Clinical Toxicology

Download as doc, pdf, or txt
Download as doc, pdf, or txt
You are on page 1of 8
At a glance
Powered by AI
The key takeaways are the general principles of toxicology including emergency stabilization, clinical evaluation, elimination and excretion of poisons, administration of antidotes, and supportive therapy and observation.

Some common causes of poisoning mentioned are overdose of drugs, chemicals, and biological substances. Acute poisoning occurs within 24-48 hours while chronic poisoning occurs over weeks, months or years.

The general principles of emergency stabilization for poisoning cases include maintaining the airway, breathing, and circulation. Other measures include treating convulsions, correcting metabolic abnormalities, treating coma, and providing recommended IV fluids.

Pharmacology (dra Dando)

Clinical Toxicology

13 February 08

POISONING  Opiates (Morphine, Novaine, Heroin, Codeine)


 Quinine
• Overdose of drugs, medicaments, chemicals o Anti-protozoal
and biological substances
• “acute” poisoning versus “chronic’ poisoning RECOMMENDED IV FLUIDS
 Acute: 24 -48 hrs of exposure  Hypotensive patients
 Chronic: weeks, months, years of  NSS
exposure  Adult for maintenance
• Father of toxicology: Paracelsus  NSS
 D5 Acetated Ringer’s solution
GENERAL PRINCIPLES
 Emergency stabilization  Pediatric for maintenance
o First thing to do  D5 0.3% NaCl (hypo)
 Clinical evaluation
o Include good Hx taking & thorough PE POISON COMMONLY ASSOCIATED WITH
 Elimination of the poison CONVULSIONS
 Excretion of the absorbed substance  Aminophylline
 Administration of antidotes  Amphetamines
o Important for certain specific poisons or  Carbon monoxide
drugs  Cocaine
 Supportive therapy and observation  Cyanide
 Disposition  Ethylene glycol
 Hypoglycemic agents
EMERGENCY STABILIZATION  Isoniazid – triad of coma, metabolic acidosis,
 Maintain adequate Airway intractable seizures
o Remove obstructions  Lead
o Conditions wherein suction cannot be  MAO inhibitors
done:  Mefenamic Acid (usual side effect: GI irritation;
- caustic substances (causes ulceration overdose: seizures)
of GI mucosa)  Opioids
- hydrocarbons (causes aspiration)  Organophosphates
 Ensure adequate Breathing/Ventilation  Phenothiazines
o Nasal cannula, intubation  Salicylates (Aspirin)
 Maintain adequate Circulation (put IV lines,  Strychnine
fluids)  Theophylline
 Treat convulsions (e.g Diazepam)  Tricyclic antidepressants
o Diazepam: 1st line of Tx for active seizures  Withdrawal of narcotics, diazepam or ethanol
and status epilepticus  Signs of ethanol withdrawal
o Irritable
 Correct metabolic abnormalities (Electrolytes,
glucose, acid-base) o Agitated
o Base: used for severe metabolic acidosis o Seizure
(Tx: Na, bicarbonate)
o Glucose: for hypoglycemia (Dextrose 50- CAUSES OF CONVULSION IN POISONED PATIENTS
50 concentration)  Direct convulsant effect of the poisons
 Cerebral hypoxia from respiratory or
 Treat coma (e.g Flumazenil)
cardiovascular depressive effect of drugs
o Flumazenil:
 Hypoglycemia
1) Tx for BZD (diazepam) overdose
2) Tx for coma (but not as first line agent)  Severe muscle spasm due to spinal o peripheral
- coma due to overdose of valium effects on the mechanism controlling muscle
tone
COMMON CAUSE OF HYPOXIA  Withdrawal reactions in patients with physical
 Alcohol dependence on abused drugs
 Cyanide  Decreased seizure threshold in an epileptic
o In silver jewelry cleaners patient
 Organophosphates
TREATMENT OF CONVULSION
o In pesticies
• Diazepam
 Carbon monoxide
joyce 1 of 8
Pharmacology – Clinical Toxicology by Dra Dando Page 2 of 8

