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‫زندگی عرصه یکتای هنرمندی ماست‪.‬‬
‫هر کسی نغمه خود خواند و ازصحنه رود‪,‬‬
‫صحنه پیوسته به جاست‪.‬‬
‫خرم آن نغمه که مردم بسپارند به یاد‪.....‬‬
‫نام درس‪:‬مسمومیت ها در اطفال‬
‫نام مدرس‪:‬روانشاد دکتر مهدخت صدر بافقی‬
‫نام ویادش جاودان باد‪.‬‬
The most common agents include:
• family member medication , cleaning solution,
plants, cosmetic.
• most ingestion occur in home(92%).
•More than 50% occurred in children <5 yr.
history:
•Product name, amount of medication, time of
exposure.
•age and weight of child
• progression of symptoms
•Medical history and underling disease
Physical examination
 Level of consciousness , vital signs
pupillary size , presence of muscle faciculation
bowel and bladder activity , cardiac arrhythmias ,
seizures , hypothermia.
 Pulmonary edema
 Certain symptoms and signs are specific .
( toxic syndromes)
toxic syndromes
Anticholnergic:
 Thirst ,flushed skin
 mydriasis
 hyperthermia ,urinary retention,
 delirium, hallucination, tachycardia
 respiratory insufficiency
Cholinergic
 Exocrin glands secration, urination
 nausea ,vomiting , diarrhea
 muscle fasciculation, weakness or paralysis
 bronchospasm , bradycardia or tachycardia ,
 convulsions , coma
 miosis
Extrapyramidal
 Tremor ,rigidity, opisthotons ,torticollis
 dysphonia ,fever , metabolic acidosis
 tachycardia ,hyperpnea
 restlessness , convulsion ,
 narcotic:
 CNS depression
 hypothermia
 hypotention
 hypoventilation
 miosis
Sympathomimetic
 Psychosis
 seizure
 mydriasis
 hypertension
 tachypnea
 hyperthermia
complication
 Coma
DD: trauma , CVA , asphexia, meningitis
 Pinpoint puils :
Opiate, organophosphate ,phenothiazines ,hloral
hydrate ,
 Dilated pupils:
cyclic antidepressant , atropine -like agents
Caustic ingestion
 Dysphagia , epigasteric pain.
 oral burns.
 low-grade fever.
 When lesion heal then strictureform .
alkalia agents :(tastless) oropharynx and esophagial necrosis.
button batteries : produce caustic injury if that remain in
esophaguse should be removed.
treatment:
 dependents on agent ingested and presence or absence
esophagial injury
 Routine use of diluent as a first aid ???
 Antibiotic if there is signs of infection .
 Dilatation of late forming strictures(2-3 weeks later) .
 Acid agents: lung , oral mucosa,esophgus and
stomach injury and necrosis.
 Mocusal and tissue damage less sever than alkali .
(Acid taste)
 Treatment: initial therapy like the alkali ingestion
 (dilution and no emesis or nutralizing)
Screening laboratory clues
 Metabolic acidosis:
 methanol, ethanol
 uremia, diabetes
 iron, isoniazid, salicylate , starvation
 Determining : Blood gases, urin PH, Na, K,
chloride, glucose, BUN, serum osmolality and
anion gap
Screening laboratory clues
 Hyper glycemia: salysilate, phenothiazide,
sympathomimetic, isoniazid, iron,
 hypoglycemia: insulin, Ethanol , propranolol,Isonizid, oral
hypoglycemic agents.
 Hypo calcemia: Ethylene glycol, fluride , oxalate
 Radiopaque substance:
iron , phenothizine , Entric coted pills, Dental amalgam,
Heavy metals, pothassium chloride
Drugs monitoring for toxicity
 Antibiotics :
aminoglycosid, chloramphenicol, vancomycin.
