group 6 plenary 6
DESCRIPTION
untarTRANSCRIPT
Name Nim
Toni periyanto 405070018
Jessica stephanie 405080007
Paramita adinda P 405080139
Maria marcella 405090007
Alexandra adeline 405090036
Obed yosia 405090050
Christine yuliani 405090055 Scribber
Reza adrian H 405090059
Ansella riska 405090085
Idha idhar dewi P 405090155 Secretary
Fany azhar A 405090180 Leader
Brigita maria A 405090255
Tutor : dr.Agnes
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
smelling liquid drink
3 hours after drinking it throw up delirium and fever
physical examination and lab
poisoned
Poisoning
• Poisoning the entry of toxic substances into the body (GI tract, inhalation / direct contact) clinical signs and symptoms of a typical.
Classification
Etiology
Onset
Self Poisoning
Attempted suicide
Accidental poisoning
Homicidal poisoning
Acute
Chronic
Target OrganLiver
HeartKidney
CNS
Chemical Material
Alcohol
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 Etiology
Pupil pin point, RR ↓ OpioidCholinesterase Inhibitor (organophosphate, carbamate insectiside)
Pupil dilatation, speed of breath decrease
Benzodiazepin
Pupil dilatation, tachycardia
Tricyclic antidepresant Amfetamine, extasy, cocaine Anticholinergic (benzeksol, benztropin)Antihistamine
Cyanosis CNS depresant drugsSubstance causes methaemoglobinemia
Hipersalivasi organophosphate, carbamate insectiside
Clinical features Etiology
Nistagmus, ataxia, cerebral signs
Anticonvulsive (fenitoin, karbamazepin)Alcohol
Extrapyramidal symptoms Phenotiazin, haloperidolMetoklopramide
Seizure Tricyclic antidepresant , anticonvulsive, teophiline, antihistamine, NSAIDPhenothiazin, isoniazid
Hypertermia Litium, Tricyclic antidepresant, antihistamine
Hypertermia & hypertension, tachycardia, agitation
Amfetamine, ecstasy, cocaine
Hipertermia & takikardi, asidosis metabolik
Salicilat
Clinical Features Etiology
Bradikardia Beta blocker, digoxin, opioid, clonidine , Ca blocker (except dihidropiridin)Organophosphat insectiside
Abdominal cramp, diarrhea, tachycardia, hallucinatiion
Withdrawal alcohol, opioid, benzodiazepin
Blood Gas Analysis
Blood gas analysis Interpretations
Respiratoric acidosis(pH < 7,3; PCO2 > 5,6 kPa)
Hypoventilation, CO2 retention, maybe because of CNS depresant
Respiratoric alkalosis(pH > 7,45; PCO2 < 4,7 kPa)
Hyperventilation maybe as response to hypoxia, drug injury (aspirin) or CNS injury
Metabolic alcalosis (pH > 7,45; HCO3 >30 mmol/l)
Uncommon in poisoning, as a effect from loosing acid or alcali excess
Metabolic acidosis(pH < 7,45; HCO3 <24 mmol/l; Base excess < -3) compensated if PCO2 < 4,7 kPa
Common in poisoning, if get worse watch for etanol, metanol, etilen glikkol poisoning
Wide anion gap Metformin, isoniazid, salycilate ,cyanide
Odor of poisoning
Smell Etiology
Aseton Isopropil alkohol, aseton
Almond Cyanide
Garlic Arsenik, celenium, talium
Broken eggs Hidrogen sulfida, mekraptan
Colors of urine
Color Etiology
Green / blue Blue methylene
Yellow-red Rimfapisin, Fe
Dark brown Fenol, cresol
White crystal Primidon
Brown Mio/ haemoglobinuria
GENERAL MANAGEMENT
• Stabilization (ABC)
• Decontamination decrease
exposure to toxins, reduces
absorption and prevent damage:– decontamination pulmonary
– decontamination eye
– skin decontamination
– GIT decontamination
• Elimination Accelerate
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 SurveyAnamnesa • 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
PE • 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
BP There is/no shock
Respiration • frequency of breath• Volume minute - Wright's spirometer• <4L/mnt O2
Confulsion CNS excitation (amphetamines), spinal cord (strychnine) or with neuromuscular (organophosphate)
Pupil Varied except in poisoning atropine and morphine
Bowel • Matching degree of awareness• III - usually negative• IV - always negative
Heart Heart rhythm abnormalities - symptoms of heart failure or cardiac arrest
Other • Acid-base balance disorders• EEG abnormalities• retention urine• Vomiting and diarrhea
DEKONTAMINATIONDecontamination GOALS : to decrease exposure to toxins, reduce absorption, and
prevent damageUse 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)
Providing an antidote
↑ elimination • 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 ↑
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
Chemical poisoningChemical poisoning
Poisoning metal and metalloid
Corrosive chemical poisoning
Hydrocarbon poisoning
Poisoning nitrogen compounds
Alcohol and glycol poisoning