o Adult: 5mg IV INFORMATION TO BE ELICITED DURING HISTORY


o Children:0.3mg/kg • Time exposure
o Only compatible fluid is blood (direct)  Needs to be very specific
• Lorazepam (Ativan)  e.g.: N-acetylcysteine, antidote for
o Adult: 2.5-10mg IV paracetamol overdose; effective only in
o Children: 0.05-1 mg/dose the first 6 hrs after ingestion
o Withdrawn from the marked d/t its  e.g. lavage of poison is only good for
associated side effects the 1st 24hours
o Short acting, long duration • Mode exposure
• Phenytoin  Rectal
o LD: 15-20mg/kg IV  Transplacental
o Adult: 50mg/min  Oral
o Children: 1mg/kg/min  Etc
o Inducer of CYP450 • Intake of other substances
o Maintenance drug • Circumstances prior to poisoning
• Pyridoxine (B6) • Current medications
o Adult: 5g IV
• Past medical history
o Children: 80-120mg/kg
• Any home remedies taken
o For INH poisoning
o Tx of convulsions due to unknown
*Organophosphate/carbamate poisoning: manifests
etiology
with DUMBEL
Hypothermia Hyperthermia POISONS WITH DELAYED MANIFESTAIONS
 Alcohol  Antihistamines Ethylene glycol 6 hours
 Barbiturates  Amphetamines o Present in anti-
 Carbon monoxide  Isoniazid freeze 12 hours
 General  Phenytoin Salicylates 36 hours
anesthetics  Salicylates Paracetamol 48 hours
 Opioids  Xanthines Paraquat 48 hours
 Phenothiazenes  Anticholinergics: Methanol
 Sedative-hypnotics Atropine o Toxic alcohol 4 weeks
 Tricyclic  Cocaine Thyroxine
antidepressants  Phenothiazines
 Quinidine *Vodka
- among alcohols, has the highest alcohol content
 Sulfonamides
- converts ethylene glycol and methanol to less toxic
form
TREATMENT OF COMA OF UNKNOWN ETIOLOGY
- amount to be given needs to be computed
• Thiamine (vit B1) 100mg IV
o Tx of Wernicke Korsakoff Synd in COMPLETE CLINICAL EVALUATION
alcoholic px  Complete physical examination
• Glucose  Evaluate general status
o Adult: 50-100ml D50-50  Examine skin
o Children:2ml/kg d10  Characterize odor of patient’s breath
o Most pts present with hypoglycemia  Auscultate the lungs
esp. in alcoholic intoxication  Listen to patient’s heart
o Wernicke-Korsakoff syndrome  Check the abdomen
 d/t sever B1 deficiency  Do a complete neurologic exam
 administer B1 first before giving  Skin changes in poisoning
glucose  Bullae: barbiturates, CO
• Naloxone  Diaphoresis: OP, salicylate, amphetamine
o Adult: 2mg IV every 3-5mins  Jaundice: paracetamol
o Children: 10mcg/kg  Dry and warm: atropine, anticholinergic
o For opiate overdose (coma)
o Expensive
 Flushed: anticholinergics, alcohol, cyanide,
atrophine odors
o Given to newborns whose mothers
 Brerath odors
underwent CS causing respiratory
difficult in their babies  Bitter: almonds, cyanide
 Fruity: DKA, isopropanol
COMPLETE CLINICAL EVALUATION  Oil of wintergreen: methylsalicylate
• Good history taking (d/t vulnerability of children)  Rotten eggs: sulfur dioxide, hydrogen sulfide
 Pears: chloral hydrate
Pharmacology – Clinical Toxicology by Dra Dando Page 3 of 8

