Presentation on theme: "General Toxicology By: Rajia Mahmoud Hejazy MD CLINICAL TOXICOLOGY Assistant professor of clinical toxicology Faculty Of Pharmacy, & Faculty of Medicine."— Presentation transcript:
General Toxicology By: Rajia Mahmoud Hejazy MD CLINICAL TOXICOLOGY Assistant professor of clinical toxicology Faculty Of Pharmacy, & Faculty of Medicine Umm Al-Qura University, KSA Benha University, EGYPT
GENERAL TOXICOLOGY Classification of poisons: I- According to their mode of action: a) Poisons with local action: They act locally producing immediate destruction of the tissues with which they come in contact e.g corrosives (except organic acids). b) Poisons with remote action: They act only after absorption without any local effects e.g plant poisons which act mainly on CNS. c) Poisons with both local and remote actions: As irritant metallic poisons (lead, Mercury, arsenic,..etc) which have a local irritant action on the tissues they come in contact for sometime and a remote action (on parenchymatous organs) after absorption.
II- According to the organs affected: The poison may be: Hepatotoxic: APAP, phosphorus, CCL 4 and arsenic, Cardiotoxic: digitalis, Nephrotoxic:mercury, ASA Neurotoxic: alcohol …. etc. III- According to the chemical nature: Acids: like H 2 SO 4, HNO 3 and H 2 CL. Alkalies: as caustic soda & caustic potash and ammonium hydroxide. N.B. The source of the poison may be considered as in cases of plant and animal poisons.
IV- According to Use – (e.g., pesticide, solvent, food additive) V- According to Effects - (e.g., cancer, mutation, liver injury) VI- According to Labeling requirements - (e.g., explosive, flammable, oxidizer) VII- According to Poisoning potential - (e.g., very or slightly toxic)
Factors affecting the severity of toxicity: Factors related I- to the person II- to the poison I- 1) Age of the person & individual suscptibility: Children and old people generally are more susceptible to the toxic agents due to decrease detoxification power. However, children can tolerate the action of atropine, but not morphine.
6 Drug rash 2) Genetic factors: Persons suffering from glucose-6-phosphate dehydrogenase deficiency are susceptible at therapeutic doses to hemolytic effect of some drugs like vitamin K and sulphonamides.
3) Personal hypersensitivity: Very small harmless doses can produce severe symptoms in sensitive patients e.g. therapeutic dose of penicillin or iodine may produce anaphylaxis in some hypersensitive patients. 4) Tolerance: Repeated intake of substances of abuse leading to the development of tolerance where the addicts can stand big dose without ill-effect. So, they have to increase the dose to get the same effect.
5) Idiosyncrasy: Abnormal response to some drugs e.g. morphine may produce convulsion instead of depression of CNS. 6) State of health : Patients suffering from liver or kidney diseases may show signs of increased toxicity of the poisons. 7) Synergism: The action of one drug may be increased if given with another drug e.g. alcohol and barbiturate.
8) Condition of the stomach: - Type of food: Fatty foods delay the absorption of arsenic while they increase the absorption of some poisons as DDT and phosphorus. - Gastric secretion: Poisoning with potassium cyanide may not be fatal in case of achlorhydria as HCL in stomach is important to form the severely toxic hydrocyanic acid. Empty or full stomach : A poison taken on full stomach has slower action than the same dose of poison on empty stomach.
II- Factors related to the poisons: 1) State of the poison. Poisons in gaseous form are more rapidly absorbed followed by liquid poisons, fine powder, then big lumps. 2) Routes of administration: The quick.. inhalation followed by IV, IM, SC, ingestion, absorption through mucous membranes, lastly absorption through the intact skin which is minimal except in some poisons as organophosphates, phenol & tetraethyl lead.
3) Dose of the poison: The bigger the dose, the more toxic the effect. However, this is NOT a general rule as big doses of metallic poison may cause severe vomiting, so eliminate most of the poison. 4) Cumulation: After repeated small doses of certain drugs, that are not readily metabolized, the effect of a single large dose is reached leading to poisoning e.g. digitalis.
Diagnosis of Poisoning: 1- History and circumstantial evidences. 2- Clinical manifestations. 3- Investigations.
1- History and circumstantial evidences: - Sudden appearance of toxic manifestations in a healthy person or a group of persons after taking certain food or drink (as food poisoning, methanol and carbon monoxide toxicity). - History of intake a poison, financial problems, psychiatric troubles, previous attempts at suicide or threatening by somebody. - Presence of bottle of tablets or insecticide near the victim. - Patients rescued from fire (CO, cyanide).
