1 supportive or symptomatic treatment 11/4/2011 management of poisons in conscious patient: 1)...

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Supportive or Symptomatic Treatment 11/4/2011

Management of Poisons in Conscious Patient:1) Establish and stabilize adequate vital signs of Patient (CV, Respiration, CNS)

2) Clinical evaluation (Lab test, blood chemistry, liver enzymes)

3) Determine the cause for the symptoms (body temperature, pupil size, breath)

4) Removal of unabsorbed or the remaining portion of poison from the site of exposure

* immediate action

*gastric emptying, (emesis, lavage,cathartics, neutralization,antidotes), * enhance elimination (diuresis, changing urine pH),

* artificial & mechanical removal of the remaining poison)

5) Supportive & Symptomatic Treatment

6) Patient Disposition

7) Poison prevention

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Supportive or Symptomatic Treatment

5) Supportive & Symptomatic Treatmenta) General treatment strategy of relieving symptoms without actually treating the cause (at this point, symptoms is treated and not the poison)

b) Regular medical treatment of each symptom separately (nausea & vomiting, bleeding, changes in body temperature, CV, seizure, convulsion) c) If the patient is suffers from acidosis, most likely is hyperkalemic ( K) & has an electrolytes imbalance (Na+ & K), Na+ level needs to be adjusted d) Adjust respiratory gases e) If bradycardia develops, an external pacemaker may be necessaryf) If sever hypotension develops, an Intra-Aortic Balloon Pumps (IABP) is inserted into the aorta to help maintaining blood pressureg) If hyperthermia develops (ASA & salicylates can produce hyperthermia & may lead to seizers in children), use of Tepid sponging (warm water) to return the child normal temperature (also used for restless, tense patient)h) Ice packs and alcohol sponging should not be used for toxic poisoning

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Disposition

• After released from hospital, patient should follow up with recommended treatment for the specific symptoms

• Legal issues should be address:– If toxicity is resulted from suicide or homicide attempted, authorities must be

notified

– Psychiatric should follow up regularly for the suicide cases

– If a child was overdosed, the case should be reported to Social Service

– Substances resulted in chronic effects, should be monitored & need follow up:• acetaminophen (APAP) may cause delayed liver damage (liver enzymes must be

monitored regularly

• Iron overdose, may cause delayed mucosal effects & clotting deficiencies

• Any slow in improvement of the condition, patient should be referred to specialist

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Poisoning Prevention (1)• Storage: medicines & chemicals should be stored safely out of reach &

out of sight of children, up high (at least 5-6 ft high) in a locked or child resistant cupboard. Many poisonings occur when a product or medicine is not in its usual storage location, when it is in use and left on a bench top or bedside table, or during transport from shop to

home.

• Safe use: Use medicines and chemicals safely. Read directions for use carefully. Do not leave them unattended whilst in use.

Separate medicines from household products. • Identification: Be sure that all products are properly labeled. Read the

label carefully before use.• Regular clean up: Clean out your medicine cupboard every several weeks.

Take unwanted and out-of-date medicines to your nearest pharmacy for disposal.

• Children tend to imitate adults, so avoid taking medicines in their presence.

• Refer to medicines by their proper names. They are not lollies.

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Poisoning Prevention (2)

• Watch the children at home: Visitors' bags may contain medicines. Keep them well out of reach of children. Also, the incidence of poisoning increases

when usual household routines are disrupted (moving being on holiday, parties and having visitors).

• Use child resistant packaging: always ask for and use household and medicines which are in child resistant packaging (e.g., blister or strip packs or

special push and turn lids).• Know what you are taken: Always take medicines in a well lit room, wear your

glasses. Follow the directions for use carefully and accurately. Do not take other peoples medicines.

• Use of house cleaning: Use appropriate protection when painting, spraying or oven cleaning. Follow the directions for use. Protect skin and eyes. Ensure

there is adequate ventilation, with air circulating continuously. Remove any contaminated clothing immediately.

• Rinsing: all empty containers from liquid medications or household products should be rinsed with water before they are thrown out.

• Keep everything in original containers and never in cups or soft drink bottles.