 Garlic: arsenic, OP  Emesis


 Mothballs: camphor (like the one in vicks)  Lacrimation
 Salivation
Bradycardia Tachycardia
 Propranolol  Iron Sympathomimetics Opiates / Narcotics
 Anticholinesterase  CO, cyanide  Mydriasis  Miosis
 Clonidine, codeine,  Organophocphate  Tachycardia  Bradycardia
Ca-channel blocker  Phenothiazine  Hypertension  Hypotension
 Ethanol  Hyperthermia  Hyperventilation
 Ethanol, ethylene
 Seizures  Coma
 Digitalis glycol
 Free-base cocaine CONDITION OR AGENTS PREDISPOSING TO
 Anticholinergics METABOLIC ACIDOSIS OR ELEVATED ANION GAP
 Antihistamines • Methanol
 Amphetamines • Ethylene gycol
 Sympathomimetics • Theophylline, toluene
 Salicylates, solvents • Alcoholic ketoacidosis
 Theopylline • Lactic acidosis

Mydriasis Miosis • Aminoglycosides

 Antihistamines  Cholinergics, • Cyanide, CO


 Antidepressants clonidine • Isoniazid, Iron
 Sympathomimetics  Opiates, • Diabetic ketoacidosis
Organophosphate • Grand Mal seizures
 Isoniazid
 Phenothiazines,
• Aspirin (salicylate)
 Anticholinergics pilocarpine, pontine
bleed • Paraldehyde, phenformin
 Sedative-hypnotics
ELIMINATION OF THE POISON
*Triad of opiate overdose: • External Decontamination – bathing of pt with
 Coma alkaline soap e.g perla, ivory, dove
 Respiratory depression • Emptying the stomach
 Pinpoint pupils o Emesis – only in adults
*pediatrics have risk for aspiration
Clinical Evaluation: o Gastric lavage – H20, NSS, Na Bicarbonate,
Check for Toxidromes activated charcoal
 Signs and symptoms taken collectively can • Limiting GI absorption
characterize a suspected toxicant o Activated charcoal
 These groups of manifestations are observed to o Demulcents (watusi) / neutralizing agents
occur consistently with particular poisons (raw egg white: to prevent absorption)
o Intractable seizures + Coma +
Metabolic acidosis = INH Poisoning SUBSTANCES NOT ABSORBED BY ACTIVATED
*Intractable seizures despite CHARCOAL
administration of diazepam  Alcohol – rapid absorption
 Cyanide
Anticholinergic / Antidepressant Toxidrome  Iron
 Hyperthermia: “hot as a hare” o Lavage with NaHCO3
 Dry mucosa: “dry as a bone”  Lithium - dialysis
 Flushed skin: “red as a beet”  Petroleum distillates (hydrocarbons)
 Dilated pupils: “blind as a bat”  Caustic agents
 Confusion / delirium: “mad as a hatter”
SUBSTANCES WITH EXTRAHEPATIC
Cholinergic Toxidrome (S&Sx of organophosphate RECIRCULATION
and carbamate poisoning) • Aspirin
 Diarrhea, diaphoresis • Cyclosporine
 Urination • Digoxin
 Miosis, muscle fasciculations • Meprobamate
 Bradycardia, bronchoconstriction • Paracetamol
• Phenothiazine
Pharmacology – Clinical Toxicology by Dra Dando Page 4 of 8

• Phenytoin  DMSA: suximer?


