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له ى ال عل ت ل ك و ت له م الس ب دا ب ن له م الس ب ول الأ رة ك ا مد ل ل ا ب ق دعاء ى ل و الأ ه ق ل ح ل اPart 1 رال. ي ب ج ل ا2 ن ع هاردة لن م ا كل ت< هن ال2 ن م ع ل ط تC اك يعاchapter . ى تI الأ دة بManagement of poisoning ل م ع ن ما ل عد كدة ناس س و الأ ه2 ن لأttt . ي لأpoison ل مV ب. ي والد1-Prevent further exposure . 2-Emergency stabilization of the patient. 3-Proper clinical evaluation . 4- Prevent further absorption . 5- Eliminate absorbed poison . 6- Antidotal therapy if available. 7- Supportive Therapy. 1-Prevent further exposure: #In therapeutic overdose(e.g. digitalis) -stop drug responsible #occupational toxicology (co ,cyanide gas) Remove from place #In homicide -keep under complete control in hospital 2-Emergency stabilization of the patient.

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Page 1: toxicology 1 doc

بسم الله توكلت على اللهبسم الله نبدأ

دعاء قبل المذاكرة األولالحلقة األولى

Part 1هنتكلم النهاردة عن الجينيرال

ده باآلتي chapterعايزاك تطلع من الManagement of poisoning

poison ألي tttألن هو األساس بعد كده لما نعملوالذي يشمل

1-Prevent further exposure .2-Emergency stabilization of the patient.

3-Proper clinical evaluation .4- Prevent further absorption .5- Eliminate absorbed poison .

6- Antidotal therapy if available.7- Supportive Therapy.

1-Prevent further exposure:#In therapeutic overdose(e.g. digitalis) -stop drug

responsible#occupational toxicology (co ,cyanide gas) Remove

from place#In homicide -keep under complete control in hospital

2-Emergency stabilization of the patient.

ABCD s resuscitation : A ==== Airway

B ==== BreathingC ==== Circulation

D ====drug induced C.N.S Depression

Airway ===ACauses of obstruction الحل

#Secretions===Suction of secretions#Posterior displacement of the tongue===pull tongue using tongue depressor or support jaw (head tilt chin left

maneuver)#Foreign body e,g artificial teeth=== Remove FB

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# Insert endotracheal tube (cuffed in comatosed patient)V.I.P.

# Tracheostomy (not need definition)B=== Breathing (Maintain respiration):

*Oxygen therapy ==Oronasal mask (Carbogen5%CO2 ,95%O2)

*Artificial respiration== Mechanical ventilation If too slow respiration i.e no chest movement or paralysis of resp.

muscles

Artificial Resp.==Mouth to mouth Breathing (at a rate of 2 mouth breath then 15 compression on chest at a rate of

100/min.)Till patient become well or you are exhausted.

C===circulation

Shock characterised by failure of the circulatory system to maintain adequate perfusion of vital organs

Hypovolaemic shock==ttt Fluid replacementNeurogenic shock ==ttt analgesic e.g. morphine

Hypotesive shock ==ttt vasopressor e.g dopamine

Signs of shock: cyanosis, hypotension.What to do:

1.Elevate legs2.Fluid replacement

3-cover with blankets4-Vasopressor drugs

D==Drug induced C.N.S depressionLevel of consciousness classified according

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Qualitative ==change of level of consciousness (lethargy ,stupor , coma)

Quantitative==change in cotent of consciousness (confusion ,delirium ,psychosis)

Coma= unarousable unresponsivenessStupor=grade of coma in which arousability only in

response to sever stimuli

Reed' s classification of coma :Grading of covsciousness G0 G1 G2 G3 G4*Response to verbal stimuli + - - - -*Response to verbal stimuli + + - - -*Deep tendon reflexes + + + - -

*Resp. or circul.depression + (intact) + + + - (lost)

Coma Cocktail 3 thingsNaloxone ,Dextrose , Thiamine

Naloxone :(0.4mg ampouls Narcan),2mg I.V =5ampouls

value:Very useful as there are synthetic & semisynthetic opiods

such as codeine ,propoxyphene for which naloxon is administered in large dose to antagonize them effectively

Dextrose:D50W for adults , D25W for children

D=dextrose W=waterThiamine(vit B1)

Dose 100mg I.V to all adult &Adolescent But not to childrenValue :

Prevent ppt of Wernick's encephalopathy in alcoholic patient

Seizures(convulsions )Management:

#airway must be kept patent+O2# Diazepam (valium)of choice

#in status epilepticus phenytoin or Phenobarbital

2- Proper clinical Evaluation

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History, physical examination & laboratory tests are used for proper clinical evaluation

3- Reduction of further absorption of the poison : 1- Eye decontamination2- Skin decontamination

3- GIT decontamination

Eye decontaminationIn corrosives: with normal saline for at least 15-20 minute.

