Acute poisoning
Self poisoning is a very common and urgent medical problem.
It is most common medical emergency in pediatric hospital
It account for 10% of all emergency home visits and about
5-10% adult medical admission in developed countries
Classification of acute poisoning.
1.Accidental
2.Intentional
Accidental poisoning—increased more in children ,confused
Elderly more in female. Frequent drugs used .Substances
include ,Home used substances like paraffin , detergent .Inhal
ed gas organic solvent glue and cleaning fluid, carbon
monoxide from incomplete combustion. Arthropod bite, scorpia
-n ,spider ,tick .poisonous fish
Intentional poisoning—Self-destruction-Suicide and parasuicid
Substances used in self intention poisoning
Drugs as they are well available ,previously substances like
Barbiturate.psychotropic drugs . The most common drugs now
Include antidepressant sedative drugs , paracetomol and aspirin
Combination of drugs constitute 60% of the cases
Diagnosis of acute poisoning
Informative service
History from patient relative ,friends
Note –In age group 15-40 years acute poisoning is most
Common cause of unconsciousness in absence of head injury
Clinical features
Main points in examination include:
1.Conscious state
2.Pupil size ,Reaction to light
3.Vital signs
4.Skin condition, dryness ,red color, pink color
5.Abnormal smell
6.examination of mouth and mucous membrane
EXAMPLES
1.pinpoint pupil ,vomiting and depressed respiration
may raise possible of Morphine overdose
2.Rapid change of conscious level ,arrest respiration may
raise possible dextropropoxyphane poisoning
3.Wide dilated pupil , bladder distention , absent bowel
sound, cardiac arrhythmias may point to tricyclic
Poisoning
4.Sweating, tinnitus ,deafness and hyperventilation may
indicate salicylate poisoning
Identification of the poison
Methods use for medico legal purpose
Code number ,appearance of drug
Chromatography can diagnose up to 90%
Confirmatory and quantitatively by gas
Chromatography and mass spectrometry
General therapeutic methods
Note; Treatment should not delayed by spending time in
attempt to identified precisely the poison involved
Note .;The main concern should be directed for;
1.Maintainance of respiration and circulation
2.Removal and inactivation of poison
Maintenance of Respiration
1.Clear airway
2.Cuff endotracheal tube
3.Transport and nurse in semi prone position
4.If depress respiration may need artificial
Respiration
5.Mechaical ventilation
6.possible use of antibiotic
Maintenance of circulation
1.Managment of arrhythmias
2.Oxygen for hypoxia
3.Cardiac resuscitation
Removal and inactivation of the poison
1.In gas poison patient should put in fresh air
2.Patient cloths should be removed if poison has
Cutanious absorption
3.When the patient is conscious and swallow the poison
Used activated charcoal
4.Emesis ,Gastric aspiration and lavage depend on
A-Level of consciousness
B-Nature of poison , contraindicate in kerosene
C-Time since ingestion it is usually up to 4 hour
extend to12 for Tricyclic and 24 for salicylate
Methods to increase poison elimination include
Forced alkaline diuresis
Peritoneal dialysis
Haemodialysis
Hem perfusion in which heparinized blood
From the patient is passed through column
Containing charcoal coated with synthetic acrylic hydro gel or
alternatively ion exchange
Resin use in barbiturate poison
Other methods
Antidotes
Examples
Cobalt edetate for Cyanide poison
Desferoxamine for iron poison
N acetyl cystine for paracetamol poison
Correction of ;
Hypothermia by rewarming
Metabolic acidosis
Epilepsy
Fluid and electrolyte disturbances
PSYCHATRIC ANALYSIS
This is important part after correction and stabilized
Patient condition
EXAMPLES OF IMPORTANT AND COMMON POISON
PARACETAMOL POISONING
The early symptoms are non
specific and include nausea,
Vomiting . After 36 hours toxic effect appears when
Blood level exceed 200 micro gram per cc in first 4 hour
More serious effects include hypotension ,hypothermia,
Metabolic acidosis .hypoglycemia .bleeding tendency
and delirium . The main danger effect is liver failure
may occur days after ingestion and cause death
Mechanism of toxicity
Liver glutathione stores become depleted so that the liver
Is unable to deactivate the toxic metabolite. Renal damage
Properly result from a mechanism similar to that which is
responsible for hepatotoxicity
Management
1.General measures
2. In moderate to sever poison ( when ingestion of 20 tablets )
10 gm . The damage can be prevented if within 12 hours
From ingestion by giving N acetyl cysteine 150 mg per kg
In 200cc 5% glucose over 15min fellow by 50mg per kg
In 500cc 5% glucose in 4, 8, and8 hours and usually 300
Mg per kg in 20 hours. Methionine in oral dose of 2.5 g
Followed by three similar doses every 4 hours if
unable to give N-acetylcysteine
3.iv glucose to manage hypoglycemia
4.Measure PT
5.Hemodialysis for renal failure
6.Liver transplantation is indicated in sever fulminanant liver
failure
TRICYCLIC ANTIDEPRESSANTS TOXICITY
Mechanism of action
Tricyclic antidepressants block the reuptake of nor
epinephrine into peripheral and intracerebral neurons ,thereby
increasing the concentration of monoamines in these areas.