• Salicylate  NAPA: N-acetyl-penicillamic acid – mercury,
• TCAD arsenic, lead
• Anticoagulants  Accelerated detoxification
• Carbamazepine  Cyanide antidote kit – available in US only
• Dapsone  Sodium nitrite and sodium thiosulfate
• Gluthetimide o Sodium nitrite: Induce
• Methamphetamine methemoglobinemia (a condition in
• Phencyclidine which the iron within hemoglobin is
• Phenobarbital oxidized from the ferrous (Fe2+) state
to the ferric (Fe3+) state, resulting in
• Piroxicam
the inability to transport oxygen and
• Theophylline
carbon dioxide)
• Organochlorines o Sodium Thiosulfate: binds with
cyanide-methemoglobin complex to
*Formalin ingestion: detoxify
 No antidote o Used in PGH, a raw material that is
 Give H2 blockers compounded and prepared
 Surgery (cut the part with ulceration) whenever it is needed
 Reduction in conversion to more toxic compounds
ENHANCEMENT OF ELIMINATION OF ABSORBED  Ethanol
SUBSTANCES o For tx of methanol and ethylene glycol
• Forced diuresis poisoning
o Mannitol 20% - osmotic diuretic  Competitive inhibition at receptor site
o Furosemide – loop diuretic
 Atropine (physiologic antidote) – for
• Alkalinization therapy organophosphate/carbamate poisoning;
o Sodium bicarbonate – for weak acids: INH inhibits the enzyme acetylcholinesterase)
poisoning  Pralidoxime (pharmacologic antidote)
• Acidification therapy (for weak bases:  Bypassing the effects of the poison
Methamphetamine/shabu)  Oxygen for CN poisoning
o Ascorbic acid  Pyridoxine for INH poisoning
o Ammonium chloride  Antibody interacting with poison
• Dialysis and hemoperfusion
 Digoxin antibody fragments (Digibind) – not
• Multiple dose activated charcoal
available locally
*Locally: nadia-nadia
INDICATIONS FOR DIALYSIS
 Snake antivernin (available in RITM)
• Amanita phalloides (mushroom) – very - species of Philippine cobra cause
dangerous and lethal causing renal failure paralysis
• Antifreeze (glycol type) - Tx: activated charcoal
o Tx: ethanol e.g. vodka via NGT; prevents
conversion to more toxic from SUPPORTIVE THERAPY
• Heavy metals in soluble compounds • Essential for poisoning patients, especially for
o Tx with EDTA or chelators critically ill
• Heavy metals after chelation • Problems in the critically ill poisoned patients
• Methanol o Depressed sensorium
o Impaired ventilation
ANTIDOTES FOR PATIENTS WITH COMA OF o Impaired cough reflexes
UNKNOWN ETIOLOGY o Prone to aspiration
• Naloxone o Immobility
• Glucose o Fluid, electrolyte and other ,metabolic
• Thiamine problems
• Intravenous fluids: replacement and
ANTIDOTE FOR PATIENTS WITH SEIZURE OF maintenance
UNKNOWN ETIOLOGY • Frequent blood and urine pH determination:
• Pyridoxine (Vitamin B6) acidification and alkalinization therapy
• Prevention of aspiration
USE OF ANTIDOTES • Prevention of decubitus
Mechanisms: • Ulcer
 Inert Complex Formation • Treatment of electrolytes, metabolic and
 Chelating agents (DMSA, NAPA) temperature problems
o Tx of heavy metal poisoning • Monitoring of vital signs
Pharmacology – Clinical Toxicology by Dra Dando Page 5 of 8

• Monitoring of input and output  Benzene (ADR: Leukemia)


GOOD SUPPORTIVE AND NURSING CARE IS  Toluene (ADR: Kidney failure due to chronic
IMPORTANT exposure)