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Agents-induced toxicity

• Hypoxia Producing Poisons – Carbon monoxide

– Cyanide toxicity

• Corrosives and house hold cleaners toxicity

• Toxicity of drug of abuse

• Toxicity of therapeutic agents and drug overdose

• Radiation toxicity

• Pesticides/Insecticides and Insect Repellants toxicity

• Rodentcidies and Herbicides toxicity

• Heavy metals toxicity

• Food Poisoning

• Natural and other environmental toxins (i.e, Radon)

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Agents-induced toxicityHypoxia Producing Poisons

Carbon monoxide (CO) poison• Endogenous & Environmental sources of CO:

• Produced endogenously in human body @ rate of 0.4 %/hr (breakdown of the heme protein)

• The level is much higher in smokers (5-10% Carboxyhemoglobin COHb)• CO produced as a result of incomplete combustion • Burning Natural gas water heater, oil, coal, gasoline (garden tools), wood

burning stove/fireplace• Faulty gas stoves, faulty space heaters, unclean chimneys, and car exhaust

– This has been used for the purpose of suicide (car exhaust)

Why CO is so treacherous: It is odorless, colorless, and tasteless know as the silent killer

*** CO poisoning cause the death of 500 persons/year & 15,000 visit to the hospital emergency room/year (CDC)

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Hypoxia Producing Poisons Carbon monoxide (CO) poison

* It has a high affinity for hemoglobin (250 times that of O2) * It will also displace O2 very rapidly & decreases O2 dissociation from hemoglobin (make O2 not readily available to the tissues, causing hypoxia

* Hypoxic hypoxia (Hypoxia to tissues as a result of hypoxia in the blood) * The brain and the heart are most affected -The brain can not perform any anaerobic reactions (depends on O2) - The final reason CO is so treacherous is because at low levels it

produces fainting.

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Hypoxia Producing Poisons Carbon monoxide (CO) poison

Symptoms of CO poisoning:* < 10% (%= the amount hemoglobin converted to carboxyhemoglobin, COHg), no

serious symptoms

• * 20% - headache, tightness across forehead, dilation of blood vessels

• * 20-30%, visual disturbances, sever headache (brain function is affected),Tachycardia, Tachypnea, Possible nausea and vomiting

* 30-40%, increased Tachycardia and Tachypnea, Syncope (fainting), inability to leave the place where the poisoning is taking place

• * 50%, while in syncope, there is an increase in neuronal activity and convulsions result, coma develops due to exhaustion of the CNS

• * 60% and higher, DEATH

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Carbon Monoxide Poisoning

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* Populations with increased sensitivity to CO (at high risk):

• o Anemic• o Females, due to having less

hemoglobin• o Children, due to their high metabolic

rate• o Chronic Obstructive Pulmonary Disease (COPD) • o Hyperthyroid sufferers due to

metabolic rate

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• * Treatment and Prevention of CO poisoning:- Resuscitate the patient (ASAP, Sustain respiration, CNS, and circulation )

– - Give pure 100% O2– - CO has a half-life of 4 hours (Carboxyhemoglobin). If we use 100% O2, we

will decrease CO half life to 40 minutes (Decreased chance for brain damage). – - It the patient is placed into a hyperbaric chamber the CO half life will be

decreased even more to 20 minutes.

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* * Treatment and Prevention of CO poisoning

* To get rid of the cerebral edema• - Use an osmotic diuretic (Mannitol)

- Give a glucocorticoid (Prednisone) to decrease inflammation

• - Due to anaerobic metabolism, acidosis may develop

• -Can lead to coma (give IV Na HCO3)

• -Can also cool the patient to decrease the demand of the CNS

• In any case, if one even suspect CO poisoning, do not hesitate to call the National Poisoning Control Center 24/7. Do not wait until is a matter of life and death

• Prevention: Install CO detector (every home should have one)

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• * Outcome of CO poisoning – § Impairment of the CNS– § Muscle Weakness– § Depression– § Parkinson’s –like symptoms – § Decreased & blurred vision– § Numbness in the extremities – § Speech impairment– § Paralysis– § various degrees of symptoms may last for up to two years after the

incident – § If exposure was the result of car exhaust fumes, then treat the CO

poisoning and also for alcohol intoxication.