DONOT USE NEUTRALIZING SUBSTANCE (heat release)

Skin decontamination1. For corrosives: use water or saline for 10-15 minute. 2. for other toxic substances: use cold water then

wash with soap.3. Some chemicals require special TTT such as:

*Lime & cement → ttt like alkali burn *Flammable metals →remove the large

particles & cover the surface with mineral oil.*Phenols (cresols) → Polyethylene.

*White phosphorus →use copper sulfate solution.(Oxidizing agent)

YOU MUST PROTECT YOURSELF FIRST

GIT Decontaminationa) Emesis

b) Gastric lavagec) Activated charcoal

d) Catharticse) Whole-Bowel irrigation

f ) Surgical decontaminationg) Local antidotes

a)EmesisIndications :

-Patient: alert (intact gag reflex).

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-Time of ingestion: not more than 4-6 hours-Poison: not adsorbed by activated charcoal.

- Sustained release or enteric-coated tablets or big lumps.

Contraindications:-Patient: absent or impaired gag reflex, heart disease,

gastric ulcers , pregnancy,….- Time of ingestion: more than 4-6 h after ingestion

- Poison: corrosives, sharp solid objects, drugs causing convulsions, volatile hydrocarbons (kerosine).

Methods used in induction of emesis*Mechanical: touch the back of the pharynx by a finger; it is used in the home if syrup of ipecac is not available.

*Drugsa) Gastric irritants : strong solution of salt or copper

sulfate this is dabgerous as prodces hypernatremia ,cooper make copper toxicity

b)Apomophine: centrally +ve CTZ , Not used now due to Depression of respiratory center

c)syrup of epicac :Origin :dried root or rhizoma(ساق) of ipecacuanha or

acminata plantPrinciple alkaloid :Emetine ,CephalineMechanism of induction of vomiting :

Act both central &peripheral central +ve CTZ ,peripheral by irritation of gastric mucosa

N.B.It must be given on full stomach so ask patient to drink

one liter of water before administration

Dose of syrup of epicac

Infant (6-12month) 5-10ml of syrup of epicac +100-150ml clear fluid

Children (1-5years) 15ml of syrup of epicac +240 ml clear fluid

Children (5-12years) 20ml of syrup of epicac +240 ml clear fluid

Over12 years 30ml of syrup of epicac +240-480 ml clear fluid

When to stop epicac ?

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The dose is given every 20-30minutes for two doses if vomiting doesn’t occur Gastric lavage or Activated

charcoal administration is decided .

b)Gastric lavagePrinciple :

Insert tube into stomach ,washing it with water or harmless solvent to remove unabsorbed poison

Indications :1- After ingestion as soon as possible

2- Useful for as long as 3hrs after ingeastion3- If delayed gastric emptying lavage useful for 12hrs4- Considered only if patient ingested life threatening

amount of toxic substance within one hour of presentation .

Contraindications:As for emesis but can be used for hysterical ,

comatosed ,or any uncooperative patient

Precautions :1- In case of C.N.S depression or pulmonary irritant

ingestion insert cuffed endotracheal tube before lavaging2-It can be performed under general anesthesia in patient

with convulsions

Procedure : Tube:150 cm long ,1.25 cm in diameter Having multiple

openings on sides &At tips.

Before inducing the tube Ask the patient to drink a glass of water if alert

Steps1- The patient lies on his left side with head lower to Avoid

Aspiration &get good washing2- Remove any foreign body from mouth (artificial

tooth ,chewing gum,..)3-lubricate the end of the tube with Glycerine then pass it smoothly to pharynx =oesophagus =stomach[If the

patient alert ask him to swallow =closure of resp.passage during swallowing ]

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4- Aspirate gastric content by irrigation syringe &keep in abottle with name of both patient &doctor ,time=sent

for analysis

5-Attach a funnel to the tube &hold it up pour water (200ml) slowly lower the funnel &let the content

Regurgitate into a bucket =Repeat it several times until fluid returned is as clear as possible

How to know that the tube is in Stomach Not in the Trachea:

** If in Trachea :1- movement of Air is heared.

2- Patient shows sudden spasmodic cough &cyanosis3- Bubbling occurs if the end of the tube is immersed in

water(expiration)

*****if the tube is in stomachAspiration brings up gastric content

You ca leave Cathertic(مسهالت),local antidote …etcc)Activated charcoal

Is considered the best method of Gastric decontaimationIt is very effective Nonspecific adsorbent

Dose : 1g/kg BW

Generally 50-100g for adult15-30g for children

+suitable amount of water (250 ml for adult )+Vigorously shaken to form a slurry

لو في البيت ممكن يضرب في الخالط ليكون عجين رقيقAdministered orally or through nasogastric tube

What do you know about Multiple(serial) dose activated charcoal?

