Toxology Source: FOMSC Vital Functions Bradycardia (PACED) • Propanolol (β-blockers), phenylpropanolamine (α-agonists) • Anticholinesterase drugs(OPC) • Clonidine, CCBs • Ethanol / alcohols • Digoxin, Darvon (opiates) Tachycardia (FAST) • F ree base (cocaine/stimulants) • A nticholinergics, antihistamines • S ympathomimetics • T heophylline (methylxanthines) Hypotension (CRASH) • C lonidine • R eserpine (antihypertensives) • A ntidepressants • S edative hypnotics • H eroin (opiates) Hypertension (CT-SCAN) • C ocaine • T heophylline, thyroid supplements • S ympathomimetics • C affeine • A nticholinergics, amphetamines • N icotine Hypothermia (COOLS) • C arbon monoxide • O piates • O ral hypoglycemics/insulin • L iquor (EtOH) • S edative hypnotics Hyperthermia (NASA) • N euroleptic malignant syndrome • A ntihistamines • S alicylates, sympathomimetics, serotonin syndrome • A nticholinergics, antidepressants Seizures (OTS SCAMPBELL) • O rganophosphates • T ricyclic antidepressants • INH, insulin • S ympathomimetics • C amphor, cocaine • A mphetamines, anticholinergics • M ethylxanthines • P hencyclidine • B enzodiazepine withdrawal, botanicals • E thanol withdrawal • L ithium, lidocaine • L ead, lindane Toxic Causes of Coma 1- Volatiles : • Methanol , Ethanol , cyanide , CO 2- Non- volatiles : • Atropine , TCA , Cocaine , CNS sympathomimetics , amphetamines , nicotine , organophosphates , carbamate , salicylates. 3- Sedatives & hypnotics : • Barbiturates & Benzodiazpine 4- Narcotics : • Opium , codeine , morphine , methadone , heroin 5- Metals : • Lead, iron encephalopathy 6- Secondary to toxins effect : • Hypoglycemia m hypoxia , hepato & nephro-toxicity Poison Organophosphate Acetaminophen Digoxin Opioids Alcohol Ethanol Methanol Anticholinergics TCA , Cocaine , Salicylates Benzodiazepines Iron Arsenic, mercury, lead CU Lectures & Osama R. El-Ghamry's Book Emesis - Centr - Cent Plant Gastric lavage Insertio waching Activated charcoal Is comb treated 2000 cm MDAC 1- Inte ent 2- GIT Cathartics (purgation) • Salin Mg sul • Sacch Whole bowel irrigation Consist cleansi glycol ( isotoni Availab • • 1) GUT Indicat 1. Drug • • • 2. Subst MDAC ( Gut dialysis ) 2) KIDNEY Objectiv ionic for resultin renal tu Indicat • • • • PH alteration & forced diuresis 3) BLOOD Indicat • • • • • • • Dialysis A) Hemodialysis B) Peritoneal dialysis, If : • Renal failure • Bleeding disorders • Vascular access problems • HD & HP not available or contraindicated Hemoperfusion Indicat • Plasma Exchange & Plasmaphoresis • • Chelators • 1 Antidotes Antidote Atropine Initial a Dose ca Pralidoxime N-acetyl cystenine loading addi=o Digoxin specific FAB fragments If dose Naloxone 0.4- 2 m Thiamine 100 mg - Ethanol 100% - Fomepizole -PO 1m -15 mg Physostigmine - adults - childr Na bicarbonate Flumazenil Deferoxamine 15 mg/ vin rise Dimercaprol (BAL) Deep IM then/1 k . GIT ral stimulation: Apomorphine • Stimul • 5mg S tral & peripheral: Syrup of ipecac. t alkaloid consists of: • Emetine & • Cephaline Action: • E • L Dose : • 3 on of tube into stomach and g it with water & saline. Amount & c N.B. Tape w bustion of organic material & d to increase surface area (1000- m 2) Action: • I • I Dose : • 1 • F s erruption of enterohepatic , teroentric circulation T dialysis . 0.25 : Dose 0.25 ne cathartics : lphate , Mg citrate , Na sulphate harides: sorbitol Action : • C i G Dose: • M • S ts of using surgical bowel- ing solution polyethylene (PEG), 60 gram in a balanced ic electrolyte salt solution. ble as : • Golytely • Colyte • C g Procedure • I • T • E tion : g remaining in the gut for long time: Sustained release preparation: T heophylline Concretions: S alicylates , Phenobarbitol Slowing GIT motility: A nticholinergic. tances with EHC: D igitalis , T CA , S alicylates ve is to alter PH making the toxin in polar or rm which is unable to cross cell membranes ng in reabsorption & enhanced excretion in ubules tions : (PSMC) P henobarbital, S alicylates, M ethotrexate C hlorpropamide, tions: Patients unstable despite maximum supportive therapy Renal compromise WHEN Toxins metabolized or excreted by kidneys Hepatic compromise WHEN Toxic substance metabolized by liver Blood Level of toxin is lethal Toxicity of agent of delayed toxicity Toxicity agent metabolized to more toxic fo Dialyzable drugs . tion The same as hemodialysis but because 1- Hight M.W. - Hig Replacement of plasma with protein so Effective for toxins that : - have high pr Compounds which unite with absorbed 1- Iron toxicity Deferoxamine (desfer Dose atropine dose (IV or IM)1-2mg (adult) 0 an repeated every 10 min. till Clear chest o 1-2g (adult) 25-50 mg/kg (childr g dose of 140 mg/kg followed by 70 mg/kg onal doses, giving a total of 72 hrs of therap e ingested in known : No. of vials=(Ingested X 0.8) / 0.6 mg (max 10mgin adults) / 0.01/kg (child) IV g IV l/kg loading dose then 0.5ml/kg/4hrs to mainta g/kg initial dose then repeated s: 2 mg in 100 ml normal saline slow iv inf ren: 0.02 mg/kg. 1 – 2 mEq/kg bolus 0.2 mg IV/3-5 min. (max. dose: 5m /kg/hr slow IV infusion (max. 6 gm) or disa e color of urine. M oily solu=on, 2-5 mg/kg/dose/4-6h for 2 12h for 7 days. T Decontamination