PLENO 6 POISONING GROUP 6

Name Toni periyanto Jessica stephanie Paramita adinda P

Nim 405070018 405080007 405080139

Tutor : dr.Agnes

Maria marcella
Alexandra adeline Obed yosia Christine yuliani Reza adrian H Ansella riska Idha idhar dewi P Fany azhar A Brigita maria A

405090007
405090036 405090050 405090055 405090059 405090085 405090155 405090180 405090255 Secretary Leader Scribber

Problem 6
A 3 year old girl is brought by her parents to the emergency departement with decrease of consciousness. About 3 hours earlier, the mother discovered her daughter was vomitting. An almost empty bottle containing a strong smelling liquid was found next to her. After wards, the girl started to talk deliriously and was feverish. No history of seizures or influenza. Physical examination results : delirious, blood pressure 90/60 mmHg, heart rate 100 bpm, RR 40 breaths/, temperature 38c, lung examination revaelascoarse crakles . Abdominal examination indicates the liver is 2cm palpable below costal arch. Pulse oximetry shows 90% of oxigen satuuration laboratory result : hb 95 g/dl, leukocyte 15000/mm3, ht 31%, trombocyte 550000/mm3, Na 128 meq/l, K 3.6meq/l Please discuss the problem!

Mind mapping
Girl 3year old
poisoned

smelling liquid drink

physical examination and lab

3 hours after drinking it throw up

delirium and fever

Learning objective
1. general poisoning 2. poisoning by etiology

LO 1 GENERAL POISONING

Poisoning Poisoning the entry of toxic substances into the body (GI tract, inhalation / direct contact) clinical signs and symptoms of a typical.

Self Poisoning Attempted suicide Accidental poisoning Etiology Homicidal poisoning Acute Classification Onset Chronic Liver Target Organ Heart Kidney CNS Alcohol Chemical Material Phenol Heavy metal Organochlorin

Diagnose
Consiousness 4 grade: Grade 1 somnolens but easy to talk to Grade 2 Sopor, wake up with minimal stimulant Grade 3 soporocomma, react with maximum stimulant Grade 4 Comma

Clinical Features depens on Etiology

Clinical features Pupil pin point, RR Etiology Opioid Cholinesterase Inhibitor (organophosphate, carbamate insectiside) Benzodiazepin

Pupil dilatation, speed of breath decrease

Pupil dilatation, tachycardia Tricyclic antidepresant Amfetamine, extasy, cocaine Anticholinergic (benzeksol, benztropin) Antihistamine Cyanosis Hipersalivasi CNS depresant drugs Substance causes methaemoglobinemia organophosphate, carbamate insectiside

Clinical features

Etiology

Nistagmus, ataxia, cerebral signs

Extrapyramidal symptoms Seizure

Anticonvulsive (fenitoin, karbamazepin) Alcohol

Phenotiazin, haloperidol Metoklopramide Tricyclic antidepresant , anticonvulsive, teophiline, antihistamine, NSAID Phenothiazin, isoniazid Litium, Tricyclic antidepresant, antihistamine Amfetamine, ecstasy, cocaine

Hypertermia Hypertermia & hypertension, tachycardia, agitation Hipertermia & takikardi, asidosis metabolik

Salicilat

Clinical Features Bradikardia

Etiology Beta blocker, digoxin, opioid, clonidine , Ca blocker (except dihidropiridin) Organophosphat insectiside Withdrawal alcohol, opioid, benzodiazepin

Abdominal cramp, diarrhea, tachycardia, hallucinatiion

Blood Gas Analysis

Blood gas analysis Respiratoric acidosis (pH < 7,3; PCO2 > 5,6 kPa) Respiratoric alkalosis (pH > 7,45; PCO2 < 4,7 kPa) Interpretations Hypoventilation, CO2 retention, maybe because of CNS depresant Hyperventilation maybe as response to hypoxia, drug injury (aspirin) or CNS injury

Metabolic alcalosis (pH > 7,45; HCO3 >30 mmol/l)

Metabolic acidosis (pH < 7,45; HCO3 <24 mmol/l; Base excess < -3) compensated if PCO2 < 4,7 kPa Wide anion gap

Uncommon in poisoning, as a effect from loosing acid or alcali excess

Common in poisoning, if get worse watch for etanol, metanol, etilen glikkol poisoning Metformin, isoniazid, salycilate ,cyanide

Odor of poisoning Smell Aseton Almond Garlic Etiology Isopropil alkohol, aseton Cyanide Arsenik, celenium, talium

Broken eggs

Hidrogen sulfida, mekraptan

Colors of urine Color Green / blue Yellow-red Dark brown White crystal Brown Etiology Blue methylene Rimfapisin, Fe Fenol, cresol Primidon Mio/ haemoglobinuria

MANAGEMENT AND THERAPY

GENERAL MANAGEMENT
Stabilization (ABC) Elimination Accelerate

Decontamination decrease
exposure to toxins, reduces absorption and prevent damage:
decontamination pulmonary decontamination eye skin decontamination GIT decontamination

spending toxins that are

circulating in the blood or in the gastrointestinal tract after> 4 hours
forced diuresis urine alkalinization acidification urine

Hemodialysis / peritoneal dialysis

antidotum

Primary Survey
Make sure the airway is open
Can be given supplemental oxygen, 12 L / min (non-rebreathing mask) Intubation when swallowing reflex -

Measurement of arterial blood gas levels and blood pH IV access

Check blood glucose levels, complete blood tests, serum electrolytes, and kidney and liver function checks

Management of coma
If the patient's response is weak / suspected drug overdose (pinpoint pupils, weak breathing) naloxone 2mg every 1-2 min s / d dose of 10-20mg max

 If suspected alcohol poisoning and malnutrition - thiamine, 100mg IM / IV with glucose control Maintain circulation circulation control and management of shock to restore volume with infusion / crystalloid sollution

Management of seizures
ECG monitor Perform gastric rinse

Installation of NGT/OGT with activated charcoal (1g/kg) mixed with 70% sorbitol solutio
Find the etiology

Secondary Survey
Anamnesa Gather information about medications used include medications that are often used Gather information from family members, friends and officers about drug use Ask and keep (for toxicological examination) residual drug and vomit Ask a history of drug allergy or a history of anaphylactic shock Awareness GCS I patients drowsiness but easy to talk II sopor, can be awakened with minimal stimulation (talking loudly, shake hands) III soporokoma, can only react with maximal stimulation (pressing sternum) IV coma, no reaction There is/no shock frequency of breath Volume minute - Wright's spirometer <4L/mnt O2

PE

BP Respiration

Confulsion
Pupil

CNS excitation (amphetamines), spinal cord (strychnine) or with neuromuscular (organophosphate)

Varied except in poisoning atropine and morphine

Bowel

Matching degree of awareness

III - usually negative IV - always negative

Heart

Other

Heart rhythm abnormalities - symptoms of heart failure or cardiac arrest Acid-base balance disorders EEG abnormalities retention urine Vomiting and diarrhea

DEKONTAMINATION
Decontamination GOALS : to decrease exposure to toxins, reduce absorption, and prevent damage Use a barrier (gloves, mask, apron) before provide help Depends on location decontamination pulmonary skin decontamination decontamination eye gastrointestinal decontamination

GI Decontamination

Give bonding material (activated carbon) Dilution Removing the stomach contents (induced vomiting, aspiration of gastric rinse)

Through the mouth (gastrointestinal decontamination)

absorption induce vomiting Giving syrup ipekak Giving apomorphine drain the stomach Performed within 1 hour after poisoning Not performed on patients poisoned acid / strong base Absorb toxins with activated carbon colon cleanse Using laxatives drug oontaining salts (Mg sulfate or Na sulphate) Alkaline diuresis increasing salicylate elimination, barbital acid diuresis is not effective Multiple doses of activated carbon drug elimination with a small volume of distribution Dialysis and toxin elimination hemoperfusi

Providing an antidote elimination

Through the Nose (Decontamination Pulmonary)

Moving patients or poisoning from contaminated indoor toxins Monitor the possibility of distress respiratory Give 100% O2 + ventilator Tracheotomy can be performed if necessary If using a Resuscitator with positive pressure Blood pressure control !

