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‫بسم الله توكلت على الله‬

‫بسم الله نبدأ‬
‫دعاء قبل المذاكرة الول‬
‫الحلقة الولى‬
Part 1
‫هنتكلم النهاردة عن الجينيرال‬
‫عايزاك تطلع من ال‬chapter ‫ده بالتي‬
Management of poisoning
‫لن هو الساس بعد كده لما نعمل‬ttt ‫ لي‬poison
‫والذي 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
#occupational toxicology (co ,cyanide gas) Remove from
#In homicide -keep under complete control in hospital

2-Emergency stabilization of the patient.

ABCDs resuscitation :
A ==== Airway
B ==== Breathing
C ==== Circulation
D ====drug induced C.N.S Depression

Airway ===A
Causes of obstruction ‫الحل‬
#Secretions===Suction of secretions
#Posterior displacement of the tongue===pull tongue
using tongue depressor or support jaw (head tilt chin left
#Foreign body e,g artificial teeth=== Remove FB
# Insert endotracheal tube (cuffed in comatosed
# Tracheostomy (not need definition)
B=== Breathing (Maintain respiration):
*Oxygen therapy ==Oronasal mask (Carbogen5%CO2
*Artificial respiration== Mechanical ventilation If too slow
respiration i.e no chest movement or paralysis of resp.

Artificial Resp.==Mouth to mouth Breathing (at a rate of
2 mouth breath then 15 compression on chest at a rate of
Till patient become well or you are exhausted.


Shock characterised by failure of the circulatory system to
maintain adequate perfusion of vital organs
Hypovolaemic shock==ttt Fluid replacement
Neurogenic shock ==ttt analgesic e.g. morphine
Hypotesive shock ==ttt vasopressor e.g dopamine

Signs of shock: cyanosis, hypotension.
What to do:
1.Elevate legs
2.Fluid replacement
3-cover with blankets
4-Vasopressor drugs

D==Drug induced C.N.S depression
Level of consciousness classified according
Qualitative ==change of level of consciousness
(lethargy ,stupor , coma)
Quantitative==change in cotent of consciousness
(confusion ,delirium ,psychosis)
Coma= unarousable unresponsiveness
Stupor=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) + + + -

Coma Cocktail 3 things
Naloxone ,Dextrose , Thiamine
Naloxone :
(0.4mg ampouls Narcan),2mg I.V =5ampouls
Very useful as there are synthetic & semisynthetic opiods
such as codeine ,propoxyphene for which naloxon is
administered in large dose to antagonize them effectively
D50W for adults , D25W for children
D=dextrose W=water
Thiamine(vit B1)
Dose 100mg I.V to all adult &Adolescent But not to
Value :
Prevent ppt of Wernick's encephalopathy in alcoholic

Seizures(convulsions )
#airway must be kept patent+O2
# Diazepam (valium)of choice
#in status epilepticus phenytoin or Phenobarbital

2-Proper clinical Evaluation
History, physical examination & laboratory tests are used
for proper clinical evaluation

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

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

Skin decontamination
1. 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)


GIT Decontamination
a) Emesis
b) Gastric lavage
c) Activated charcoal
d) Cathartics
e) Whole-Bowel irrigation
f ) Surgical decontamination
g) Local antidotes

Indications :
-Patient: alert (intact gag reflex).
-Time of ingestion: not more than 4-6 hours
-Poison: not adsorbed by activated charcoal.
- Sustained release or enteric-coated tablets or big lumps.

-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.
a) 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(‫ )ساق‬of ipecacuanha or
acminata plant
Principle alkaloid :Emetine ,Cephaline
Mechanism of induction of vomiting :
Act both central &peripheral central +ve CTZ ,peripheral
by irritation of gastric mucosa
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
When to stop epicac ?
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 lavage
Principle :
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 ingeastion
3- If delayed gastric emptying lavage useful for 12hrs
4- Considered only if patient ingested life threatening
amount of toxic substance within one hour of
presentation .

