Transcript 1-2 mg/kg
مسمومیتهاي شايع داروئی منابع -1- Goldfrank’s Toxicologic Emergencies 2015 2- www.emedicine / Emergency Medicine / Toxicology فراواني مسموميت ها ی دارويی Mixed drug ingestion مواد مخدر –مواد محرک ضد افسردگي سه حلقه اي أنتي سايكوتيكها بنزو ديازپين ها بتابلوکرها مسكن ها Tricyclic antidepressant poisoning داروهاي ضد افسردگي داروهاي ضد افسردگي آ مي تريپتيلين -نورتريپتيلين...ما پروتيلين -آموكساپين > 1 g : Life treatening )one pill can kill (children شروع عالئم سريع ) خطرناکترين لحظات 2-1ساعت اول پس از خوردن تا 6ساعت ) تغيير وضعيت ناگهانی Clinical manifestations Delirium, Hallucination, Hypertermia, …. Hypotension Ventricular Tachycardia Wide QRS (> 0.10 s) Tricyclic Antidepressants Symptoms 1- Midriasis ; Tachycardia 2- Coma, 3- Delirium 4- Seizures 5- Hypotension 6- QRS > 0.1s ; R avR >= 3 mm ; Right Axis deviation ; Arrhythmias (VT) ECG is the single most important test to determine diagnosis and prognosis Management of TCA poisoning 1- ABCD ( Antidote) A:Airway compromise (Artificial airway, Intubation) B: Breathing difficulties (Oxygen, Intubation, Mechanical ventilation) C:Circulation Problems (IV line; ECG, Manage hypotension, VT) D: Drugs (Coma : Thiamine- Glucose-Naloxone – Oxygen) Antidote: Sodium Bicarbonate Hypotension Arrythmia, Wide QRS > 0.1 s, R avR 3 mm Seizure (wide QRS) 1-2 mEq / kg bolus , Infusion (50-150 mEq / L D5W) + repeated bolus (ABG) End point: Serum pH ( 7.45-7.55) Seizure: Diazepam 0.1-0.2 mg/kg (5-10 mg), Midazolam 0.1 mg/kg, NaHCO3 Hyotension: N.S., NaHCO3, Norepinephrine (0.10.2 ug/kg/min), Dopamine (10-20 ug/kg/min) Wide QRS, R/avR>3 mm: NaHCO3 Coma: Glucose, Naloxone, Thiamine Delirium: Benzodiazepines Ventricular Arrhythmias (VT) NaHCO3 (1-2 meq/kg) 5 min Lidocaine: 1-1.5 mg/kg slow IV bolus over 2-3 min up to 3 mg/kg total infusion: 1-4 mg/min IV IO/ET Monitor: ECG PH: 7.45-7.55 Management of TCA Poisoning ABCD , Antidote Gastric Lavage (GL) Activated Charcoal(AC) 1 g/kg, 50-100 g urine toxicology screen Contraindicated medications beta-blockers, calcium channel blockers, class IA (procainamide, quinidine, disopyramide, moricizine), class IC (flecainide, propafenone), and possibly class III (bretylium, amiodarone, sotalol) antidysrhythmics. Management of TCA Poisoning Rapidly transport all patients with possible TCA ingestion to the hospital because clinical deterioration often occurs rapidly after overdose. Supplemental oxygen and airway support (Intubation,..) Intravenous access, Cardiac monitoring Rapid glucose determination (finger stick) GL + Activated charcoal Sodium bicarbonate should be considered in life-threatening circumstances in the pre-hospital setting. Antipsychotics Large toxic to therapeutic ratio Clinical manifestations Antichlinergic (midriasis, Tachycardia,….) receptor blocking (Hypotension, Miosis):Chlorpromazine CNS (Coma, seizure,…) Dystonic reaction (Thiotexene, halloperidol, Perphenazine, Trifluperazine,..) Cardiovascular (Mesoridazime, Thioridazine, Chlorpromazine, Halloperidol) Respiratory depression ( Coma) Management ABCD اكسيژن ساكشن كردن+ لوله گذاري داخل تراشه (Counsciousness( بررس ي نيازبه گلوكز (Respiratory depression , pin point pupil ) نالوكسان Gastric Evacuation 1 g/kg دادن زغال فعال Close Observation; Supportive treatment Seizure: Diazepam 0.1-0.2 mg/kg (5-10 mg), Midazolam 0.1 mg/kg Hyotension: N.S., Norepinephrine (0.1-0.2 ug/kg/min), Dopamine (10-20 ug/kg/min) Coma: Glucose, Naloxone, Thiamine Dystonic reaction: Diphenhydramine or Biperdine or Benzodiazepine (alternative) Wide QRS: NaHCO3 Benzodiazepine Poisoning CNS Depression (Somnolence, Stupor, Coma), Miosis, Ataxia Deep Coma, respiratory arrest (rare) Symptoms of BZD overdose may include the following Dizziness Confusion Drowsiness Blurred vision Anxiety Agitation Findings on physical examination may include the following: Nystagmus, Slurred speech Ataxia, Coma, Hypotonia Weakness, impairment of cognition Amnesia, Paradoxical agitation urine toxicology screen Managment of BZD Poisoning ABCD Antagonist: Flumazenil pure BZD overdose + verbally unresponsive +no history of long-term BZD use or seizure disorder not recommended for use by pre-hospital personnel Contraindication (past history of seizure, co ingestion with drugs induced seizure e.g. TCA; BZD addiction) Decontamination within 1-2 h of ingestion Gastric Lavage + Activated charcoal Flumazenil 0.1-0.2 mg IV over 15-30 sec IF no response after 30 sec, administer 0.3 mg over 30 sec 1 min later Rarely patient may require titration up to total dose 5 mg; IF no response after 5 min, sedation unlikely to be secondary to benzodiazepines Beta-Adrenergic Receptor Antagonists In use for nearly 50 years. treating hypertension and other cardiovascular disorders migraine headaches, anxiety, and various other disorders. As a result of their expanded use, the incidence of overdose with these agents has also increased. Table 1-1* B-Adrenergic Receptor Antagonist Pharmacologic Profile Agent Acebutolol Atenolol Esmolol Metoprolol Labetolol Nadolol Pindolol Propranolol Sotalol Timolol ß Lipid selective Solubility yes yes yes yes No No No No No No low low low moderate moderate low moderate High low moderate Elimination Half- Life 3-4 hours 6-9 h. 10 minutes 3-4 h 5h 14-24 h 3-4 h 3-6 h 12 h 4 -5 h Clinical Manifestations of B-Adrenergic Antagonist Toxicity System Manifestations Cardiovascular Brady cardia, conduction delays, hypotension Central Nervous System Coma, seizures Pulmonary Bronchospasm(unusual) Metabolic Acidosis, hypoglycemia, Hyperkalemia Increased PR intervals Loss of atrial activity Atrioventricular junctional rhythm Widening of the QRS complex Atrioventricular block Asystole prolonged QT interval: sotalol overdose. VF, VT: uncommon (sotalol) Diagnosis History Clinical presentation ECG, ABG/VBG serum glucose and potassium levels. Treatment end points HR>60 SBP>90mmHg Evidence of good organ perfusion Evidence of good organ perfusion (improved mentation or urine output) Mangement ABCD Bradycardia Atropine (1 mg..>3 mg) Pace Mangement (Hypotension) Isotonic IV fluid (20 mL/kg) Glucagon (5-10 mg IV slow) (50-150 mcg/kg IV over 1 minute) Infusion: 3-5 mg/hr or 50-100 mcg/kg/hr IV titrate to response Epinephrine for hypotension, bradycardia Unresponsive to atropine or pacing: 2-10 mcg/min by IV infusion or 0.1-0.5 mcg/kg/min (7-35 mcg/min in 70 kg patient); titrate to response Calcium Chloride (1g IV central line/ over 10-20 min (emergent 5 min) slow infusion Insulin: 0.1-1 U/kg/h + Hypertonic glucose (10%,20,%, 50% 1 g/kg, check BS/30min) (Dextrose infusion of 10-75 g/h may be required) Dopamine (5-20 ug/kg/min),Norepinephrine (0.1-0.2 ug/kg/min) Insulin-Glucose should be considered for overdoses that are refractory to crystalloids, glucagon, and catecholamine infusions. monitoring serum glucose and potassium levels Monitoring must be conducted regularly during high-dose insulin therapy and for up to 24 hours after its discontinuation. Dextrose supplementation is typically required to maintain euglycemia Benzodiazepines : if seizures occur. Hemodialysis : severe cases of atenolol overdoses because atenolol is less than 5% protein bound and 40-50% is excreted unchanged in