2- Clinical manifestations (signs and symptoms): - Vital signs: Temp, Pulse, BP,Respiratory rate Breath odour, Pupil, Skin Recorded in initial evaluation & repeated regularly.
*Mydriasis: Dilated & reactive: CNS stimulants nicotine opoid withdrawal Dilated & fixed: Anticholinergics late in any poisoning brain stem lesion
Skin: *Needle tracks in IV drug abuse *Bullous lesions in prolonged coma with prolonged pressure and skin hypoxia e.g. sedative hypnotics (especially barbiturates) & CO *Flushing anticholinergics (flushed & hot), alcohol (flushed & cold) *Diaphoresis (CANOS) C: carbamates A: alcohol withdrawal N: nicotine O:organophosphates, S: salicylates, (D.D. hypoglycemia).
*Red: CO & cyanide *Cyanosed: CNS depressants *Jaundiced: (appi) arsenic, phosphorous, paracetamol, iron *Petechiae & ecchymosis e.g. salicylates. *Patches or eschars around the mouth in corrosives.
Clinical examination: 1-Respiratory system: Wheeze, pulmonary edema *Wheezing: (due to bronchospasm) ipcco e.g. irritant gases & fumes, paraquate, carbamates, cholinergics organophosphates. *Pulmonary edema: cardiogenic or non-cardiogenic - Cardiogenic: (left ventricular failure) e.g. calcium channel blockers, beta blockers, tricyclic antidepressants. - Non-cardiogenic: (due to factors increasing the pulmonary capillary permeability) ipcons irritant gases & fumes, prolonged coma of CNS depressants as opiates & barbiturates (due to prolonged hypoxia) carbamates, organophosphates. nicotine, salicy.
CNS : *Coma: abpo a: alcohols, atropine b: barbiturates p :phenol o:organophosphates, opiates *Convulsion: prolonged coma of CNS depressants as opiates & barbiturates (due to prolonged hypoxia) lead, arsenic (encephalopathy) oxalic acid (decalcification) organophosphates (early stage of CNS stimulation) CNS stimulants: strychnine; nicotine, cocaine. amphetamine phenol, atropine, ergot, cyanide,
Abdomen: *Adynamic ileus e.g. Anticholinergics *Distened abdomen may indicate GIT perforation from inorganic corrosives.
3- Investigations: They are done to assess: -base line of the patient -follow up target organs e.g. blood gases, electrolytes, glucose, liver & renal function tests, ECG and X-ray.
Common radiopaque medications: (BETA CHIP) B-Barium E-Enteric coated tablets: ASA, theoSR T-Tricyclic antidepressants A-Antihistamines. C-Chloral hydrate, cocaine, calcium, condoms (contains tablets, or Body Packers). H-Heavy metals I- Iodides P-Phenothiazines
b) Chemical detection: (Analytical toxicology) The most important evidence of poisoning is by chemical analysis. A) In the living: Samples are taken from vomitus, gastric lavage, blood, urine and stool. B) In the dead: - Blood from femoral, axillary or iliac veins. - Stomach and intestine. - Organ samples -Vitreous humor if there is difficulty in blood sampling particularly in putrefaction. -CSF.
General lines of treatment of poisoned patient (6)
Good supportive care is the backbone of any successful therapy of poisoned patients: 1- Prevent further exposure to the poisons.1- Prevent further exposure to the poisons. 2- Emergency and supportive measurements.2- Emergency and supportive measurements. 3- Decontamination.3- Decontamination. 4- Enhancement of excretion.4- Enhancement of excretion. 5- Administration of toxin-specific (physiological) antidotes.5- Administration of toxin-specific (physiological) antidotes. 6- Symptomatic treatment.6- Symptomatic treatment.
1-Prevent Further Exposure To The Poisons: *In industrial or agricultural exposure → removed from the polluted area. *In cases of toxic inhalants → removal of the patient to fresh air and giving oxygen. *In suspected suicidal cases → the patient hospitalized and observed to prevent another trials. *During medical treatment if toxic manifestations appear → the drug should be stopped immediately
2. Emergency and Supportive Measures : ABCD’s
2. Emergency and Supportive Measures : The first step is to recognize and treat life threatening conditions (A, B, C, D): A=Airway. B= Breathing. C= Circulation. D= Disability i.e. assess neurological status, level of consciousness and convulsion.