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Hypoxia Producing Poisons

2) Cyanide Poisoning • Cyanide is 1st isolated in pure form in 1786 by

Scheele from the dye Prussian blue• Its sever toxicity was also discovered by

Scheele (was killed when inhaling the vapor)• One of the most rapidly acting lethal poisons

known to the public– i.e., homicidal disasters as the Jonestown massacre

33 years ago– Cyanide-laced Tylenol in Chicago in 1982

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Cyanide Poisoning

• Cyanide (CN- ) negatively charged ion• It present either in the gas form as Hydrogen

Cyanide (HCN), as a liquid or solid forms as Cyanide salts

• At physiological pH 7.4 (unbound), in present in the form of HCN

• HCN Can be formed when acid added to a Cyanide salt

• It is concentrated in the RBC than in plasma (100:1) • In RBC, 92-95% CN- is bound to Hb

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Cyanide Poisoning Sources of exposure

1) Industry: • electroplating (HCN gas or particulates in the air)

• Extraction of Ores (gold and silver)

• Metal processing

• Manufacturing of plastics, pesticide, rodentcidies

• Hair removal from hides (in tanning industry)

• In pressure-treated wood (lumber)

• Acetonitrile: a chemical widely used in laboratories & some cosmetic removal is metabolized to CN when ingested

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2) Plants: (food/dietary supplements) – Many plants (fruit pits of Apricot, Bitter Almond, Peach,

Plum) containing Amygdalin a cyanogenic glycoside, a cyanide producing substance (glucose, benzaldehyde + CN)

– The enzyme -glucosidase (found in these plants and in human GI tract) will hydrolyze the glycosides HCN

– Amygdalin (active ingredient in Laetrile) is hydrolyzed by the enzyme emulsin (in GI) HCN

– CN poisoning will develop if the kemels (i.e. Almond) is eaten raw

– Once the kemels are processed, destroying the emulsin and CN poisoning will not occur

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3: Combustion: - Small amount is endogenously produced in human body (Vit B12 metabolism) - Polyurethane, a commonly used in modern plastic

furniture, release CN on combustion– Silk and wool will release CN during fires– Smoke inhalation, death will be due to both CO & CN– Cigarette smoking (each release 150-200 g of HCN)– Burning pressure treated wood in close place will

release HCN gas

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Cyanide PoisoningMechanism of Action

• Toxicity occurs by either respiratory, PO and dermal routes.

• Produces cytotoxic hypoxia (interferes with cell metabolism in the presence of normal blood and O2 supply) = metabolic inhibitor.

• HCN binds to heme iron in the cytochrome oxidase (a-a3) (has high affinity for Fe+++) forming a complex

• This complex inhibits the final step of oxidative phosphorylation where O2 is used for the production of ATP

• Aerobic metabolism stops (cells will not be able to use Q2), Patient essentially suffocates

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Cyanide PoisoningMechanism of Action

• Cyanide inhibits mitochondrial cytochrome oxidase , thus blocks electron transport, resulting in decreased oxidative metabolism and oxygen utilization

• Lactic acidosis occurs as a consequence of anaerobic metabolism (accumulation of Lactic acid).

• Most affected cells are at the heart & CNS

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Cyanide Poisoning Symptoms

• Acute:– Depends on the dose, route of exposure &

duration• CNS (most sensitive), headache, nausea,

vomiting, confusion, restlessness & anxiety, tachypnea with convulsion (are immediate, within few min)

• Severe poisonings progress to tachycardia and tachypnea, comma, fixed dilated pupils and death (occur within minutes)

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• Acute• Skin/Ocular:

– In sever poisoning, skin is cold – Cyanosis may be develop late– Retinal veins and arteries may appears similar in color

• CVS: (required higher dose than that of CNS dose)– Tachycardia followed by bradycardia– Hypotension followed by peripheral vascular collapse – Abnormal ECG & pulmonary edema

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• Chronic: – Long-term CN exposure Occupational –related,

heavy smoker will cause headache, dizziness, nausea, or vomiting, psychosis

– Tobacco Amblyopia: visual impairment not due to

lesion & abnormalities in the optic disk, but due to direct effect of CN on the eye

• (Vit B12a) improve visual acuity in some patients)