Indications: In theophyllin overdose &if threatening amount of

Phenobarbital,Carbamazepine ,Quinine ,Dapsone or Aspirine is ingested.

Mechanism : It can enhance elimination of absorbed toxins through

@Interruption of enterohepatic or enteroenteric circulation e.g. theophylline ,Phenobarbital ,salicylates

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b)Gastro intestinal dialysis whereby the drug back diffuse from the higher serum levels ,through the intestinal villi&

into the lower intraluminal concentrations.

Contraindications

1- Presencce of diminished bowel sounds,ileus &bowel obstruction

2-Prior to endoscopy after corrosive ingestion3-In poorly absorbed poisons :cyanide, ethanol

methanol,iron ,strong acids &alkalies

d) Cathartics : two groups are present :

1) saline cathartics :e.g. sodium sulphate ,magnesium sulphate

2) Saccharides :e.g.e.g. sorbitol (is the cathartic of choice )

Contraindication:Ingestion of corrosive, sever diarrhea,ileus ,serious

electrolyte imbalance &bowel injurye)Whole bowel irrigation

It is a useful safe &rapid method to empty the gut in 4-6 hours .It produces a through cleansing of the entire

intestinal tractMethod :

By use of High molecular weight polyethelene glycol (PEG) and isosomlar electrolyte solution (sodium sulphate) are

used as isotonic solutions for WBI and available as Golytely & Colyte

Indications: Ingestion of massive amounts of highly toxic drugs .

Ingestion of large amounts of drugs in patients presenting late(more than 4 hours)

Ingestion of drug packets by body packers (cocaine filled packets ) (تجار المخدرات)

Ingestion of substances not adsorbed by activated charcoal

Contraindications:- G.I.T Haemorrhage ,perforation ,ileus

&obstruction

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- Inadequate air way protection .

f) Surgical decontamination:

Surgical removal of concretions of sustained release tablets (e.g .Theophylline, Aspirin ,Carbamazepin)

from the stomach . The concrations are fragmented or via

gastroendoscopy to be followed by activated charcoal and W.B.I.

Indications : Concretion of sustained-release tablets .

Drug packets by body packers or body stuffers Patients with bowel obstruction

When there is a contraindication to gut decontamination.

g) Local antidotes: 1- Adsorbents : Activated charcoal

2-Dilution&Neutralization:dilution with fluids (water or milk)

But note that :If Alkali (any strength ) or weak acid caustic ,the oral

dilution with cold fluids immediately after exposure may reduce oropharyngeal & gastric mucosal damage as it

reduce the contact time with tissues .If strong acid :It is contraindicated due to production of heat &gases which lead to more destruction of tissues

3-precipitation مهمe.g. tannic acid for= alkaloids e.g opium

Albumin water =mercuryMagnesium sulphate=Carbolic acid

Calcium hydroxide =oxalic acid

4 -oxidation potassium permanganate solution =oxidize most

alkaloids e.g.Atropincupper sulphate =phosphorus

5- Reduction

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e.g. sodium formaldhyde sulphoxylate =è reduce mercuric chloride to metallic mercury which is less soluble &thus

non absorbable.

METHODS FOR ELIMINATION OF THE ABSORPED POISON

(1) Forced diuresis and PH alteration.(2)Hemodialysis .

(3) Peritoneal dialysis.(4)hemofiltration .(5)plasmapheresis .(6)Hemoperfusion .

(7) Gut dialysis.(8) Plasma perfusion.

(9) Hyperbaric oxygen.(10) Exchange transfusion.

(11) Cardio pulmonary bypass.

Forced diuresis and PH alteration

AIM: PH alteration of urine to enhance renal excretion by increasing the amount of ionized form of the drug in

urine AS*when the drug in the non ionized form is easily diffuse

across the tubular membrane and reabsorbed*when the drug is ionized form it will be trapped in renal

tubules and easily excreted

INDICATIONSIn toxicity with drug that are:(1) Weak acid or weak base

(2) Low protein binding(3) Have limited metabolism(4) Have high renal clearance

(5) Have small volume of distribution

COMPLICATIONS

(1) Fluid overload

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(2) Pulmonary oedema(3) Cerebral oedema