A) Airway opening & clearance: Airway opening: Triple airway maneuver: (Head tilt, jaw thrust, Mouth opening) If there is any suspicion of neck injury: Place the patient in left lateral position with the head downwards which allows the tongue to fall forwards and vomitus or secretions to drain out of the mouth.
Airway clearance: a- Finger sweep technique to remove any F.B. or denture. b- Suctioning of the mouth and oropharynx to remove secretions.
B) Breathing support: a) Airway devices b) Assist ventillation by giving oxygen c) Active ttt.
Airway devices : 1-oropharyngeal or nasopharyngeal airway devices 2-ETT, 3-Tracheostomy 1-Oropharyngeal or nasopharyngeal airway devices: placed in the mouth or to lift the tongue and push it forward
Endotracheal intubation (ETT): In Comatosed patient. Advantages : - It protects the airway & prevents aspiration and obstruction. - It allows for mechanically- assisted ventilation. Some emergency drugs can be given through it e.g. naloxone, atropine and epinephrine
-Cricothyrodotomy or tracheostomy: In upper airway obstruction (ETT can not be INSERTED)
b- Assist ventillation: (oxygen) Indication PO 2 60 mmHg. Don’t wait until apniec Methods: 1- Mouth-to-mouth ventilation. 2- Mouth-to-mask ventilation (this method is more hygienic). 3- Bag and mask ventilation 4-Bag and tube ventilation 5-Mechanical ventilation (used when resuscitative efforts are prolonged).
The greatest contributor to death from drug overdose or poisoning is respiratory failure Toxic causes of respiratory failure: I Central causes: such as opiates, barbiturates, alcohols ….. II Peripheral causes due to 1-airway obstruction 2-Neuromuscular block 3-Paralysis of respiratory muscles
c- Active treatment: Bronchospasm, pneumonia, pulmonary edema, specific antidote. 1-Administer bronchodilators if there is wheezing or ronchi: - B 2 - agonists e.g. sulbutamol inhalation. - Aminophylline slowly IV if the above is not effective. 2-Treat pneumonia with the following: - Antibiotics if there is evidence of infection. - Corticosteroids (if it is a chemical-induced pneumonia). 3-Treat pulmonary edema with the following: -Avoid excessive fluid administration. -Administer supplemental oxygen. -Diuretics. 4-Consider specific antidotes e.g. Naloxone can reverse respiratory depression in a patient with opiate overdose.
C) Circulatory support: (5) 1-Check blood pressure and pulse rate and rhythm: Perform CPR if there is no pulse. Treat shock and arrhythmia if present. Hypotension treatment: –Normal saline fluid challenge, 20 mL/kg up to 2 liter or S BLP 100 mm/Hg –Vasopressors if still hypotensive as dopamine or dobutrex –PRBC’s if bleeding or anemic Hypertension treatment: –Nitroprusside, beta blocker, or nitroglycerin –With tachycardia: do not give BB alone, you can worsen HTN if it is caused by alpha adrenergic stimulation as with cocaine
C) Circulatory support: (5) 2-Begin continuous ECG monitoring: This is essential for comatosed patients and patients with cardiotoxicity. 3-Establish an intravenous line. 4- Draw blood for routine studies. 5-Foly’s catheter is placed in the bladder if the patient is seriously ill (shocked, convulsing or comatosed). Obtain urine for routine and toxicologic testing and measure hourly urine output
D)Disability Once ABC are addressed, the neurological status should be assessed, mainly: level of consciousness & convulsions. I-level of consciousness: a)Coma and b)stupor Stupor: is a grade of unconsciousness in which the patient can be aroused (awakened) only by painful stimuli. Coma: is a state of prolonged unconsciousness in which the patient can not be aroused by painful stimuli. The level of consiuosness is evaluated roughly by the responsive scale AVPU: A=awake and alert. V= respond to verbal stimuli. P=respond to pain. U= unresponsive
Reed’s classification of the level of consiousness Circul.RespReflexesPain response Consious level stage Normal IntactArousable Asleep 0 Normal Intact Withdrawal Comatose I Normal IntactNone Comatose II Normal AbsentNone Comatose III Shock cyanosed AbsentNone Comatose IV
Causes of coma : (5) *Toxic *Traumatic *Pathologic *Environmental *Hysterical Toxic causes: Generalized CNS depression (e.g. ethanol, opiates, sedative-hypnotics). As a postictal phenomenon (after a drug-induced seizure) (e.g. anticholinergics). Hypoglycemia (e.g. insulin, oral hypoglycemic drugs). Cellular hypoxia (e.g. CO, cyanide). Traumatic Causes head injures. Pathologic causes: Liver & renal failure. Infections as encephalitis or meningitis.