urine. Nadolol, sotalol, and atenolol (low lipid solubility, low protein binding) reportedly are removed by hemodialysis. Acebutolol is dialyzable. Consider hemodialysis or hemoperfusion only when treatment with glucagon and other pharmacotherapy fails. Cardiac pacing: Cardiac pacing may be effective in increasing the rate of myocardial contraction. cardiac pacing for patients unresponsive to pharmacologic therapy torsade de pointes unresponsive to magnesium Resuscitation should be aggressive and prolonged. Gastric lavage may be beneficial if the patient presents to the ED within 1-2 hours of ingestion. Activated charcoal Although most useful if used within 4 h of ingestion, repeated doses may be used, especially with ingestions of sustained-released agents. Adult:1 g/kg PO up to 50-100 g Pediatric: 1-2 g/kg PO , up to 15-30 g 35 با تشكر Glucagon can enhance myocardial contractility, heart rate, and atrioventricular conduction; Load: 50-150 mcg/kg IV over 1 minute, THEN 3-5 mg/hr or 50-100 mcg/kg/hr IV; titrate infusion to achieve adequate clinical response Dopamine 5-15 mcg/kg/min IV (medium dose): May increase heart rate, and cardiac contractitlity 20-50 mcg/kg/min IV (high dose): May increase blood pressure and stimulate vasoconstriction; may not have a beneficial effect in blood pressure; may increase risk of tachyarrhythmias May increase infusion by 1-4 mcg/kg/min at 10-30 min intervals until optimum response obtained Titrate to desired response calcium Beta-blocker Overdose, Refractory to Glucagon & High Dose Vasopressor Calcium chloride 1000 mg IV bolus via central line over 10-20 min (emergent 5 min) Insulin-Glucose The currently recommended regimen is a 1 U/kg of an insulin bolus followed by continuous infusion of 1-10 U/kg/h, but boluses of up to 10 U/kg and continuous infusions as high as 22 U/kg/h have been used with good outcomes and minimal adverse events. Dextrose infusion of 10-75 g/h may be require Acetaminophen Commonest drug used DANGEROUS , PEOPLE DON’T KNOW IT YOU FEEL WELL AND THEN THE LIVER FAILURE SETS IN.. NAPQI (TOXIC mtetabolite) Glutathione Toxic dose: 7.5 g , 150 mg/kg Acetaminophen poisoning Phase 1 (0-24 h) Asymptomatic Anorexia, Nausea or vomiting, Malaise serum transaminases levels 12 hours postingestion Phase 2 (18-72 h) Right upper quadrant abdominal pain, anorexia, nausea, vomiting, rise in serum transaminases Phase 3 (72-96 h) Hepatic necrosis with continued abdominal pain, Jaundice , Coagulopathy, Hepatic encephalopathy, Renal failure, Fatality Phase 4 (4 d to 3 wk) Complete resolution of symptoms (7-10 days), or death, Complete heaptic recovery (3-6 months) Acetaminophen ingestion should be considered as a potential cause of illness in patients who present with hepatic dysfunction of unknown etiology. Acetaminophen crosses the placenta, and the fetal liver is able to elaborate NAPQI by 14 weeks of gestation. A delay in treating pregnant patients with antidotal therapy is associated with fetal demise. Acetaminophen Overdosemanagement ABCD ( usually well systemically) Gastric lavage, Activated charcoal Antidote: N-Acetylcysteine, IV (20 h) Shown to be advantageous if given in the first 8 hours Early administration of NAC, within 8 hours of ingestion, is nearly 100% hepatoprotective NAC should be administered if the patient presents close to or later than 8 hours after an acute ingestion or if the patient is pregnant. Follow up ارگانو فسفره موارد استفا د ه براي از بين بردن حشرات در كشاورزي پاراتيون ؛ ديازينون ؛ ماالتيون بعنوان گازهاي جنگي گاز جنگي سارين ؛ سومان فارماكو كينتيك جذب :گوارشي ؛ پو ستي ؛ تنفسي ؛ چشمي متابوليسم :كبد دفع :دفع متابوليتها از طريق ادرار نيمه عمر دفعي 2/89 :ساعت در ماالتيون و 1/2روز در متيل پاراتيون مكانيسم اثر مهار كننده غير قابل برگشت آنزيم كلين استراز شروع عال ئم :در طي چند دقيقه تا چند ساعت -1عالئم موسكاريني افزايش ترشح بزاق (سيالوره) ،اشكريزش ابريزش از بيني تعريق ميوز اسهال ،درد شکمی بی اختياری ادرار و مدفوع برادي كاردي ؛ هيپو تانسيون -2عالئم نيكوتيني ضعف فاسيكوالسيون……….