Skin contamination

Remove the patient's clothing, shoes and other accessories

rinse immediately with water to dilute and cleanse the toxins at least 10 minutes dried

Contamination Eyes

Open eyelids - irrigation (distilled water or NaCl 0.9%) for 15 minutes Do not shed a chemical antidote hot eye damage Cap with sterile gauze

Refer to ophthalmologist
Contamination stings or bites of venomous animals If exposed could prevent spreading by using tourniquets in the bite wound up giving that specific antidotesIt can also perform local cooling using ice cubes prevent spreading

ANTIDOTE

Lo 2 chemical poisoning food poisoning plant poisoning animal poisoning heavy metal poisoning

CHEMICAL POISONING

Poisoning gases, vapors, and chemical dust Poisoning metal and metalloid

Corrosive chemical poisoning

Chemical poisoning

Hydrocarbon poisoning Toxicity of hydrocarbons containing halogen

Poisoning nitrogen compounds

Alcohol and glycol poisoning Other chemical poisoning

POISONING GAS

Poisoning Gas, Steam, and dust Chemicals

caused by:
carbon monoxide chlorine gas ammonia gas carbon dioxide hydrogen cyanide Hydrogen sulfide and carbon disulfide sulfur oxides methane Butane gas - propane nitrogen gas nitrogen dioxide ozone gas phosgene formaldehyde hydrogen fluoride osmium tetroxide vanadium pentoxide manganese cadmium oxide chromate zinc chloride mercury

Carbon monoxide
info carbon monoxide poisoning if symptom Produced by the incomplete combustion of materials - carboncontaining materials from machinery and motor vehicles through inhalation Limit exposure to <1000 ppm dyspnea Headache, weakness, blurred vision, nausea, vomiting, red mucous membranes, respiratory rate, and pulse increases, convulsions, coma subsequent shock, respiratory depression, arrhythmias, and death > 1000 ppm: unconsciousness, respiratory failure, and death if inhaled > 1 hour Levels of carbon monoxide inside, the air around must be below exposure limits

complication Cerebral and pulmonary edema, myocardial infarction / stroke prevention

info emergency action Avoid contact later, the patient had to be removed Oxygen 100%

Antidot
General action

Oxygen
Keep the body temperature normal TD patients Reduce cerebral edema 1g/kg mannitol as a solution of 20% Overcoming edema sererbral prednisolone 1 mg.kg IV or IM every 4 hours Inflammation of the lungs caused by bacterial infection specific chemotherapy drugs Reduce neurological complications 2-4 week break Overcome convulsions diazepam 0.1 mg / kg IV slowly land

Gas Klor
info
Gas klor poisoning symptom Used as a drinking water disinfectant and household bleach Through inhalation irritation, cough, dyspnea, and pneumonia Irritation and burning sensation in the affected tissue, cough, vomiting, and bad breath are typical conjunctivitis of the eye without serious corneal damage Keep the alive Poisoning by inhalation avoid further contact Actions supportive and symptomatic medication

action

carbon Dioxide
info symptom action Dyspnea, headache, visual disturbances, tinnitus, tremor, and unconscious Move the patient to the open space Give artificial respiration If necessary inpatient hospital

Ammonia gas
info Ammonia gas Explosives, plastics, fertilizers, and as a refrigerant cooling device Is corrosive, damaging the cells direct irritation of the mucous membranes Through inhalation pulmonary edema and pneumonia Limit exposure: 25 ppm Inhalation: irritation of the upper respiratory tract, with coughing, vomiting, mucous membranes of the nose and pharynx red Large dose: shortness of breath, pulmonary edema, cyanosis, and rapid but weak pulse Eyes: corneal haziness eyes flush with water immersion 15 minutes inhaled remove from contaminated indoor Overcome pulmonary edema and narrowing of the esophagus

Poisoning if symptom

emergency Special case

Hidrogen Sianida
info Poisoning if Through inhaled breathing becomes rapid, TD down, convulsions and eventually a coma, paralyzed because all cells Limit exposure: 20 ppm Acute unconscious immediately, convulsions and death within 1-15 minutes Chronic dizziness, weakness, pulmonary congestion, conjunctivitis, loss of appetite and weight loss, and mental deterioration Move into the room that is not contaminated Amyl nitrite by inhalation Give artificial respiration with 100% oxygen

Clinical manifestation

emergency

Antidot

Sodium nitrite 3% in IV, discontinue if systolic BP <80mmHg Give 25% solution of sodium thiosulfate IV Dikobalt edetat WITH INITIAL dose of 300-600 mg

HIDROCARBON

Hidrocarbon
Definition an organic compound composed of carbon and hydrogen atoms

Material

mixture of aliphatic chains (straight) and aromatic rings (benzene)

Epidemiology

Poisoning most children pd ( 50%). Mostly aged under five year age groupings common with someone aged 1-2 yrs.

clasification
low viscosity aliphatic gasoline kerosene Mineral oil seal mineral spirits High viscosity aliphatic asphalt diesel oil fuel oil "Fat" (grease) lubricant tar Aromatic (v low) Benzen Toluen Terpentin Silen halogenated hydrocarbons Karbon tetraklorida Metilen klorida Trikloroetana trikloroetilen

Patofisiologi

penetration of the mucous membranes, damage the airway epithelium, alveolar septa, and reduce the number surfactan trigger hemorrhage, pulmonary edema, or collapse of the lung. number <1 ml of pulmonary aspiration can cause significant damage. death as aspiration + 2.5 ml of the lung (gastric + 350 ml). in addition, the amount of 1 ml / kg kerosene can cause cns depression mild - moderate, carditis, damage to liver, adrenal gland, kidney, and erythrocyte abnormalities.eritrosit

Clinical pharmacology and toxicology

Aspiration !!!! Related to the viscosity (and voltage) surface compounds: the lower the viscosity - the greater the risk of aspiration hydrocarbons irritate the airway and cause edema, spasm bronkiulus. Hydrocarbons v.low wide spread over the surface of the small airways and alveoli. Dissolving properties of this material intregritas damage cell membranes produce an inflammatory reaction (hyperemia, vascular thrombosis, hemorrhage, edema) Dissolving the surfactant layer alveolar collapse and atelectasis

Clinical pharmacology and toxicology

Ingestion H.alifatik absorption through the gastrointestinal mucosa is less Aromatic very good Sistemic Toxicity does not occur The effect may be due to hypoxia CNS H.alifatik v.increased aspiration hazard is not significant and is not absorbed from the gastrointestinal tract.

Manifestasi clinic

Breathing
GIT

Respiratory

Cough :often Rarely : dyspnea is usually associated with severe aspiration Burning / irritation of the mouth and throat belch nausea and vomiting abdominal pain diarrhea Fever and smell "gasoline" in the mouth tachypnea rhonchi Cyanosis SSP (associated with the ingestion of aromatic hydrocarbons) SSP Depresi

Kerosene Poisoning
Effects on acute exposure to kerosene Skin contact: dry, irritation can, cause rash Skin absorption: rare Eye contact: irritation, may cause permanent damage Inhalation: irritation, headache, dizziness, drowsiness, intoxication Ingestion: headache, dizziness, drowsiness, intoxication Effects of chronic exposure to kerosene in In general: chapped skin, dermatitis, liver damage / adrenal gland / renal and erythrocyte abnormalities Carcinogenic: seen in experimental studies in mice, in humans no data recorded Reproductive system: no data recorded

Signs & symptoms

Estimated toxic dose of 120-150 mL : 2 teaspoons when aspired aspiration in the lungs - pulmonary, gastrointestinal irritation, central nervous system depression with respiratory depression, vomiting, aspiration with the result dyspnea, asphyxia, pulmonary edema, pneumonitis and sometimes sometimes seizures Investigation:

Laboratory Routine blood, urine routine Radiology: the thorax. Best 1.5 - 2 hours after exposure Patients with pneumonia will generally appear in the photo on the 6-18 hours, but it had also been reported recently looked after 24 hours Procedure Monitor respiratory system inhaled oxygen Salbutamol: when a nascent breathing disorders Antibiotics: when you have an infection arises, it is not recommended as prophylaxis Hydrocortisone: first recommended, now rarely performed Antacids: to prevent irritation of the gastric mucosa Granting dilution of milk or other ingredients Anus and perineum should be cleaned immediately to avoid irritation (skin burn) secondary In case of respiratory failure, mechanical ventilation can be done

Complications

aspiration pneumonitis. Spread through the penetration of the mucous membranes, damage the airway epithelium, alveolar septa, and surfactan : amount of bleeding, pulmonary edema, or collapse of the lung. Total <1 ml of pulmonary aspiration in significant damage. Death may occur due to aspiration as much as + 2.5 ml of the lung (gastric + 350 ml). In addition, the amount of 1 ml / kg of kerosene may cause CNS depression mild - moderate, carditis, damage to liver, adrenal gland, kidney, and erythrocyte abnormalities (rare systemic effects are not absorbed in the number >> on sal tract, Kerosene excreted through urine)

insektisida
Organofosfat
DDPV Diazinon Malation Paration

Insektisida

Karbamat

Karbaril Baygon

Organoklorin

Aldrin BHC DDT Dieldrin Endrin Klordran Tiodan Toksifen

ORGANOPHOSPHATE AND CARBAMATE INSECTICIDES

Principles of Disease Highly lipid soluble and are readily absorbed via dermal, gastrointestinal (GI), and respiratory routes. Organophosphorus pesticides work by persistently inhibiting the enzyme acetylcholinesterase

PESTICIDES IN DIFFERENT MEDIA

Air -Respirable particles contaminated with pesticides - Respirable aerosols during spraying - Vapour from volatile residues of pesticides
Hand-to-mouth behaviour - Crawling on the ground - Dermal contact

soil

water Pesticides in drinking water: tap, well food -Crops routinely sprayed: fruits, vegetables, grains -Bioaccumulation in animals and products fish, meat, eggs, dairy

ROUTES OF EXPOSURE
Ingestion Breastfeeding Accidental ingestion Residues in food Mouthing Indoor and outdoor spraying Occupational exposure Accidental contact Occupational exposure Residues on surfaces Contaminated clothing Medical use: scabies, head lice

Inhalation

Dermal absorption

Because of the global penetration of organophosphorus compounds, inhibition occurs at tissue sites:
- true acetylcholinesterase represented by erythrocyte - circulating pseudocholinesterase in plasma

Inhibition of cholinesterase results in the accumulation and subsequent prolonged effect of acetylcholine at a variety of neurotransmitter receptors : - sympathetic and parasympathetic ganglionic nicotinic sites - postganglionic cholinergic sympathetic - parasympathetic muscarinic sites - skeletal muscle nicotinic sites - CNS sites

Clinical Features
This syndrome represents postganglionic acetylcholine-induced hollow end-organ general hypersecretion.