 Immuno suppression :
methotrexide , cyclospurine
 Antipyretic:
Acetaminophen , salycilate
 Others: digoxin, lithium, theophylin, anticonvulsant
serotonin
treatment
Supportive care
1-ABC 100%O2 ,naloxane,glucose 1g/kg IV .
 Diuresis

Hemoperfusion: rarly used in small children
 Most liquid drugs absorbed within 10 min and
solid within 1-2hr
treatment
 Prevention absorption :
1.
Activated charcoal
2.
3.
Gastric lavage
Cathartics
4.
5.
Diuresis
Hemoperfusion
6.
Dialysis:
methanol, ethylen glycol, salycylate, theophylin
Treatment(con)
Gastric lavage:
 Not documented efficacy in children.
 Remove only a fraction of gastric contents.
 It should only used in older children and selected
situations
treatment
 Prevention absorption
 syrup ipeca : ??
(Potentially complication without improve clinical outcome)
 onset emesis after 20-30 min and several episodes over 1-2
hr.
 10 CC for small children 15CC =1-12years ,30 CC older
children.
 Remove 1/3 stomach content.
 when ingestion is < 60 minute and air way protected
 not be used as a general treatment.
Treatment(con)
 Contraindication ipeca :
 minimaliy toxic agents
 prior vomiting
 air way unprotected
 caustic agents, hydrocarbon , agent cause the rapid
onset CNS or cardiovascular symptoms
 foreign body
treatment
Activated charcoal:prevent toxin absorption.
 single dose25-50g small children 50-100g> 12yr. Repeated
doses in serious poisoning.
 25% of patients experience one episode of vomiting.
 most benefit achieved within 1 hour of ingestion.
 Ineffective against : caustic ,corrosive , hydrocarbon ,
heavy metals, glycols and water – insoluble
compounds
Treatment(con)
Cathartics:
( sorbitol 1g/kg, magnesium citrate250cc/kg ).???
 combination with activated charcoal is not
recommended (essential nelson)
 complication: Electrilyt imbalance and dehydration
Emergency Antidotes
 Poison
Mercury ,arsenic, gold
Methyl alcohol
Nitrites
Opiates
antidotes
BAL
Ethyl alcohol +dialysis
methylene blue
naloxan
dose
5mg/kg
1ml/kg
1-2 mg/kg
0.1 m g /kg- 2
Emergency Antidotes
Poison
organophosphate
antidotes
Atropin
paralydoxime
Sympathomimetic
agents
phentolamin
β-blocking
dose
0.02- 0.05mg/kgIV
20-50 mg/kg
Acetaminophen
 Acute toxic dose200mg/kg in children < 12 yr.
 Repeated doses more than recommended may lead hepatic
injury.
 Children <6yr unlikly develop significant toxicity .
 1-2 hr of ingestion activated charcoal
 antidot started as soon as possible ,oral N- acetylcysteine
may be benefit if started 24-36 hr after ingestion
stages in clinical course of Acetaminophen toxicity
 1-
½-24 hr
anorexia ,nausea ,vomiting ,pallor
 2-
24-48hr
abdominal pain, bilirobin , PT↑
hepatic enzyme ↑
 3
72-96 hr
 4-
4days- 2 weeks
anorexia , nausea , vomiting ,
peak liver abnormality
resolution of hepatic dysfunction
↑or complete or liver failure
salicylates
 Nausea , vomiting, gastric irritation
 hyperventilation, Respiratory alkalosis
 dehydratoin
 prograssive metabolic acidosis
 Agitation, counfusion are common.
 Hyperglycemia, or hypoglycemia.
 Pulmonary edema
salicylates ( treatment)
 Activated charcoal.
 Rehydration , correction electrolyte.
 Large quantities of Potassium , and bicarbonate.