(4) Acid base disturbance(5) Electrolyte imbalance

INVESTIGATION(1)Plasma drug concentration

(2)Fluid balance(3)Central venous pressure

(4)Electrolytes , Serum sodium, Potassium. calcium and magnesium

ACID DIURESIS INDICATIONS

Amphetamine .strechnine. Quinidine and phencyclidineMETHOD

500ML dextrose 5%+ 500ml saline 0.9%+

75ml ammonium chloride 2% give over 6 hours

ALKALINE DIURESISINDICATIONS

Salicylates phenobarbital and phenoxyacetate herbicideMETHOD

500ml dextrose 5%+500ml saline 0.9% +

500ml Na bicarbonate 1.26% over 3_4 hours

HEMODIALYSISOnly eliminate drugs or toxins which can pass easily

across the dialysis membranei.e characterized by

A) low molecular weightB) high water solubility

C) small volume of distribution(high plasma concentration)

INDICATIONS

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1)Several clinical intoxications with vital signs abnormalities such as apnea, hypotension that do not

respond to supportive care.2)Impaired normal excretion routes e.g renal failure3)progressive clinical deterioration and presence of

complications such as aspiration pneumonia4)prolonged coma with complications5)presence of underlying diseases .

6)ingestion of alethal dose of poison .7)ingestion of large dose of toxin that is metabolized to more toxic metabolites such as methanol and ethylene

glycol .8)drug produce delayed toxicity e.g paraquat.

CONTRAINDICATIONS1) Presence of antidotes

2)Coagulopathy3)Cardiogenic shock

4) Non dialyzable toxins

COMPLICATIONS1) Hypotension

2) Electrolyte and Osmolar imbalance3) Hypoxemia

4) Vascular access Complications5) Spontaneous Bleeding

6) Infections7) mechanical Complications

8)sever anaphylactic9)sudden death fromMachine malfunction,

Electrocution& Coagulopathy

3-HemoPerfusionBlood is pumped through a cartridge of absorbent material

(activated charcoal or resins)Indications: -

The same as in hem dialysis, but hemoperfusion is not limited by the high molecular weight, protein binding or

poor water solubility of the toxin because charcoal or resin can adsorb these toxins

Contraindication: -

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Similar to those for hem dialysisComplications: -

Similar to those for hem dialysis + thrombocytopenia, leucopenia and hypocalcaemia

4- Peritoneal dialysis :-Peritoneal dialysis operates on principles similar to those

of hem dialysis diffusions of toxins from mesenteric capillaries across the peritoneal ( membrane into dial sate

dwelling in the peritoneal cavityIndications: -

1- Patients with acute renal failure2- Patients with bleeding disorders

3- Patients with venous access problems4- Hem dialysis is not available

5- Patients for whom hem dialysis andhemoperfusion are contraindicated

Method: - Through a catheter inserted intraperitoneally , adialysate

fluid is instilled and 1-2 liters is exchanged each hours

Complications: - 1- Pain

2- Hemorrhage3- Leakage

4- Inadequate drainage5- Perforation of viscera6- Bacterial peritonitis

7- Arrhythmias8- Volume depletion or overload

9- Hyperglycemia and electrolyte disorders10- Pneumonic and pleural effusion

5- Gut dialysis :-

(Serial activated charcoal)Gut dialysis enhances elimination of the toxins that havea) significant enterohepatic or enter enteric circulation

b) limited protein bindingc) small volume of distribution

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6- Hyperbaric oxygen (HBO): -

Hyperbaric oxygen ( HBO ) has been used in the management of carbon monoxide ( CO ) and cyanide

( CN ) poisoning , it is also used in other poisoning such as barbiturates , mushrooms , hydrocarbons and oregano phosphates HBO needs special hyperbaric chambers

which aren’t available in most hospitals of EgyptHBO dramatically displaces CO from hemoglobin as well as the tissue sites , myoglobin and city chromes it reduces

the elimination half lives of blood CO-Hb from 250 minutes at room air to 22 minutes at 3 atom of 100 % oxygen

Complications :-

1- Traumatic rupture of tympanic membrane2- Acute sinusitis3- Optic neuritis

4- Pneumonia thorax5- Oxygen toxicity

6- Seizures7- Safety hazards (explosions , fire……etc )

7- Exchange Transfusion : -

It is the method by which the patient’s blood is removed and replaced with fresh whole blood

Double – exchange transfusion :- Is an amount of blood equivalent to twice the patient’s total blood volume is exchanged the only indication for

this method is sever methaemoglobinemia not responding to ethylene blue therapy

Specific antidotal TherapyChelating agents

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Are organic compounds that react with heavy metal ions to form firmly bound complexes (chelates)

We are going to study:B.A.L

E.D.T.APenicillamine

DeferroxamineD.M.S.A.

1-B.A.L.B.A.L=British anti-lewisite (lewisite is the gas of war)

Mechanism of Action: It acts by fixing the metal ions which have high affinity for

SH group forming a relatively harmless &poorly dissociable ring compounds ‘chelates ‘ that prevent the poison from inactivating the SH containing respiratory

enzymes .