late C.T.Z of medulla oblongata S.C. / ac=on: 3-5 min. Early vomi=ng (within 30 minutes): due to the direct local irritant action of on Late vomi=ng (aGer another 30 minutes) : due to central stimulation of the (C.T.Z) 30 ml for adults , 15 ml for children & 5- 10 ml f • If voming does not occur aer 30 min • If still no vomiting, gastric lavage shoul ipecac from the stomach (emetine is ca composition of fluid: • 10 ml/kg/ lavage of 0.9% saline- up to • Con=nue lavage =ll clear (3000ml). water lavage might produce hyponatremia. It works by adsorption of toxins from the gut be It interrupt the enterohepatic & circulation of t 1g / kg Then 0.5g/kg at 4-6 hr intervals Freshly repared by adding powder to 250 ml wa slurry then taken orally or via nasogastric tube. (oral) r 4h - 0.5 gm/kg/1 – 5 (NGT) 0.5 gm/kg/hr – 5 Catharsis is produced by osmotic retention of flu intrluminal bulk of fluids, activates GIT motility GIT contents Mg sulphate: adult 15 – 20 gm Sorbitol : adult 1ml/kg ( 70% soul=on) Consists of using surgical bowel-cleansing glycol (PEG),60 gram in a balanced isotoni e: It is administered by nasogastric tube or o The solution is administered at a rate of : • 0.5 L/h in c • 2 L/h for a End point when the stools are clear Enhancement of elemination e. (oral) 4hr - 0.5 gm/kg/1 – 0.25 : Dose (NGT) 0.5 gm/kg/hr – 0.25 PH alteration by alkalinization or acidifi Alkalinization of the urine • NaHCO3 (1-2mEq/kg) is mixed in 5 % saline (15ml/Kg) infuse i.v. over 3 to 4 • to maintain urine volume at 3-6 ml/Kg 7.5 to 8 orm Drugs with delayed toxicity • Paracetamol • Ethanol • Organophosphate Drugs metabolized to more toxic drug • Methanol • Ethylene glycol • Paraquat e the charcoal can adsorb the toxin , hempe gh protein binding - Poor water solubility olution Plasma exchange / Replacemen rotein binding & - poorly dialyzed or filte d poisons ( Metallic poisons ) to form Chel ral) : has high affinity to ferric iron & hemo • Rationale: Hypo • D50W ( 50 -100 • DDx – hypoglyc - Tox insu - Non-tox • Cautions : diabe • Co-factor for py dehydrogenase • Decreased leve - chronic liv malnutritio • Deficiency - We - Ophthalmo • Dose: 100 mg IV • Pure opioid ant • Diagnostic and t • Dose: 0.4- 2 mg 0.05mg/kg(child) or ATROPINISATION. ren) g q4h for 17 py 6 V, IM, SC ain level at 100mg/dl fusion over 10 min. mg) appearance of 2 days , Contraindic 1- Organopho 2- Phenol 3- Iron 4- Corrosives n gastric mucosa, for infants (6 months & 2 y.) nutes, the dose is repeated. ld be carried out to remove ardiotoxic component). o 400ml in adults. 1- Organopho 2- Corrosives efore absorption toxic metabolites. ater and shaken to form 1- Iron 2- Lithium 3- Corrosives uid in GIT with increases leading to propulsion of 1- Iron 2- Corrosives solution polyethylene ic electrolyte salt solution orally. children < 5 years & adults. n ) ) Substances poorly adsorb C austics & corrosives H ydrocarbons A cids & Alkalies & A C hlorine, Iodine L ithium I ron C yanide E thylene glycol fication of urine. dextrose/0.5 4 h g/h & urine PH at Dialyzable drugs (LET ME • Lithium • Ethylene glycol • Theophylline • MEthanol • Salicylates • Atenolol • Valproic acid • Potassium, Par gs erfusion can be performed in toxins chara y nt of plasma with crystalloid solution pl ered as phenytoin lates which are non toxic & rapidly excrete osiderin (doesn't affect trasferrin , cytoch Coma Cocktail 1- Dextrose oglycemia common cause of ↓LOC 0cc IV ) or D25W 2-4cc/kg in peds cemia : ulin, oral hypoglycemic, EtOH, salicyla sepsis, hyperthermia, hepatic failure etic or hyperosmolar pts, cerebral infa 2- Thiamine yruvate dehydrogenase, and α-ketoglu e.(Vit B1) els in: ver ds, folate deficiency, malabsorption on, EtOH intake ernicke’s encephalopathy : oplegia,Nystagmus, Ataxia, Altered m V 3- Naloxone tagonist, used for reversal of acute into therapeutic g (max 10mgin adults) / 0.01/kg (child) 4- Oxygen GIT decontam not indicated because it's a rapidly cated with : osphate osphate bed : ( CHACLICE ) s Alcohols E SAV P) l raquat acterized by: lasmaphoresis. ed in urine. hrome & heme ) ates e, myxedema arct utarate n, mental status oxication ) IV, IM, SC mination d in Ethanol absorbed
10
Embed
Toxology - MedicoNotesmediconotes.com/freenotes/clinical/Summaries_of_Toxology.pdf · N.B. Tape water lavage might produce hyponatremia. adsorption of toxins from the gut before absorption
This document is posted to help you gain knowledge. Please leave a comment to let me know what you think about it! Share it to your friends and learn new things together.
2. Substances with EHC: Digitalis , TCA , Salicylates
Objective is to alter PH making the toxin in polar or
ionic form which is unable to cross cell membranes
resulting in � reabsorption & enhanced excretion in
renal tubules
Indications : (PSMC)
Phenobarbital,
Salicylates,
Methotrexate
Chlorpropamide,
Indications:
Patients unstable despite maximum
supportive therapy Renal compromise WHEN
Toxins metabolized or excreted by kidneys Hepatic compromise WHEN
Toxic substance metabolized by liver Blood Level of toxin is lethal Toxicity of agent of delayed toxicity Toxicity agent metabolized to more toxic form
Dialyzable drugs .