Bradycardia is a classic sign of the cholinergic syndrome, but the increased release of norepinephrine from postganglionic sympathetic neurons precipitated by excess cholinergic activity at sympathetic ganglia may result in normal or even tachycardic heart rates (nicotinic effect).

A combination of sympathetic stimulation, involvement of the N-methyl-d-aspartate receptor, and enhanced acetylcholine concentrations seizures

Because the diaphragm is affected, cholinesterase poisoning leads to respiratory arrest.

Clinical Features

Treatment
Treatment is directed toward four goals: (1) decontamination, (2) supportive care (3) reversal of acetylcholine excess at muscarinic sites (4) reversal of toxin binding at active sites on the cholinesterase molecule

Organochlorine
Mechanism:
Interfering ion transport through the membrane Na and K axonal

Toxin dose: 15-30gr DDT, Endrin 1 '5 gr Signs and symptoms:

Seizures, tremors, coma. Then comes the paralysis

Treatment: Symptomatic. Rinse the stomach and leave MgSO4 30 g

Phenobarbital 100-200mg Diazepam 5-10 mg IM or IV

OTHER CHEMICAL POISONING

Acids and strong bases

MECHANISMS OF TOXICITY
Toxicity by strong acids is due to the type of coagulation necrosis that tend to limit further damage While the strong base that is liquefactive cause necrosis (degeneration structure of solid to liquid or semi-liquid) and continues to penetrate into the deeper tissues, causing considerable damage extensive

ESTIMATED DOSE TOXICITY

No specific toxic dose. The concentration of the substance or material the solution pH can be an indicator of the potential for serious damage

SIGNS AND SYMPTOMS

Corrosive

THERAPY
Are symptomatic: give milk. When ingested in concentrated solution, do not rinse the hull Endoscopic whenever possible to assess the degree of damage

Borax (boric acid)

MECHANISMS OF TOXICITY
There are no known mechanisms of toxicity for certain boric acid. boric acid is distributed throughout the network and the possibility of working as a general cellular poisons System is the organ most frequently affected are GIT, brain, liver and kidneys

ESTIMATED DOSE TOXICITY

Acute: 1-3g in neonates, infants 5g, 20g in adults

SIGNS AND SYMPTOMS

Vomiting, diarrhea, decreased body temperature, feeling weak, headache, rash erythemateous

THERAPY
Symptomatic: Forced diuresis

Gasoline
SIGNS AND SYMPTOMS
Inhalation or oral: nausea, vomiting, headache, vision impaired, drunk, coma, respiratory depression and central depression

THERAPY
Symptomatic: epinephrine and nor-epinephrine should not be granted because it can cause ventricular fibrillation Mechanism was unknown and the dose

Bromide (Karbromal, bromosolvalum)

MECHANISM KERCUNAN
Bromide ions displace chloride ions on the membrane transport systems, specifically in the CNS With high levels of bromide, the effect of depression on the membrane progressively debilitating neuron transmission

ESTIMATED toxic dose

Adults: 3-5g; oral more than 10-20g (+)

SIGNS AND SYMPTOMS

Acute: rare, because spewed

THERAPY
If possible give oral: NaCl or NH4Cl 6g/day HCT 2x25 mg or 1-2ml IM salirgan

Phenol
MECHANISMS OF TOXICITY
Phenol causes protein denaturation and penetrate well into tissue Phenol is corrosive to the eyes, skin and respiratory tract Systemic absorption may cause CNS stimulation (CNS toksikasi mechanism is unknown

Toxic dose
1g

SIGNS AND SYMPTOMS

Corrosive (oral and intestinal mucous cells), severe pain, vomiting, coma and shock Kidney damage

THERAPY
Symptomatic: give milk. Rinse carefully hull, if any use olivariu

Formalin
mechanism Cause precipitation of proteins and cause the type of coagulation necrosis in the exposed tissue. The form is very soluble gas and cause local irritation if inhaled upper respiratory tract and may cause spasm of the statements contained and laryngeal edema Metabolism of formic acid metabolic acidosis Formalin is known to be carcinogenic in humans Inhalation 100ppm called dangerous 30 mL of 37% formalin solution can lead to death In the eyes of eye irritation Inhalation coughing, wheezing, pulmonary edema Ingestion korosive damage to the hull Metabolic acidosis can occur due to accumulation of formic acid Inhalation maintain airway and give oxygen and 4-6 hours of observation Overcome coma and shock. Provide drip to replace fluids hilangkarena gastroenteritis Overcome metabolic acidosis with sodium bicarbonate Oral rinse stomach. Do not induced emesis karen corrosive

Toxic dose Sign & symptoms

Therapy

Potassium Permanganate
Mechanisms of toxicity: corrosive Signs and symptoms:
Crystal: working corrosive (solution: no danger), vomiting, weak pulse, cold skin, collapse, edema of glottis

Therapy:
Give the egg whites, milk and laksan Rinse the hull in preparation for tracheotomy

FOOD POISONING

Hazards in food
Physical: glass, stone, metal, wood, etc Chemical: - natural toxins - residues - metals - toxins formed during food processing Microbiological: pathogenic microorganisms (bacteria, viruses, parasites, etc)

Foodborne Diseases

Infections

Intoxications

Toxicoinfection

Invasive Infection

Chemical Poisoning

Poisonous Plant Tissues

Poisonous Animal Tissues

Microbial Intoxications

Other

Neurotoxins

Enterotoxins

Intestinal Mucosa

Systemic

Mycotoxins (Fungal Toxins)

Algal Toxins

Bacterial Toxins

Other Tissues or Organs (Muscle, Liver, Joints, Fetus, Other)

Diarrhogenic

Emetic

Enterotoxins

Neurotoxins

Other

Risk
High risk ppl : Geriatry Pregnancy child
High risk food : meat and meat products; milk and dairy products; fruit. If these foods

becomcontaminated with
food-poisoning micro organisms and conditions allow them to multiply, the risk of food-poisoning increases.

Factors affecting food poisoning

Some common factors leading to food poisoning include: preparation of food too far in advance; storage at ambient temperature; inadequate cooling; inadequate reheating; under cooking;

inadequate thawing.

More common factors leading to food poisoning include: consuming raw food; improper warm holding (i.e. holding hot food below 63C); infected food handlers; contaminated processed food; poor hygiene.

Symptoms of food poisoning

Food poisoning can be mild or severe.

The symptoms will be different depending on what type of bacteria is responsible.

Common symptoms include: severe vomiting; diarrhoea; exhaustion; headache; fever; abdominal pain; tiredness.

Preventing
Tips for buying food include: it is illegal to sell food that has passed its use by date; dented, blown or rusted cans of food should not be purchased; frozen food which has frozen together in the pack should not be purchased; do not buy food where the packaging has been damaged; only shop in clean and hygienic storesTips for transporting food back home: buy chilled and frozen foods at the end of the shopping trip; keep frozen and chilled foods cold, by using cool boxes/bags and packing these types of foods together; cooked and uncooked foods should be kept separate; dry and moist foods should be packed separately; household chemicals should be packed separatelyTips for storing food in the home: food should be unpacked as soon as possible; old stocks of food should be used before buying new ones (first in, first out theory); store food in the correct place, i.e. dry food, in cool, dry clean places and chilled food in the refrigerator

The Main Food Poisoning Bacteria

Type of food Where the Onset time poisoning bacteria come from
Salmonella Raw meat, eggs, poultry, animals 6 - 72 hours

Symptoms

Abdominal pains, diarrhoea, fever, vomiting, dehydration Abdominal pain, diarrhoea Vomiting, abdominal pains, lower than normal temperature

Clostridium perfringens

Raw meat, soil, 8 - 72 hours excreta, insects 1 - 6 hours

Staphylococcu Skin, nose, s aureus boils, cuts, raw milk

Incidents of Food Poisoning in PDO

Date Place People Type of Food Affected Poisoning 23 12 32 75 Source

June '98 Marmul April '99 April '99 Fahud RAH Club

Salmonellosis Unknown Shigellosis Shigellosis Unknown Unknown

May '01 Toco Camp Saih Rawl

Salmonellosis Unknown

Name Campylobacter

RF Meat and poultry.