Toxicity of hydrocarbons containing halogen
Poisoning gases, vapors, and chemical dust
Other chemical poisoning
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
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
– nitrogen dioxide– ozone gas– phosgene– formaldehyde– hydrogen fluoride– osmium tetroxide– vanadium pentoxide– manganese– cadmium oxide– chromate– zinc chloride– mercury
info
carbon monoxide
Produced by the incomplete combustion of materials - carbon-containing materials from machinery and motor vehicles
poisoning if •through inhalation•Limit exposure to <1000 ppm
symptom •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
complication Cerebral and pulmonary edema, myocardial infarction / stroke
prevention •Levels of carbon monoxide inside, the air around must be below exposure limits
Carbon monoxide
info
emergency action
•Avoid contact later, the patient had to be removed•Oxygen 100%
Antidot Oxygen
General action •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 Used as a drinking water disinfectant and household bleach
poisoning •Through inhalation irritation, cough, dyspnea, and pneumonia
symptom Irritation and burning sensation in the affected tissue, cough, vomiting, and bad breath are typical conjunctivitis of the eye without serious corneal damage
action •Keep the alive•Poisoning by inhalation avoid further contact•Actions supportive and symptomatic medication
carbon Dioxideinfo
symptom •Dyspnea, headache, visual disturbances, tinnitus, tremor, and unconscious
action •Move the patient to the open space•Give artificial respiration•If necessary inpatient hospital
Ammonia gasinfo
Ammonia gas Explosives, plastics, fertilizers, and as a refrigerant cooling deviceIs corrosive, damaging the cells direct irritation of the mucous membranes
Poisoning if Through inhalation pulmonary edema and pneumoniaLimit exposure: 25 ppm
symptom •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
emergency • eyes flush with water immersion 15 minutes•inhaled remove from contaminated indoor
Special case Overcome pulmonary edema and narrowing of the esophagus
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
Clinical manifestation
•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
emergency •Move into the room that is not contaminated•Amyl nitrite by inhalation•Give artificial respiration with 100% oxygen
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
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.
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 •Cough :often•Rarely : dyspnea is usually associated with severe aspiration
GIT •Burning / irritation of the mouth and throat•belch•nausea and vomiting•abdominal pain•diarrhea•Fever and smell "gasoline" in the mouth
Respiratory •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, intoxicationEffects 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
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, intoxicationEffects 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 systeminhaled oxygenSalbutamol: when a nascent breathing disordersAntibiotics: when you have an infection arises, it is not recommended as prophylaxisHydrocortisone: first recommended, now rarely performedAntacids: to prevent irritation of the gastric mucosaGranting dilution of milk or other ingredientsAnus and perineum should be cleaned immediately to avoid irritation (skin burn) secondaryIn 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
InsektisidaInsektisida
OrganofosfatOrganofosfat
KarbamatKarbamat
OrganoklorinOrganoklorin
DDPVDiazinonMalationParation
DDPVDiazinonMalationParation
KarbarilBaygonKarbarilBaygon
AldrinBHCDDT
DieldrinEndrin
KlordranTiodan
Toksifen
AldrinBHCDDT
DieldrinEndrin
KlordranTiodan
Toksifen
ORGANOPHOSPHATE ANDCARBAMATE 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
soil Hand-to-mouth behaviour- Crawling on the ground- Dermal contact
water Pesticides in drinking water: tap, wellfood -Crops routinely sprayed: fruits, vegetables, grains
-Bioaccumulation in animals and products fish, meat, eggs, dairy
ROUTES OF EXPOSUREIngestion •Breastfeeding
• Accidental ingestion• Residues in food• Mouthing
Inhalation •Indoor and outdoor spraying• Occupational exposure
Dermal absorption •Accidental contact• Occupational exposure• Residues on surfaces• Contaminated clothing• Medical use: scabies, head lice
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 FeaturesThis 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.