Indication
The same as hemodialysis but because the charcoal can ad
1- Hight M.W. - High protein binding
Replacement of plasma with protein solution
Effective for toxins that : - have high protein binding &
Compounds which unite with absorbed poisons ( Metallic poisons ) to form
1- Iron toxicity � Deferoxamine (desferal) : has high affinity to ferric iron & hemosiderin (doesn't affect trasferrin , cytochrome & heme )
Dose
nitial atropine dose (IV or IM)� 1-2mg (adult) 0.05mg/kg
Dose can repeated every 10 min. till Clear chest or
1-2g (adult) 25-50 mg/kg (children)
loading dose of 140 mg/kg followed by 70 mg/kg q4h for 17
addi=onal doses, giving a total of 72 hrs of therapy
edema of vipers • Antibiotics and antitetanic serum
Care of the wound • Cleansing, debridement of n
vascular impairment follow
Treatment Supportive & Symptomatic treatment
Prevention of further exposure
ComaCocktail if coma.
Monitoring of cardiac functions.
ComaCocktail if coma.
benzodiazepines or barbiturates.
reat. Phosphokinase & urine myoglobin level. IV fluids, alkalization of urine & mannitol to avoid acute tubular necrosis.
rarely needs intervention. cold compresses
catheterization
Folinic acid (1mg/kg i.v. up to 50 mg/dose) followed by folic acid are
needed for conversion of formic acid to co2 and water.
is a strong inhibitor of alcohol dehydrogenase (15mg/kg).
: for dehydration.
: should be used to correct acidosis. (1 to 2 mEq/kg)
If seizure occur diazepam 5 to 10 mg i.v. over 2 to 3 min repeated every 10 to 15 min
as needed to a maximum of 30 mg.
alcoholic ketoacidosis by dextrose . Hypokalemia or hypomagnesemia should be corrected.
Diazepam 5 to 20 mg i.v. every 4 h in mild symptoms.
Diazepam 10 to 20 mg i.v. every 20 min un=l moderate symptoms resolve. Diazepam 10 to 40 mg i.v. every 20 min un=l severe symptoms resolve up to 200mg total dose.
Cardiovascular support - Control seizures
wash with undiluted polyethylene glycol or copious amount of water
remove from contaminated area & given 100% humidified oxygen
resuscitation and removal of the offending agent.
Obtain empty bottles and calculate amount of elemental Fe ingested
Deferoxamine
Intracellular Fe outside mitochondria.
mitochondrial free iron and further preventing lipid peroxidation
(poorly absorbed from GIT), IV is the preferred.
( max. 6 gm ) un=l urine returns to normal color or
+Deferoxamine = Ferrioxamine
Ferrioxamine excreted in urine (also dialyzable)
up to 1 gram
“vinrose”color to urine Compare color of urine pre and post Deferoxamine
If test Positive, start chelation
If test Nega=ve &no symptoms for 6hrs, pta=ent may be discharged
Negative Deferoxamine test by itself does not rule out Fe toxicity
Dose: 1 vial IM & 1 vial IV (A dose/ 4hrs if serum toxin persists
Snake Bite
Immobilization of the affected limb Light tourniquet may be applied proximal to site of the bite
It neutralizes the venom but don't reverse local injury It should be given within the first 4 hours to prevent local injury Skin sensitivity test must be done before administration.
to be repeated according to the severity
It is given in normal saline up to 1: 1 dilu=on .
IV Fluids for hypotension Blood for bleeding and hemolysis
Fresh frozen plasma to replenish coagulation factors Artificial ventilation for the paralytic syndrome of Cobra or the pulmonary
Antibiotics and antitetanic serum
ment of necrosed tissues and fasciotomy if peripheral
nt follow limb edema and compartment syndrome.
Treatment (don’t forget antidotes)
GIT decontamination
1- Activated charcoal.
- Emesis &
- Gastric lavage
are contraindicated
IV fluids, alkalization of urine & mannitol to avoid acute tubular necrosis.
1- Activated charcoal
repeated doses of
prevent further absorption.
2- Gastric emptying procedures
are useful even up to 12 hrs
after ingestion.
(due to slowed GIT absorption).
acid are
is a strong inhibitor of alcohol dehydrogenase (15mg/kg).
If seizure occur diazepam 5 to 10 mg i.v. over 2 to 3 min repeated every 10 to 15 min
Preventing further absorption
1- Emetics
2- Gastric lavage
Hypokalemia or hypomagnesemia should be corrected.
Diazepam 10 to 40 mg i.v. every 20 min un=l severe symptoms resolve up to 200mg total dose.
Gastric decontamination
NOT INDICATED
because ethanol absorbed rapidly
N.B. It is poorly absorbed to activated charcoal
BUT If ethanol intoxication is associated
with another toxic agent decontamination
and activated charcoal are indicated.
Control seizures
wash with undiluted polyethylene glycol or copious amount of water
100% humidified oxygen
1- Gastric lavage
Repeated lavage if there is no
esophageal injury followed by
administrated of olive oil or
vegetable oil and can followed
by 2- Cathartic
NO Emetics
r preventing lipid peroxidation
IV is the preferred. ( max. 6 gm ) un=l urine returns to normal color or
If test Nega=ve &no symptoms for 6hrs, pta=ent may be discharged
1- Gastric lavage :
preferred method
2- Whole Bowel Irrigation
with Poly ethylene glycol (GoLytely)
to remove iron tablets from gut
- Adults �1.5-2.0 liters per hr.
- children �25 ml/kg/hr
- Con=nue for 5 hours
Gastric lavage with Bicarbonate ,
Phosphate or Deferoxamine not
recommended (why ?? )
N.B. • Ipecac is less favored agent.
