. Esophageal obstruction .
1- Erythema, edema and erosions of the oropharynx.
2- Psedomembrane formation may be present over the mucosa . b. Pyloric stenosis .
3- Hypotension, tachycardia and changes in mental
ment status. c. Squamous cell carcinoma of the esophagus.
4- Respiratory distress . d. Vocal cord paralysis .
5- Sepsis may develop secondary to bacterial colonization of devitalized tissue.
Pathophysiology: I. Classic (Adult) botulism:
The human oral lethal dose is 1 μg/kg from the toxin. • Symptoms & signs develop within 12 – 36 hrs aGer inges=on.
• Severity of disease depends on type of toxin (type A gives most severe picture).
• Botulinum toxin binds to specific receptors on the mucosal surfaces of gastric 1) Initial vague & GIT symp. 2) Neurological manifestations
and small intestinal epithelial cells where endocytosis followed by
• Malaise, • Cranial nerve palsy:
transcytosis permits release of the toxin on the serosal cell surface.
- III, IV, VI, VII, IX, XI, XII.
• Release into the systemic circulation allows uptake into presynaptic
• Dizziness, - Abducens (VI) or oculomotor (III) nerve palsy
acetylcholine containing neurons.
(frequently resulting in strabismus).
• As a result, cholinergic transmission at all acetylcholine-dependent
dependent synapses • Diplopia & blurred
• Dysphonia , Dysarthria, Dysphagia.
in the peripheral nervous system is impaired. vision
However, there is no effect on central nervous system or axonal conduction. • Bilateral symmetrical descending flaccid paralysis of:
• Diarrhea or constipation 1. Limbs
- Toxins are distributed to target sites via hematogenous dissemination • Nausea, vomiting,
2. Resp. muscles & diaphragm
- Toxins act on the presynaptic part of neuromuscular junctions leading to • No sensory loss
decreasing the amount of ACH release 3) Anticholinergic manife. • Normal mental status
see the scheme • Death from respiratory failure
II. Infant Botulism : III. Wound botulism :
• Affected children are younger than 1 year of age (usually 1–33 months). • The “classic” presentation of wound botulism is a patient injured in a
• Constipation is the first sign of infant botulism, followed by motor vehicle crash who sustains a deep muscle laceration, crush injury, or
- Hypotonia, compound fracture treated with open reduction.
- Generalized
eneralized Weakness, • The wound iss typically quite dirty and usually associated with inadequate
- Poor sucking, débridement,, subsequent purulent drainage AND local tenderness.
tenderness
- Weak cry.
• Ophthalmoplegia, Clinical picture:
• Loss of facial grimacing, • 4 to 18 days later cranial nerve palsies AND the other neurologic findings
• Dysphagia, typical of botulism may appear.
• Diminished gag reflex, • Fever associated
ed with tthe tissue infection.
• Poor anal sphincterr tone, • Typical gastrointestinal
intestinal signs of food-related botulism are usually
usuall absent.
• Respiratory failure are also present, fever & enteric symptoms ms do no
not occur.