4.Environmental causes: Hypothermia or hyperthermia. 4. Hysterical: No organic cause, normal vital signs, and negative investigations. Complications of coma: - Loss of protective airway reflexes, resulting in airway compromise which is a major cause of death. -Hypotension. -Hypothermia. -Rhabdomyolysis.
Treatment of coma (7) 1- Support ABC. 2- Give coma Coktail: DONT Administer supplemental O 2 Dextrose, Naloxone and Thiamine:
a) Dextrose is given to all patients with depressed consciousness. Child : 25 % (1-2 ml/kg) I.V. Adolescent/Adult: 50 % (1 ml/kg) I.V. b) Naloxone is given to all patients with depressed respiration. - Child: 0.01 mg/kg I.V. - Adolescent/Adult: 0.4 mg I.V. (amp= 200µgm/Kg) up to 2 mg I.V. can be repeated max 10 mg. if no response, repeat the dose every 2 min. till a total dose of 10 mg. c) Thiamine is given to malnourished and chronic alcoholic patients. - It is not given routinely to children. 100 mg I.M.
3- Control convulsions if they are present: 4- Correct any temperature, electrolyte, or acid-base disturbance. 5- If suspecting a brain lesion, perform a CT scan and treat accordingly. 6- Continuous care of the comatosed: a)Care of respiratory system: Frequent suctioning, antibiotics. b) Care of G.I.T.: Antacids, lactulose. c) Nutritional support: Tube feeding d) Removal of excreta: Urine and stools removal. e) Care of the skin: Frequent changing PP f) Care of the eyes: Antibiotic eye drops& ointment). 7-Consider specific antidotes e.g. flumazenil for benzo.
II-Convulsions: (6) *Toxic *Traumatic *Pathologic *Metabolic *Idiopathic *Environmental Toxic causes: 1-Convulsions due to Withdrawal from alcohol or sedative hypnotic drug. 2-Convulsions due to Decalcification of the blood e.g. oxalic acid poisoning → tetanic convulsions 3-Convulsions due to Poisons acting on CNS.
Poisons acting on the cerebrum → muscular hyperactivity. E.g. Amphetamine, cocaine, caffeine & atropine. - Poisons acting on the brain stem → clonic convulsions i.e. contraction and relaxation of the muscles.e.g. picrotoxinPb - Poisons acting on the spinal cord → tonic convulsions i.e. sustained hypertonia of the muscles.e.g. as strychnine - Poisons → cerebral anoxia.e.g. cyanide.
-Metabolic causes: hypoglycemia, hyponatremia, hypocalcemia, or hypoxia. -Traumatic causes: head trauma with intracranial injury. -Idiopathic epilepsy -Exertional or environmental hyperthermia. Pathologic causes: -CNS infection: meningitis or encephalitis,febrile seizures in children.
Complications of convulsions: 1- Any seizures can cause airway compromise, resulting in apnea or pulmonary aspiration. 2- Multiple or prolonged seizures may cause severe metabolic acidosis, hyperthermia, rhabdomyolysis, and brain damage.
Treatment of convulsions: 1-Maintain an open airway and assist ventilation. 2- Use one or more of the following anticonvulsants: Diazepam (Valuim): mg/kg IV (5-10 mg) IM or IV Lorazepam (ativan) 2 mg IV, may repeat as needed. Short acting barbiturates or ultrashort acting as Pentothal sodium: 0.5 – 1 gm, slowly IV. Phenobarbital: 10-15mg/kg slowly IV infusion over minutes. Phenytoin: the anticonvulsant of last choice for most drugs induced seizures. Dilantin (phenytoin)10 mg/kg IV
3- Decontamination Skin Eye Lungs GIT
I-Skin decontamination Indications: 1- Cases of Corrosives to prevent skin injury. 2- Toxins that are readily absorbed through the skin (e.g. organophosphorous insecticides, paraquat, phenol, oxalic acid, …etc); to prevent systemic absorption. Steps of decontamination: a) Wear protective clothes & gloves. b) Remove the patient’s contaminated clothing. c)Flush exposed areas with copious quantities of taped water or saline for at least 30 minutes. Use soap for oily substances.