Uses: It is the physiological antidote of poisoning with

heavy metals e.g. Arsenic, Mercury, Antimony, Antimony, and Gold &Bismuth.

It is of little value in ttt of lead poisoning because it only chelate lead ions present in the blood while the ions in the bones &tissues are too firmly bound to be

mobilized by it BAL is not used in iron poisoning because BAL – iron

complex is even more toxic than the unchelated iron.

Dose : Deep I.M. injection of 10% BAL in peanut oil is given in a

dose of 2.5 mg/kg body weight every 4-6 hours for 2 days then every 12 hours for 7-10 days.

Why deep? To avoid abscess formation

EDETA EDETA&EDETA salts :[ Na2 EDETA &Ca Na2 EDETA ] Ca salts are used because rapid I.V. administration of

Na2 EDETA result in hypocalcemic tetany .This is the reflection of high affinity of EDTA for calcium.

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CaNa2EdETA can chelate any metal that has a greater affinity for EDETA than has calcium & can

thus replace calcium from the complex Lead has high affinity for EDETA than calcium &can

replace calcium in the complex forming a poorly dissociable chelate which is harmless &excreted in

urine. Mercury poisoning responds poorly to ttt with Ca Na

2 EDETA in vitro because it doesn’t pass into areas of mercury

Dose: CaNa2 edetate injection 20%solution 1g. (5ml)in 250-

500 ml of 5% glucose in water or saline solution slowly by IV drip over a 1 hour period ,twice daily for

3-5 days The drug is then withheld for 2 days to allow

redistribution of the lead, thus increasing the amount of metal available for chelation.

Dicobalt Edetate (Kelocyanor) It is a cobalt salt that forms a relatively nontoxic

stable ion complex with cyanide. Dose :

300mg I.V Followed immediately by 50 ml of 50% glucose I.v this may be repeated after 5 minutes if there is no

response . Side effects :Vomiting ,urticaria ,facial &neck

edema ,hypotension ,chest pain &anaphylactic shock .

Penicillamine :It posses one SH group

It is prepared by hydrolic degradation of penicillin . It is an effective chelator of Copper ,Mercury, zinc

&lead that promotes their excretion in urine It is well absorbed from G.I.T so it can be given orally

.

Dose : Penicillamine capsules :250 mg/capsules the usual

dose is 1-2 capsules (250-500mg) every 6 hours on empty stomach to avoid interference by dietary

metals .

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Deferoxamine ( Desferal ) It is the chemically modified metal free ligand from

streptomyces pilosus . It has high affinity for ferric ions ,& very low affinity

for calcium It readily competes for the iron of ferritin

&hemosiderin ,butthe iron of transferring is very minimally affected

Dose: Deferroxamine mesylate 500mg ampules .

1g is given I.M ,followed by 500 mg every 4hours for two doses .

The dose can be repeated at 4 or 12 hours intervals ,depending on clinical response ,but a total

of 6g/24 hours shouldn't be exceeded In case of acute iron toxicity ,8g has to be given by

nasogastric tube to be followed by IM injection described above

DMSA (Succimer) DMSA is relatively selective orally active water

soluble chelating agent It can be used in ttt of lead , arsenic ,organic

&inorganic mercury poisoning . It is more effective than I.V. CaNa2-EDTA in lowering

blood lead level , restoring red cell gamma aminolevulinic acid dehydratase (ALA-D)activity ,and

increasing urinary lead excretion .

Dose 10 mg /kg/8hrs orally for 5 days followed by 10mg/kg/12 hr for 14 days to delay the eventual

rebound in blood lead concentration.

Advantages of DMSA1- It is less toxic

2- Orally active&highly effective .3- Relatively specific i.e. doesn't significantly chelate

ca ,Mg,Fe, Cu, &Zn.4- Given safely to patient with G6Pd deficiency while

BAL can cause hemolysis

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5- Iron supplementation can be given concomitantly with DMSA without any adverse effects ,while BAL –

Iron complex is a potent emetic

تطبيقعايزين نطبق اللي خدناه

تعالو ناخد حاجة بسيطة األولزي األسبرين مثال

الخطوات بتاعتنا ايه؟1-2-3-4-5-6-7-

كويس

1-Prevent further exposure .

لو واحدة منتحرة مثال نحطها تحت المالحظة لو غير كده نكتب الخطوة وجنبها شرطة علشان تعرف المصحح أنك

عارف الخطوات ألن كل عنصر عليه درجة

2-Emergency stabilization of the patient. Safeguard against لو العيان صاحي خالص شرطة أو تقول

respiration

3-Proper clinical evaluation .هيقولك شرب أسبوسيد مثال علشان ألوانه جذابة لألطفال

4- Prevent further absorptionEmesis,Gastric lavage هل ينفع أعمل

ينفع أستخدم فحم منشط هل5- Eliminate absorbed poison .

