First Flashcards
Contraindications of emesis:
Corrosives: for fear of perforation of esophagus or stomach.
Coma: for fear of suffocation or aspiration pneumonia.
Convulsions: as vomiting and patient manipulation may stimulate
convulsions.
Kerosene (volatile hydrocarbons) for fear chemical pneumonitis.
Chronic poisoning.
Cardiac and elderly patients and vascular insufficiency.
Infants below the age of 6 months (immature gag and airway protective reflexes).
Contraindications of gastric lavage:
[are the same as for emesis] except:
* Coma & volatile hydrocarbons — Lavage is allowable after inserting a cuffed endotracheal tube to prevent aspiration pneumonia.
- Convulsions— Lavage can be performed under general anesthesia.
- Cardiac dysrhythmias must be controlled before gastric lavage is initiated, as insertion of the tube may create vagal response — cardiac arrest.
Activated Charcoal is ineffective (poorly adsorb) in some poisons as:
C– Cyanide and Corrosives.
H–Heavy metals (Iron, Lead, Arsenic and Mercury).
A–Alcohols.
R—Rapid onset or absorption poisons (Cyanide and Strychnine).
C—Chlorine and iodine.
O-Others insoluble in water (Substances in tablet form).
A–Aliphatic and poorly adsorbed hydrocarbons (petroleum distillates).
L–Lithium
indications of Multiple-Dose Activated Charcoal (MDAC)
for poisoning that:
Show enterohepatic circulation (TCA, Digitalis and Barbiturates)
Stick to the stomach (Salicylate).
Slow gut motility (Barbiturates & Morphine)
Whole Bowel Irrigation contraindications
Unprotected airway or compromised airway.
Bowel obstruction, ileus, or perforation.
Clinically significant GIT bleeding.
Intractable vomiting.
Unstable vital signs.
Signs of leakage of illicit drug packets (e.g. tachycardia, hypertension, hyperthermia in a patient who has ingested cocaine packets),
surgical consult should be obtained in this circumstance.
Alkalization of urine for
elimination of acidic drugs e.g. salicylates and barbiturates.
Using: (NaHCos) urine pH 7.5-8.0.
Acidification of urine for
For elimination of alkaline drugs e.g. Amphetamine, Quinidine and PCP.
Using: (NH4Cl)
Antidotes of Anticholinergic
- Physostigmine for atropine and antihistaminics
- lt reverses the peripheral & central anticholinergic effects.
- Itis indicated in severe cases.
- It should be given under cardiac monitoring & should not be given as a constant infusion for a long time.
- It is contraindicated with wide QRS complex, bradycardia, asthma and bowel or bladder obstruction.
- Sodium bicarbonate in case of TCAs: indicated for
- Conduction defects.
- Arrhythmias.
- Metabolic acidosis.
Mechanism:
Alkalinization: promotes dissociation of the tricyclic antidepressant from sodium channels.
Increased plasma sodium: helps to drive sodium through sodium channels.
indications of extracorporeal removai of poison:
1-Severely intoxicated patients (coma, hypotension, metabolic disturbances)
2-Toxic serum drug level
3- Progressive clinical deterioration.
Common opioid drugs:
Morphine is only injected & has no smell. It is used for relieving intense
pain such as pain associated with some cancers.
- Codeine is an antitussive (suppress the cough reflex)
1- Heroin is a semisynthetic derivative of morphine, with analgesic properties superior to morphine and cough-suppressant properties
superior to codeine. Heroin is 2-4 times more addictive than morphine; it is
neither used medically nor manufactured legally.
2- Fentanyl, meperidine, methadone and tramadol are synthetic opioids.
- Fentanyl is 25-50 times more potent than heroin and 50-100 times more potent than morphine.
- Tramadol is a centrally acting synthetic analgesic with opioid-like effects
Mechanism of action of opioids
They exert their effects by interacting with specific opioid receptors.
- Opioids interact with [mu, kappa and delta receptors] causing a mixture of stimulations and depressions but mainly depressions.
- Tramadol binds to p-opioid receptors only. It also inhibits the reuptake of noradrenaline and serotonin.
Treatment of opioid toxicity
24&25
Clinical presentations of opioid toxicity
The classic triad of opioid toxidrome is CNS depression, respiratory depression, and miosis.
. CNS manifestations:
-The patient feels euphoria (sense of wellbeing and relief of pains) due to depression of Sensory cortex followed by dysphoria (distress,
anxiety and fear).
- Gradual deterioration of consciousness (drowsy, stupor then
comatose) due to depression of Consciousness.
- Cyanosis due to depression of respiratory center.
- Circulatory collapse due to depression of vasomotor center.
-Vomiting due to stimulation of vomiting center.
-The pupils are constricted pin pointed pupil (ppp) and non- reactive due to stimulation of Pupillo-constrictor center.