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Cyanide Poisoning

Management

For prevention: small doses of Na+ Nitrite: (Sequesters CN before it gets into the cells)

• * Give a mild nitrite by inhalation (2 pearls of Amyl Nitrite (crushed and rubbed on the face)

• * Several drugs are used:– 1) Amyl nitrite (by inhalation), followed by– 2) Na nitrite (by IV), initial dose 300 mg/adult– * these combination will convert Hb to methemoglobin and the

formation of Fe+++ heme– * The Fe+++ will bind to CN forming a stable complex

Cyanmethemoglobin– * As a result the free CN in circulation will ↓

• Be careful with the Nitrites, massive vasodilation and server hypotension are possible

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Cyanide Poisoning

Management

– * Permanent & irreversible intoxication of CN is by IV injection of Na thiosulfate

– -25% Na + Thiosulfate 50ml, IV (Provides Sulfur for the• enzymes Rhodanase)

• - The enzyme Rhodanase converts CN to Thiocyanate (inactive) which is excreted in the urine

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Cyanide Poisoning

Laetrile

• * Used to be found in health food stores as a nutritional supplement for malignancy– *Obtained from the kemels of peaches, apricots, and almonds

• * Contain amygdalin (a cyanogenetic glycoside), CN is liberated by the enzyme, emulsin (which works better in alkaline pH)

– - Used in more than 22 countries for cancer treatment (falsely)

– - It kills cancerous and normal cells - Children have a higher incidence of toxicity because they have a more alkaline environment in their GI

- 2-3 tablets are lethal

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Toxicity induced by household chemicals

1. Corrosive Alkalis

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1. Corrosive Alkalis

Occurs most often in Toddler’s and children • *Alkalis are present in many household products:

– Liquid plumber, Drano, Oven cleaners, Glass cleaners (ammonia), Dishwasher detergents, Lye, Drain openers, Alkaline batteries

Alkaline batteries are dangerous to children because they are small and easily swallowed.

Alkaline dissolve tissues– Liquefy membrane by interacting with proteins to form water

soluble salts & lipids through saponification• * Solubilized cellular membranes

• - Protein, Na, K, Salt• -Very penetrative & cause perforation

•

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1. Corrosive Alkalis • * Penetrating effect:

-Least: sticking together of esophagus walls –stricture• - Worst: perforation of membranes if swallowed

• ·At high dose Alkalis, can produce either an immediate death to a delayed death

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• Acute effects:• - Severe irritation of the eye, skin and other dermatoses• Eye: disintegration and sloughing of the conjunctival and

corneal epithelium, corneal opacification, edema, ulceration)• Skin: severe burn, deep skin ulceration, loss of hair• mucous membrane: corrosion of the lips, mouth, tongue and

pharynx,

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Toxicity induced by household chemicals 1. Corrosive Alkalis

• Chronic effects: Esophageal strictures may occur in small doses, which can lead to

respiratory distress. Burns (can be 1st to 3rd degree burns) causing skin scaring Permanent corneal opacification Dehydration which can lead to immediate death (From traumatic

shock and severe pain that leads to cardiovascular and CNS collapse)

Delayed death (24-48 hours later), (Due to internal injury caused by perforation)

If the alkalis ingested is a small amount and make it into the stomach, usually the acid will neutralize the toxin.

If ingestion occurred, usually bloody emesis will be seen and the patient will be unable to swallow so drooling may result.

•

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• Management• *Removal from exposure ASAP• *Flushing the eyes and skin with lots of water• *Use of an antibiotics ointment to prevent ocular adhesions• *Nothing should be given by mouth to dilute the poison (unless

the patient is in the act of swallowing) • * If is already swallowed, give diluted vinegar or fruit juice to

balance GI pH, followed by administering eggs or gelatin, followed by stomach emptying where possible

• *Stomach intubation’s is not recommended because the possibility of penetrating of the abdomen

• * If the alkalis were spilled onto the body, use Morphine to reduce the pain and IV fluids should be given to reduce shock

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• * Treatments of esophageal stricture, Antibiotics (Penicillin or Ampicllin) Prednisolone to decrease inflammation of the esophagus Feed with a gastric tube 2-3 days after the ingestion Use special catheters (which have Mercury on the end which

slide down the esophagus by gravity and do not have to be pushed forcefully).