• No activated charcoal (Poor Fe
binding) • No emetics
• No cathartics
A dose/ 4hrs if serum toxin persists)
1- Gastric lavage
2- Emetics
ic syndrome of Cobra or the pulmonary
ipheral
A- First aid measures
B- At hospital I- Stabilization of the patient
II- Antidote (Best given in the first 4 h but can s=ll be given as late as 24 hours
Indications: All children, and senile patients Adults presenting with any of the systemic
Patients with previous cardiovascular disease, hypertension or diabetes
Dose : Adult : 3 - 5 amp slow IV or IM aGer nega=ve skin sensi=vi
minutes if signs still progress or do not regress
Pediatric: The same dose as adults (Dose is not related to
power of the circulating venom)
III- Supportive treatment
- Pain killers : NSAIDs & Local anesthesia.
- Corticosteroids:
Indications : Stridor , Myocarditis
- IV vasodilators (Na nitroprusside, hydralazine or prazocin
- Mechanical ventilation :
Indications : Respiratory failure, Non cardiogenic pulmonary edema in which PEEP mode is used.
- Dehydration, hypotension and shock
- IV fluids
- Dobutamine if cardiogenic sho
- Anticonvulsants e.g. diazepam - Malignant hyperthermia : Cooling meas
GIT decontamination Enhancement of elemination
Activated charcoal.
are contraindicated
Activated charcoal &
repeated doses of AC to
prevent further absorption.
Gastric emptying procedures
en up to 12 hrs
(due to slowed GIT absorption).
Preventing further absorption by:
Hemodialysis. Indication
• Blood methanol level is 25 mg/dl
or severe acidosis. • Persistent fluid and electrolyte
disturbances despite treatment.
• Visual symptoms, or renal failure.
There is no role for peritoneal dialysis or
hemoperfusion in the management of
methanol poisoning.
Gastric decontamination
NOT INDICATED
ethanol absorbed rapidly .
poorly absorbed to activated charcoal
If ethanol intoxication is associated
another toxic agent decontamination
and activated charcoal are indicated.
Hemodialysis.
Gastric lavage :
Repeated lavage if there is no
esophageal injury followed by �
olive oil or
and can followed �
NO Emetics
- Treat acid-base disorders
- Treat methemoglobinemia:
If > 30% → ingest methylene blue
If > 70% → exchange transfusion
method
Whole Bowel Irrigation
with Poly ethylene glycol (GoLytely)
to remove iron tablets from gut
2.0 liters per hr. 25 ml/kg/hr
Con=nue for 5 hours
Gastric lavage with Bicarbonate ,
Phosphate or Deferoxamine not
(why ?? )
Ipecac is less favored agent.
No activated charcoal (Poor Fe
Dialysis
Scorpion Sting
Best given in the first 4 h but can s=ll be given as late as 24 hours ) :
All children, and senile patients Adults presenting with any of the systemic
Patients with previous cardiovascular disease, hypertension or diabetes
5 amp slow IV or IM aGer nega=ve skin sensi=vity test to be repeated every 30
signs still progress or do not regress The same dose as adults (Dose is not related to body weight but to neutralizing
power of the circulating venom)
Local anesthesia.
Myocarditis , Non cardiogenic pulmonary edema, Cranial palsy
Na nitroprusside, hydralazine or prazocin): To control hypertension.
Non cardiogenic pulmonary edema in which PEEP mode is used.
Dehydration, hypotension and shock
genic shock 2ry to myocardi=s complicates the picture
measures and chlorpromazine
Enhancement of elemination
Indication :
Blood methanol level is 25 mg/dl
Persistent fluid and electrolyte
disturbances despite treatment. Visual symptoms, or renal failure.
There is no role for peritoneal dialysis or
hemoperfusion in the management of
Hemodialysis.
base disorders
Treat methemoglobinemia: → ingest methylene blue → exchange transfusion
Dialysis
All children, and senile patients Adults presenting with any of the systemic manifest. Patients with previous cardiovascular disease, hypertension or diabetes
ty test to be repeated every 30
body weight but to neutralizing
, Cranial palsy
Non cardiogenic pulmonary edema in which PEEP mode is used.
picture
Digitalis
Salicylates
1- ABCS
2- GIT decontamination
3- Elimination from blood
4- Symptomatic &
supportive TTT.
Acetaminophen
1- GIT decontamination
2- Antidote
Psychotropic drugs
1- Anti-psychotics
2- Antidepressants
3- Lithium
4- Sedative &
hypnotics
- Barbiturates
- Benzodiazepines
• Assessment of the case
• Electrolyte disturbance
- Hyperkalemia (never use Calcium
- Hypokalemia
- Hypomagnesaemia: MgSo
• Manage dysrhythmia :
- Lidocaine and phenytoin are antiarrhythmic drugs of
- Severe bradyarrhythmias are treated with atropine, electrical pacing
is used in unresponsive patients
- Verapamil is useful for SVT’s
- MgSo4
- Cardioversion should be limited to patients with life
arrhythmias and used at the lowest
• Digoxin-specific antibody Fab fragments (Digibind®)
purified from sheep IgG, rapidly bind to circulating digoxin and are indicated in:
ABCS: Pulmonary edema (Intubate),
Symptomatic & Supportive Care : • Fluid/electrolyte management
- Rehydrate with 0.9% saline
- Urinary output : 2
- Be careful with
• Coma: care of coma
• Convulsions: give succinylcholine with artificial respiration & oxygen
( avoid the use of a CNS depressant)
• Hypoprothrombinemia : vitamin K , Fresh blood or platelet transfusion.
• Hypoglycemia: glucose 50%
• Hyperthermia: Sponge bath, fans, cold water submersion
• Pulmonary edema: Oxygenation , Intubation
AGer 4 hrs : Antidote : N-Acetylcysteine
Mechanism ofaction : - It acts by increasing glutathione concentration to bind the toxic metabolite
- It serves as a source of slupher , so it increases conversion of paracetamol to its
sulphate metabolite � decrease formation of other
Oral NAC dose: loading dose of 140 mg/kg followed by 70 mg/kg q4h for
I.V. NAC dose : Given if oral NAC failed
- 150mg/kg in 20 min. � then 50 mg/kg in 4 hr.