2. CVS manifestations
- Slow full pulse due to stimulation of vagal center.
1. Respiratory manifestations:
- Non-cardiogenic pulmonary edema.
- Slow deep respiration due to stimulation of vagal center.
2. Gastrointestinal manifestations:
- Constipation and diminished bowel sounds.
Clinical presentations of CNS depressants
Barbiturates and benzodiazepines
1. CNS manifestations:
« Confusion, memory deficit, poor judgment, vertigo, slurred speech,
and ataxia.
¢« — Mild drowsiness up to coma.
¢ Barbiturates coma characterized by being deep & prolonged (may
last for days), with slow weak pulse, slow shallow respiration, hypotension
and hypothermia, Muscle flaccidity with diminished reflexes and may end
in respiratory failure (central asphyxia).
« Benzodiazepines coma is Low-grade coma (in most comatose
patients arousal occurs within 12-36 hrs. following an acute overdose).
2. CVS manifestations:
Hypotension due to direct myocardial depression & vasodilatation.
3. Respiratory manifestations:
¢R.C. depression (in barbiturates only) which results in hypoventilation
& apnea.
¢ Pneumonia (in barbiturates only) which may occur due to:
¥ Prolonged coma.
Y Inhibition of the protective reflexes (cough reflex).
¥ Aspiration pneumonia following vomiting of gastric contents.
¢ Non-cardiogenic pulmonary edema in (barbiturates only).
«ln rare cases respiratory arrest may occur following rapid IV
administration in benzodiazepines.
1. Skin manifestations:
¢ Blisters “bullae” over pressure points.
2. Renal manifestations in barbiturates only:
Renal failure due to:
¢ Hypotension — decreased perfusion.
¢ Rhabdomyolysis (due to prolonged coma).
Differential diagnosis of opioid
الجدول صفحة 24
Mechanism of action of
Both act by enhancing the binding of y-aminobutyric acid (GABA) to GABA receptors. GABA receptors inhibit post-synaptic nerve impulse transmission.
Barbiturates causing GABA dependent chloride-channels to stay open for a longer period of time, while benzodiazepines causing chloridechannels to open more frequently.
investigations of opioid
- Routine investigations.
- Toxicological screening.
- ECG: arrhythmias.
- Chest X-ray: pulmonary edema in cases of opioid overdose.
Differential diagnosis Medications associated with coma and
blisters:
¢ Barbiturates.
° Carbon monoxide.
¢ TCA (Amitriptyline & Imipramine).
Investigations of CNS depressants
- Routine investigations:
- Renal function test in cases of barbiturates: Acute renal failure. - Toxicological screen.
- CPK in cases of barbiturates: t (due to rhabdomyolysis).
- Chest X-ray in cases of barbiturates: pneumonia and noncardiogenic pulmonary edema.
Treatment of CNS depressants
p27/28.
Supportive treatment: ABC.
GIT decontamination:
*Emesis: not recommended since rapid neurologic deterioration is known to occur.
*Gastric Lavage: with cuffed endotracheal tube up to several hours after the overdose due to decreased GIT motility.
* Activated charcoal.
* MDAC: in phenobarbital toxicity only (enterohepatic circulation).
3. Elimination of the poison from blood:
*Forced alkaline diuresis: for long acting barbiturates only (less bound
to plasma proteins than short acing and mainly excreted in the urine).
* Hemodialysis and hemoperfusion have been successfully utilized in all
types of barbiturate overdoses (most effective for long-acting
barbiturates)
Hemodialysis and hemoperfusion are ineffective in benzodiazepines
(high protein binding & large volume of distribution).
¢Charcoal hemoperfusion is more effective than hemodialysis only in
barbiturates.
mechanism of action of inorganic corrosives
p30
clinical presentation of inorganic corrosives
GIT:
Severe pain of lips, mouth and stomach.
Excessive salivation.
Dysphagia
Vomiting.
Symptoms and signs of GIT perforation.
Respiratory system:
Cough.
Dyspnea.
Hoarseness, stridor and respiratory distress due to edema of
vocal cords.
Bronchoconstriction.
Pulmonary edema.
Chemical pneumonitis.
Skin:
oChemical burns and eschars.
Eye
Corneal ulcers.
Conjunctival irritation with lacrimation.
Photophobia and severe burning pain.
4. Significant exposures:
May also result in gastrointestinal absorption of the acidic substances
leading to:
¢ Significant metabolic acidosis.
* Acute renal failure.
complications of inorganic corrosives
1) Acute:
- Airway obstruction
- Shock (due to pain)
- Vomiting lead to dehydration
- GIT perforation.
2) Late:
- Stricture leading to cachexia.
3) Remote:
- Carcinoma of esophagus.
investigations of inorganic corrosives
1.Laboratory Tests:
Routine lab investigation: -
ABG: metabolic acidosis.
Renal function test: ARF.