 Urine PH 7-7/5 ( using bicarbonate IV)
 Dialysis in sever cases
Antidepressant( TCA, SSRI)
 Block reuptake serotonin , dopamin , norepinephrin
 Myocardial depression ,dysrhythmia
½-6 hr
 CNS effect 1/3 (lethargy , coma, drowsiness ),seizure
 Anticholinergic effect. tachycardia ,mydriasis ,
 Hypertension ( no treatment ).
 hypotension (rare but poor prognosis).
Antidepressant( TCA, SSRI) treatment
 ABC
Emesis is contraindication( aspiration ,after onset CNS deprassion)
 Activated charcoalshould be used .
 Sodium bicarbonate ( to treat and prevent dysrhythmia)
and if unresponsive…….. Lidocaine used .
 Fluid therapy for hypotension.
 Bezodiazepine for seizure.
 Asymptomatic patient observe and ECG monitoring for 6
hr.
Cholinsterase inhibitor ( organophosphate and carbamate)
 Prevent degradation acetylcholine , bind to cholinesterase
and inactiveted it .
 muscarin signs: emesis, urinary and fecal incoutinence,
drooling , bronchospasm, miosis, hypotention ,
bradycardia.
 Nicotinic signs: muscle weakness , tremor , fasciculation,
 hypertention ,hypoventilation , tachycardia ,
dysrehythmia,
 CNS effects ; confusion, seizure , coma .
Cholinsterase inhibitor ( organophosphate)
 Treatment:
1. ABC
activated charcoal
3. Fluid and electrolyte replacement .
4. antidotes ( significant organophophate poisoning both
antidotes is necessary) .
even with treatment neurologic symptoms may occur and
may be persist .
2.
Treatment( con) Antidotes
1- Atropin infusion :
 blocks acetylcholine receptor .
( reversing the CNS and muscarinic effect)
2- paralidoxime :
 breaks the bond between organophosphate and enzyme
,librating enzyme, degrading organophosphate
Acute hydrocarbon risk assessment
 Systemic and pulmonary toxicity
Hydrocarbon ingestion result in systemic but more
often pulmonary toxicity,
Systemic: carbon tetrachloride, benzen, trichloroethylene.
Local toxicity: kerosen, furniture polish, signal oil , gasolin
Non toxic : tar asphalt, motor oil , lubricant, baby oil
hydrocarbon
1. Aspiration pneumonia:
(Low vicosity : gasolin, kereson , naphta , lamp oil ).
Cough, fever (10 days),leukocytosis , chest Xray ( may
normal 6-12hr)
2. Systemic symptoms : most hydrocarbon can cause
transient CNS depression. Few have renal toxicity
,carbon tetrachloride produce hepatic toxicity.
Hydrocarbon ( treatment)
 Emesis is contraindicacated.
 Activated charcoal is not useful.
 in pneumonit respiratory treatment is supportive.
 Corticosteroid avoided .
 Prophylacttic antibiotics should not be given.
 Respiratory failure treated with standard ventilation
(ECMO ?)