- Dura=on of I.V regime is 48 h.
A) General measures :
1- ABC & ComaCocktail if coma
2- ABG , Cardiac monitoring , Serum electroly
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
2- Hypotension: Respond to Ringer's lactate or normal saline
If failed : a adrenergic
3- Cardiotoxicity :
• Direct current cardioversion used in : SVT , VT , Torsade de points
• Defibrillation followed by lidocaine used in : ventricular fibrillation.
• Lidocaine is the 1st
line agent , if fail we use phenytoin.
4- Acute dystonia: Diphenylhydramine (Benadryl)
5- Parkinsonism: anti-parkinsonism drugs
6- NMS : Dantrolene - Bromocriptine
A) General measures : As above
B) Specific TTT :
a- Alkalinization is the first line treatment
arrhythmias & hypotension.
A bolus of NaHCO3 mEq/kg is given over several minutes.
b- Management of complicating factors :
1- CNS depression & coma � Supportive care
2- Hypotension: Respond to Ringer's lactate or normal saline
If failed : a adrenergic agonist ( Phenylephrine ).
3- Cardiotoxicity :
• Alkalinization is the most effective TTT for cardiac arrhythmias and for
sinus tachycardia with widened QRS > 0.10 second.
• Alkalinization + Pacemaker for third degree heart block.
• Drugs to be avoided
4- Acidosis : treated by alkalization of urine
5- Hyperthermia : cooling the patient.
A) General measures : As above ( + Serial estimation of lithium level )
B) Specific treatment : main line of treatment is :
- Sodium polystyrene sulfonate
- Furosamide
C) Symptomatic treatment :
1- In mild to moderate cases with serum level < 4 meq/L
• Good hydration with IV infusion of normal saline.
After the patient is rehydrated fluid administration should be
continued with half normal saline until toxicity is resolved.
• Maintenance of electrolyte
2- Severe toxicity : TTT of Coma
A) General measures : As above
B) Specific TTT :
• CNS depression.
• Flumazenil (anexate)
• Treating withdrawal
Therapeutic Drugs
never use Calcium)
Hypomagnesaemia: MgSo4 .
Lidocaine and phenytoin are antiarrhythmic drugs of first choice
Severe bradyarrhythmias are treated with atropine, electrical pacing
is used in unresponsive patients
Verapamil is useful for SVT’s
Cardioversion should be limited to patients with life-threatening
arrhythmias and used at the lowest effective energy level
specific antibody Fab fragments (Digibind®) :
purified from sheep IgG, rapidly bind to circulating digoxin and are indicated in:
( see lecture )
tends to improve as serum salicylate level
Fluid/electrolyte management : Rehydrate with 0.9% saline
Urinary output : 2-3 mL/kg/hr
Be careful with elderly/renal/cardiac patients
give succinylcholine with artificial respiration & oxygen
( avoid the use of a CNS depressant)
vitamin K , Fresh blood or platelet transfusion.
Sponge bath, fans, cold water submersion
Oxygenation , Intubation (tends to improve as serum salicylate level
Acetylcysteine (NAC)
It acts by increasing glutathione concentration to bind the toxic metabolite
It serves as a source of slupher , so it increases conversion of paracetamol to its
decrease formation of other toxic metabolite.
dose of 140 mg/kg followed by 70 mg/kg q4h for
Given if oral NAC failed (Increased risk of anaphylactic response.)
then 50 mg/kg in 4 hr. � then 100mg/kg in 16 hr.
Dura=on of I.V regime is 48 h..
if coma ( Intubation if severe R.D. / Assisted ventilation with PEEP )
With CNS depression or mild respiratory depression : Initial dose should be low 0.1 mg i.v.
depression mg i.v.
with no response aGer 2-3 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)
Clinical assessment for evidence of co-ingestions.
Patients with acute paranoia or toxic psychosis :
The drug should be stopped The progress of symptoms observed Support & gentle sedation with a benzodiazepine Heavy user may need antidepressant medication
Addiction TTT : behavioral & group therapy.
Others
Secure the patient’s airway .ageal and gastric tissue.
Monitor vital signs closely. Perforation . Preparation of the patient for surgery
Monitor fluid & electrolyte status and pH. Patient is to keep fasting until endoscopy is performed. Serial evaluation is performed .
Pain killers as morphine
Shock measures: IV fluids , Blood transfusion and crystalloids.
biotics , to guard against infection
H2 blockers or proton pump inhibitors to minimize acid secre=on
Total Parenteral Nutrition (TPN) for at least three weeks.
in severe hemorrhage & in perforation
Esophageal bypass surgery
Dilatation of esophageal strictures
Repair of bronchoesophageal fistula
Gastrotomy for feeding purposes.
� Irrigate with running tap water for 2 min.
Oxygen, aerosol thrapy with B2 s=mulant &
Drug dependence & drug abuse
good anticonvulsant activity)
Never use beta blockers as they exaggerate alpha stimulation & worsen hypertension.
maintain urine output of at least
If ingested :
1- Activated charcoal
2- Gastric Lavage
good anticonvulsant activity)
or Na nitroprusside.
rehydration, and time to metabolize drug.
arrhythmia (lidocaine & Na bicarb,), unstable patients should be defibrillated.
Na bicarbonate & hydration & maintain urine output of at least
uphoria, alertness, hypersexuality The increased activation of dopaminergic
to the feelings
As the cocaine dose increases, :
(Direct CNS effects)
Hallucinations) :
rise to
(depletion
or dysregulation of dopamine):
choreoathetoid movements
due to
hypertension, vasospasm,coagulopathies
dysregulated
syndrome :
aGer usage for up to 24 hrs (dopamine
lethargy, want to sleep, trouble
initiating and sustaining movement.
Atherogenesis, Coagulation, and
Ischemic Cardiac Events :
Mechanisms :
hypertension and tachycardia increase
myocardial oxygen demand.