فلج عضالت تاكيكاردي هيپر تانسيون ميدرياز -3عال ئم سيستم عصبي مركزي اضطراب گيجي كما تشنج دپرسيون مركز تنفس و قلبي ABCD لوله گذاري داخل تراشه در صورت ترشحات فراوان اكسيژن آنتي دوتها : -1 آتروپين :باعث از بين رفتن عالئم موسكاريني و سيستم عصبي مركزي مي شود . آتروپين تا زماني داده ميسود كه ترشحات خشك شوند و يا عال ئم مسموميت با آتروپين ظاهر شود. -2 پراليدوكسيم Management of OPs Poisoning ABCD (Intubation, Suctioning , Oxygen, MV) Antidotes: Atropine (Adult 1-2 mg IV, repeat every 1-5 min. Children, 0.01 mg/kg Infusion 0.02-0.08mg / kg/h (depends on patient) Pralidoxime :Adult 1-2 g / 200 cc Normal saline IV/30 min Continued infusion Up to 500 mg / h Gastric Lavage + Activated charcoal + Dermal Decontamination Opioid poisoning مواد مخدر ترياك هروئين بوپرنورفین متادون ترامادول ديفنوکسیالت Pharmacokinetics 1- GI tract : Methadone, Diphenoxylate, Opium Peak effects generally are bioavailability :60-79% : methadone IV, Inhalation: 1-5 minutes (Heroin) 2. Nasal mucosa: Heroin Nasal insufflation: 10-15 minutes (Heroin) 3. IV, Inhalation, smoking Heroin PO: 90 minutes 4. Rectal mucosal Methadone (Dolophine) excellent oral bioavailability (to 100%). Metabolism: 90% metabolized in the liver and intestines ……> excreted almost exclusively in feces ( an advantage in patients with renal insufficiency or failure), <10% unchanged High lipid solubility, it is redistributed to the fat tissues, and has a very long elimination phase, with a half-life of up to 150 hours. Methadone (Dolophine) The metabolism of methadone is always variable. Methadone is metabolized by CYP3A4 primarily and CYP2D6 secondarily; CYP3A4 expression can vary up to 30-fold, and there can be genetic polymorphism of CYP2D6, ranging from poor to rapid metabolism. Methadone (Dolophine) its analgesic action (4-8 hours) is significantly shorter than its elimination half-life (up to 150 hours), and patient self-directed re-dosing and a long half-life may lead to the potential of respiratory depression and death. lack of awareness of its metabolism its long half-life…….> increase in the deaths associated with this medication. Risk of Torsades de Pointes, a potentially fatal arrhythmia, Congenital QT prolongation, high methadone levels (usually over 200 mg per day), conditions that increase QT prolongation (hypokalemia and hypomagnesemia) Pharmacokinetics A single day’s maintenance dose in a tolerant dult can cause life-threatening respiratory depression in an adult who is not tolerant, and as little as 10 mg can be fatal in a child. Tramadol (Ultram) absorbed rapidly one fifth to one tenth as potent as morphine. max dose: 400 mg/24 hrs decrease dose in elderly & renal impaired May enhance risk of seizures Caution should be exercised when combining tramadol with MAOIs, neuroleptic agents, and other drugs that lower the seizure threshold. Heroin Adulterants When heroin first enters the U.S., it may be 95% pure, by the time it is sold, it is 3 to 5% pure. Heroin combined with cocaine is called “speedballing.” Iran heroin has strychnine, Lactose, mannitol, quinine, Talcum powder, starch, curry powder Other adulterants: Caffeine, Acetaminophen, Phenobarbital, … IVDU related infections Botulism: Subcutaneous or IM