هستعمل معاه أي نوعمعروف أن األسبرين حمض إذن هستخدم قلوي

مل لثالثة محاليل 500مل جلوكوز أو دكستروز 500

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. في المائة9مل سالين 500مل بيكربونات صوديوم 500

ionizable ,prevent reabsorbtion وكلمتين عن6- Antidotal therapy if available.

مفيش اذن شرطة

7-Supportive Therapy.

معروف أن األسبرين بيرفع درجة الحرارة و بيزود الحموضة وممكنيعمل

Haematemsisإذن هعمله إيه

كمادات ميه ساقعةZintac

مضادات الهستامين علشان الحساسيةولو دخل في

Pulmonary edemaأديله أكسجين من

Endotracheal tube

تطبيق تانيCO poisoningالخطوات بتاعتنا ايه؟

1-2-3-4-5-6-7-

ماشي

1-Prevent further exposure. لو أنت في قلب الحدث أول حاجة أنك تخرج المصاب من المكان ألن

تركيز أول أكسيد الكربون بيكون أعلى في طبقات الجو السفلى

طب افرض مثال أن التعرض كان بكمية بسيطة والشخص جالك وقالك أناأغمى علي½ خالص طالما فايق أحطه تحت المالحظة

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2-Emergency stabilization of the patient.أهتم بالتنفس بتاعه

إفرض أنا لوحدي ومش معايا أنبوبة أكسجين وال حاجة أعمل إيهairway patent &prevet obstruction أشوف

وأعمل له تنفس صناعي لحاد ماتيجي عربية اإلسعاف

طيب تصرفي إيه كطبيب في المستشفىEndotracheal entubation& mechanical entillation

*100% oxygen*hyperbaric oxygen

اإلتنين مع بعض

3-Proper clinical evaluation .historyمن ال

هيقول لك كان بيتدفى في يوم شتى ومقفل عليه أو في جراش ومشغل بنزين و مقفل عليه مثال او منتحر داخل عربيته

مقفل القزاز برده ومدخل خرطوم البنزين من فتحة أو البوتاجاز كان بينفس وبعدين شغلنا الشعلة يقوم يحصل احتراق غير

كامل ومثلها سخان الغاز برده4- Prevent further absorption .

شرطة مفيش5- Eliminate absorbed poison .

شرطة مفيش6- Antidotal therapy if available.

شرطة مفيش

7- Supportive Therapy.ممكن ايه

Warm patient with blanketsBlood transfusion

Part 2

Corrosives

General characters:–هنجيب األعراض من فوق لتحت من أول الفم وبعدين الحنجرة والبلعوم

معدة -أمعاء–مرئ

1- Immediate sever local destructive action

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2- Immediate sever burning pain in mouth,osophagus ,&stomachطب ليه مفيش ألم بعد المعدة

ألن حصلPyloric spasm

3- Immediate sever vomiting except carbolic acidBecause has local anesthetic action &inhibit CTZ

Vomitus is at first of gastric content then dark due to formation of acid or alkaline haematin +mixed with

shreds of gastric mucosa4- Dehydration & circulatory collapse

Shock (Neurogenic ,Hypovolemic)5- Diarrhea with Alkali Liquefaction of intestinal

mucosa while with acid there is pyloric spasm constipation

6- If inhaled there will be Laryngitis &Laryngeal edema +swelling of tongue+hoarsnesss of voice

Dyspnea &choking is common

7- Pneumonitis ,Pulmonary edema

8-ttt

1-Prevent further exposure .2-Emergency stabilization of the patient.

Keep patent airway patent+O2 ±tracheostomylaryngeal obstruction by glottic edema علشان

3-Proper clinical evaluation4- Prevent further absorption .

Emesis هو بيرجع أصال No activated charcoal (mask tissues during

endoscopy due to its blackish discolouration) No stomach Wash because tissues are

macerated Risk of perforation No Neutralization (Exothermic reaction)

No Na bicarbonate Release Co2 distension &perforation

Best antidote is milk : Dilute the corrosive Physical

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Demulcent because rich in protein coagulation separate tissues from corrosives Act as buffer amphoteric i.e

Act as alkali in presence of acid Act as acid in presence of alkali

5- Eliminate absorbed poison .6- Antidotal therapy if available.