DISPOSITION CAUSTIC AGENTS


• Observation at the emergency room: atleast  Alkali (ph > 7) Strong alkali: ph >10
24hrs may be warranted  No antidote (only supportive): H2 blockers, PPI
• Frequent reevaluation  Sodium hypochlorite
• Psychiatric evaluation: suicidal patients and  Sodium hydroxide (e.g liquid sosa)
substance abusing patients  “LIhiya” (pang-green ng suman)
• Childhood poisoning: evaluate for possible child  Main Tx: surgical
abuse or neglect Pathology: liquefaction necrosis (esophagus and
• Family counseling and education intestine)
• Physical or sexual abuse among women
• Domestic violence  Acids (ph < 7) Strong acid: ph <4
 Hydrochloric acid
TOP TEN POISONS (All Ages) IN-PATIENT STATISTICS  Acetic acid
National Poison Control and Information Service UP-PGH  Benzalkonium chloride
YEAR 2006 (N=847) NUMBER PERCENTAGE
Pathology: Coagulation necrosis
1. Ethanol – alcohol 95 11.2
withdrawal pts  Others
2. Kerosene (Gaas) 87 10.3  Phenol (e.g. Lysol)
3. Sodium Hypochlorite 62 7.3  Cyanide salts: Silver jewelry cleaner
(Zonrox) - mixed with Na Hydroxide
4. Mercury (thermometer) 45 5.3
5. Jewelry Cleaner (Cyanide) 35 4.1
6. Hydrochloric acid 27 3.2 PHARMACEUTICAL AGENTS
(Muriatic)
 Paracetamol
7. Methamphetamine (Shabu) 19 2.2
8. Paracetamol 16 1.9  Toxic dose: 150-200mg/kg
9. Mixed Pesticides (Baygon) 15 1.8  Toxic metabolite: NAPQI (N-acetyl-p-
10. Jathropa seeds (cause 15 1.8 benzoquinone imine)
hemorrhagic gastritis)  GI, liver and renal damage (4 stages)
 Antidote: N-Acetylcysteine
*Na Hydroxide: Liquid sosa
 Preparation: IV – usual route (e.g. Hydranap)
TOP TEN POISONS (All Ages) TELEPHONE REFERRALS
Oral – in sachet
National Poison Control and Information Service UP-PGH Inhalation
YEAR 2006 (N=2,682) NUMBER PERCENTAGE  Average 50-kh man who ingests 15-20 tablets
1. Kerosene 192 7.2 (500 mg) causes toxic injury
2. Sodium Hypochlorite 131 4.9
3. Mixed Pesticides (Baygon) 118 4.4  Iron
4. Elemental Mercury 90 3.4
 Toxic Dose: 20mg/kg
5. Paracetamol 64 2.4
6. Silica gel (shoes) – 62 2.3  GI, CVS, CNS manifestations (4 stages)
nontoxic, causes mild GI  EGD
manifestation  Antidote: Deferroxamine
7. Jewelry Cleaner 57 2.1
 Causes severe bleeding and hypotension
8. Ferrous Sulfate 53 2.0
9. Hydrochloric acid 48 1.7  e.g. Flintstones, Gummy bears – contains iron
10. Isoniazid 42 1.6 which can cause toxicity

HYDROCARBONS  Isoniazid (INH)


 Kerosene (Gaas)  Toxic Dose: 80-100mg/kg
 Chemical pneumonitis  Triad of INH toxicity: seizures, coma, metabolic
acidosis
o Presents with cough  cyanosis  seizures
 Aspiration pneumonia  Antidote: Pyridoxine (Vitamin B6)
 Treatment: Pen G or other beta-lactams (for
pneumonia)  Aspirin
 No antidote  Acetylsalicylic acid: 100mg/kg (children),
200mg/kg(adults)
 Easily absorbed
 Methylsalicylate: 50-500mg/kg or 4ml
(1.4mg/ml)
 Solvents
 Aliphatic hydrocarbons  Vomiting, tinnitus (first thing to manifest),
 Aromatic hydrocarbons metabolic acidosis, seizures, coma, renal failure
Pharmacology – Clinical Toxicology by Dra Dando Page 6 of 8

