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2 مسمومیتهاي شايع داروئیمنابع -1- Goldfrank’s Toxicologic Emergencies 2015 2- / Emergency Medicine / Toxicology

3 فراواني مسموميت ها ی داروییMixed drug ingestion مواد مخدر –مواد محرک ضد افسردگي سه حلقه اي أنتي سايكوتيكها بنزو ديازپين ها بتابلوکرها مسكن ها

4 Tricyclic antidepressant poisoning داروهاي ضد افسردگي

5 داروهاي ضد افسردگي > 1 g : Life treateningآ مي تريپتيلين - نورتريپتيلين...ما پروتيلين -آموكساپين > 1 g : Life treatening one pill can kill (children) شروع علائم سريع )خطرناکترین لحظات 1-2 ساعت اول پس از خوردن تا 6 ساعت ) تغییر وضعیت ناگهانی

6 Clinical manifestationsDelirium, Hallucination, Hypertermia, ….

7 Hypotension Wide QRS (> 0.10 s) Ventricular Tachycardia

8 Tricyclic Antidepressants Symptoms1- Midriasis ; Tachycardia 2- Coma, 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

9 Management of TCA poisoning1- 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)

10 Antidote: Sodium BicarbonateHypotension Arrythmia, Wide QRS > 0.1 s, R avR  3 mm Seizure (wide QRS) 1-2 mEq / kg bolus , Infusion ( mEq / L D5W) repeated bolus (ABG) End point: Serum pH ( )

11 Seizure: Diazepam 0.1-0.2 mg/kg (5-10 mg), Midazolam 0.1 mg/kg, NaHCO3Hyotension: N.S., NaHCO3, Norepinephrine ( ug/kg/min), Dopamine (10-20 ug/kg/min) Wide QRS, R/avR>3 mm: NaHCO3 Coma: Glucose, Naloxone, Thiamine Delirium: Benzodiazepines

12 Ventricular Arrhythmias (VT)NaHCO3 (1-2 meq/kg) 5 min Lidocaine: 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:

13 Management of TCA PoisoningABCD , Antidote Gastric Lavage (GL) Activated Charcoal(AC) g/kg, g urine toxicology screen

14 Contraindicated medicationsbeta-blockers, calcium channel blockers, class IA (procainamide, quinidine, disopyramide, moricizine), class IC (flecainide, propafenone), and possibly class III (bretylium, amiodarone, sotalol) antidysrhythmics.

15 Management of TCA PoisoningRapidly 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.

16 Antipsychotics Large toxic to therapeutic ratioClinical 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)

17 Management ABCD Close Observation; Supportive treatment اكسيژنلوله گذاري داخل تراشه + ساكشن كردن بررسي نياز به گلوكز ((Counsciousness نالوكسان (Respiratory depression , pin point pupil ) Gastric Evacuation دادن زغال فعال 1 g/kg Close Observation; Supportive treatment

18 Seizure: Diazepam 0.1-0.2 mg/kg (5-10 mg), Midazolam 0.1 mg/kgHyotension: N.S., Norepinephrine ( ug/kg/min), Dopamine (10-20 ug/kg/min) Coma: Glucose, Naloxone, Thiamine Dystonic reaction: Diphenhydramine or Biperdine or Benzodiazepine (alternative) Wide QRS: NaHCO3

19 Benzodiazepine PoisoningCNS Depression (Somnolence, Stupor, Coma), Miosis, Ataxia Deep Coma, respiratory arrest (rare)

20 Symptoms of BZD overdose may include the followingDizziness Confusion Drowsiness Blurred vision Anxiety Agitation

21 Findings on physical examination may include the following:Nystagmus, Slurred speech Ataxia, Coma, Hypotonia Weakness, impairment of cognition Amnesia, Paradoxical agitation urine toxicology screen

22 Managment of BZD PoisoningABCD 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

23 Flumazenil 0.1-0.2 mg IV over 15-30 secIF 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

24 Beta-Adrenergic Receptor Antagonists

25 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.

26 Table 1-1* B-Adrenergic Receptor Antagonist Pharmacologic Profile

27 Clinical Manifestations of B-Adrenergic Antagonist ToxicitySystem Brady cardia, conduction delays, hypotension Cardiovascular Coma, seizures Central Nervous System Bronchospasm(unusual) Pulmonary Acidosis, hypoglycemia, Hyperkalemia Metabolic

28 Increased PR intervalsLoss of atrial activity Atrioventricular junctional rhythm Widening of the QRS complex Atrioventricular block Asystole prolonged QT interval: sotalol overdose. VF, VT: uncommon (sotalol)

29 Diagnosis History Clinical presentation ECG, ABG/VBGserum glucose and potassium levels.

30 Treatment end points HR>60 SBP>90mmHgEvidence of good organ perfusion Evidence of good organ perfusion (improved mentation or urine output)