II. Eyes Indications: 1- Corrosive agents and hydrocarbon solvents that can rapidly damage the cornea. 2-Toxins that are readily absorbed through the skin can also be absorbed through the conjunctiva. Steps of decontamination: a) Flush exposed eyes with copious quantities of taped water or saline for up to 20 minutes. b)Ophthalmologic consultation is a must in patients with serious injury.
III. Inhalation Indications: 1. Irritating gases and fumes e.g. chlorine gas. 2. Toxins that are absorbed thorugh the respiratory tract e.g. CO, cyanide, hydrogen sulphide, organophosphorus insecticides. ((هام
Steps of decontamination: a) Ensure adequate respiratory protection for yourself and other care providers (wear protective mask). b) Remove the victim from exposure to fresh air. c) Care of respiration is started after cleaning the mouth, administer humidified O 2 (if available) and assist ventilation (if necessary). Tracheostomy or ETT may be needed. Observe for evidence of upper respiratory edema (manifested by stridor and hoarse voice) and a later non-cardiogenic pulmonary edema (manifested by dyspnea, tachypnea and hypoxemia).
A-Emesis: This is one of the most convenient methods used to get rid of the poison from the stomach. Emetic used : Syrup of ipecac Syrup of ipecac is the emetic of choice in both children over the age of 6 months and in adults. Ipecac is the dried root of Cephalus ipecaquanha plant that contains the active alkaloids emetine & cephaline.
It causes vomiting through 2 phases: Early vomiting (within 30 minutes): due to the direct local irritant action of ipecac on gastric mucosa, Late vomiting (after another 30 minutes) is the result of central stimulation of the chemoreceptor trigger zone. Dose: 30 ml for adults, 15 ml for children and 5 – 10 ml for children between 6 months and 2 years. If vomiting does not occur after 30 minutes, the dose is repeated. If still no vomiting, gastric lavage should be carried out to remove ipecac from the stomach (as it is toxic). NB: Manual digital stimulation or apomorphine are unsafe and should not be used.
Contraindications of emesis: 1) Substance: -Convulsants -Corrosives (inorganic) - Hydrocarbons -Sharp objects (needle, pin) 2) Patients: -Unconscious or comatosed patient. -Decreased gag reflex. -Severe CVS disease or emphysema or respiratory distress. -Recent surgical intervention. -Hemorrhagic tendencies. - Previous significant vomiting before this moment. - Under 6 months of age (gag reflex not well developed). -Pregnancy.
Advantages of emesis: -It is generally less traumatic than gastric lavage which is unpleasant to most people and must be done by qualified trained physician. -Emesis can recover particles that are too large to pass through the openings of gastric lavage tube.
Decrease Absorption: B. Gastric lavage a. provides immediate recovery of gastric contents. It Does not reliably remove pills and pill fragments b. Efficacy after the first hour or two is questionable c. Risk of Aspiration, so airway has to be protected (LLD position with some Trendelenberg or for a lethargic patient with a depressed gag, endo-tracheal intubation). d. Contraindicated as emesis (Rule of Except) in most hydrocarbon ingestions and in caustic ingestions
Decrease Absorption: C.Activated Charcoal Drug may adsorb into the charcoal and thereby prevent absorption in the first place. Useful for some drugs that undergo substantial enterohepatic recirculation, or small volume of distribution or low protein binding and are highly adsorbed by charcoal. Dose usually 1-2 g/kg orally or naso- gastric tube (Patient must be awake or intubated.
Decrease Absorption: C.Activated Charcoal – Multiple doses may be given: 0.5 g/kg every 2h h or 20g every 2 h for up to 48 h Indication of Repeat-dose activated charcoal –Very large ingestions of toxic substance –Sustained release and enteric coated preparations Carbamazepine, phenobarbital, phenytoin Salicylate, theophylline, digitoxin
Activated Charcoal Not good for: –Lithium –Iron –Alcohols –Lead –Hydrocarbons –Caustics –N.B. Recent studies suggest that activated charcoal alone is just as effective as gut emptying followed by charcoal (gut dialysis).