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 lavaging
2-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
1- The patient lies on his left side with head lower to Avoid
Aspiration &get good washing
2- 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 ]
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
** If in Trachea :
1- movement of Air is heared.
2- Patient shows sudden spasmodic cough &cyanosis
3- Bubbling occurs if the end of the tube is immersed in
*****if the tube is in stomach
Aspiration brings up gastric content
You ca leave Cathertic(‫)مسهلت‬,local antidote …etc
c)Activated charcoal
Is considered the best method of Gastric decontaimation
It is very effective Nonspecific adsorbent
Dose :
1g/kg BW
Generally 50-100g for adult
15-30g for children
+suitable amount of water (250 ml for adult )
+Vigorously shaken to form a slurry
‫لو في البيت ممكن يضرب في الخلط ليكون عجين رقيق‬
Administered orally or through nasogastric tube

What do you know about Multiple(serial) dose activated
Indications: In theophyllin overdose &if threatening
amount of Phenobarbital,Carbamazepine ,Quinine
,Dapsone or Aspirine is ingested.
Mechanism:It can enhance elimination of absorbed toxins
@Interruption of enterohepatic or enteroenteric circulation
e.g. theophylline ,Phenobarbital ,salicylates
b)Gastro intestinal dialysis whereby the drug back diffuse
from the higher serum levels ,through the intestinal villi&
into the lower intraluminal concentrations.


1- Presencce of diminished bowel sounds,ileus &bowel
2-Prior to endoscopy after corrosive ingestion
3-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
2) Saccharides :e.g.e.g. sorbitol (is the cathartic of
choice )
Ingestion of corrosive, sever diarrhea,ileus ,serious
electrolyte imbalance &bowel injury
e)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 tract
Method :
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
• 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

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

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  ‫مهم‬
e.g. tannic acid for= alkaloids e.g opium
Albumin water =mercury
Magnesium sulphate=Carbolic acid
Calcium hydroxide =oxalic acid

potassium permanganate solution =oxidize most
alkaloids e.g.Atropin
cupper sulphate =phosphorus
5- Reduction
e.g. sodium formaldhyde sulphoxylate = reduce mercuric
chloride to metallic mercury which is less soluble &thus
non absorbable.


(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

In 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

(1) Fluid overload
(2) Pulmonary oedema
(3) Cerebral oedema
(4) Acid base disturbance
(5) Electrolyte imbalance

(1)Plasma drug concentration
(2)Fluid balance
(3)Central venous pressure
(4)Electrolytes , Serum sodium, Potassium. calcium and

 Amphetamine .strechnine. Quinidine and
 500ML dextrose 5%+
 500ml saline 0.9%+
 75ml ammonium chloride 2% give over 6 hours

Salicylates phenobarbital and phenoxyacetate herbicide
500ml dextrose 5%+
500ml saline 0.9% +
500ml Na bicarbonate 1.26% over 3_4 hours

Only eliminate drugs or toxins which can pass easily
across the dialysis membrane
i.e characterized by
A) low molecular weight
B) high water solubility
C) small volume of distribution
(high plasma concentration)

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 failure
3)progressive clinical deterioration and presence of
complications such as aspiration pneumonia
4)prolonged coma with complications
5)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.

1) Presence of antidotes
3)Cardiogenic shock
4) Non dialyzable toxins

1) Hypotension
2) Electrolyte and Osmolar imbalance
3) Hypoxemia
4) Vascular access Complications
5) Spontaneous Bleeding
6) Infections
7) mechanical Complications
8)sever anaphylactic
9)sudden death fromMachine malfunction,
Electrocution& Coagulopathy

Blood is pumped through a cartridge of absorbent material
(activated charcoal or resins)
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
Similar to those for hem dialysis
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 cavity
1- Patients with acute renal failure
2- Patients with bleeding disorders
3- Patients with venous access problems
4- Hem dialysis is not available
5- Patients for whom hem dialysis and
hemoperfusion are contraindicated
Through a catheter inserted intraperitoneally , adialysate
fluid is instilled and 1-2 liters is exchanged each hours

1- Pain
2- Hemorrhage
3- Leakage
4- Inadequate drainage
5- Perforation of viscera
6- Bacterial peritonitis
7- Arrhythmias
8- Volume depletion or overload
9- Hyperglycemia and electrolyte disorders
10- Pneumonic and pleural effusion

5- Gut dialysis :-

(Serial activated charcoal)
Gut dialysis enhances elimination of the toxins that have
a) significant enterohepatic or enter enteric circulation
b) limited protein binding
c) small volume of distribution
6- Hyperbaric oxygen

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 Egypt
HBO 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 membrane
2- Acute sinusitis
3- Optic neuritis
4- Pneumonia thorax
5- Oxygen toxicity
6- Seizures
7- 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 Therapy
Chelating agents
Are organic compounds that react with heavy metal ions
to form firmly bound complexes (chelates)
We are going to study:

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 .