• Cocaine-induced vasoconstriction :
1- stimulation of the α-adrenergic
receptors in smooth muscle cells
in the coronary arteries
2- � endothelin-1, which is a
powerful vasoconstrictor
3- � nitric oxide, which is
Thus, cocaine decreases oxygen supply
-Enhanced coagulation and impaired
thrombolysis . mediated by :
1- � in plasminogen-activator
inhibitor thereby impairing clot
2- �in platelet count, platelet activation,
platelet hyper-aggregability.
3- � levels of C-reactive protein, von
Willebrand factor, and fibrinogen
cocaine use is associated with premature
coronary atherosclerosis and thrombosis.
Cardiovascular GIT
Orthostatic hypotension,
sinus bradycardia
ventricular arrhythmias
- Reduced motility
- Reduced bowel sound
Anorexia , malnutrition &
weight loss
Dermatology Hypothermia
Flushing & urticaria.
Skin boils, cellulitis &
needle tracks are in I.V
Complications
Noncardiogenic pulmonary edema.
& abscesses. Pulmonary emboli & peripheral emboli. Endocarditis and aspiration pneumonia. Prolonged or unusual seizures. Rhabdomylosis with or without compartmental
Active metabolites of meperdine has convulsant activity.
Metabolites of propoxyphene has cardiotoxic activity
On Respiratory system:
Smoking marijuana delivers
does smoking tobacco, causing :
1- Asthma & bronchitis
2- cancers of the respiratory tract (mouth, larynx, sinuses, lung)
On Heart:
1- ↑ heart rate &
2- ↑ risk of a heart a[ack
On Immune system:
Immunosuppressive
On Reproductive system:
Reduced fertility in chronic users is a result of
Oligospermia, Abnormal menstruation, and D
- Males: ↓ testosterone levels
- Females: ↓ FSH & LH, and affect the menstrual cycle.
- Crosses placental barrier :
Lower birth weight.
childhood cancer.
Neurobehavioral Effects
1- underachievement
2- deficits in cogniti
3- and lack of energ
ecrease airway resistance &
conductance
� IOP (Ac=ng on CB1 receptors in the ciliary body)
CVS � � : hypertension, tachycardia, vasospasm�
Brain
1- cerebral infarction,
2- Intraparenchymal & subarachnoid hemorrhage.
Heart
3- myocardial ischemia or infarction �4- Dysrhythmias
5- aortic dissection
Lung
6- Noncardiogenic pulmonary edema
occur due to pulmonary vessels severe
vasospasm, acidosis , hypoxia.
Intestine
7- ischemic colitis..
If the drug is wrongly administered in the artery it will
produce severe vasospasm & limb ischemia.
CVS :
Atherogenesis, Coagulation, and
ic Cardiac Events :
hypertension and tachycardia increase
induced vasoconstriction : adrenergic
receptors in smooth muscle cells
in the coronary arteries 1, which is a
powerful vasoconstrictor nitric oxide, which is vasodilator.
, cocaine decreases oxygen supply
Enhanced coagulation and impaired
activator inhibitor thereby impairing clot lysis.
platelet activation, and
aggregability.
reactive protein, von
Willebrand factor, and fibrinogen
cocaine use is associated with premature
coronary atherosclerosis and thrombosis.
Heart • Chest pain or discomfort
• myocardial infarction is a common
concern, Many will have an ischemic
cardiac event,
• Congestive heart failure.
• Dilated cardiomyopathy,
cocaine use is associated with
repeated subclinical ischemic events.
• Infective endocarditis might occur
due to I.V. drug abuse.
• Dysrhythmias
- Cocaine blocks neuronal Na channels
- Cocaine also blocks cardiac potassium
channels � QTc prolongation .
Pulmonary :
• Smoked cocaine � bronchospasm
• Pneumothorax,
pneumomediastinum, and
pneumopericardium
• Noncardiogenic pulmonary edema
• exacerbates reversible airway disease
• hemorrhagic alveolitis
• pulmonary infarction
Abdomen : • local ischemia of the gastrointestinal tract
� later may perforated ulcer
• Ischemic colitis
• Intestinal infarction
• Bowel obstruction such as vomiting or
distension might suggest body packing
Endocrinology
motility
bowel sound
Anorexia , malnutrition &
- Reduced ADH,
- Abnormal hypothalamic
pituitary adrenal axis
- Abnormal hypothalamic
gonadal axis (decreased libido, irregular menses)
Hypothermia
Withdrawal symptoms
Rhabdomylosis with or without compartmental syndrome. Active metabolites of meperdine has convulsant activity. Metabolites of propoxyphene has cardiotoxic activity
See the picturein the general
scheme.
In chronic toxicity
Smoking marijuana delivers more particulates to the lower respiratory tract than
, causing :
Asthma & bronchitis cancers of the respiratory tract (mouth, larynx, sinuses, lung)
& blood pressure (++sympathetic)
↑ risk of a heart a[ack
Immunosuppressive
Reduced fertility in chronic users is a result of :
Oligospermia, Abnormal menstruation, and Decreased ovulation
↓ testosterone levels & sperm count ↓ FSH & LH, and affect the menstrual cycle.
Factor contributing to injury1- 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
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: • 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, 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 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
ost come from the (foxglove) plant. The drugs have a low therapeutic index
Factors affecting distribution:
With thiazide or loop diuretics)
binding to Na/k ATPase
inhibits binding (K reverses toxicity in hypokalemic patient).
Pregnancy & hyperthyroidism:
digoxin binding sites
miodarone
1- Regulation of Ca concentration:- Inhibiting the ability of the myocyte to actively pump Na
(membrane-bound Na-K-ATPase pump )
gradient � consequently, the ability of the Na
calcium out of the cell.
- Further, the higher cellular Na
Na+/Ca
2+-exchanger � increasing intracellular Ca
Results :
• Desited: + intropic effect
• Side effect : Tachyarrhythmias
2- Decreased heart rate, by 2 mechanisms :- Increased myocardial contraction leads to
� thus increasing the efficiency of contraction
�resulting improved circulation
then reduces peripheral resistance
heart rate.
- Vagal tone is also enhanced, so the heart rate decreases and myocardial oxygen
demand diminishes.