2. Radiology:
Chest X-ray: pneumothorax, pneumomediastinum and pleural effusion.
Abdominal X-ray: pneumoperitoneum
3. Endoscopy
Done for grading the esophageal and gastric lesions to guide therapy.
*Contraindicated in airway obstruction and in cases of
perforation.
° Should be done within 24-48 ho
treatment of inorganic corrosives
32/33
the combination of hypochlorite
the combination of hypochlorite with an acid or
ammonia produces chlorine and chloramine gases, respectively
causing ocular and respiratory tract irritation:
as
a) Difficulty breathing
b) Coughing
c) Bronchospasm
d) Rarely pulmonary edema.
actions and clinical presentation of Carbolic acid (phenol)
34
causes of death in phenol toxicity
2 R failure
1-Early: respiratory failure due to respiratory center depression.
2-Late: renal failure.
investigations of phenol
1-Routine lab investigation:
ABG for
Respiratory alkalosis.
Metabolic acidosis follows.
Kidney function test for Acute renal failure.
2-Urine analysis: oliguria with albumin, blood and casts in urine. The urine turns green on exposure to air.
3-Met-hemoglobin level.
4-ECG: Arrhythmias
treatment of phenol
35
Mechanism of action of Digoxin
- Slows conduction through the atrioventricular (AV) node.
-It inhibits Na+—Ka+ ATPase in the cardiac muscle fibers — increased intracellular Na+ and Ca+ and increased extracellular Ka+.
Clinical presentation of digoxin
CVS manifestations:
-Tachyarrhythmias and bradyarrhythmia’s.
- Hypotension
Other manifestations:
-GIT: (the first to occur) nausea, vomiting, colic and diarrhea.
- Visual: blurring, halos (yellow / green halos).
-CNS: headache, drowsiness, and disorientation.
-Hyperkalemia may occur (in acute digitalis toxicity), but hypokalemia may be seen in chromic patients
treatment of digoxin toxicity
40
investigations of digoxin
. Routine investigations.
- Hyperkalemia in acute toxicity
- Hypokalemia in chronic toxicity.
- Kidney function tests: (renal impairment alters elimination of digoxin).
- Serum caicium levels because hypercalcemia induce serious arrhythmias
Toxicological screening (Digoxin level):
ECG and continuous cardiac monitor.
mechanism of toxicity of acetaminophen
is caused by the active metabolite NAPQI, which can lead to oxidant cell injury, hepatic failure and death.
clinical presentation of aceminophen
p 41
phases 1-5
investigations of acetaminophen
liver function tests
renal function test
ABG
blood glucose level
serum paracetamol levels
treatment of acetaminophen
42
Aspirin on Gastrointestinal System:
nausea and vomiting due to direct irritation on gastric mucosa
mechanism of action and clinical presentation of aspirin
43&44
Aspirin on Central Nervous System:
o Alterations in mental status, cerebral edema and seizures
o Tinnitus:
Aspirin on respiratory system
Acute lung injury (ALI).
- Non cardiogenic pulmonary edema
As on Cardiovascular System:
sinus tachycardia.
- Hypotension due to hypovolemia.
treatment of aspirin
كله الا انتيدوت
clinincal presentation of iron
48
Investigations of iron
- Routine lab investigation:
- ABG: metabolic acidosis.
- Hepatic functions tests:
- ‘enzymes and bilirubin. - Serum iron levels:
The most suitable time for assessing serum iron is 4 - 6 hrs post ingestion
due to delayed absorption:
- Serious toxicity: 500 yg/dL
- Fatal toxicity: 1000 ug/dL - Deferoxamine challenge test:
(Change urine color after single IM Deferrioxamine dose indicates presence
of iron in urine, which is chelated by Deferrioxamine). - Abdominal x-ray: Radiopaque iron tablets could be detected.
treatment of iron toxicity
supportive
gastric lavage with ammonium chloride and antidote
deferoxamine
Mechanism of action of iron poisoning
1.Local:
- GIT: Corrosive effect on mucosal tissue and may cause hemorrhagic necrosis and perforation.
2.Remote:
Iron causes oxidative stress and inhibits several key metabolic enzymes. Reactive oxygen species (ROS) oxidize membrane-bound lipids and cause loss of cellular integrity and tissue injury.
1. Liver:
Free iron accumulates first in the Kuppfer cells then hepatocytes localizing in mitochondria producing periportal necrosis.
2. Cardiovascular system:
i. Iron produces hypotension and shock (iron or ferritin causing massive post arteriolar dilatation leading to venous pooling).
ii. Iron has direct myocardial depressant effect.
3. Metabolism:
lron produces metabolic acidosis due to:
i. Conversion of ferrous iron to ferric iron with subsequent release of hydrogen ions (major role).
ii. Disruption of mitochondrial function forcing anaerobic respiration
(lactic acids & other organic acids).