 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.

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 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.
 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
 Mercury poisoning responds poorly to ttt with Ca Na 2
EDETA in vitro because it doesn’t pass into areas of
 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 .

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 ,but
the iron of transferring is very minimally affected
 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 .

 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 DMSA
1- 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
5- Iron supplementation can be given concomitantly
with DMSA without any adverse effects ,while BAL –
Iron complex is a potent emetic
‫عايزين نطبق اللي خدناه‬

‫تعالو ناخد حاجة بسيطة الول‬
‫زي السبرين مثل‬
‫الخطوات بتاعتنا ايه؟‬


‫‪1-Prevent further exposure .‬‬

‫لو واحدة منتحرة مثل نحطها تحت الملحظة‬
‫لو غير كده نكتب الخطوة وجنبها شرطة علشان تعرف المصحح أنك‬
‫عارف الخطوات لن كل عنصر عليه درجة‬

‫‪2-Emergency stabilization of the patient.‬‬
‫‪ Safeguard against‬لو العيان صاحي خلص شرطة أو تقول‬

‫‪3-Proper clinical evaluation .‬‬
‫هيقولك شرب أسبوسيد مثل علشان ألوانه جذابة للطفال‬

‫‪4- Prevent further absorption‬‬
‫‪ Emesis,Gastric lavage‬هل ينفع أعمل‬
‫هل ينفع أستخدم فحم منشط‬
‫‪5- Eliminate absorbed poison .‬‬
‫هستعمل معاه أي نوع‬
‫معروف أن السبرين حمض إذن هستخدم قلوي‬
‫مل لثلثة محاليل ‪500‬‬
‫مل جلوكوز أو دكستروز ‪500‬‬
‫مل سلين ‪ .9‬في المائة ‪500‬‬
‫مل بيكربونات صوديوم ‪500‬‬

‫‪ ionizable ,prevent reabsorbtion‬وكلمتين عن‬
‫‪6- Antidotal therapy if available.‬‬
‫مفيش اذن شرطة‬

‫‪7-Supportive Therapy.‬‬

‫معروف أن السبرين بيرفع درجة الحرارة و بيزود الحموضة وممكن‬
‫إذن هعمله إيه‬
‫كمادات ميه ساقعة‬
‫مضادات الهستامين علشان الحساسية‬
‫ولو دخل في‬
‫‪Pulmonary edema‬‬
‫أديله أكسجين من‬
‫‪Endotracheal tube‬‬

‫تطبيق تاني‬
‫‪CO poisoning‬‬
‫الخطوات بتاعتنا ايه؟‬


‫‪1-Prevent further exposure.‬‬
‫لو أنت في قلب الحدث أول حاجة أنك تخرج المصاب من المكان لن‬
‫تركيز أول أكسيد الكربون بيكون أعلى في طبقات الجو السفلى‬

‫طب افرض مثل أن التعرض كان بكمية بسيطة والشخص جالك وقالك أنا‬
‫ي خلص طالما فايق أحطه تحت الملحظة‬
‫أغمى عل ّ‬

‫‪2-Emergency stabilization of the patient.‬‬
‫أهتم بالتنفس بتاعه‬
‫إفرض أنا لوحدي ومش معايا أنبوبة أكسجين ول حاجة أعمل إيه‬
‫‪ airway patent &prevet obstruction‬أشوف‬
‫وأعمل له تنفس صناعي لحاد ماتيجي عربية السعاف‬
‫طيب تصرفي إيه كطبيب في المستشفى‬
Endotracheal entubation& mechanical entillation
*100% oxygen
*hyperbaric oxygen
‫التنين مع بعض‬

3-Proper clinical evaluation .
‫من ال‬history
‫هيقول لك كان بيتدفى في يوم شتى ومقفل عليه‬
‫أو في جراش ومشغل بنزين و مقفل عليه مثل 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 برده‬
4- Prevent further absorption .
‫شرطة مفيش‬
5- Eliminate absorbed poison .
‫شرطة مفيش‬
6- Antidotal therapy if available.
‫شرطة مفيش‬