administrations (26 case of botulism in California; impure form of heroin : black tar heroin) Tetanus: users of quinine-adulterant heroin more likely to develop tetanus than no-quinine-adulterant heroin (extensive tissue destruction by SC or IM quinine) IVDU related infections Hepatitis B & C HIV Malaria American trypanosomiasis (Chagas disease) Leishmaniasis (Spanish IVDU) Syphilis Non viral infections Usually staphylococci (75%) and/or streptococci from skin Anaerobes from mouth Faecal organisms from groin area Fungi from lemon juice Contaminants from drugs Anaerobes with muscle popping Murphy EL et al. J Inf Dis 2001; 33: 35-40 Bassetti S, Battegay M. Infection 2004; 32: 163-9 Generalised infections Bacteraemia (septicaemia) Pneumonia & lung abscess Endocarditis (heart valves) Other deep abscesses Septic arthritis Osteomyelitis etc NEUROLOGICAL COMPLICATIONS Coma without complications Hypercapnia, hypoxia, cardiorespiratory arrest Most recover & discharged Coma with neurological sequelae -Seizures -Acute delirium -Delayed post anoxic encephalopathy (residual weakness, cognitive impairment, spasticity) -Involuntary movement disorder (Parkinsonism, dystonias) Deaf ness NEUROLOGICAL COMPLICATIONS Brain edema, myelin damage, astrocytic, globus pallidus cysts reduced neuronal populations. Diagnosis (1) hypoxia 1- history 2- clinical presentation (2) early stages of Lomotil poisoning when the atropine * specific toxidromes 1- decreased respiratory rate, effects predominate a. miosis cyanosis, (3) after the b. Apnea, CNSof depression use naloxone 2- hypoxia on pulse oximetry, c. respiration depression most opioid-related deaths, the most specific (4)potentially after the use of a co-ingestant sign 3- hypercarbia or hypoxia on * Noncardiogenic pulmonary edema (NCPE) (Heroin, cyclic antidepressants). Mydriasis (sympathomimetics, ABG. methadone) (Tachycardia, Tachypnea, …)(CXR) 3- screening technique : * qualitative(urine) Positive results are observed up to 36-48 hours post-exposure, but wide variations are possible depending upon test sensitivity, dose, route, and the patient's metabolism. Management General Mx Specific Mx Aggressive airway management use of Naloxone are the mainstay of therapy. Naloxone Life threatening (cyanosis): 1- Respiratory support: Oxygen, Bag-vlave-mask, positioning, suctioning 2- Naloxone: 0.4-2 mg (IV, IT, SC, IM, IL, SL)..…………….> Correct respiratory depression Intubation and ventilation Children: 0.1 mg kg Non life threatening: (RR < 14 without cyanosis or res. Arrest,..) Respiratory support: Oxygen, Bag-vlave-mask Addict: Initial 0.05 mg…> Correct respiratory depression Non-addict: 0.4 mg….> Correct respiratory depression Altered mental status: Glucose [0.5-1 g/kg (DW 50% in adult, 20% children, 10% neonate)] Thiamine ICU, pulseoxymetery, ABG or VBG Wards: Close observation (Parents or friends,….) Gastric evacuation (kind, route, time,..) Activated charcoal : 1 g /kg Body packers: Whole bowel irrigation (poly ethelene glycole) Multiple dose of AC : Non-cardiogenic pulmonary edema Heroin, Methadone Tachypnea, tachycardia, ..... Intubation + ventilation (PEEP) Dx and Treat 1-3 min onset of action 5-10ofmin max effects Indications ENDOTRACHEAL 1- long-acting 10-30 minopiates half-life INTUBATION: (methadone30-90 ,diphenoxylate,…) min duration of if there is no response to the Naloxone action 2-Recurrent Res. Dep 3-Large initial dose of Naloxone Route of administration : 4-Body-packer IV ,IM ,SC ,ET ,IL ,SL 5-Suicidal attempt Ingestion (consider addiction) 6-Children 7-Low Staff support Treatment DRUG ABUSE Drugs Drugs refer