7- Supportive Therapy.لو فيه مثال

Pulmonary edema ,shockأتصرف

Cause of deathA-Early ''Immediate ''

*Shock ,collapse :due destructive action on mucosa(Neurogenic due to sever pain

Hypovolemic due to vomiting & diarrhea )**Asphyxia :due to choking from acute oedema of

glottis caused by irritating fumes e.g. Ammonia ,nitric ,acetic acid

B-Late*Gastric perforation ,Peritonitis : in case of deep

ulceration reaching muscle layer**Cashexia ,Emaciation :from chronic starvation

resulting from cicatricial contraction of oesophagus ,stomach ,pylorus or impaired gastric

function

أنواع المواد األكالةأحماض غير عضوية حمض الكبريتيك والهيدروكلوريك والنيتريك*

أحماض عضوية كربوليك وأسيتيك وأوكزاليك**القلويات صوديوم وبوتاسيوم هيدروكسيد والمبيضات***

أمالح أكالة باريم كلوريد وأنتيموني تراي كلوريد****

هنبدأ باألحماضوأدي أول جدول

بس حضرتك اللي هتكتبه ألن المنتدى ال يقبل الجداول خانات4هنعمل جدول

هنقارن بين األحماض الغير عضوية الكبريتيك والهيدروكلوريك والنيتريكو خانة وجه المقارنة

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أول حاجة هي الFatal dose

H2SO44-5 ml. of commercial acidHcl15ml.of conc. acidNitric7ml of conc. acid

Fatal periodH2SO4can be rapid (12-48hrs) due to shock from

pain ,Asphyxia by odema of tha glottis ,Syncope due to collapse &dehydration or delayed (few days or few

weeks)Due to gastric perforation ,peritonitis pulmonary complication &chronic starvation due to

oesophageal ,gastric perforationHclas above

Nitric as aboveColour of ishures

H2SO4Blackish Brown متفحمHclpinkish Red

NitricYellow due to formation of xanthoproteinsClinical picture

هنكتب ف الثالثة (ممكن تكتب اللي فوق )Immediate sever burning pain

Immediate sever vomitingThirst &corrosion in lips

# 3 CConstipation (Because Acid)

CollapseCold Clammy skinوهنزود في النيتريك

More volatile Irritate airway passage, Edema of glottisCoughing, Dyspnea

Pulmonary complications as bronchitis ,bronchopneumoniaTreatment

هنقول نفس الكالم فوقبس هنزود

Egg white or olive oil can be used as demulcent Morphine 5-15 mg IV for sever pain ,shock

I.V. fluids for dehydration ,correction of electrolyte imbalance

Nutrient enemata can be used Surgical ttt graft operation in oesophageal stricture

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Post mortemنفس الكالم ف الثالثة Necrosis of mm

Lesions in larynx ,esophagus, stomach may show haemorrhage with altered blood

Antemortem or postmortem perforation in stomach may occur

With HCL +dirty white to ashy grey nccrosis of mucosa .

الجدول التانيالله المستعانهنقارن بين

Carbolic &oxalicاألول كلمتين ع الفنيك قبل ما نقول الجدول

أهم حاجة واحنا بنذاكر الToxicologyهي أنك تعرف

target organالوتعرف ال

Mechanism of actionوأنت هتقول الباقي لوحدك

Carbolicمن اسمه هنطلع بيؤثر على ايه

cCNS حرفr renal حرفcCVS حرف

CNSعلىStimulation followed by depressionوعلشان نتفق بعد كده أي حاجة هتالقي فيها

Stimulation on CNSهنقول

Irritability, Restlessness, AnxietyAgitation, Hallucinations, Convulsions

وأي حاجة فيهاDepression

هنقول

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Lethargy, Apathy, Somnolence, Confusion, Sleep, stupor, Coma

وبالمرة هيكون سبب الوفاةCirculatory collapse, Resp. Failure(RC depression)

ألنها هتتكرر بعد كده كتير فمش كل شوية هنقعد نقول كالم مش شكلبعضه(زي ما بقول لك كده هنحط الكلمتين دول وهيطلعو صح)

Renal علىDirect toxic nephritis (Acute Glom.Nephritis)

Renal failure with oliguria or even anuriaUrine contain Blood &albumin cast, Turns Green on Exposure to air due to formation of Hydroquinone

(oxidative product of phenol)

CVS علىMyocardial depression

Ventricular arrhythmias, Rapid, weak, irregular pulseMarked hypotension, Subnormal temperature

نرجع للمقارنة بتاعتناهنقارن من حيث

SourcesFatal dose

Fatal periodAction

Clinical pictureTreatment

Post mortem picture

CarbolicSourcePhenol is used as disinfectant ,insecticide &in

Some outpatient Pediatric surgery .Phenique contains 2-5%phenol

It is also present in CresolNB It can be absorbed from intact skin

OxalicSourcein Bleaches &metal cleaners &many plants

especially citrus fruit &rhubarb leaves

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CarbolicFatal dose3-6 gmOxalicFatal dose15-30gm

CarbolicFatal periodabout 4 hrsOxalicFatal period15 min (fatal decalcification )

10 days (renal failure )