31 Mangement ABCD Bradycardia Atropine (1 mg..>3 mg) Pace

32 Mangement (Hypotension)Isotonic IV fluid (20 mL/kg) Glucagon (5-10 mg IV slow) ( mcg/kg IV over 1 minute) Infusion: 3-5 mg/hr or mcg/kg/hr IV titrate to response Epinephrine for hypotension, bradycardia Unresponsive to atropine or pacing: 2-10 mcg/min by IV infusion or mcg/kg/min (7-35 mcg/min in 70 kg patient); titrate to response Calcium Chloride (1g IV central line/ over min (emergent 5 min) slow infusion Insulin: U/kg/h + Hypertonic glucose (10%,20,%, 50% 1 g/kg, check BS/30min) (Dextrose infusion of g/h may be required) Dopamine (5-20 ug/kg/min),Norepinephrine ( ug/kg/min)

33 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

34 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.

35 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 g Pediatric: 1-2 g/kg PO , up to g

36 با تشكر

37 Glucagon can enhance myocardial contractility, heart rate, and atrioventricular conduction;Load: mcg/kg IV over 1 minute, THEN  3-5 mg/hr or mcg/kg/hr IV; titrate infusion to achieve adequate clinical response

38 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 min intervals until optimum response obtained Titrate to desired response

39 calcium Beta-blocker Overdose, Refractory to Glucagon & High Dose Vasopressor Calcium chloride 1000 mg IV bolus via central line  over min (emergent 5 min)

40 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 g/h may be require

41 Acetaminophen Commonest drug used DANGEROUS , PEOPLE DON’T KNOW ITYOU FEEL WELL AND THEN THE LIVER FAILURE SETS IN.. NAPQI (TOXIC mtetabolite) Glutathione Toxic dose: 7.5 g , 150 mg/kg

42 Acetaminophen poisoningPhase 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)

43 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.

44 Acetaminophen Overdose-managementABCD ( 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

45 ارگانو فسفره موارد استفا د ه براي از بين بردن حشرات در كشاورزيپاراتيون ؛ ديازينون ؛ مالاتيون بعنوان گازهاي جنگي گاز جنگي سارين ؛ سومان

46 فارماكو كينتيك جذب : گوارشي ؛ پو ستي ؛ تنفسي ؛ چشمي متابوليسم : كبددفع : دفع متابوليتها از طريق ادرار نيمه عمر دفعي : 2/89 ساعت در مالاتيون و 2/1 روز در متيل پاراتيون

47 مهار كننده غیر قابل برگشت آنزيم كلين استرازمكانيسم اثر مهار كننده غیر قابل برگشت آنزيم كلين استراز شروع علا ئم : در طي چند دقيقه تا چند ساعت

48 1- علائم موسكاريني ابريزش از بيني تعريق ميوز اسهال، درد شکمیافزايش ترشح بزاق (سيالوره)، اشكريزش ابريزش از بيني تعريق ميوز اسهال، درد شکمی بی اختیاری ادرار و مدفوع برادي كاردي ؛ هيپو تانسيون

49 2- علائم نيكوتيني فاسيكولاسيون……….فلج عضلات تاكيكاردي هيپر تانسيونضعف فاسيكولاسيون……….فلج عضلات تاكيكاردي هيپر تانسيون ميدرياز

50 3- علا ئم سيستم عصبي مركزياضطراب گيجي كما تشنج دپرسیون مركز تنفس و قلبي

51 ABCD لوله گذاري داخل تراشه در صورت ترشحات فراوان اكسيژن آنتي دوتها: 1- آتروپين : باعث از بين رفتن علائم موسكاريني و سيستم عصبي مركزي مي شود. آتروپين تا زماني داده ميسود كه ترشحات خشك شوند و يا علا ئم مسموميت با آتروپين ظاهر شود. 2- پراليدوكسيم

52 Management of OPs PoisoningABCD (Intubation, Suctioning , Oxygen, MV) Antidotes: Atropine (Adult 1-2 mg IV, repeat every 1-5 min. Children, 0.01 mg/kg Infusion mg / 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

53 Opioid poisoning

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58 مواد مخدر ترياك هروئين بوپرنورفین متادون ترامادول دیفنوکسیلات

59 Pharmacokinetics 1- GI tract : Methadone, Diphenoxylate, OpiumPeak effects generally are IV, Inhalation: 1-5 minutes (Heroin) Nasal insufflation: minutes (Heroin) PO: 90 minutes 1- GI tract : Methadone, Diphenoxylate, Opium bioavailability :60-79% : methadone 2. Nasal mucosa: Heroin 3. IV, Inhalation, smoking Heroin 4. Rectal mucosal

60 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.

61 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.

62 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.

63 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)

64 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.