to a non food substance that is deliberately taken to produce some physiological or psychological effect Stimulants Amphetamines Quickly develop a tolerance Found in diet pills Students, truck drivers use them to stay awake When the drug wears off you suddenly fall asleep Avoid the experimental stage and use it for a specific reason which increases the chance for addiction Depression occurs during withdrawal Must deal with psychological addiction Acute overdose of amphetamines Central nervous system Change of mental status, disorientation, and headache, Dyskinesias, Agitation, Stroke Cardiovascular Chest pain, Palpitations Gastrointestinal Dry mouth, Nausea and vomiting, Diarrhea Genitourinary - Difficult micturition Skin/cutaneous Diaphoresis, Erythematous painful rashes, needle marks, Infected deep ulcerations (ecthyma) Ocular - Mydriasis Seizures, hypertension, tachycardia, hyperthermia, psychosis, hallucinosis, stroke, and fatality Stimulants Methamphetamines Ice, crystal Euphoria, stimulant, and anorectic effects Effects felt in first 7 seconds after smoked, injected, pills or snort Effects last several hours The euphoria produced by methamphetamine appears similar to that produced by cocaine. taken orally, IV, or smokable form Patients who inhale the smokable form of methamphetamine (ice): immediate euphoria similar to that of crack cocaine, but the effects may last much longer. Methamphetamines synthesis from inexpensive and readily obtainable chemicals has led to the widespread increase in abuse of this dangerous drug. Methamphetamine lacks much of the peripheral stimulant properties of amphetamine while still offering euphoric and hallucinogenic properties. These actions are similar to those of cocaine; however, while effects of cocaine last for 10-20 minutes, duration of amphetamine action is much longer, lasting as long as 10-12 hours. Chronic use: Wt loss, Psychological addiction (Withdrawal see fatigue, depression), Infections Stimulants Cocaine Can be Originally : relieve fatigue Very addictive Snorted Injected Ingestion Effects do not last long Repeat dose in 5-30 min especially for heavy users Cocaine enters the United States in the form of a hydrochloride salt Crack is produced when the hydrochloride molecule is commonly removed by ether extraction, which frees the basic cocaine molecule, the socalled freebase. Heating does not destroy freebase, these are physical properties that allow it to be smoked. Crack is lipid soluble and therefore rapidly absorbed in the pulmonary capillaries. The term crack characterizes the crackling sound heard when cocaine freebase is smoked. Crack may be smoked in a pipe bowl or in a cigarette Smoking crack bypasses the vasoconstriction that results when cocaine is snorted; therefore, the effects are similar to taking cocaine IV. Crack smokers may aggressively inhale against a small pipe and then perform a Valsalva maneuver before exhaling against pursed lips or forcefully blow the drug into a partner's mouth. These techniques are reputed to enhance the euphoria of cocaine. Cocaine / Crack Absorbs from mucous mbr, IV Onset 1-2 minutes, ½ life = 60 min passive inhal./breast milk seizure blocks reuptake of neurotransmitters on presyn, nerves (Accumulation of Epi, Nor, Dopa, Serot) and is a fast Na channel blocker (prolongs QRS) Cocaine / Crack, Clinical CNS: mood elevation, hallucination, tremor, hyper , mydriasis, Seizures Resp.CV: Hypertension, ACS (Acute Coronary Syndrome) 02 demand, coronary artery const. Myocardial infarction, chest pain. Prolonged QRS, QT, VT, VF Platelets: Aggregation, activation Cocaine and Alcohol become the most common combination forms a metabolite, Cocaethylene, which is less potent than cocaine but has longer half life (3-5X longer) risk of sudden death increases to as high as 20 times than with cocaine use alone Stimulants Crack/ cocaine Very addictive Combines cocaine with baking soda and heated in a pipe and vapors inhaled into the lungs May be combined with heroin or methamphetamine and given IV a speedball In both cases, the second drug is used to supplement, rather than substitute, the primary drug. Cocaine / Crack Treatment ECG monit (troponin) Benzodiazepine (no phenothiazine) “MONA” greets all patients: Morphine, O2, Nitroglycerin 0.2 – 0.5 mcg/kg/min ASA / Heparin Na H CO3 1 – 2 mcg/Kg No ß-blocker (antagonize cocaine ß adrenergic stimulation and vasodilation) Ecstasy MDMA (ecstasy, XTC, Adam, E, X, clarity, Stacy) MDMA is available as a tablet, capsule, powder, and liquid; most commonly is used in tablet form Dancing Tablet Each tablet contains 50-100 mg of MDMA ($20-25) Effective doses: 1-2 mg/kg (initial effects in 30-60 min, Peak effects at 90 minutes and may persist 4-8 h) Severe hyperthermia has been reported at doses of 4-5 mg/kg Central nervous system Change in mental status, seizures, Anxiety, paranoia, Increased psychomotor activity, restlessness, Hyperthermia, hot flashes, Headache, Ataxia, Blurred vision, halos, Syncope Cardiovascular Palpitations , Chest pain Gastrointestinal Dry mouth, Nausea, vomiting, Abdominal cramping, Anorexia Skin Diaphoresis, Piloerection Urinary retention, difficulty voiding, Sexual dysfunction ABCs: ETI and MV (seizures, cardiovascular instability, or trauma) (oxygen, IV access, cardiac monitoring) A bedside glucose determination (altered mental status) Place the patient in a calm quiet room Agitation or disruptive behavior: benzodiazepines and/or physical restraints acute toxicity by ingestion (GID + activated charcoal) Whole bowel irrigation (body packing of drugs is suspected) Severe hyperthermia (aggressive cooling measures and adequate fluids) Obtain a rectal temperature. Morbidity is directly related to the severity and duration of hyperthermia. Undress the patient. Apply evaporative cooling with water and a fan. Apply ice packs to the groin and axilla. Iced gastric lavage may be considered. Control shivering with a benzodiazepine. Antipyretics are not useful. Hypertension: benzodiazepine refractory symptoms or signs of end-organ damage, (nitroprusside or nitroglycerin) Pregnancy testing in patients with overdose. MDMA, like all amphetamines, can be toxic to the fetus and may induce miscarriage or premature labor Ecstasy Parkinsonian symptoms, shaking with movement chronic depression Strong psychological addiction Marijuana 5000 year old history Used as a pain reliever before aspirin Euphoria, heightened sensory experience THC active ingredient, fat soluble and may stay in body tissue for a month High probability of psychological dependence, low probability of physical dependence Used for glaucoma, chemotherapy and AIDS patients Marijuana Long term effects Chronic bronchitis and damage to lungs Lung cancer Lower testosterone levels and abnormalities in sperm count Alters menstrual cycle, low birth weight infants Damages the immune system با تشكر Nalterexone *latency to onset (oral tablet 15-30 min.) *duration of action 24-72 hours *peak effect (6-12 hours) opioid receptor antagonist. It is longer acting than naloxone Plasma half-life of 8 to 12 hours versus 0.5 to 1.5 hours, Naltrexone, like naloxone, can stimulate the cardiovascular system.