Action :Carbolic

Local action يشبه المواد الكاوية مع بعض اختالف When applied to the skin or ingested intense pain &blanching of the area with superficial ulcers

Followed by* Local anesthetic action tingling &numbness, may

cause complete anesthesia**denaturation of ptns causing coagulative necrosis so it

is a general protoplasmic poison***Can cause gangrene if applied to the skin for a period

of timeRemote action

Mentioned CNS, CVS, RENAL

OxalicLocal action

1- Local corrosive action on alimentary tract2- With production of gastroenteritis

Remote actionأول ما تسمع أوكزاليك على طول يجي علي بالك الكالسيوم

Oxalic acid chelates ionisable calcium from the blood symptoms Related to hypocalcaemia

When large fatal dose is taken it produce fatal decalcification of blood

Also calcium Oxalate crystals Plug Renal Tubules Renal Failure within 10 days Death occurs

Clinical pictureCarbolic

Burning sensation in mouth,oesophagus ,stomach followed by Tingling due to local anesthetic action No or scanty vomiting due to local anesthetic

action Ishures colour

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Around mouth BrownishAt mouth & oesophagus WhitishWith characteristic aromatic odour

من الحاجات اللي بيؤثر عليها عندنا ايهCNS at first anxiety then followed by coma with

cyanosisالكالم اللي قولناه فوق

CVSPulse

Bl.PressureTemperature

Respir.*Pupils constricted reactive

(N.B. in Morphine Poisoning pinpoint pupil Irreactive )Arrhythmia

Large dose coma with unrecordable blood pressure ,Resp. arrest ,death

Delayed death from acute Renal failure

Oxalic حاجات3هنتكلم على

األولى It has local corrosive effect Sever pain in mouth ,esophagus ,stomach +sever vomiting &haematemsis+oxalate crystals in vomitus

+Diarrhea (dehydration ,collapse )خللي بالك أن ده حمض وعمل

Diarrheaعلى العكس من باقي االحماض

التانية Large fatal dose Death in few minutes due to

fatal decalcification as Ca is necessary for muscle contraction &nerve coduction So cause of death is

CNS depression & Myocardial depressionالتالتة

Sublethal doseSymptoms &signs are of hypocalcemia as

#Muscle twitches ,Ms cramps, tetany#Cardiac arrhythemia, convulsions

#Shock, stupor, comaCa oxalate crystals are deposited in Bl.vessels ,Kidney ,liver heart ,lungs

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Renal tubules Oliguria or even anuria Death from Uremia

Urine contain Ca oxalate crystals +blood +albumin

TreatmentCarbolic

1-Prevent further exposure .2-Emergency stabilization of the patient.

3-Proper clinical evaluation .4- Prevent further absorption .

Skin decontamination with extensive irrigation using H2O then Olive Oil

Gastric DecontaminationEmesis: Not contraindicated Because we said scanty

vomiting or no vomiting at allStomach wash: Is allowed No fear of perforation due to

coagulative necrosis wall is thickStomach wash is done using water then olive oil as it

dissolves phenol &prevent its absorptionAfter lavaging you can leave olive oil in the stomach as local antidate that retard absorption of any remaining

phenol Also we can leave Mg sulphate to ppt poison as Mg sulpho carbolate

5- Eliminate absorbed poison .Dialysis isn't beneficial here so ttt is mainly supportive

6- Antidotal therapy if available.7- Supportive Therapy.

Supportive in comaالمقصود هنا مش الكوما كوكتيل اللي قولنا عليه

المقصود أن لو العيان ده فضل عندي في المستشفي مغمى عليهProlonged Comaتانية Measures فيه

1- Maintenance of body temp. by blankets2- Frequent change in patient's position with rubbing

skin with alcohol to avoid bedsores3- Prophylactic antibiotic safe guard against

bronchopneumonia4- Regular catheterization for liability of retention of

urine5- Maintenencce of Fluid &electrolyte balance especially

Potassium

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#Safeguard against resp.#ttt of shock

#symptomatic ttt# Follow up this patient For fear of oesophageal stricture

Oxalic

1-Prevent further exposure .2-Emergency stabilization of the patient.

Here it is life saving to give this patient Calcium gluconate I.V.to prevent hypocalcemia

Also rapidly make patient orally drink calcium lactate water and /or milk to supply large amount

of calcium to inactivate Oxalate by forming an insoluble calcium oxalate in the stomach . lime

3-Proper clinical evaluation .4- Prevent further absorption

mentioned aboveGastric lavage is done with lime water (Ca hyhroxide)

5- Eliminate absorbed poison .Hemodialysis may be life saving as it prevents acute renal

failure &also help to correct hypocalcemia6- Antidotal therapy if available.

7- Supportive symptomatic Therapy.