65 Tramadol (Ultram) absorbed rapidly65 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. Mechanism of action mu opiate receptor binding weak inhibition of NE & 5-HT 1 Ultram equivalent to 1 Tylenol #3

66 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, …

67 IVDU related infectionsBotulism: 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)

68 IVDU related infectionsHepatitis B & C HIV Malaria American trypanosomiasis (Chagas disease) Leishmaniasis (Spanish IVDU) Syphilis

69 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

70 Generalised infectionsBacteraemia (septicaemia) Pneumonia & lung abscess Endocarditis (heart valves) Other deep abscesses Septic arthritis Osteomyelitis etc

71 NEUROLOGICAL COMPLICATIONSComa 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

72 NEUROLOGICAL COMPLICATIONSBrain edema, myelin damage, astrocytic, globus pallidus cysts reduced neuronal populations.

73 Diagnosis (1) hypoxia (2) early stages of Lomotil poisoning when the atropine effects predominate (3) after the use of naloxone (4)potentially after the use of a co-ingestant (sympathomimetics, cyclic antidepressants). 1- history 2- clinical presentation * specific toxidromes a. miosis b. CNS depression c. respiration depression most opioid-related deaths, the most specific sign * Noncardiogenic pulmonary edema (NCPE) (Heroin, methadone) (Tachycardia, Tachypnea, …)(CXR) 3- screening technique : * qualitative(urine) Positive results are observed up to hours post-exposure, but wide variations are possible depending upon test sensitivity, dose, route, and the patient's metabolism. 1- decreased respiratory rate, Apnea, cyanosis, 2- hypoxia on pulse oximetry, 3- hypercarbia or hypoxia on ABG. Mydriasis

74 Aggressive airway managementGeneral Mx Specific Mx Aggressive airway management use of Naloxone are the mainstay of therapy.

75 Naloxone Life threatening (cyanosis):1- Respiratory support: Oxygen, Bag-vlave-mask, positioning, suctioning 2- Naloxone: 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

76 Altered mental status: Glucose [0Altered 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 :

77 Non-cardiogenic pulmonary edemaHeroin, Methadone Tachypnea, tachycardia, ..... Intubation + ventilation (PEEP)

78 Treatment Indications of ENDOTRACHEAL INTUBATION:1- long-acting opiates (methadone ,diphenoxylate,…) 2-Recurrent Res. Dep 3-Large initial dose of Naloxone 4-Body-packer 5-Suicidal attempt Ingestion (consider addiction) 6-Children 7-Low Staff support Treatment Dx and Treat min onset of action 5-10 min max effects 10-30 min half-life 30-90 min duration of action Route of administration : IV ,IM ,SC ,ET ,IL ,SL Indications of ENDOTRACHEAL INTUBATION: if there is no response to the Naloxone

79 DRUG ABUSE

80 Drugs Drugs refer to a non food substance that is deliberately taken to produce some physiological or psychological effect

81 Stimulants Amphetamines Quickly develop a toleranceFound 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

82 Acute overdose of amphetaminesCentral 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

83 Stimulants Methamphetamines Ice, crystalEuphoria, 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.

84 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 minutes, duration of amphetamine action is much longer, lasting as long as hours. Chronic use: Wt loss, Psychological addiction (Withdrawal see fatigue, depression), Infections

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92 Cocaine enters the United States in the form of a hydrochloride saltStimulants Cocaine Originally : relieve fatigue Very addictive Can be 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

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94 Crack is produced when the hydrochloride molecule is commonly removed by ether extraction, which frees the basic cocaine molecule, the so-called 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.

95 Cocaine / Crack Absorbs from mucous mbr, IVOnset 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)

96 Cocaine / Crack, ClinicalCNS: 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

97 Cocaine and Alcohol become the most common combinationforms 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

98 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.

99 Cocaine / Crack TreatmentASA / Heparin Na H CO3 1 – 2 mcg/Kg No ß-blocker (antagonize cocaine ß adrenergic stimulation and vasodilation) ECG monit (troponin) Benzodiazepine (no phenothiazine) “MONA” greets all patients: Morphine, O2, Nitroglycerin 0.2 – 0.5 mcg/kg/min

100 Ecstasy

101 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 mg of MDMA ($20-25) Effective doses: 1-2 mg/kg (initial effects in min, Peak effects at 90 minutes and may persist 4-8 h) Severe hyperthermia has been reported at doses of 4-5 mg/kg

102 Central nervous systemChange 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

103 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.

104 Hypertension: benzodiazepinerefractory 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

105 Ecstasy Parkinsonian symptoms, shaking with movementchronic depression Strong psychological addiction

106 Marijuana 5000 year old history Used as a pain reliever before aspirinEuphoria, 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

107 Marijuana Long term effects Chronic bronchitis and damage to lungsLung cancer Lower testosterone levels and abnormalities in sperm count Alters menstrual cycle, low birth weight infants Damages the immune system

108 با تشكر

109 Nalterexone *latency to onset (oral tablet 15-30 min.)*duration of action 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.