* Esophageal replacement:– Previously, a portion of the colon was used – Recently, a Reserve (inverted) gastric tube replacement is

performed – A portion of the stomach is formed into a tube to act like the

esophagus (Continuity is not broken and the blood supply is not interrupted)

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• Batteries • ·Alkaline • · Toddler’s favorite are attracted to their size • · If swallowed and there is no obstruction, the batteries will not

burst and leak their contents• · If the battery is excreted into the feces, no action should be taken• · Observe the child for 24-48 hours, if the battery is not passed,

then an x-ray should be performed • · If the battery is obstructed, the alkaline content may leak and

perforation may occur.• · At this point, the battery should be removed by surgery •

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2) Strong or concentrated Acids • Source of exposure:• - Any acid solutions used for cleaning brick,

garage (concrete) or bathroom floor• - Acids will not affect the lipids of the

membrane, but will cause coagulation of the proteins

• - The penetrative power is much less then the alkalis

• - Acids produce more charring (burning) and cause more pain

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2) Strong or concentrated Acids

Pathology a) Acute Toxicity:• - If ingested: ==►burning in the mouth, esophagus, stomach

with pain, nausea & vomiting • - If inhaled: ==► coughing, burning in the throat, inflammation

of the nose, eye laryngeal spasms, pulmonary edema

• - Dermal: skin burn, dermatitis

b) Chronic Toxicity:- Prolong exposure to diluted solutions ==►dermatitis, tooth erosion

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2) Strong or concentrated Acids

Duration of Symptoms:• - 7-14 days depending or the rout of exposure

Treatment:• - Flush the skin, eye with H2O• - If inhalation is the rout, use 60-100 % O2• - For lung inflammation ==► use steroids (i.e.

Prednisolone) • - For GI ==► use milk of magnesia (as an antacid

and laxative)

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3) Phenols Source of Exposure:

- Disinfectants, (at homes, hospitals, school,….), cleaning solutions- Occupational exposure (manufactures, packing, distribution, storage or use)

- In some skin medication, vaccine, inks

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3) Phenols Pathology

a). Acute Toxicity:– - dark-colored urine– - mucous membrane whiting– - skin numbness, necrosis– - GI disturbance– - CNS effects

b). Chronic Toxicity:- Similar to acute, but resulted from long term and

repeated exposure

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3) Phenols• Duration of exposure:• - If seizure developed ==► death due to respiratory OR

cardiac collapse• - If hepatic & renal failure developed ==►death occurs after

several days

• Pathology:• - esophagus appears tanned• - cerebral edema• - cardiac dilation• - degeneration of glomerular and tubular cells of the kidney

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3) Phenols• Treatment:• - Dermal: wash skin, eye with H2O (for at least 15

minutes)

• - If seizure developed ==►control with diazepam or Phenobarbital

• - If ingested ==►Do not induce vomiting. Do not dilute (may absorption). Give polyethylene glycol solution or activated charcoal with Sorbitol. wash stomach repeatedly with 25% bicarbonate

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Radiation Toxicology

• Source of Radiation:• 1) Cosmic, radiation present in environment, radio active

materials in soil, rocks,….• • 2) X-Ray diagnostics, dental, industry, T.V., industrial X-ray

machine, cobalt treatment for cancer, other 238PU•

3) Radioactive Pharmaceutics: used for diagnostic purpose and/or treatment (e.g., 131 I), in vivo or in vitro, in RadioImmunoAssay (RIA) kit

4) Reactors: operate on the basis of nuclear fission, in peace time, they produce energy and power

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Factors affecting toxicity:1) Depend on the types of particles (α, Causing high degree of cell damage, β or γ )2) Dose and frequent of exposure3) Whole body irradiation vs. partial exposure4) Type of elements (radium, tritium)

5) t1/2

6) Tissue uptake and concentration7) Type of tissue exposed

Toxic effects: Radiation react with H2O to form free radicals Free radical interact with cell molecules

The result changing in cell function

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• Toxic effects:* Radiation react with H2O to form free radicals

• * Free radical interact with cell molecules The result changing in cell function