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
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
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
Toxic dose •Inhalation 100ppm called dangerous •30 mL of 37% formalin solution can lead to death
Sign & symptoms •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
Therapy •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
Formalin
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
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
Poisonous Animal Tissues
Poisonous Plant Tissues
Chemical Poisoning
Intoxications
Microbial Intoxications
Other Neurotoxins Enterotoxins
Toxicoinfection Invasive Infection
Intestinal Mucosa
Systemic Other Tissues or Organs
(Muscle, Liver, Joints, Fetus,
Other)Mycotoxins(Fungal Toxins)
Algal Toxins Bacterial Toxins
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 63ºC);• 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 foodsshould 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
3
Type of foodpoisoning
Where thebacteria comefrom
Onset time Symptoms
Salmonella Raw meat,eggs, poultry,animals
6 - 72 hours Abdominal pains,diarrhoea, fever,vomiting, dehydration
Clostridiumperfringens
Raw meat, soil,excreta, insects
8 - 72 hours Abdominal pain,diarrhoea
Staphylococcus aureus
Skin, nose,boils, cuts, rawmilk
1 - 6 hours Vomiting, abdominalpains, lower thannormal temperature
The Main Food Poisoning Bacteria
6
Date Place PeopleAffected
Type of FoodPoisoning
Source
June '98 Marmul 23 Salmonellosis Unknown
April'99
Fahud 12 Shigellosis Unknown
April'99
RAH Club 32 Shigellosis Unknown
May '01 TocoCampSaih Rawl
75 Salmonellosis Unknown
Incidents of Food Poisoning in PDO
Name RF Sign & Symptoms
Campylobacter Meat and poultry. 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.
E Coli 0157 Raw meat and dairy products.
Diarrhoea, which may contain blood, can lead to kidney failure or death.
Listeria Monocytogenes
Unpasteurised milk and dairy products, cook-chill foods, pate, meat, poultry and salad vegetables
Ranges from mild, flu-like illness to meningitis, septicaemia, pneumonia. During pregnancy may lead to miscarriage or birth of an infected baby.
Name RF Sign & Symptoms
Bacillus cereus Rice, meat, seafood, salads, potatoes, and noodles
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.
Clostridium botulixnum
Inadequately processed canned meat, vegetables and fish (faulty canning)
Onset 24 – 72 hours. Voice change, double vision, drooping eyelids, severe constipation. Death within a week or a slow recovery over months.
Salmonella Raw meat, poultry and eggs, and raw unwashed vegetables.
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.
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 ; ChickenGram - rodKilled by high temperatures
Sign & Symptoms 12-36 hours ; low grade fever ; abdominal pain ; diarrhea; chills
Diagnose • patient history• stool culture• Microscopic examination
• leukocytes• occult blood
Treatment • 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
Clostridium botulinum
• Four different types• food borne• infant• wound• undetermined
Resistant heating, freezing, ionizing radiation
Destroyed by boiling >120 degrees for >20 min
Toxin • Very powerful : 0.5 nanograms (lethal)• Heat sensitive : 80 degrees for 30 min
Sign & symptoms • 12-48 hrs (14 days)• N/V/D• abdominal distention• constipation (as disease progresses)• Neurologic disturbances : dysarthria, dysphagia, dry mouth
With disease progression
descending paralysis ; respiratory weakness; respiratory failure ; oculobulbar symptoms
Treatment • stabilization of airway• history• upper and lower GI decontamination• trivalent antitoxin
• (ABE)• watch for hypersensitivity
• call CDC
DD • 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
Treatment / profilaksis
Ventilatory assistance and supportive careBotulinum 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 necessaryVaccine 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
Treatment • mild• self limiting• death is rare
• elderly• debilitated
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.