7- Supportive Therapy.
‫ممكن ايه‬
Warm patient with blankets
Blood transfusion

Part 2


General characters:
– ‫هنجيب العراض من فوق لتحت من أول الفم وبعدين الحنجرة والبلعوم‬
‫أمعاء‬- ‫مرئ –معدة‬

1- Immediate sever local destructive action
2- Immediate sever burning pain in mouth,osophagus
‫طب ليه مفيش ألم بعد المعدة‬
‫لن حصل‬
Pyloric spasm
3- Immediate sever vomiting except carbolic acid
Because 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 mucosa
4- Dehydration & circulatory collapse
Shock (Neurogenic ,Hypovolemic)
5- Diarrhea with Alkali Liquefaction of intestinal
mucosa while with acid there is pyloric spasm 
6- If inhaled there will be Laryngitis &Laryngeal edema
+swelling of tongue+hoarsnesss of voice
Dyspnea &choking is common

7- Pneumonitis ,Pulmonary edema


1-Prevent further exposure .
2-Emergency stabilization of the patient.
Keep patent airway patent+O2 ±tracheostomy
‫ علشان‬laryngeal obstruction by glottic edema
3-Proper clinical evaluation
4- Prevent further absorption .

Emesis ‫هو بيرجع أصل‬

• 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

Best antidote is milk :

• Dilute the corrosive Physical
• 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 مثل‬
Pulmonary edema ,shock

Cause of death
A-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
*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 الكالة‬
*‫أحماض غير عضوية حمض الكبريتيك والهيدروكلوريك والنيتريك‬
**‫أحماض عضوية كربوليك وأسيتيك وأوكزاليك‬
***‫القلويات صوديوم وبوتاسيوم هيدروكسيد والمبيضات‬
****‫أملح أكالة باريم كلوريد وأنتيموني تراي كلوريد‬

‫هنبدأ بالحماض‬
‫وأدي أول جدول‬
‫بس حضرتك اللي هتكتبه لن المنتدى ل يقبل الجداول‬
‫ خانات‬4 ‫هنعمل جدول‬
‫هنقارن بين الحماض الغير عضوية الكبريتيك والهيدروكلوريك والنيتريك‬
‫و خانة وجه المقارنة‬

‫أول حاجة هي ال‬
Fatal dose
H2SO44-5 ml. of commercial acid
Hcl15ml.of conc. acid
Nitric7ml of conc. acid
Fatal period
H2SO4can 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 perforation
Hclas above
Nitric as above
Colour of ishures
H2SO4Blackish Brown ‫متفحم‬
Hclpinkish Red
NitricYellow due to formation of xanthoproteins
Clinical picture
‫) هنكتب ف الثلثة )ممكن تكتب اللي فوق‬
Immediate sever burning pain
Immediate sever vomiting
Thirst &corrosion in lips

Constipation (Because Acid)
Cold Clammy skin
‫وهنزود في النيتريك‬
More volatile Irritate airway passage, Edema of glottis
Coughing, Dyspnea
Pulmonary complications as bronchitis ,bronchopneumonia
‫هنقول نفس الكلم فوق‬
‫بس 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
• Nutrient enemata can be used Surgical ttt graft
operation in oesophageal stricture

Post mortem
‫نفس الكلم ف الثلثة‬
• 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 التاني‬
‫الله المستعان‬
‫هنقارن بين‬
Carbolic &oxalic
‫الول كلمتين ع الفنيك قبل ما نقول الجدول‬
‫أهم حاجة واحنا بنذاكر ال‬
‫هي أنك تعرف‬
‫ال‬target organ
‫وتعرف ال‬
Mechanism of action
‫وأنت هتقول الباقي لوحدك‬
‫من اسمه هنطلع بيؤثر على ايه‬
‫ حرف‬cCNS
‫ حرف‬r renal
‫ حرف‬cCVS

Stimulation followed by depression
‫وعلشان نتفق بعد كده أي حاجة هتلقي فيها‬
Stimulation on CNS
Irritability, Restlessness, Anxiety
Agitation, Hallucinations, Convulsions