‫‪Snake bite‬‬
‫‪ ‬خصوصیات سم مار‬
‫پلي پپتیدها ‪ ،‬آنزیمهاي پروتئولیتیكوتوكسینها‪ ،‬نوروتوكسیك ‪ ،‬سیتولیتیك‬
‫‪ ‬عالئم كلینیكي سیستمیك ‪:‬‬
‫ترس و وحشت ‪ :‬تهوع‪ ،‬استفراغ‪ ،‬اسهال‪ ،‬سنكوپ‪،‬تاكیكاردي ‪ ،‬پوست سرد و مرطوب‪،‬‬
‫فاسیكوالسیون عضالني‪ ،‬بندرت شوك‬
‫عالئم موضعي‪:‬‬
‫محل نیش مار ‪ :‬درد فوري و در ‪ %90‬موارد‬
‫ادم ‪:‬ادم درطي نیم ساعت و گاهي چند ساعت بعد‬
‫تاول‪ :‬در طي چند ساعت‪ ،‬لنفاژیت‪ ،‬غدد لنفي حساس‬
‫خفیف‪ ،‬متوسط ‪ ،‬شدید‬
‫ارزیابي بر اساس ‪:‬عالئم لوكال‪ ،‬سیستمیك‪ ،‬انعقادي‬
‫‪Guidelines for assessing‬‬
‫‪ ‬خفیف‪ :‬ادم ‪ ،‬اریتم یا اكیموز و بدون عالئم سیستمیك و مشكالت انعقادي‬
‫‪ ‬متوسط ‪:‬‬
‫ادم پیشرونده باالتر از محل گزش‬
‫تهوع ‪،‬استفراغةپارستزي اطراف دهان و هیپوتانسیون خفیف‬
‫عالئم خفیف انعقادي‬
‫‪ ‬شدید‪:‬‬
‫ادم سریع ‪،‬اریتم و یا اكیموز در تمام عضو‬
‫هیپوتانسیون شدید‪،‬تاكیكاردي ‪،‬تاكي پنه‪،‬تغییر سطح هوشیاري‬
‫مشكالت واضح انعقادي‪ ،‬ترومبوسیتوپني و خونریزي خودبخود‬
‫‪treatment‬‬
‫‪ ‬آیا مار سمي بوده؟‬
‫‪ ‬بیحركت كردن عضو‬
‫‪ ‬تورنیكه ممكن است ایسكمي را تشدید كند‪.‬‬
‫‪ ‬گذاشتن یخ و انسیزیون موضع ممكن است باعث آسیب بافت بشود‪.‬‬
‫‪ ‬زخم باید تمیز شود ‪ ،‬تتابولین‬
‫‪ ‬در اورژانس‪:‬‬
‫كنترل راه هوایي‪ ،‬تنفس‪ ،‬گردش خون‪ ،‬گرفتن رگ‪،‬‬
‫گرفتن شرح حال‪:‬‬
‫زمانگزش ‪ -‬خصوصیات مار‪،‬شرایط مدیكال همراه ‪ ،‬حساسیت دارویي و غذایي‪ ،‬سابقه‬
‫مارگزیدگي و درمان آن‬
‫‪treatment‬‬
‫‪ ‬معاينه فيزيكي‪:‬‬
‫‪ ‬معاینه قلبي‪ ،‬ریوي‪ ،‬نورولوژیك‪ ،‬توجه به محل گزش‬
‫‪ ‬اندازه گیري قطرمحل گزش وتكرار اندازه گیري هر ‪ 15-20‬دقیقه تا توقف تورم‬
‫‪ ‬گرفتن نمونه خون جهت‪ PTT,PT,CBC -‬فیبرینوژن ‪ ،FDP ،‬گروه خون ‪ ،‬اوره ‪ ،‬كراتینین‬
‫‪ ‬تجويز آنتي ونوم‪(:‬در طي ‪ 4‬ساعت و حد اكثر ‪ 12‬ساعت پس از گزش )‬
‫اثر اوقات در طي چند دقيقه ودر تمام مواقع در طي ‪ 6‬ساعت عالمت دار ميشود‪.‬‬
‫اكثر بچه ها درجه ‪2‬ويا ‪ 3‬مسموميت بوده و اكثر اوقات نياز به آنتي ونوم و با مقدار زيادتر‬
‫دارند‬
‫كنترل اولیه‬
‫ابتدا ‪ 10-5‬ويال )‪ ( crifab antivenin‬در صورت كنترل ‪ 2 ،‬ویال در فواصل ساعات‬
‫‪ 6‬و ‪12‬و‪18‬‬
‫گزیدگي با مار ‪coral‬نیاز به ‪ 5-3‬ویال آنتي ونوم پروفیالكسي دارد‪.‬‬
‫ايمونيزاسيون كزاز‬
‫آنتي بيوتيكدرصورتعوارض باكتلاير‬
classification of envenomation
 Grade0 : no envenomation
 Grade 1 mild : local swelling and pain
 Grade 2 moderate: swelling, pain or echymosis
progressing beyond the site
Mild systemic or laboratory manifestation
 Grade 3 sever: sever systemic finding and labratory
scorpion
Patogenesis:
 Hyaluronidase ,sertonin, histamin and neurotoxin
 neurotoxin bind to presynaptic membranes and
release acetylcholin and stimulation of both
sympathetic and parasympathetic nervous systems.