GI Decontamination Decrease Absorption: D. Cathartics –Hasten passage of ingestions or AC –Contraindications: obstruction, ileus, child 5y, corrosives –10% magnesium citrate 3ml/kg or 70% sorbitol 1-2 …./kg (not used now) –Severe fluid loss, hypernatremia, hyperosmolarity, renal failure with Mg catharatics, nausea & abdominal pain
GI Decontamination Decrease Absorption: E.Whole bowel irrigation Poly Ethylene Glycol ( movicol)-1 to 2 liters/hour until the material is recovered or the effluent is clear –Used for: Large ingestions, SR or EC tablets, packers (ex. cocaine) –Contraindications: obstruction or ileus –Complications: Aspiration, nausea, may decrease effectiveness of charcoal
Enhanced Elimination Urinary manipulation –Forced diuresis can cause fluid overload(CHF, Pulm Edema) –Alkalinization as in salicylate poisoning Hemodialysis, Hemoperfusion less dependent on molecular size, solubility, and protein binding, achieves greater clearance rates for most drugs
Enhanced Elimination Peritoneal dialysis, Hemofiltration less invasive than above, used for a continuous removal over time in a non- critical patient. Role in acute poisonings is unclear.
Enhanced Elimination Does the patient need it? –Severe intoxication with a deteriorating condition despite maximal supportive care –Usual route of elimination is impaired –A known lethal dose or lethal blood level –Underlying medical conditions that can increase complications
Antidotes AcetaminophenN-acetylcysteine (Mucomyst) Organophosphates Atropine, PAM (Toxoguanin) Anticholinergicphysostigmine Arsenic, mercury dimercaprol (DMSA) Benzodiazepinesflumazenil (Anexate) Beta blockersglucagon Calcium channel block calcium Carboxyhemoglobin (CO)100% O2, HBO Cyanidenitrite, Na thiosulfate ( Lilly kit) Digoxindigoxin antibodies (FAB) Physostigmine:-- Side effects: seizures, vomiting, diarrhea, abdominal cramping indications: tachydysrhythmias with hemodynamic compromise, intractable seizures or severe agitation or psychosis. Contraindications: conduction disturbances, prolonged QRS, PR
Antidotes Ethylene glycolfomepizole, HD Heparinprotamine sulfate Irondeferoxamine (dysferal) Isoniazidpyridoxime (Vit. B6) Methanol fomepizole, HD Methemoglobinmethylene blue Opioidsnaloxone (narcan) Salicylatealkalinization, HD TCA’ssodium bicarbonate WarfarinFFP, vitamin K Fresh Frozen Plasma
Toxidromes A group of typical signs and symptoms consistently associated with exposure to a particular type of toxin
Cholinergics Muscarinic only in 1-Organophosphates –Irreversibly bind cholinesterases 2- Carbamate –Reversibly bind cholinesterases, poor CNS penetration Muscarinic and nicotinic effects 1-Pesticides, nerve agents –Military personnel –Field workers, crop dusters –Truckers –Pest control, custodial workers O
Cholinergics Antidote –Atropine for muscarinic effects –Pralidoxime reverses phosphorylation of cholinesterase Irreversibly bind cholinesterases – acetylcholine supply increases and you exhaust the postsynaptic neuronal transmission in the CNS and PNS Muscarinic – parasympathetic effects Nicotinic – gives you muscular effects O
Anticholinergic Toxidrome DRY m.m ( thirsty ),& throat ( hoarseness ) DRY Flushed skin Mydriasis, blurred vision, loss of accommodation EYE Fever HIGH Tachycardia HIGH Hypertension HIGH Decreased bowel sounds S.Ms Urinary retention S.Ms Mental status changes ( hallucination, excitation ) CNS St. Seizures CNS St. Ataxia CNS St. Amanita muscaria mushroom
Antihistamines Antidepressants Atropine Antipsychotic (HOT as a hare) Hyperthermia (RED as a beet) Flushed (DRY as a bone) Dry skin (BLIND as a bat) Dilated pupils (MAD as a hatter) Hallucinations (Flappy as a bird) Tachycardia (Full as Container) Urinary retention
NICOTINIC TOXIDROME: (recalled by the days of the week): Saturday: Seizures Sunday: Somnolent Monday: Miosis Tuesday: Tachycardia Wednesday: Weakness Thursday: Tremors Friday: Fasciculations
References Poisoning & Drug Overdose, California Poison Control System. KR Olson, 3 rd edition, Appleton & Lange, Emergency Medicine Board Review Series. L Stead, Lippincott Williams & Wilkins, Emergency Medicine, A comprehensive study guide. Tintinalli, 6 th edition, McGraw Hill, 2008.
How to generally manage a toxic patient The most famous toxidromes, & antidotes Prescribe the ideal treatment for toxic patient