Sign & Symptoms Onset 2 11 days. Fever, headache and dizziness for a few hours, followed by abdominal pain. This usually lasts 2 7 days and can recur over a number of weeks

Clostridium perfringens

Raw meat, cooked meat dishes and poultry.

Onset 8 22 hours. Abdominal pain, diarrhoea and nausea. This usually lasts 12 48 hours.
Diarrhoea, which may contain blood, can lead to kidney failure or death. Ranges from mild, flu-like illness to meningitis, septicaemia, pneumonia. During pregnancy may lead to miscarriage or birth of an

E Coli 0157

Raw meat and dairy products. Unpasteurised milk and dairy products, cook-chill foods, pate, meat, poultry and salad vegetables

Listeria Monocytogenes

Name Bacillus cereus

RF Rice, meat, seafood, salads, potatoes, and noodles

Sign & Symptoms Ranges nausea and vomiting and abdominal cramps and has an incubation period of 1 to 6 hours . This usually lasts less than 24 hours after onset. Onset 24 72 hours. Voice change, double vision, drooping eyelids, severe constipation. Death within a week or a slow recovery over months. Onset 12 36 hours. Headache, general aching of limbs, abdominal pain and diarrhoea, vomiting and fever. This usually lasts 1 7 days, and rarely is fatal.

Clostridium botulixnum

Inadequately processed canned meat, vegetables and fish (faulty canning) Raw meat, poultry and eggs, and raw unwashed vegetables.

Salmonella

Staphylococcus aureus

Meat, dairy products and poultry.

Onset 1 6 hours. Severe vomiting, abdominal pain, weakness and lower than normal temperature. This usually lasts 6 24 hours.

Salmonella

Outbrakes associated with grade A eggs. Preparation of Poultry. Sources : Chocolate mousse ; Ceasar salad ; Chicken Gram - rod Killed by high temperatures 12-36 hours ; low grade fever ; abdominal pain ; diarrhea; chills patient history stool culture Microscopic examination leukocytes occult blood Supportive fluid and electrolyte NO antibiotics does not alter the severity prolongs the carrier state Do NOT give anti-motility drugs lead to intestinal perforation

Sign & Symptoms Diagnose

Treatment

Clostridium botulinum

Four different types food borne infant wound undetermined heating, freezing, ionizing radiation boiling >120 degrees for >20 min Very powerful : 0.5 nanograms (lethal) Heat sensitive : 80 degrees for 30 min 12-48 hrs (14 days) N/V/D abdominal distention constipation (as disease progresses) Neurologic disturbances : dysarthria, dysphagia, dry mouth

Resistant Destroyed by Toxin Sign & symptoms

With disease progression Treatment

descending paralysis ; respiratory weakness; respiratory failure ; oculobulbar symptoms stabilization of airway history upper and lower GI decontamination trivalent antitoxin (ABE) watch for hypersensitivity call CDC

DD

Treatment / profilaksis

Neuromuscular disorders Stroke syndrome Myasthenia gravis Guillain-Barre syndrome (Miller-Fisher variant) Tick paralysis Atropine poisoning Paralytic shellfish/puffer fish poisoning Diagnosis based on clinical presentation with subsequent laboratory confirmation Ventilatory assistance and supportive care Botulinum antitoxin Trivalent equine product against types A,B, and E available from CDC Most effective if given early Antibiotics for wound botulism Penicillin Recovery may be prolonged with supportive care necessary Vaccine investigational not available

Staphylococcus aureus

Enterotoxins Found : protein rich foods : ham, poultry, fish, milk and other dairy improper food handling

Mechanism

entrotoxin acts as a superantigen stimulates intense cytokine production toxic shock like syndrome

Sign & Symptoms

2-6 hrs abdominal pain N/V/D

mild self limiting death is rare elderly debilitated

Treatment

JengKOL

not well for people outside indonesia, because not many cultures that used jengkol as food ingredients. Jengkol itself is a kind of beans (Pithecolobium lobatum). : = 9:1 (Highest 4-7 years old) intoxication occurs depends on individual susceptibility to jengkolic acid

Symptoms

caused by obstruction of urinary tract by jengkolic acid crystal. Complains in 5-12 hours after eating jengkol. Fastest 2 hours, the latest after 36 hours. abdominal pain/discomfort after eating few jengkol Vomit , colic pain at micturition. Urine volume also decreased, even can be anuria. hematuria can be found. Also urine and breath smells jengkol. In urine examination with microscope, can be found jengkolic acid crystal that being seen as sharp needle or sometimes agglutinated as bound or rosette
Parents told us, after hours eat jengkol, sign and symptoms appear
mild (vomit, abdominal/flank pain only) advice to drink a lot and giving

LAB
Diagnose

sodium bicarbonate.
severe (oliguria, anuria, hematuria and can't drink), hospital or opname

and receive Sodium bicarbonate in 5 % glucose I.V (adult and child doses 2-5 mEq/kgBB with Natrium bicarbonat IV for 4-8 hours.
Antibiotik (if suspect secundary infections)

Prognose Advise

Bonam, still have some patient die cause acute kidney failure Dont EAT JENGKOL

Cassava (Singkong)

Root and leaf of cassava have hydrocyanate acid (HCN). HCN + cytochrome oxydase cytochrome oxydase HCN compleks, (oxydation in the tissu would be inhibited) HCN cyanmethemoglobin, toxic respiratory cel, disruption to the process of oxidation enzymes Enzim distruption tissue, neuron cell cant take the O2 Venous blood is bright red as arterial blood More quantity death due to respiratory failure initially heat to the abdomen, nausea, dizziness, spasms, weak breathing fast and short Smelly breath and vomit bitter almond smell Fainting, seizures, weakness, sweating, eyes bulging wide pupils without reaction Mouth foam mixed with the color of blood Skin color brick red (light skin), cyanosis usually (-) appears Test Giunard u / cassava picric acid color change yellow to red (15minutes ~ 3 hours) Commonly same toxin eliminated (vomited, rinse the hull(gaster), antidot amil/na nitrit, Na-tiosulfat Na-nitrit NaCN bind prevent damage to cells ferisitokrom oxidase enzyme Na-tiosulfat NaCN bind stable tiocynatat excretion through the lungs, saliva, urine Na-nitrit 3% ml iv slowly, Na tiosulfat 10% IV slowly (0.5mL/kgBB/x or 10-50ml) if Na nitrit (-), Na tiosulfat is fine O2 th suportif & antidotum (t.u O2 high tension/CPAP) Ok O2 competitive against bond ferisitokrom oxidase enzyme with cyanide

Sign & symptoms

Treatment

Advise

Processing HCN : peeled tubers with - washed - dried, soaked, heated PATPI (Perhimpunan Ahli Teknologi Pangan Indonesia): Bulbs soaked with 8% salt solution in 3 days , or Tuber slices heated in boiling water 30 min > effective How linase enzyme (-) Active If the consumption of cassava alone FR low protein calori, & iodium

Bongkrek (tempe bongkrek, asam bongkrek) Etiology Symptoms

Bongkrek acid from tempe bongkrek (manufacture with coconut pulp fermentation and peanuts) coconut pulp bongkrek acid (Pseudomonas cocovenenan) iron pedestal Clostridium botulinum contamination Mild : headache, nausea, Abdominal pain, anoreksia, diplopia, ptosis, Strabismus severe : Respiratory and circulatory failure, seizure, death

Treatment

Spesific Antidot not yet.

Prevent further absorption of toxins and accelerate the excretion Rinse the hull Catharsis General improvement IV plasma liquid & NaCl IV glukosa activated charcoal u / impaired circulation and respiration. Ne

PLANT POISONING

Mushroom Groups
Early onset of symptoms (04 hours postingestion) Late onset of symptoms (>6 hours postingestion) No symptoms (edible).

Mushrooms with serious toxicity and potential for death are in the group that have late onset of symptoms.

Management of Mushroom Exposure

Identification of the mushroom mycologists or a poison center may be helpful. If a specimen is available stored in a paper bag at room temperature for delivery. A digital picture can be taken and e-mailed. Vomitus.

Prognosis
The prognosis depends on the specific species.

Group/Toxin GI toxin

Structurally related to

Symptoms nausea, vomiting, diarrhea, and abdominal cramps 0.53 hours after ingestion, and typically last 24 hours.