LAB In urine examination with microscope, can be found jengkolic acid crystal that being seen as sharp needle or sometimes agglutinated as bound or rosette
Diagnose Parents told us, after hours eat jengkol, sign and symptoms appearmild (vomit, abdominal/flank pain only) advice to drink a lot and giving 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 Bonam, still have some patient die ‘cause acute kidney failure
Advise Don’t 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 can’t take the O2 Venous blood is bright
red as arterial blood
Sign & symptoms
• 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)
Treatment • 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
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)
Bongkrek acid from tempe bongkrek (manufacture with coconut pulp fermentation and peanuts)
Etiology • coconut pulp bongkrek acid (Pseudomonas cocovenenan)• iron pedestal Clostridium botulinum contamination
Symptoms • 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
Mushroom Groups
• Early onset of symptoms (0–4 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.
• CNS effects are associated with two groups of mushrooms, ibotenic acid/muscimol and psilocybin.
Group/Toxin
Structurally related to
Symptoms Treatment
GI toxin •nausea, vomiting, diarrhea, and abdominal cramps•0.5–3 hours after ingestion, and typically last 24 hours.
supportive, with good outcome expected
Ibotenic acid and muscimol
glutamic acid and GABA
•Lethargy, hallucinations, seizures, or severe agitation•1 to 2 hours after ingestion
Seizures, supportive care produce a good outcome
Muscarine •Acetylcholine•Does not cross the blood-brain barrier
salivation, lacrimation, urination, defecation, gastroenteritis, and emesis (SLUDGE)
•Atropine•Pralidoxime is KI acetylcholinesterase inhibition is not involved
Coprine blocking acetaldehyde dehydrogenase
flushing, nausea, vomiting, and headache occur 30 minutes - several days after ingestion
supportive
Psilocybin serotonin and lysergic acid diethylamide (LSD)
most often used as a drug of abuse
coprinus atramentarius agaricus xanthodermus agaricus californicus
amanita muscaria
clitocybe dealbata
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, high-dose 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/orellanine
•Begin 1 to 2 days after ingestion•Nausea, vomiting, abdominal pain, and headache•Renal toxicity manifests days to weeks after these initialsymptoms and can progress to chronic renal failure.
Red Clover
• Description: purplish red clover head, hairy stem, 3 leaved segments, pale ring on leaves
• Poisonous parts: all• Found: all over US, in
fields
• Signs of poisoning:– Excessive salivation– Bloating– Diarrhea– Blindness– Abortion– Laminitis
Foxglove
Signs of poisoning:• Colic• Bloody feces• Poor appetite• Pain• Frequent urination• Irregular heartbeat • Possible convulsions
prior to deathOne bite is fatal
http://www.freefoto.com/preview.jsp?id=12-57-51&k=Foxglove+-+Digitalis
Poinsetta
Signs of poisoning:• Skin
– Redness and swelling – Blistering
• Gastrointestinal– Stomach pain – Diarrhea
•Poinsettas have low toxicity
http://www.schaefergreenhouses.com/poinsettia.html
http://www.schaefergreenhouses.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
• Signs of toxicity occur when large amount are ingested
• Symptoms may last 3-10 days
• Death occurs with 85% of horses showing signs
http://www.ansci.cornell.edu/plants/horselist.html
OleanderDescription: • Woody evergreen bush,
grows up to 30’ tall• Leaves
– leathery & pointed leaves– grow opposite each other in
groups of 3
– arranged in whorls • Flowers
– grow in clusters at the ends of branches
– white, pink, purplish, red
http://www.ansci.cornell.edu/plants/horselist.html
http://www.ansci.cornell.edu/plants/horselist.html
Oleander
•Takes only 1 ounce of leaves to kill a horse
http://vet.purdue.edu/depts/addl/toxic/color52.htm
OleanderSigns of Poisoning:• Diarrhea• Trembling• Cold extremities• Paralysis• Coma• Cardiac arrest followed
by death
• Scientific Name: Nerium oleander
• Poisonous Parts: all (do NOT burn—smoke 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
http://www.ansci.cornell.edu/plants/horselist.html
http://www.ansci.cornell.edu/plants/horselist.html
**Horses must consume plant over a 2 week period—sometimes plant is in hay
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