 Activated charcoal / hemodialysis (causes coma,  Naphthalene – causes hemolytic anemia in


seizure) G6PD deficiency pts
 Camphor – most toxic
PESTICIDES  Para-dichlorobenzene – deodorizer (e.g.
 Organophosphates Albatross)
 Malathione - least toxic, causes
 Chlorpyrifos slight gastric irritation
 SSx: DUMBELS
HEAVY METALS
 Carbamates  Mercury (a.k.a Asoge)
 SSx: DUMBELS  Sources:
 Elemental: “quicksilver” metal, cinnabar
 Pyrethroids ore, dental amalgam, apparatus,
 DEET (diethyltolbutamide) thermometers
- present in insect repellants (e.g. lotions)  Inorganic: antiseptics, vaccines
- causes seizures esp in children >2 y/o (merthiolate)
 Permethrin  Organic: contaminated waters from
- anti-pediculosis and scabies: cause seizure industrial waste products, air, soil
(methylmercury)
 Rodenticides
 Zinc Phosphides Small-scale mining practices
 Coumatetralyl  bleeding (Tx: vitamin K) = residue after panning operation where most of the
water are removed
 Herbicides = no personal protective device is provided
 Chemical pneumonitis = route of entry is skin

MIIXED PESTICIDES (e.g. Baygon) Mercury in Thermometer


“There is approximately 1 gram of mercury in a typical
 Carbamates
fever thermometer. This is enough mercury to
 Propoxur
contaminate a lake with a surface area of about 20
acres, to the degree that fish would be unsafe to eat”
 Pyrethroid
 Cyfluthrin *Mercury is not actually absorbed if GI is intact but can
 Transfluthrin cross BBB after 24-48 hrs
 S/Sx: DUMBELS *Tx: cathartics
 Treatment: Atropine, Activated Charcoal
 Organic Chemicals: Methylmercury

Effects of Pesticides:
- Endocrine disruption (cause problems in
reproduction and immune system)
- Neurodevelopmental effects (e.g autism,
cerebral palsy, mental retardation)
- Immune system (can cause cancer)

NON-PHARMACEUTICALS
 Silica gel – gastric irritant
 Chinese herbal meds (e.g. Ma-Huang – has
pseudoephedrine and ephedrine: precursor of
methamphetamine)
 Button batteries
- in <7 y/o, the diameter of intestine is >1.5 cm
- can obstruct trachea, pyloric sphincter
*Mercury vapor – amalgam fillings are chief sources of
- endoscopy is done to get it manually
exposure to mercury vapor
 Watusi
 Yellow phosphorus – most dangerous Minamata Disease (d/t high levels of methyl mercury
(protoplasmic: cause severe hypotension and in big fishes, e.g. tuna)
hypoxia) In 1932, Nippon Chisso Hiyu started to operate an
 Trinitrotoluene (present in dynamite and bombs) acetaldehyde acetic venyl chloride manufacturing plant
 Potassium nitrate using mercury as a catalyst. The plant had been
 Potassium chlorate directly discharging its industrial waste into Minamata
 Moth balls Bay for 36 years with no adequate facilities.
Pharmacology – Clinical Toxicology by Dra Dando Page 7 of 8

 A higher proportion of learning disabilities was


In 1958, Chisso redirected the outlet drainage canal found among school-aged children with
from Minamata Bay into the tributary of the Minamata biological parents who ere lead poisoned as
River which resulted in the contamination of a wider children 50 years previously
area of Yatshushiro Sea.  Source: paints, lipstick, gasoline, hair dyes

Increase in number of vaccines  Arsenic Poisoning


recommended for routine use in infants
 Keratotic lesions  cancerous
 Patients from Bangladesh dig a well