• Symptoms:• * Anorexia, nausea, vomiting, diarrhea, apathy,

headache, fever, tachycardia, anemia

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• Delayed effects: Mutation Sterility• * Carcinogenesis Alopecia• * Shorten life expectancy (due to cancer) Cataract

• Treatment Blood transfusions• * Antibiotics• * Supportive

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• Preventive measures• * Don’t smoke, eat or drink while handling

radioactive materials• * Wear protective clothes• * No radiation exposure during pregnancy• * Use Pb shield for X-ray• * Keep distance from α, β• * Every thing should be prepared under a

designated hood, disposed correctly

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Principle of ToxicologyDecember 2, 2011

Agents-Induced ToxicityI. Natural Substances

• Animal source Fish (Puffer fish)• Plant source (Wild Mushroom)

II. Heavy Metals• Lead (Pb)

III. Drug of Abuse• Amphetamine• MDMA• Cocaine

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Toxicity induced Natural Substances

1) Animal Sources (fish)– More than 700 species of marine fishes

are toxic (due to injury OR after ingested by human):

• Some have tissue that are toxic at all

times, • other are toxic at a specific period/areas

and • some have specific organs that are toxic • Most potent marine toxin is Tetrodotoxin

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1) Fish (Puffer fish)• Fish-induced human

poisoning: • Globe fish = puffer fish, contains a

potent and deadly toxin called tetrodotoxin.

• The toxin is concentrated mainly in the eggs (ovaries), liver and skin.

• The organs containing toxins even after careful removal, there are still chances that the flesh of the fish will be contaminated.

• The toxin cannot be destroyed by drying, cooking, or freezing.

• The toxin can affect a person’s central nervous system, and in extreme cases, can cause death.

• There is no specific antidote at present

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1) Puffer Fish

Tetrodotoxin– Is found in some puffer fish, amphibian species, octopus – There are > 100 types of Puffer fish, (at least 50 are poisonous) – Lethal dose is very steep (e.g., in mice):

• Minimal lethal dose = 8ug/kg• LD99 = 12ug/kg

• Mechanism of Action:• -blocks Na+ channels ( which are presents in every excitable

tissue)• - nerve and muscle blockade paralysis • - produce hypotension & respiratory distress • - Tetraodotoxin can lead to death• - Many of the reported death in Japan was due to suicidal

use of it

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1) Puffer FishClinical signs of Toxicity:– Very rapid (5-30 min), muscle weakness paralysis– Pallor– Numbness of the lips, tongue, throat (tingling or pricking) salivation– Change in HR (bradycardia, dyspnea, cyanosis shock

death

Treatment:– O2 & IV fluid (S Saline solution + dextrose)– For the paralysis (due to Ach) & Salivation atropine

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2) Plants (Mushrooms)

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2) Plants (Mushrooms)* Wild mushrooms induced different types toxicity in

human 1) Mushroom produce GI discomfort & rapid nausea (w/in 3-4

hrs), emesis & diarrhea dehydration, hypovolemic, shock

2) Mushroom-evoked sweating ( muscarine, not affected by cooking), also may cause nausea & vomiting, blurred vision

3) Mushroom evoked Hallucination (symptoms appears + 2 hrs), hyperthermia, loss of consciousness, severe symptoms = alcohol intoxication

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2) Plants (Mushrooms)4) Mushroom-induced delirium/sleep & coma (symptoms w/in

20-90 min), w/in 60min drowsiness, dizziness sleep, followed by motor activities, tremor

5) Mushroom-induced disulfiram-like effects = alcohol intoxication, headache, nausea & vomiting,pain (for up 3 days)

6) Mushroom-induce headache (delayed effect after 6-8 hrs, onset is sudden), may cause liver necrosis, pt recover w/in 2-6 days

7) Mushroom-induced polydepsia, polyurea (3 days later, lasts 3-17 days)

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Heavy Metals-Induced Toxicity

• Heavy metals:– Lead (Pb)– Mercury (Hg)– Cadmium (Cd)– Arsenic (As)– Iron (Fe++)– Gold– Platinum – Beryllium– Chromium – Nickel (Ni)

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Heavy Metals-Induced ToxicityLead (Pb)