Treatment supportive, with good outcome expected

Ibotenic acid and muscimol Muscarine

glutamic acid and GABA Acetylcholine Does not cross the blood-brain barrier

Lethargy, hallucinations, seizures, or severe agitation 1 to 2 hours after ingestion salivation, lacrimation, urination, defecation, gastroenteritis, and emesis (SLUDGE) flushing, nausea, vomiting, and headache occur 30 minutes - several days after ingestion most often used as a drug of abuse

Seizures, supportive care produce a good outcome Atropine Pralidoxime is KI acetylcholinesterase inhibition is not involved supportive

Coprine

blocking acetaldehyde dehydrogenase

Psilocybin

serotonin and lysergic acid diethylamide (LSD)

CNS effects are associated with two groups of mushrooms, ibotenic acid/muscimol and psilocybin.

coprinus atramentarius

agaricus xanthodermus agaricus californicus

clitocybe dealbata

amanita muscaria psilocybe cubensis

Cyclopeptide Most mushroom related deaths in the United States Severe nausea,vomiting, diarrhea, and abdominal cramping, begin 6 to 24 hours postingestion. Hepatic toxicity followed by other end-organ involvement may ensue over the next several days to weeks Noninvasive: silibinin, thioctic acid, activated charcoal, highdose penicillin, dexamethasone, etc. Invasive: diuresis, hemodialysis, hemoperfusion, hemofiltration, plasmapheresis, and hepatic transplantation. Gyromitrin Commonly are mistaken for edible mushrooms as they look similar to Morchella species (morel) mushrooms Metabolites of this toxin cause GABA neurotransmitter depletion similar to isoniazid toxicity, leading to excitatory CNS effects headaches, agitation, and seizures, nausea, vomiting, and possible hepatotoxicity. The onset of symptoms is at least 6 hours after ingestion. Antidote: pyridoxine

Orelline/orell Begin 1 to 2 days after ingestion anine Nausea, vomiting, abdominal pain, and headache Renal toxicity manifests days to weeks after these initial symptoms and can progress to chronic renal failure.

amanita phalloides gyromitra esculenta

cortinarius orellanus

Red Clover
Signs of poisoning: Excessive salivation Bloating Diarrhea Blindness Abortion Laminitis

Description: purplish red clover head, hairy stem, 3 leaved segments, pale ring on leaves Poisonous parts: all Found: all over US, in fields

Foxglove
Signs of poisoning: Colic Bloody feces Poor appetite Pain Frequent urination Irregular heartbeat Possible convulsions prior to death

http://www.freefoto.com/preview.jsp?id =12-57-51&k=Foxglove+-+Digitalis

One bite is fatal

Poinsetta
http://www.schaefergreenhouse s.com/poinsettia.html

Poinsettas have low toxicity

Signs of poisoning: Skin

Redness and swelling Blistering

Gastrointestinal
Stomach pain Diarrhea
http://www.schaefergreenhouse s.com/poinsettia.html

Oak Tree
Poisonous Parts: acorns, young leaves Found: all over US Signs of poisoning:
Bloody diarrhea Abdominal pain Kidney & liver damage Frequent urination Thirst Anorexia
http://www.ansci.cornell.edu/plants/horselist.html

Signs of toxicity occur when large amount are ingested Symptoms may last 3-10 days Death occurs with 85% of horses showing signs

Oleander
Description: Woody evergreen bush, grows up to 30 tall Leaves
leathery & pointed leaves grow opposite each other in groups of 3 arranged in whorls

http://www.ansci.cornell.edu/plants/horselist.html

http://www.ansci.cornell.edu/plants/horselist.html

Flowers
grow in clusters at the ends of branches white, pink, purplish, red

Oleander

http://vet.purdue.edu/depts/addl/toxic/color52.htm

Takes only 1 ounce of leaves to kill a horse

Oleander
Signs of Poisoning: Diarrhea Trembling Cold extremities Paralysis Coma Cardiac arrest followed by death

Scientific Name: Nerium oleander Poisonous Parts: all (do NOT burnsmoke is also toxic) Found: NOT in MI, found in southern US & on the west coast

http://en.wikipedia.org/wiki/Oleander

Horsetail
Signs of Poisoning: Trembling Muscular rigidity Diarrhea Rapid pulse Cold extremities Coma and death if feed source is not removed
**Horses must consume plant over a 2 week period sometimes plant is in hay

http://www.ansci.cornell.ed u/plants/horselist.html

http://www.ansci.cornell.edu/plants/horselist.html

Bracken Fern
Signs of poisoning: Loss of coordination Depression Blindness Stand in braced position with legs apart Death may occur if horse not removed from source of plant

http://www.fcps.k12.va.us/StratfordLandingE S/Ecology/mpages/bracken_fern.htm

Horses must eat plant for a month to see toxicity signs

Red Maple
Poisonous parts: wilted or dried leaves, bark Found: eastern half of US Signs of poisoning:

http://www.fcps.k12.va.us/StratfordLandin gES/Ecology/mpages/red_maple.htm

Severe anemia Weakness Depression Pale mucus membranes Dark brown urine Abortion Death due to RBC unable to transport oxygen to tissues

ANIMAL POISONING

Animal Toxins
Arachnids - Scorpions, Spiders, Ticks Insects Snakes Lizards Fish, and frogs

Example Puffer Fish

Tetrodotoxin 100 different species of puffer fish Tetrodotoxin used by fish to discourage consumption by predators Low dose of tetrodotoxin produces tingling sensations and numbness around the mouth, fingers, and toes As little as 1 to 4 mg of the toxin can kill an adult

Arachnids Scorpions, Spiders, Ticks

Scorpions Stinger low toxicity Spider bites Widow spiders - Neurotoxin Brown or Violin - Tissue Damage Ticks Neurotoxin Transmits other diseases

Insects

Moths and caterpillars Irritating to eat Ants Proteins, formic acid Irritation to allergic response Honey bees Proteins Swelling, allergic response Wasps Formic acid
Lizards Irritating to eat Snakes Vipers Rattlesnakes, Water moccasins, Copperheads Complex enzymes Tissue necrosis, allergic response, shock Elapidae Cobras, Kraits, Coral Snakes Proteins Neurotoxin, paralysis Shellfish (filter-feeding mollusks) Mussels, clams, oysters, scallops Jelly fish, anemona, coral Sea Snail (cigua) and some fish, oysters and clams Puffer Fish (fugu, blowfish, toadfish,some frogs, starfish, octopus Tuna, shark, sword fish (mercury)

Reptiles

Marine Animal

THE CHARACTERS: MILDLY VENOMOUS ANIMALS

Non-life-threatening except by anaphylactic shock in those that are allergic. Wasps, bees, ants, most spiders, most scorpions, etc.

THE CHARACTERS:
DANGEROUSLY VENOMOUS ANIMALS

Life-threatening. Need to seek medical attention. Bark scorpion, black widow, brown spider, gila monster, coral snake, rattlesnakes.

TYPES OF VENOM
Hemolytic: affects circulatory system (hemo = blood) by destroying blood cells and vessels. Symptoms include severe pain, swelling, discoloration, and local tissue death. Shock can occur. Example: most rattlesnakes.

Rattlesnake bite picture source http://www.venomous.com/snake/armpic.jpg

TYPES OF VENOM
Neurotoxic: affects nervous system (neuro). Symptoms may include local pain, headache, lethargy, paralysis and occasionally death by circulatory arrest or respiratory paralysis. Usually no swelling, discoloration, or tissue death. Examples include Black Widow, Scorpions, and Coral Snake.

Other:
Gila Monster toxin causes pain. Brown (Recluse) Spider toxin destroys proteins, thus tissues.

WHY BE VENOMOUS?
1. Subdue Prey: allows predator to reduce chance of injury and to eat larger prey. 2. Defense: protects animal from predators and other potential threats. 3. Digest Food: venom is modified saliva, produced by modified salivary glands. Most contain compounds that aid in digestion (thought to be the original use of venom).

WHY NOT BE VENOMOUS?

1. Takes Special Equipment: requires glands to produce toxins and often specialized apparatus for injecting venom (teeth, modified ovipositor, etc.). 2. Takes Energy and Materials: toxins are expensive to produce.

AVOID USING TOXIN

Hide (use cryptic coloration): camouflage.
Warn (use aposematic coloration): bright, memorable colors and/or patterns.