PLANT TOXINS
 Jathropa Seeds
 Contents: toxalbumins = ricin (toxic content
causing hemorrhagic gastritis), curcin, tannic
Potential increased exposure of infants to mercury from acid
thimerosal in vaccines  Effects: abdominal pain, nausea, vomiting,
hepatic injury, muscle twitching, weakness,
Ethyl Mercury salvation, sweating, dehydration, hemorrhagic
= in children receiving thimerosal in vaccines, the half- gastritis
life of ethyl mercury in blood was 7-10 days or 1/7 to  Tx: activated charcoal
1/5 as long as that of methyl mercury
= a WHO advisory committee recently concluded that it CYANIDE
is safe to continue using thimerosal in vaccine - inhibits cytochrome oxidase
- CNS Effects: shock, profound lactic acidosis
Mercury (Pink Disease) - Toxic blood level: >0.5 mcg/ml
Acrodynia
- Acrodynia is a rare idiopathic chronic toxic  Cyanogen-containing plants
reaction to elemental or inorganic mercury  Linamarin in cassava cake – associated Sxs:
exposure, which occurs mainly in young DUMBELS
children. It is characterized by pain in the
extremities and oink discoloration with
 Cyanide salts
desquamation of the skin
 Metal polishing (jewelry cleaners)
Uncommon Syndrome “Pink Disease”
 Cyanide Antidote Kit
 Pain in the extremities  Amyl nitrite, sodium nitrite, sodium thiosulfate
 Pinkish discoloration and desquamation
 Hypertension RED TIDE POISONING
 Sweating  Diarrheic shellfish poisoning
 Insomnia, irritability, apathy  Okadaic acid (OA) and its derivatives
 Considered as idiosyncratic reaction
 Amnesic or encephalopathic shellfish
Adverse Effects of Mercury poisoning
 Elemental  Domoic acid
- acute necrotizing bronchitis pneumonitis,
insomnia, forgetfulness, loss of appetite, tremor,  Paralytic shellfish poisoning
erethism, renal toxicity  Saxitoxin and gonyautoxin (GTX)
 Inorganic
- corrosive effects: GI ulceration, perforation,  Neurotoxic shellfish poisoning (NSP)
hemorrhage, acrodynia, renal toxicity
 Brevetoxin
 Organic
- CNS: paresthesia, ataxia, muscle spasticity Department of Health
- Infants: psychomotor retardation, blindness, Criteria for Detecting PSP
deafness, seizure, cerebral palsy
 Ataxia +
- Behavioral and learning delays: deficits in
 Additional 2 Motor Distrubances +
language, attention and memory
- Dysphagia
- Inability to stand
 Lead (a.k.a tingga) - Vomiting
 Pregnant women and their developing fetuses - Dyspnea
are at high-risk because lead readily crosses the - Paralysis
placenta  Additional 2 Sensory Disturbances
 For every 10mcg/dl increase in BLL, children’s IQ - Dizziness
dropped by 4-7 points - Headache
- Lightheadedness
Pharmacology – Clinical Toxicology by Dra Dando Page 8 of 8

- Paresthesias REMEMBER THE DONT’S:


- Dysthesia  Do not induce vomiting in the following situations:
- Hot flashes - drowsy and comatose patients
- Numbness - poor gag reflex
- ingestion of corrosive and hydrocarbon
Specific Treatment - if the ingestion has occurred for more than one
With known or suspected toxin hour
- late pregnancy (last 3 months of pregnancy)
- presence of heart disease

 Do not give milk or vinegar


(-) Respiratory Distress (+) Respi Distress :milk is not a universal antidote

Observe for 24 hrs

Asymptomatic (-) Respi Failure (+)


Respi Failure

Discharge NaHCO3 q 5 hr NaHCO3 q 5


hrs x 24h

Observe x 24 hrs
Ventilatory support

Respi Distress Test dose of


edrophonium

With Response

Public Health Issues


 Reporting to DOH
 Shellfish / Fish Advisory
 Monitoring of other possible patients
 Monitoring of levels of toxins in the area (BFAR)

SUBSTANCE ABUSE
Sedatives
 Diazepam (Valium)
 Lorazepam (Ativan)
 Flunitrazepam (Rohypnol)
 Sleeping Pills (Stinox, Unisom)

*Ecstasy
- side effect: bruxism
- causes seizure, severe dehydration
- more toxic than shabu

Smoking and Alcohol

FIRST AID MANAGEMENT OF POISONING CASES


GOAL OF TREATMENT:
- to limit absorption of poison
- remove from toxic environment
- decontamination Maneuvers

You might also like