Clinical manifestation
 Most sting cause immediate local reaction .(mild burning
to sever pain)
 Severe envenomation causes autonomic dysfunction
within 1 hr.
 Symtoms :
Agitation,irritability,salivation,bluredvision,
hypertension, tachycardia,tachypnea and nystagmus.
Rarely in smal children respiratory failure,convulsion or
coma.
‫‪Clinical manifestation‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫عالئم سیتمیك ‪:‬تب ‪ ،‬تعریق‪ ،‬افزایش بزاق‪ ،‬پوست سرد و مرطوب‪ ،‬تاكیكاردي و تاكي پنه‬
‫عالئم عصبي‪ :‬بیقراري ‪ ،‬گیجي ‪ ،‬خواب آلودگي ‪ ،‬افزایش رفلكسها‪ ،‬همي پلژي‪ ،‬تشنج‪ ،‬كوما‬
‫ریه‪ :‬ادم ریه قطع تنفس‪ ،‬فلح عضالت تنفس‬
‫كلیه‪ :‬تغییراتحجم ادرار‪،‬هماتوري‪،‬هموگلوبینوري‪ ،‬نارسایي كلیه‬
‫خوني‪:‬همولیز ‪ ،‬ترمبوز عروق و گانگرن‬
‫رقلبي ‪ ،: CHF :‬تغییرات فشار خون‬
‫گوارش‪:‬افزایش دفعات اجابت مزاج ‪ ،‬خونریزي گوارشي‪ ،‬تهوع و استفراغ ‪،‬پانكراتیت‬
‫مرگ و میر در اطفال و افراد مسن ‪ ،‬از چنددقیقه تا ‪ 2‬روز ‪ ،‬اغلب در ‪ 12‬ساعت اول‬
‫علت مرگ ‪ :‬اثر سم روي ‪ ،CNS‬مركز تنفس‪ ،‬میوكاردیت‪ ،‬نارسایي قلب‪ ،‬آریتمي‪ ،‬خونریزي‬
Scorpion envenomation
 Grade 1: local discomfort and paresthesia.
 Grade 2: pain and parestesia extend up the extremity.
 Grade 3: cranial nerve dysfunction, dysphagia, roving
eyes, facial , paresthesia, restlessness.
 Grade 4: cranial nerve dysfunction ,drooling,
uncontrollable eye movements, faciculation ,
opisthotonos, convulsion,wheezing, hyperthermia
,cyanosis
treatment
 Localized pain:
ice and analgesics.(pain deminish within 24hr)
hospital admission: Sever envenomation + autonomic
instability.
 Symptoms resole within 24-48hr
 In cardiopulmonary compromise should be given
antivenin. (complete resolution symptoms within 1
hr)
‫‪treatment‬‬
‫‪ ‬اطالع از عقربهاي منطقه‬
‫‪ ‬تسكين درد با ليدوكائين‪ ،‬گذاشتن يخ ‪ ،‬شستشوي محل زخم ‪ ،‬استامينوفن ت‬
‫‪ ‬تورنيكه‪ ،‬انسيزيون و ساكشن مؤثر نيست‪.‬‬
‫‪ ‬آنتي ونوم‪ :‬در عالئم شديد سيستميك‬
‫‪ ‬كلسيم‪:‬در كرامپ عضالني‬
‫‪ ‬تشنج‪:‬ديازپام‪ ،‬فنوباربيتال‬
‫‪ ‬هموليز‪: :‬تزريق خون ‪+‬مايعات كافي و قليائي كردن ادرار‬
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