Some useful terms

Nocturnal: active at night (e.g., scorpions) Diurnal: active during daylight hours (e.g., gila monsters) Crepuscular: active during dawn and dusk (e.g., deer tend to be most active around sunrise and sunset)

Snake Bite
Snakes are nocturnal reptiles

RATTLESNAKE SENSE ORGANS

Nostrils to smell Eyes: to see

Pit Organ to sense heat

Body to feel ground vibrations

Cont >>

 SNAKE BITE

Snake Venom

There are over 3,000 species of snakes on the Planet, but only 15% are considered to be dangerous Snakes are found on every continent except Antarctica Every State except Alaska, Hawaii, and Maine are home to at least 20 venomous snake species Each year there are 45,000 incidents of snake bites in the U.S. 7,000 - 8,000 are from venomous snakes On average 10 people die each year Snake Venom is a Toxin (Hemotoxin Neurotoxin, or Cytotoxin) ; A varied form of saliva It is excreted through a modified parotid salivary gland Located on each side of the skull Behind the eye Combination of proteins and enzymes Hemotoxic: Family: viperidae ; e.g. vipers (Cerastus) Neurotoxic: Family: Elapidae e.g. cobra (Naja haj haj; Naja nigrocollis) Myotoxic: Sea snakes

According to the dominant venom:

Hemotoxic venom:

Dominant in viper snake venom Have high MW Mainly composed of hemolysin, thromboplastine, cardiotoxin Can cause: hemolysis, destruction of vascular endothelium, cerebral hge., intestinal hge., hypotension & shock, tissue necrosis, & DIC is considered

Neurotoxic venom

Dominant in cobra venom 50-75% have low MW Act mainly on neuromuscular junctions -> weakness, dangerous when affect respiratory muscles -> respiratory failure
Non-poisonous: U-shaped as any animal Poisonous: either: Complete: 2 punctures due to fangs (more dangerous) Incomplete: 2 parallel tailed scratches(less dangerous Generally bite is more dangerous at night & during summer Defense bite: at day time Business bite: at night, usually envenominated & dangerous

According to shape:

According to time of Poisonous Biting:

SNAKE VENOM

90% protein by dry weight and most of these are enzymes 25 different enzymes have been isolated from venoms and 10 of these occur frequently in most venoms Synergistic effects: different venoms contain different combinations of enzymes causing a more potent effect than any of the individual effects (very similar to drug synergism) Generally speaking, venoms are either neurotoxic, hemotoxic or cytotoxic and the enzymes in the venom are responsible for these effects Snake venom consists of proteins, enzymes, substances with a cytotoxic effect, neurotoxins and coagulants. Phosphodiesterases are used to interfere with the prey's cardiac system, mainly to lower the blood pressure. Phospholipase A2 causes hemolysis through esterolysis of red cell membranes and promotes muscle necrosis.[1] Snake venom inhibits cholinesterase to make the prey lose muscle control. Hyaluronidase increases tissue permeability to increase the rate that other enzymes are absorbed into the prey's tissues.

 The most common types of enzymes are

Amino acid oxidases and proteases are used for digestion. Amino acid oxidase also triggers some other enzymes and is responsible for the yellow color of the venom of some species. Snake venom often contains ATPases which are used for breaking down ATP to disrupt the prey's energy fuel use. proteolytic, phospholipases, and hyaluronidases Proteolytic Enzymes: digestive properties Phospholipases: degrade lipids Hyaluronidases: speed venom spread through the body
Start 15-45 minutes after biting Local: fang mark (2 punctures), pain, redness, hotness, swelling,& may wet gangrene (generally less prominent than with hemotoxic venom) Systemic: 1st sign is ptosis & numbness in lips & tongue giddiness heaviness in bitted limb salivation & vomiting blurred vision dysarthria dysphagia bradypnea convulsions coma & death due to resp. failure Local: prominent and include: fang marks, severe pain, redness, ecchymosis, hotness, edema and swelling of affected limb & dry gangrene Systemic: nausea, vomiting hypotension with rapid weak pulse bleeding from mucous membranes acute renal failure due to hemoglobinuria coma and death due to circulatory collapse

Neurotoxic Venom

Hemotoxic Venom

First aid:

Reassurance of patient is important First step is to examine the site of bite and decide if the bite is poisonous or not to avoid unnecessary use of polyantivenom as it is risky and expensive Immobilize the affected limb Stop venom absorption as possible using tourniquet proximal to bite (just enough to obstruct lymph drainage not venous drainage) and make 2 small incisions over fang marks, and suction Dont use ice fomentations to avoid gangrene or give aspirin to avoid bleeding

Specific treatment:

Antivenoms can be classified into monovalent (when they are effective against a given species' venom) or polyvalent (when they are effective against a range of species, or several different species at the same time). We use polyantivenom
envenominated bite with systemic manifestations Why poly- & not mono-antivenom: because we have many species & the exact type of bitted snake may be not known Dose: depends on severity of bite not age or body size so, a pediatric dose equal an adult dose: mild give 3-5 vials moderate give 5-10 vials severe cases give 10 vials & maintain with more vials according to situation

INDICATION

DANGEROUSLY VENOMOUS ANIMALS:

REPTILES

coral snake: member of cobra family. Has highly toxic venom but small fangs and mouth so difficult to bite humans. Nocturnal. Neurotoxic.
Identified by the phrase: red and yellow kill a fellow (notice how red band touches yellow bands); versus red and black friend of Jack (nondangerous snakes have red touching black).

DANGEROUSLY VENOMOUS ANIMALS:

REPTILES Rattlesnakes: 11 species (17 subspecies) of rattlesnakes in Arizona

DANGEROUSLY VENOMOUS ANIMALS:

ARACHNIDS (8-legged)
bark scorpion: of 30 AZ species of scorpion, only the bark scorpion sting is considered lifethreatening. Identified by long, thin pincers. Climbs, is nocturnal, and is neurotoxic. Bark scorpion
Compare pincer shapes

Stripe-tailed scorpion

Scorpion

SCORPION VENOM

Arthropods : all of them are poisonous ; venoms are more potent than that of snakes & numerically more than snakes 9 species are known in Libya, 2 of them are more abundant & more dangerous Generally, more dangerous & causing more morbidity & mortality in children. Generally more toxic, more variability of specific toxins & more multiplicity of antigens than snake venom Consists of amino acids, peptides & small proteins (mainly neurotoxin, nephrotoxin, cardiotoxin, hemolytic toxin,histamine, serotonin, anti-ACh-esterase) & enzymes as phospholipases, hyaluronidases, phosphodiesterase

Age & body size of the victim Species & size of scorpion The amount of venom injected Site & number of stings Individual susceptibility to venom
Neurotoxin: block voltage-gated Na+ & Ca++ channels prolonged action potential & excessive release of catecholamine adrenergic manifestations Anti-cholinesterase accumulation of Ach cholinergic manifestations Thus, this will lead to marked CV effects

Local CVS

severe intense pain edema & ecchymosis numbness & tenderness sinus arrhythmias Hypertension Atrial extrasystol & PVC pulmonary edema ischemic changes in ECG

CNS

Other

CV complications are more in children with increased LDH & CPK agitation, paresthesia ,irritability & (restlessness, severe involuntary shaking &jerking extremity due to somatic skeletal neuromuscular dysfunction). cerebral edema convulsions & coma nausea & vomiting hypothermia blurring of vision, ptosis, tongue fasciculation slurred speech .( cranial nerve dysfunction) marbling of skin (VC of bl. Ves.) Priapism diaphoresis, tearing

Respiratory

Respiratory arrest and loss of protective airway reflexes are common causes of mortality. Pulmonary edema has been described and may be secondary to cardiogenic causes and to increased capillary permeability. Cerebral infarction, cerebral thrombosis, and acute hypertensive encephalopathy have been described with a variety of Buthidae scorpion envenomations. Sympathetic overdrive symptoms predominate, causing tachycardia, hypertension, hyperthermia, and pulmonary edema. Parasympathetic symptoms include hypotension, bradycardia, salivation, lacrimation, urination, defecation, and gastric emptying

Brain

Autonomic effects

Physicological

The signs of the envenomation are determined by the scorpion species, venom composition, and the victim's physiological reaction to the venom.

First Aid

like snake but, it is mandatory to control local pain (use local anaesthesia) to make the patient calm which is very important procedure in management use polyantivenom as in snake

Systemic

Supportive
Symptomatic

support CV functions to avoid complications use Haloperidol to control agitation ; use diazepam in convulsions ; use diuretics in pulmonary edema

 Do not apply tourniquets, as the toxins are small and move extremely rapidly away from the site of the sting. A tourniquet will not help the wound, and could cause more harm if applied incorrectly. Do not attempt to cut the wound and suck out the poison. This can cause infection or transfer the venom into the bloodstream of the person attempting to remove the poison.

DANGEROUSLY VENOMOUS ANIMALS:

ARACHNIDS (8-legged) black widow: Nocturnal, makes strong, messy web. Neurotoxic.