Results :
• Desited: � heart rate �• Side effect : Bradyarrhythmias
Organophosphates Mechanism of action :
otent cholinesterase inhibitors
0.05 g/ 70 kg
60 g/ 70 kg
• Organophosphorous compounds bind to
� overabundance of acetylcholine in the synapse
• By time the compound undergoes a conformational change
enzyme irreversibly resistant to reactivation.
• Carbamate compounds unlike organophosphates, are
inhibitors.
Mechanism of action :
Factor contributing to injury :
Esophagus begins to ulcerate at pH
12 . Acids with pH 2 or less cause
Large volume result in greater direct
injury and potential for perforation &
injury to other organ system. High
volumes enhance the risk of emesis,
viscosity
have prolonged tissue contact and
The passage of caustic through
normal anatomic narrowing
contact time in these areas.
result in penetrating injury
increases the
Preexisting state of the stomach :
in the stomach
affords immediate dilution effect on the
in the
stomach induce buffering effect on
acid or alkalies and help to prevent
empty stomach
of the
full stomach
curvature.
a. Alkaline agents :
- Produce tissue injury by
difficult to treat.
- Fat & protein are saponified, resulting in deep tissue destruction.
- Further injury is caused by
b. Acids :
- Cause damage to the tissue by
protective eschar. • Coagulation of tissue impedes penetration of acid to deeper
layers.
First, damage is superficial resulting in sloughing of extensive
areas of the stomach lining with resulting perforation .
• Despite the eschar
systemic acidosis & decreased cardiac output.
• Hydrofluoric acid is unusual in that it cause
Clinical picture
A. History :-
• Trying to determine the following
a. Type & concentration of caustic ingested
b. Time of ingestion .
c. Quantity of agent ingested .
d. If accidental versus intentional .
• Should determine if : a. Vomiting has occur
b. A diluent has been administered .
• Attempts should be made to obtain
B. Symptoms :-
1- Pharyngeal pain .
2- Dysphagia, sridor, drooling, and vomiting.
3- Chest & abdominal pain, respiratory distress and shock reflect severe tissue
damage .
- A caustic ingestion in adults is usually intentional and severe .
C. Physical examination :-
1- Erythema, edema and erosions of the oropharynx.
2- Psedomembrane formation may be present over the mucosa .
3- Hypotension, tachycardia and changes in ment
4- Respiratory distress .
5- Sepsis may develop secondary to bacterial colonization of devitalized tissue.
Pathophysiology:
The human oral lethal dose is 1 μg/kg
• Botulinum toxin binds to specific receptors on the mucosal surfaces of gastric
and small intestinal epithelial cells
transcytosis permits release of the toxin on the serosal cell surface.
• Release into the systemic circulation
acetylcholine containing neurons.
• As a result, cholinergic transmission
in the peripheral nervous system
However, there is no effect on central nervous system
- Toxins are distributed to target sites via hematogenous dissemination
- Toxins act on the presynaptic part of neuromuscular junctions leading to
decreasing the amount of ACH release
Gram +ve anaerobic bacillus that
Food contaminated with C. botulinum
often does not
putrefied because of the action of
organisms are saccharolytic and not
ytic, food contaminated with
toxin type E may look and taste normal.
Spores withstand 100 c for hours.
royed by boiling for 10 min. or
II. Infant Botulism :
• Affected children are younger
• Constipation is the first sign
• Ophthalmoplegia,
• Loss of facial grimacing,
• Dysphagia,
• Diminished gag reflex,
• Poor anal sphincter tone,
• Respiratory failure are also
Mechanism of action
Regulation of Ca concentration: Inhibiting the ability of the myocyte to actively pump Na
+ from the cell
ATPase pump ) � decrease the Na+ concentration
consequently, the ability of the Na+/Ca
2+-exchanger to move
the higher cellular Na+ is exchanged by extracellular Ca
2+ by the
increasing intracellular Ca2+
.
+ intropic effect (Increased contractility of the cardiac muscle)
Tachyarrhythmias
Decreased heart rate, by 2 mechanisms : Increased myocardial contraction leads to �a decrease in end-diastolic volume,
efficiency of contraction (increased ejection fraction )
resulting improved circulation �leading to reduced sympathetic activity, which
reduces peripheral resistance �Together, these effects cause a reduction in
ed, so the heart rate decreases and myocardial oxygen
� myocardial oxygen demand diminishes
Bradyarrhythmias
Mechanism of action :
compounds bind to and inhibits � acetylcholinesterase
overabundance of acetylcholine in the synapse. By time the compound undergoes a conformational change (aging) renders the
enzyme irreversibly resistant to reactivation.
compounds unlike organophosphates, are transient cholinesterase
Mechanism of action :
roduce tissue injury by liquefaction necrosis, which devastating and
Fat & protein are saponified, resulting in deep tissue destruction.
urther injury is caused by thrombosis of blood vessels.
Cause damage to the tissue by coagulation necrosis, resulting in
of tissue impedes penetration of acid to deeper
First, damage is superficial resulting in sloughing of extensive
areas of the stomach lining with resulting perforation .
eschar, the acid can be absorbed resulting in
systemic acidosis & decreased cardiac output.
Hydrofluoric acid is unusual in that it cause liquefaction necrosis
Clinical picture
following :
a. Type & concentration of caustic ingested
b. Time of ingestion .
c. Quantity of agent ingested .
d. If accidental versus intentional .
a. Vomiting has occur
b. A diluent has been administered .
to obtain the product container .
Dysphagia, sridor, drooling, and vomiting.
Chest & abdominal pain, respiratory distress and shock reflect severe tissue
A caustic ingestion in adults is usually intentional and severe .
Erythema, edema and erosions of the oropharynx.
Psedomembrane formation may be present over the mucosa .
Hypotension, tachycardia and changes in mental status.
Sepsis may develop secondary to bacterial colonization of devitalized tissue.