‫وأي حاجة فيها‬
Lethargy, Apathy, Somnolence, Confusion, Sleep, stupor,
‫وبالمرة هيكون سبب الوفاة‬
Circulatory collapse, Resp. Failure(RC depression)

‫لنها هتتكرر بعد كده كتير فمش كل شوية هنقعد نقول كلم مش شكل‬
‫)بعضه)زي ما بقول لك كده هنحط الكلمتين دول وهيطلعو صح‬
‫ على‬Renal
Direct toxic nephritis (Acute Glom.Nephritis)
Renal failure with oliguria or even anuria
Urine contain Blood &albumin cast, Turns Green on
Exposure to air due to formation of Hydroquinone
(oxidative product of phenol)

‫ على‬CVS
Myocardial depression
Ventricular arrhythmias, Rapid, weak, irregular pulse
Marked hypotension, Subnormal temperature

‫نرجع للمقارنة بتاعتنا‬
‫هنقارن من حيث‬
Fatal dose
Fatal period
Clinical picture
Post mortem picture

SourcePhenol is used as disinfectant ,insecticide &in
Some outpatient Pediatric surgery .
Phenique contains 2-5%phenol
It is also present in Cresol
NB It can be absorbed from intact skin

Sourcein Bleaches &metal cleaners &many plants
especially citrus fruit &rhubarb leaves

CarbolicFatal dose3-6 gm
OxalicFatal dose15-30gm

CarbolicFatal periodabout 4 hrs
OxalicFatal period15 min (fatal decalcification )
10 days (renal failure )
Action :
Local action ‫يشبه المواد الكاوية مع بعض اختلف‬
• 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 time
Remote action
Mentioned CNS, CVS, RENAL

Local action
1- Local corrosive action on alimentary tract
2- With production of gastroenteritis
Remote action
‫أول 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 picture
• Burning sensation in mouth,oesophagus ,stomach
followed by Tingling due to local anesthetic action
• No or scanty vomiting due to local anesthetic
• Ishures colour
Around mouth Brownish
At mouth & oesophagus Whitish
With characteristic aromatic odour
• ‫من الحاجات اللي بيؤثر عليها عندنا ايه‬
CNS at first anxiety then followed by coma with
‫الكلم اللي قولناه فوق‬
*Pupils constricted reactive
(N.B. in Morphine Poisoning pinpoint pupil Irreactive )
Large dose coma with unrecordable blood pressure
,Resp. arrest ,death
Delayed death from acute Renal failure

‫ حاجات‬3 ‫هنتكلم على‬
• 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
‫على العكس من باقي الحماض‬
• 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 depression
• Sublethal dose
Symptoms &signs are of hypocalcemia as
#Muscle twitches ,Ms cramps, tetany
#Cardiac arrhythemia, convulsions
#Shock, stupor, coma
Ca oxalate crystals are deposited in Bl.vessels
,Kidney ,liver heart ,lungs
Renal tubules Oliguria or even anuria Death from
Urine contain Ca oxalate crystals +blood +albumin

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 Decontamination
Emesis: Not contraindicated Because we said scanty
vomiting or no vomiting at all
Stomach wash: Is allowed No fear of perforation due to
coagulative necrosis wall is thick
Stomach wash is done using water then olive oil as it
dissolves phenol &prevent its absorption
After 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 coma
‫المقصود هنا مش الكوما كوكتيل اللي قولنا عليه‬
‫المقصود أن لو العيان ده فضل عندي في المستشفي مغمى عليه‬
Prolonged Coma
‫ فيه‬Measures ‫تانية‬
1- Maintenance of body temp. by blankets
2- Frequent change in patient's position with rubbing
skin with alcohol to avoid bedsores
3- Prophylactic antibiotic safe guard against
4- Regular catheterization for liability of retention of
5- Maintenencce of Fluid &electrolyte balance especially
#Safeguard against resp.
#ttt of shock
#symptomatic ttt
# Follow up this patient For fear of oesophageal stricture

1-Prevent further exposure .
2-Emergency stabilization of the patient.
Here it is life saving to give this patient Calcium
gluconate 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 above
Gastric 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 hypocalcemia
6- Antidotal therapy if available.
7- Supportive symptomatic Therapy.