Black Widow Spider

Arthropods & only female bite is clinically significant The spider venom contains a potent neurotoxin which destroy cholinergic nerve terminals with massive release of ACh especially at motor end plates causing severe muscle spasm & also, affect adrenergic nerve terminals that may cause increase in sympathetic outflow Local: bite usually painless & local reaction is very rare in the form of pain, redness, edema & itching Systemic: develop 1-3 hours ranging from mild affection to serious troubles & mostly in the form of severe muscle spasm leading to chest & abdominal pain, tremors & muscle fasciculation followed by muscle weakness hypertension nausea, vomiting & salivation First line of treatment is to give IV calcium gluconate which control pain and abdominal cramps & considered as antidote Other lines of therapeutic intervention include Latrodectus antivenin, diazepam, methocarbamol & opioid analgesics The antivenin is reserved for patient with severe cramps refractory to other therapy because it is an equine antivenin & may cause severe hypersensitivity and should be given very carefully with close patient observation

Clinical Manifestations

Treatment

DANGEROUSLY VENOMOUS ANIMALS:

ARACHNIDS (8-legged) brown spider: thin, spindly spider with three pairs of eyes in semicircle (difficult to see). May have violin-shaped marking on cephalothorax (head). Bite causes tissue damage.
Compare to Wolf Spider which is not deadly marking

DANGEROUSLY VENOMOUS ANIMALS:

REPTILES
Gila monster: only other known venomous lizard in the
world is Mexican beaded lizard (in Mexico). Diurnal, but spends 98% of time in burrow; peak activity in spring when hunting nestlings/eggs. Has leaky skin. Venom for defense (pain) only.

HEAVY METAL POISONING

BACKGROUNDS Exactly what constitutes a "heavy metal" ? (Debate) which elements should properly be classified ? (Debate) Some authors atomic weight, others point to those metals with a specific gravity of greater than 4.0, or greater than 5.0. The actinides may or may not be included. Most recently metals and semimetals with potential human or environmental toxicity. This definition includes a broad section of the periodic table under the rubric of interest. heavy metal toxicity is an uncommon diagnosis Some elements may have very different toxic profiles depending on their chemical form Metals may be contaminants in dietary supplements, or they may leech into food and drink stores in metal containers like lead decanters Metal toxicity may complicate some forms of drug abuse. Classic examples of environmental contamination include the Minimata Bay disaster and the current epidemic of arsenic poisoning in South East Asia. In the 1950s, industrial effluent was consistently dumped into Japans Minimata Bay, and mercury bioaccumulated to exceedingly high concentrations in local fish

Pathophysiology
(For the most) heavy metals bind to oxygen, nitrogen, and sulfhydryl groups in proteins alterations of enzymatic activity. This affinity of metal species for sulfhydryl groups serves a protective role in heavy metal homeostasis as well. Increased synthesis of metal binding proteins in response to elevated levels of a number of metals is the body's primary defense against poisoning.

Epidemiology (United States)chronic lead exposure is the most commonly encountered. (The National Health and Nutrition Examination Survey (NHANES III)) 1988-1990 0.4% of persons aged 1 year and older had blood levels of lead of 25 mcg/dL or higher. aged 1-5 years, an estimated 1.7 million children had blood levels greater than 10 mcg/dL (The syndrome of childhood plumbism) Mortality/Morbidity relatively uncommon. It possible failure to recognize and treat heavy metal toxicities Encephalopathy is a leading cause of mortality in patients with both acute and chronic heavy metal toxicity.

Race In the United States African American population

Sex Little or no difference in prevalence exists. Age Generally, children are more susceptible to the toxic effects of the heavy metals and are more prone to accidental exposures. For adults, only about 10% of the ingested dose is absorbed. In contrast, children may absorb as much as 50% of an ingested dose.

Clinical Presentation
History most critical aspect of diagnosing heavy metal toxicity. A complete history includes questions about potential occupational exposures, hobbies, recreational activities, and potential environmental exposure. A complete dietary history should be taken (ingestion of fish, seafood, and seaweed products since these will frequently be implicated as dietary sources of organic (and relatively nontoxic) mercury, arsenic, or both. Herbal medications and dietary supplements are also potential sources of heavy metal exposure. Many Ayurvedic and Chinese patent medicines contain heavy metals. Most acute presentations of heavy metal toxicity involve industrial exposure. The ingestion of nonfood items such as paint chips, toys, and ballistic devices has also been implicated as the source of metal exposure in several cases.

Clinical Presentation
Physical Examination Focus on the most commonly involved organ systems: the nervous, gastrointestinal, hematologic,[7] renal, and integumentary systems. Nausea, persistent vomiting, diarrhea, and abdominal pain are the hallmark of most acute metal ingestions. Dehydration is common. Metal salts are generally corrosive. Encephalopathy, cardiomyopathy, dysrhythmias, acute tubular necrosis, and metabolic acidosis are also commonly seen with acute, high-dose exposures to most metals. Encephalopathy and peripheral neuropathies may occur within a few hours to days of acute high-dose exposure. A classic presentation of chronic metal exposure includes anemia, Mees lines (horizontal hypopigmented lines across all nails), and subtle neurologic findings. Because it is relatively common, any combination of GI complaints, neurologic dysfunction, and anemia should prompt a search for lead toxicity.

Differential Diagnoses
Alcohol and Substance Abuse Evaluation Anemia, Acute Anemia, Chronic Anemia, Sickle Cell Cardiomyopathy, Dilated Disk Battery Ingestion Encephalitis Guillain-Barr Syndrome Hypothyroidism and Myxedema Coma Long QT Syndrome Pediatrics, Limp Pediatrics, Status Epilepticus Shock, Hypovolemic Shock, Septic Toxicity, Arsenic Toxicity, Carbon Monoxide Toxicity, Iron Toxicity, Lead Toxicity, Mercury Toxicity, Thallium

Work up Laboratory Studies samples should be sent in metal free containers. abstain from seafood and seaweed products (arsenic and mercury) several days to 1-2 weeks. Complete blood cell count (CBC) with peripheral smear Basophilic stippling (not specific for lead toxicity, observed in arsenic toxicity, sideroblastic anemia, and thalassemia) The anemia of lead toxicity may be normocytic or microcytic. Renal function tests Urine analysis (look for proteinuria) Liver function studies Imaging Studies Abdominal radiographs . Radio-opacities demonstrable in the gastrointestinal tract Large. helpful in confirming the diagnosis and need for surgical intervention to limit the exposure. Other Tests ECG abnormalities may provide diagnostic clues in metal toxicity.

Treatment & Management

Emergency Department Care Decontamination Removal of the patient from the source of exposure Treatment may include whole-bowel irrigation with polyethylene glycol electrolyte solution if radiographic evidence of retained metal (toys, coins, paint chips) is present. Resuscitation: Good supportive care is critical.

Medication
Chelation agents (sulfhydryl)

Dimercaprol (British Anti-Lewisite; BAL) DOC in the treatment of lead, arsenic, and mercury toxicity. IM injection only
Edetate calcium disodium (Calcium Disodium Versenate) Second-line Begin therapy 4 h after BAL is given. Only given IV, and continuous infusion is recommended. Not recommended with renal failure.

Penicillamine (Cuprimine, Depen) Treatment of arsenic poisoning

Arsen
Pharmacokinetics Absorption through the gut varied as medicine Distribution: depending on duration of administration and the type Stored in the liver, kidney, heart and lung As high levels in hair and nails because of the high content of sulfhydryl in keratin Eliminated through feces, urine, sweat, breast milk, hair, skin and lungs Mechanism of action Arsenate is an uncoupler of oxidative phosphorylation in the mitochondria. Works associated with the substitution of arsenate competitive with inorganic phosphate ester form allows for rapid arsenate hydrolyzed (process arsenolisis)

Farmako & Toksik

The cardiovascular system GI A small dose of inorganic As mild vasodilation Larger doses capillary dilatation and increased capillary permeability most evident in the area splanik Myocardial damage and hypotension appear later A small dose of inorganic mild hyperemia splanik Doses greater capillary plasma transdusi vesicles on gastrointestinal mucosal The presence of tissue damage and the cathartic effect of fluid due to increase in the intestinal lumen causing increased peristalsis and diarrhea like rice water Cause damage to the kidney capillaries, tubuli and glomeruli oliguria with proteinuria, hematuria and silinderuria In acute, As is vesikan (causing vesicles) As low dose ingested inorganic chronically causes vasodilatation skin, hyperkeratosis, especially on the palms and heels and hyperpigmentation on the body, legs and arms Chronic exposure to inorganic peripheral neuritis. In severe cases, the spinal cord can be affected As organic ingested acutely toxic dose central depression without gastrointestinal symptoms Muscle weakness occurs in the feet and hands, and if continued reduced tendon reflexes and muscle atrophy occur

Kidney Skin

The nervous system

Blood

As inorganic influence and change the composition of the bone marrow cells Haematological evaluation revealed anemia to leukemia usually mild to moderate, eosinophilia may be found