1 μg/kg from the toxin.
specific receptors on the mucosal surfaces of gastric
and small intestinal epithelial cells � where endocytosis followed by
transcytosis permits release of the toxin on the serosal cell surface.
circulation allows uptake into presynaptic
acetylcholine containing neurons.
cholinergic transmission at all acetylcholine-dependent synapses
in the peripheral nervous system is impaired.
However, there is no effect on central nervous system or axonal conduction.
Toxins are distributed to target sites via hematogenous dissemination
Toxins act on the presynaptic part of neuromuscular junctions leading to
decreasing the amount of ACH release
Affected children are younger than 1 year of age (usually 1–3 months).
is the first sign of infant botulism, followed by �
- Hypotonia,
- Generalized Weakness,
- Poor sucking,
- Weak cry.
r tone,
are also present, fever & enteric symptoms do no
Clinical manifestation of
from the cell
concentration
exchanger to move
by the
Increased contractility of the cardiac muscle)
diastolic volume,
(increased ejection fraction )
to reduced sympathetic activity, which
Together, these effects cause a reduction in
ed, so the heart rate decreases and myocardial oxygen
.
Acute
• (Brady-dysrhythmias)
• GIT manifestations • lethargy, confusion, and
weakness • Hyperkalemia, why?
• Cardiac effects:
- The common cardiac side effect is
- Characterized by : slowing of atrioventricular conduction associated with
atrial arrhythmias.
• Gastrointestinal effects:
Anorexia, nausea, and vomiting.
• Central nervous system effects:
Headache, fatigue, confusion, blurred vision, alteration of color perception,
and halos on dark objects.
1- Muscarinic Effects (DUMBELSS
2- Nicotinic Effects (MMATCH)
3- CNS effects (2C 2D
C onfusion D epression : Respiratory &
S eizures
H eadache
M alaise
acetylcholinesterase
renders the
transient cholinesterase
which devastating and
of tissue impedes penetration of acid to deeper
First, damage is superficial resulting in sloughing of extensive
acid can be absorbed resulting in
liquefaction necrosis .
1- Acute inflammatory stage :
- During the first 4 to 7
- First, Edema and Erythema , followed by
- Perforation & Acidosis may occur .
Early endoscopy is recommended within 24 to 48h .
2- Granulation stage :- - Starts at about day 4 and ends at 7 days aGer inges=on .
- Fibroplasia results in the formation of
down of collagen over the denuded areas of mucosal sloughing.
3- Perforation :-
- between days 7 & 21 but may occur earlier.
- The tissue is the weakest & the risk of perforation is highest .
4- Cicatrization stage :
- Starts at 3 weeks and may persist for years.
- Dense fibrous tissue formation occurs at variable rates .
- Overproduction of scar tissue results in stricture formation .
Course of complication
Chest & abdominal pain, respiratory distress and shock reflect severe tissue
Sepsis may develop secondary to bacterial colonization of devitalized tissue.
1-Acute complications :-
a. Upper airway obstruction and injury .
b. GI hemorrhage .
c. Esophageal &
d. Sepsis .
e. Tracho
2- Peri-esophageal complications secondary to perforation
a. Mediastinitis
b. percarditis
c. pleuritis.
d. Tracheobronch
e. Esophago
3- chronic complications`:-
a. Esophageal obstruction .
b. Pyloric stenosis .
c. Squamous cell carcinoma of the esophagus.
d. Vocal cord paralysis .
specific receptors on the mucosal surfaces of gastric
where endocytosis followed by �
dependent synapses
or axonal conduction.
Toxins act on the presynaptic part of neuromuscular junctions leading to
I. Classic (Adult) botulism:
• Symptoms & signs develop
• Severity of disease depends on type of toxin (type A gives most severe picture).
1) Initial vague & GIT symp.
• Malaise,
• Weakness,
• Dizziness,
• Diplopia & blurred
vision
• Diarrhea or constipation
• Nausea, vomiting,
•
••
•••
3) Anticholinergic manife.
see the scheme
3 months).
eneralized Weakness,
ms do not occur.
III. Wound botulism :
• The “classic” presentation of wound botulism is a patient injured in a
motor vehicle crash who sustains a deep muscle laceration, crush injury, or
compound fracture treated with open reduction.
• The wound is typically
débridement, subsequent
Clinical picture: • 4 to 18 days later�cranial nerve palsies
typical of botulism may appear.
• Fever associated with t
• Typical gastrointestinal
Clinical manifestation of toxicity
Chronic
lethargy, confusion, and
• arrhythmia
• GIT manifestations
• Visual (yellow vision)
• Confusion, Delirium,
hallucination • Hypokalemia, why?
The common cardiac side effect is arrhythmia,
slowing of atrioventricular conduction associated with
Anorexia, nausea, and vomiting.
Central nervous system effects: eadache, fatigue, confusion, blurred vision, alteration of color perception,
los on dark objects.
(DUMBELSS) see the scheme
(MMATCH) see the scheme
D SHM) :
onfusion C oma D isorientation
epression : Respiratory & circulatory centers
eizures
eadache
alaise
Time course of injury
Acute inflammatory stage :-
4 to 7 days.
rythema , followed by � thrombosis & cellular necrosis .
cidosis may occur .
Early endoscopy is recommended within 24 to 48h .
Starts at about day 4 and ends at 7 days aGer inges=on .
Fibroplasia results in the formation of granulation tissue with the lying
down of collagen over the denuded areas of mucosal sloughing.
between days 7 & 21 but may occur earlier.
The tissue is the weakest & the risk of perforation is highest .
at 3 weeks and may persist for years.
Dense fibrous tissue formation occurs at variable rates .
Overproduction of scar tissue results in stricture formation .
Course of complication
a. Upper airway obstruction and injury . b. GI hemorrhage . c. Esophageal & gastric perforation . d. Sepsis . e. Tracho-bronchial necrosis, atelectasis.
esophageal complications secondary to perforation
a. Mediastinitis b. percarditis c. pleuritis. d. Tracheobronch-oesophageal fistula e. Esophago-aortic fistula .
- a. Esophageal obstruction . b. Pyloric stenosis . c. Squamous cell carcinoma of the esophagus.