Source of exposure:- Lead-based paints in older homes, - household dust, - drinking water (if you have lead pipes), and contaminated soil - leaded gasoline

If lead accumulates- Pb in the body mimics Ca++- Pb will be stored in the bone like Ca++- It has three compartments: Bone (t1/2 = 20-30 years), blood and soft tissue (t1/2= few weeks-3 mo) - In children, more Pb is deposited in the bone due to growth

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Acute Effects:- when level > 50ug/dl Pb encephalopathy - If 60-80ug/dl in the blood, then seizures will develop- infant, toddlers, young children are more susceptible to Pb than adult

Chronic Effects:If Pb in blood is 2-10ug/dl, no seizures but the patient will develop:– Poor appetite, anemia– ↓ attention span– ↓IQ, ↓ memory– Altered behavior– Often mistaken for ADD

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Pb at high dose may cause:– Airway stricture– Can produce death by local effect– If patient survives initially, death can still occurs 2-3 days later

from Peritonitis

Management of Lead Poisoning (by Chelation)- Succimer (DMSA) (chelating agent)- Succinic acid, taken PO, and does not chelates Ca++ or Zn++- British Anti Lewisite (BAL) for acute toxicity- Ca++ Na2 EDTA- Ca++ Na2EDTA + BAL used when Pb in blood > 70ug/dl

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Toxicity induced by Drug of Abuse

• Drug of Abuse:– Amphetamine– Methamphetamine– MDMA– Cocaine– Cannabis (e.g., Marijuana, Hashish)– LSD– Nutmeg– Glue sniffing

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1) Amphetamine- A CNS stimulus, DA agonist

-Has limited therapeutic use (Narcolepsy)

Source of Exposure: – Prescription over dose– Illicit street drug– Common route of exposure (PO, IV)

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1) AmphetamineAcute Toxicity: (CNS, CVS, GI):1) CNS: Restlessness, dizziness, tremor, hyperactive reflexes, anxiety,

talkativeness,irritability, insomnia, confusion, hallucination, panic state, suicidal OR homicidal tendencies, headache, seizure, coma

2) CVS: Cardiac arrhythmias, anginal pain, hypertension OR hypotension, circulatory collapse,

sweating

3) GI: dry mouth, metallic taste, anorexia, nausea, vomiting, diarrhea, abdominal cramp

Chronic Toxicity: Same as acute symptoms, but more sever + toxic psychosis, abnormal mental activities,

wt loss, dementia

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1) Amphetamine• Duration of Symptoms:

– Acute: for up to 2 hrs– Chronic: 2-3 wks after withdrawal– The Amphetamines cause psychological &

physical addiction – They show cross tolerance with each other

and with stress

Pathology: Brain hemorrhage

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1) AmphetamineDiagnosis:– History of Amphetamine use– Detecting amphetamine & metabolites in urine– Presence of any of the symptoms

Treatment:– Emetic/Gastric lavage to remove drug from stomach– Acidified the urine by ascorbic acid (urine pH<5)

excretion of amphetamine– If hypertension developed, use nitroglycerine, Na

nitrite to lower BP

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2)M D M A

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2) MDMA

MDMA=

3,4, MethyleneDioxyMeth Amphetamine

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2) MDMAMDMA

=3,4, MethyleneDioxyMethAmphetamine

= Is known as designer drug

Street Names:* Ecstasy * XTC * Adam * E, *X, * Clarity * Stacy

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2) MDMA

* It is an illegal drug

* Listed by DEA in schedule I category of the Controlled Substance

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2) MDMA• Source of exposure:

– Street, illegal, available in tablet (50-100 mg) $20-25), capsules, powder & liquid

– Distributed & used openly in bars & nightclubs in TX, AR & southwest

– Could be purchased via toll-Free 800- number– Sold in little bottles at convenient stores under the label

“Sassyfras” extracted from Sassyfras oil – 80-90 % of the world MDMA manufactured in Belgium and

Holland– Russian-Israeli & Eastern European chemists are now the main

producing and distributing of MDMA

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2) MDMAFrequency of use: USA:

– as of 2004, 11 Million age 12 Y and older used MDMA at least once– from 1995-2005, the use 970% – in 1993, 2% of all US college students used MDMA within 12 Month– In Stanford Univ, 39% of all undergraduate used MDMA at least once– MDMA use in 8th grade by 52% & in 10th grade 58% & in 12th

grade 67%

International:In England, 6% aged 14-15 & 31% aged 16-25 Y used MDMA,

500K-1 M used MDMA every weekend – Widely used in Spain, Portugal, Australia, India,… – 3% of all European adult had tried MDMA

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2) MDMAAcute effect: CNS, CVS, GI (w/in 30 min, w=in 90 min))

(immediately after ingestion OR after the euphoric high subsided and they tried repeated dosing OR co-ingestion with other drugs e.g., alcohol, marijuana, heroin, cocaine)

• Central nervous system - Change in mental status, seizures- Anxiety, paranoia- Increased psychomotor activity, restlessness, Ataxia- Hyperthermia, hot flashes- Headache- Blurred vision, halos- Syncope

• Cardiovascular (1/10 of Amph) Gastrointestinal/Urinary:- Palpitations - Dry mouth, Nausea & vomiting- Chest pain - Abdominal cramping, anorexia

- Urinary retention/sexual dysfunction

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2) MDMAChronic Toxicity:

– Serotonin (5-HT) syndrome hyperthermia, mental changes, alter muscle tone and/or rigidity, hyponatremia ( Na+)

– Cerebral hemorrhage– Hepatotoxicity, liver failure, alters liver enzymes

Long-term neuropsychiatric effects

due to permanent damage of the 5-HT system depression, anxiety, panic attack, insomnia, difficulty concentrating, short-term memory impairment

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2) MDMA Diagnosis:

– History of drug use– Detecting MDMA & metabolites (MDA) in urine– Presence of any of the symptoms

Treatment:– Emetic/Gastric lavage to remove MDMA from stomach– Cool room (environmental) to reduce hyperthermia– Treat seizures with benzodiazepine. – If hypertension developed, use nitroglycerine, Na

nitrite to lower BP

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Toxicity of Drug of Abuse3) Cocaine

Source of Exposure:– Most potent naturally occurring CNS stimulus– Alkaloid extract from Erythroxylun Coca– Sold as an illicit street drug– Street names e.g., coke, snow, flake, Cadillac or champagne of

drugs, gold dust, speedball (heroin+cocaine)

Abuse Pattern:– Sniffing/snorting (chopped crystals into fine powder (t1/2=75 min)– Smoking (Crack, tiny crystalline pieces in cigarette, water pipe)

(rocks, free –base cocaine in pipe) (t1/2= 45-48 min)– IV: a combination with heroin (t1/2 = 50-55 min)– 25 mg iv = 100 mg sniffing (Δ 15-20 min), PO (Δ 50-90 min)

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Medical Use:– Mucous membrane anesthesia – Vasoconstriction (2-4 min, ear, nose & throat surgery)

Acute Toxicity: CNS & CVS, Respiratory CNS: Anxiety, headache, tremor, clonic & tonic, seizure, cold sweatCVS: hypotension, weak & rapid pulse rate

Respiratory failure

Chronic Toxicity: Facial pallor, sunken eyes, tremor, Mydriasis

Duration of symptoms: death occurs 20-30 min after acute large dose, recovery occurs 1-2 hrs after low-

mild dose

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Pathology:– Cardiac dilation, sign of asphyxia, mal nutrition

Diagnosis: – History of use– Identification of the drug/its metabolites in urine

Treatment:– Seizure Diazepam (DOC), Short acting barbiturate (IV), 2nd choice – Hyperthermia ice bath, hypothermic blankets, or cool room – To control respiration artificial respiration to maintain O2 content in

blood (ASAP)

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• Cocaine & Pregnancy:– Cocaine Babies:

• New born babies to cocaine user mothers have– Low birth weight– Low (smaller) brain– Increase malformation (birth defect)– Low IQ, learning & memory– Depression of interactive behavior– Poor response to external stimuli

– Spontaneous abortion (e.g., after IV)• Due to placenta vasoconstriction• Due to uterine contraction

1 supportive or symptomatic treatment 11/4/2011 management of poisons in conscious patient: 1)...

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