Liver

As a number of inorganic and organic As highly toxic to the liver and cause fatty infiltration, central necrosis and liver cirrhosis Damage generally occurs in the liver parenchyma, but in some cases the clinical picture is very similar to the obstruction of the bile duct (perikolangitis and obstruction of bile sal sal smaller)
As lead break chromosomes in human leukocyte cultures and is teratogenic in hamsters

Carcinogenesis and teratogenesis

Information Acute arsenic Early symptoms: poisoning Sense uncomfortably within the abdomen burning lips narrowing of the throat hard to swallow severe stomach pain projectile vomiting severe diarrhea Chronic arsenic poisoning Early signs: Weakness muscle pain skin pigmentation hyperkeratosis edema Other symptoms: Oliguria proteinuria hematuria anuria Skeletal muscle spasms thirsty shock fluid loss continues Other symptoms:
Breath and sweat smell of garlic hypersalivation Hiperhidrolisis Stomatitis Lacrimation Paresthesia dermatitis Vitiligo hepatomegaly bile duct obstruction impaired renal function peripheral neuritis Encephalopathy Damaged spinal TLG

Information Treatment 1.Koreksis intravascular fluid volume 2.Fix hypotension with dopamine IV 3.Chelation therapy dimerkapol 4.Continued p enisilamin Chronic Toxicity: 1.Dimerkapol & penicillamine kidney dialysis for severe arsenic nephropathy

MERKURI
Information The main forms Hg vapor Salt Hg of Hg (elemental Hg) The most volatile Irritants and toxins that are very strong Pharmacokineti Inhalation of Difficult to cross cs mercury vapor that the blood brain / quickly across the placenta membrane brain In excretion in sec urine / feces Organic Hg

Complete lbh absorbed more fat soluble krna intestine and less corrosive to the intestinal mucosa Cross the blood brain / placenta neurological effects and teratogenic Fecal excretion sec

Information Hg vapor (elemental Hg) Toxicity Symptoms within bbrp jm: Weakness Shiver Metallic taste Nausea and vomiting Diarrhea Cough Blown Fgsi severe pulmonary disorders Chronic exposure: Toxicity arising slow especially neurological symptoms vegetative syndrome astenik Continuous exposure: Tremor psychological change eretism Salt Hg Pd corrosive effects of the intestinal mucosa: Hematoschezia Local Effect: Stomatitis metallic taste with irritation ginggiva Breath odor Wobbly tooth Systemic effects: Necrosis of renal toxicity renal tubuli with oliguria / anuria LBH prominent glomerular damage Organic Hg Neurological Disorders: Impaired vision (scotoma and constriction field penglihatgan) Ataxia Paresthesia Neurastenia Hearing loss Dysarthria Mental deterioration Tremor Motor disorders Paralysis

Treatment

Information Hg vapor (elemental Salt Hg Hg) End of exposure Immediate action on special attention to fluid and electrolyte pulmonary function balance and status aid breathing hematologikus chelation therapy emesis pd conscious with dimerkapol patients rinse the hull Activated carbon and magnesium sulfate (cathartic) to limit further absorption lbh chelation therapy with dimerkapol / penicillamine hemodialysis on decreased kidney

Organic Hg Penicillamine body made it easy excretion dr tp HSL dissatisfy therapy KI: dimerkapol

Manganese
Manganese cyclopentadienyl trikarbonil & methyl manganese cyclopentadienyl material additional gasoline Drinking water contaminated wells manganese poisoned manganese chronicle Many be used on industry steel mill production potassium permanganate, bat factory battery dried in inhalation Limit exposure:
Steam: 1 mg / m 3 Dust: 5 mg / m 3

S&S
Chronicle Inhalation Lethargy Bronchitis acute Edema Nasopharyngitis Disruption extra pyramidal Pneumonia Ill head Itching Hands & feet you Dermatitis Impaired libido Disruption sleep Swelling liver Symptom Parkinsonism

 Handling
Stop further contact Antidote:
Calcium disodium edetat (repair damage to the liver and respiratory systems)

Overcome CNS symptoms of poisoning:

Levodopa PO 3 x 1g / hr - 8 g / hr Hidroksitriptopan 3g / hr

Zinc and Zinc Chloride

Steam zinc:
On welding Pemotogan metal Thaw metal mix zinc

Limit exposure:
Steam Zinc: 5 mg / m 3 Steam zinc chloride: 1 mg / m 3

Cause pulmonary edema and damage channel breath

 Zinc and Zinc Chloride

Signs & symptoms:
Fever and chills Mm Aching muscles Weakness Pulmonary Edema Cyanosis dyspnea

Handling:
Overcome pulmonary edema that occurs Give prednisone 25-30 mg / day po Antipyretic Break

Yellow Phosphorus
Soluble in fat, very toxic, and on fire if contact with air Be used as: poison insects, rodenticides, manufacturing fertilizer, fireworks Effect:
Ruin network Disrupting metabolism carbohydrate, protein, fat in liver Hinder glycogen deposits and increases fat deposits in liver

Acute oral mell Acute skin mell 1-2 hours Dry out on skin Mmd skin on fire Arrhythmias Breath smelling onions 1-2 hr Death on time coma Improve by: mmd, jaundice, hepatomegaly, TD turu n, oliguria, hypocalcemia, hypoglycemia

Acute inhalation mell 1-3 hr (phosphine & phosphide) Mm Agency tired, cough Jaundice Paresthesias, ataxia, tremor Diplopia TD down Pulmonary Edema Collapse Arrhythmias heart Convulsions, coma Death of 4 hr-2 mgg

Chronicle Ill gear Swelling jaw Necrosis mandible Eas

 Emergency action
Mell mouth:
Depletion side demgan water 5-10 L Try for gag If there contamination on skin / eye rinse with water min 15 min

Action general:
Overcome edema and shock Give solution calcium gluconate 10% 10 ml iv (set level serum calcium) Infusion solution glucose 5% 1-4 L / hr in water / solution of 10% invert sugar in water Diet with carbohydrate high can po Overcome failed liver
1

Timbal
symptom(akut) :
Colicky abdominal pain Constipation Headache Irritability Diagnosis :
Blood lead level :
< 10 mcg/dL nontoxic 10 25 mcg/dL impaired neurobehavioral development in children 25 50 mcg/dL headache, irritability, subclinical neuropathy 50 70 mcg/dL moderate toxicity 70 100 mcg/dL severe poisoning

Severe intoxication comma & seizure Chronic intoxication:

Learning disorders (in children) Motor neuropathy (eg. Wrist drop)

Microcytic anemia with basophilic stippling Elevated free erythrocyte protoporphyrin

 Emergency and supportive measures :

Encephalopathy patent airway, treat coma and convulsion Recent acute ingestion whole bowel irrigation, endoscopy, or surgical removal

Specific treatment :
Severe toxicity edetate calcium disodium (EDTA) 1500 mg/m2/kg/d (approximately 50 mg/kg/d) in four to six divided doses or as a continuous intravenous infusion. Some clinicians also add dimercaprol (BAL) 4-5 mg/kg intramuscularly every 4 hours for 5 days Less severe toxicity edetate calcium disodium (EDTA) (dosage as above); mild to modereate intoxication succimer (DMSA) 10 mg/kg orally every 8 hours for 5 days, then every 12 hours for 2 weeks

Iron poisoning
Iron overdose can present with: Nausea vomiting. Abdominal pain and diarrhoea. Possible gastrointestinal bleeds. Serious overdose, which causes hepatocellular necrosis Gastric outflow obstruction, which may be a late complication. Iron poisoning needs urgent treatment with emergency admission and desferrioxamine (IV) as an antidote.

Cadmium poisoning
Toxic by inhalation and ingestion and also, although occurring rarely, absorption through the skin. Symptoms develop 12-36 hours after inhalation Presents with: Metallic taste and increased salivation. Nausea, vomiting and diarrhoea. Impaired sensation. Difficulty breathing, cough, chest pain.

 Complications Pneumonitis pulmonary oedema. Chronic exposure may cause: Anemia emphysema or renal failure cadmium may be a risk factor in the development of prostate or lung cancer. At present there is no effective therapy for cadmium poisoning, and treatment is supportive and symptomatic. It is hoped that some of the newer chelating agents may help in reducing cadmium levels in the body.

Conclusion
we have learned about the classification, pathophysiology, signs symptoms, diagnosis, investigation, management of poisoning based on etiology:
Chemical Food Plant Animal Heavy metal

Reference
Sudoyo Aru W, Setiyohadi B, Alwi I, dkk, editor. Buku Ajar Ilmu Penyakit Dalam. Jilid I Edisi V. Jakarta: Interna Publishing , 2009 Isselbacher KJ, Braunwald E, Wilson JD, Martin JB, Fauci AS, Kasper, editors. Harrisons principles of internal medicine. 14th ed. New York : McGraw Hill, 2001. Ganiswara SG, Setiabudy R, Suyatna FD, Purwantyastuti, editor. Farmakologi dan terapi. Edisi IV. Jakarta: FK UI, 1995