• Horses must eat plant for a month to see toxicity signs
http://www.fcps.k12.va.us/StratfordLandingES/Ecology/mpages/bracken_fern.htm
Red Maple• Poisonous parts: wilted
or dried leaves, bark• Found: eastern half of
US • Signs of poisoning:– Severe anemia– Weakness– Depression– Pale mucus membranes– Dark brown urine– Abortion– Death due to RBC unable to
transport oxygen to tissueshttp://www.fcps.k12.va.us/StratfordLandingES/Ecology/mpages/red_maple.htm
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
Example – Puffer Fish
ArachnidsScorpions, Spiders, Ticks
Scorpions – Stinger – low toxicitySpider bites
Widow spiders -– Neurotoxin Brown or Violin -– Tissue Damage
Ticks – Neurotoxin – Transmits other diseases
Insects Moths and caterpillars – Irritating to eatAnts – Proteins, formic acid – Irritation to allergic responseHoney bees – Proteins – Swelling, allergic responseWasps – Formic acid
Reptiles Lizards – Irritating to eatSnakes
Vipers – Rattlesnakes, Water moccasins, Copperheads – Complex enzymes – Tissue necrosis, allergic response, shockElapidae Cobras, Kraits, Coral Snakes – Proteins – Neurotoxin, paralysis
Marine Animal Shellfish (filter-feeding mollusks)Mussels, clams, oysters, scallops
Jelly fish, anemona, coral Sea Snail (cigua) and some fish, oysters and clamsPuffer Fish (fugu, blowfish, toadfish,some frogs, starfish, octopusTuna, shark, sword fish (mercury)
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)
RATTLESNAKE SENSE ORGANS
Eyes: to see
Nostrils to smell
Body to feel ground vibrations
Pit Organ to sense heat
Cont >>
• SNAKE BITE • 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 • 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
• According to the dominant venom:
• Hemotoxic: Family: viperidae ; e.g. vipers (Cerastus)
• Neurotoxic: Family: Elapidae• e.g. cobra (Naja haj haj; Naja nigrocollis)
• Myotoxic: Sea snakes
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 venom50-75% have low MWAct mainly on neuromuscular junctions -> weakness, dangerous when affect respiratory muscles -> respiratory failure
According to shape: • Non-poisonous: U-shaped as any animal• Poisonous: either:
Complete: 2 punctures due to fangs (more dangerous)
Incomplete: 2 parallel tailed scratches(less dangerous
According to time of Poisonous Biting:
Generally bite is more dangerous at night & during summer• Defense bite: at day time• Business bite: at night, usually envenominated &
dangerous
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.
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.
• The most common types of enzymes are
• proteolytic, phospholipases, and hyaluronidases• Proteolytic Enzymes: digestive properties• Phospholipases: degrade lipids• Hyaluronidases: speed venom spread through the body
Neurotoxic Venom 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
Hemotoxic Venom • 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
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
• Don’t 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
INDICATION • 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
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 (non-dangerous 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 life-threatening. Identified by long, thin pincers. Climbs, is nocturnal, and is neurotoxic.
Bark scorpion Stripe-tailed scorpion
Compare pincer shapes
Scorpion • 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.
SCORPION VENOM
Generally more toxic, more variability of specific toxins & more multiplicity of antigens than snake venomConsists 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 victimSpecies & size of scorpionThe amount of venom injectedSite & number of stingsIndividual 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 severe intense pain edema & ecchymosisnumbness & tenderness
CVS sinus arrhythmias
Hypertension
Atrial extrasystol & PVC
pulmonary edema
ischemic changes in ECG
CV complications are more in children with increased LDH & CPK
CNS • agitation, paresthesia ,irritability & (restlessness, severe involuntary shaking &jerking extremity due to somatic skeletal neuromuscular dysfunction).
• cerebral edema → convulsions & coma
Other 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.
Brain • Cerebral infarction, cerebral thrombosis, and acute hypertensive encephalopathy have been described with a variety of Buthidae scorpion envenomations.
Autonomic effects
• Sympathetic overdrive symptoms predominate, causing tachycardia, hypertension, hyperthermia, and pulmonary edema.
• Parasympathetic symptoms include hypotension, bradycardia, salivation, lacrimation, urination, defecation, and gastric emptying
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
Systemic use polyantivenom as in snake
Supportive support CV functions to avoid complications
Symptomatic 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 Black Widow SpiderSpider
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
Clinical Clinical ManifestationsManifestations
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
Treatment 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
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.
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 diagnosisSome elements may have very different toxic profiles depending on their chemical formMetals may be contaminants in dietary supplements, or they may leech into food and drink stores in metal containers like lead decantersMetal 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 Japan’s 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/Morbidityrelatively uncommon. It possible failure to recognize and treat heavy metal toxicitiesEncephalopathy is a leading cause of mortality in patients with both acute and chronic heavy metal toxicity.
RaceIn the United States African American population
SexLittle or no difference in prevalence exists.
AgeGenerally, 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.
• 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.
Clinical Presentation
Differential Diagnoses
• Alcohol and Substance Abuse Evaluation
• Anemia, Acute• Anemia, Chronic• Anemia, Sickle Cell• Cardiomyopathy, Dilated• Disk Battery Ingestion• Encephalitis• Guillain-Barré 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 Studiessamples 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 testsUrine analysis (look for proteinuria)Liver function studiesImaging StudiesAbdominal radiographs .Radio-opacities demonstrable in the gastrointestinal tract Large. helpful in confirming the diagnosis and need for surgical intervention to limit the exposure.
Other TestsECG 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
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)
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
Farmako & Toksik
The cardiovascular system
•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
GI •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
Kidney •Cause damage to the kidney capillaries, tubuli and glomeruli oliguria with proteinuria, hematuria and silinderuria
Skin •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
The nervous system
•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
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)
Carcinogenesis and teratogenesis
•As lead break chromosomes in human leukocyte cultures and is teratogenic in hamsters
Information
Acute arsenic poisoning
Early symptoms: •Sense uncomfortably within the abdomen •burning lips •narrowing of the throat •hard to swallow •severe stomach pain •projectile vomiting •severe diarrhea
Other symptoms: •Oliguria •proteinuria •hematuria •anuria •Skeletal muscle spasms •thirsty • shock fluid loss continues
Chronic arsenic poisoning
Early signs: •Weakness •muscle pain •skin pigmentation •hyperkeratosis •edema
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 of Hg
•Hg vapor (elemental Hg)
•Salt Hg •Organic Hg
•The most volatile •Irritants and toxins that are very strong
Pharmacokinetics
•Inhalation of mercury vapor that quickly across the membrane brain
•Difficult to cross the blood brain / placenta •In excretion in sec urine / feces
•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
Toxicity Hg vapor (elemental Hg) Salt Hg Organic Hg
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
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
Neurological Disorders: •Impaired vision (scotoma and constriction field penglihatgan) •Ataxia •Paresthesia •Neurastenia •Hearing loss •Dysarthria •Mental deterioration •Tremor •Motor disorders •Paralysis
Information
Treatment Hg vapor (elemental
Hg) Salt Hg Organic Hg
•End of exposure •special attention to pulmonary function •aid breathing •chelation therapy with dimerkapol
•Immediate action on fluid and electrolyte balance and status hematologikus •emesis pd conscious patients •rinse the hull •Activated carbon and magnesium sulfate (cathartic) to limit further absorption lbh •chelation therapy with dimerkapol / penicillamine • hemodialysis on decreased kidney
•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&SChronicle Inhalation
•Lethargy •Edema •Disruption extra pyramidal
•Bronchitis acute •Nasopharyngitis •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 Acute inhalation mell Chronicle 1-2 hours • Mmd • Arrhythmias • Breath smelling
onions 1-2 hr • Death on time
coma • Improve by:
mmd, jaundice, hepatomegaly, TD turu n, oliguria, hypocalcemia, hypoglycemia
•Dry out on skin skin on fire
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
•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
• Severe intoxication comma & seizure
• Chronic intoxication:– Learning disorders (in
children)– Motor neuropathy (eg.
Wrist drop)
• 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
– 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. Harrison’s 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