These drugs also have antimuscarinic actions and class1
antiarrhythmic activity
Clinical features
Usually appear 1 hour after ingestion .Drowsiness, sinus
tachycardia, dry mouth , dilated pupils, urinary retention
increased reflexes ,and extensor plantar responses are the
most common features of mild poisoning .Sever toxicity
leads to coma often with divergent strabismus and fit
plantar, oculocephalic and oculovestibular reflexes may be
temporary abolished. An ECG often show wide QRS
Interval .Metabolic acidosis and respiratory depression
Occur in sever condition .
Management
Majority improve with supportive therapy
Small percent may need mechanical ventilator in 1st 24-48
hours ,.supraventicular and ventricular tachycardia should
be treated with sodium bicarbonate 8.4% 50 cc iv over 2
minutes ,even if there is no acidosis. In addition good
oxygenation , correction of acidosis and control of fits
Should undertaken
CARBON MONOOXIDE POISONING
The source is usually improperly maintained and poorly
Ventilated heating system. The affinity of HB to CO is
240 times than O2. CO with HB form Carboxyhemoglobin
So reducing oxygen-carrying capacity of the blood and
Cause tissue hypoxia . In addition CO inhibit cytochrome
oxidase
Clinical features
In 10% concentration of COHB , the symptom may be
mistaken as viral infection . In concentration of 10-30%
symptoms include headache and dyspnea ,In COHB
concentration > 30% coma and convulsions occur. Skin
color changes to pink.
Management
1.Removal of the patient to fresh air
2.High flow rate O2
3.Endotracheal intubation and mechanical ventilation
in patient who had coma
4.Hyperbaric O2 used in coma patient and if COHB
Concentration>40% or pregnant with >20%
ASPIRIN POISONING
Young children are more susptable to toxic effect
than adult. Many children may present with coma
50mg per100cc blood concentration indicates
Moderate to sever aspirin toxicity .Tinnitus ,deaf
-ness and blurred of vision , restlessness and sweating
may herald more specific and serious manifestation
Hyperventilation related to metabolic acidosis with
Increase in basal metabolic rate .This follow by respi
-ratory alkalosis, sever dehydration and hypokalamia
which herald cardiac arrest.
Management
1.General measures
2.Gastric lavage is feasible for 24 hours
3.Forced alkaline diuresis
{2 liters of fluid per hour for 3 hours}
A. 0.5 lit normal saline
B.1 lit glucose water 5%
C. 0.5 lit NaHCO3 1.26%
D .KCL
3gm
4.If forced alkaline diuresis is not feasible because
of renal or cardiac arrest then peritoneal or
Hemodialysis is indicated
5.Hemodialysis is treatment of choice in sever toxicity
When blood level more than 700mg per lit
ORGANOPHOSPHORUS COMPOUNDS TOXICITY
Used as insecticide ,pesticide in agriculture field
Presentation related to cholinergic effect and include
Sweating, increased salivation , nausea vomiting
Twitching convulsion ,,bronchospasm and pulmonary
edema
Management
1. Removal of patient cloths and wash with water
2.General measures
3.Atropin sulphate in dose of 3 mg per kg till dilated pupil
And full atropinization
4.Specific antidote Pradioxime 30mgperkg iv not exceed
300mg then 8mg per kg over hour infusion
BENZODIAZEPAM TOXICITY
Presentation includes drowsiness dizziness hypotension
And respiratory derangement and depression may all occur
But toxic effect usually extremely mild. Treatment is
Usually supportive and general measures is sufficient
flumazenil 0.5 mg i.v. should be administered in an
adult and this dose may be repeated if necessary
CYANIDE POISONING
Cyanide and its derivatives are used widely in industry
Cyanide reversibly inhibits cytochrome oxidase so
Cellular respiration ceases
Presentation --Symptoms within seconds and death
Within minutes when exposed to gas while ingestion
May take 1 hour for presentation. Initial symptom s
are non specific and include a feeling of
Constriction in the chest and dyspnea ,coma ,convulsion
and metabolic acidosis , pink skin, hypoventilation
Treatment
1.O2 and general measures
2.Dicobalt edetate 300mg iv may be repeated
Alternatively hydroxycobalamine 5g i.v
Other method is to give sodium nitrite 300mg iv
And sodium thiosulphate 12.5 g i.v
BARBITURATE POISONING
Absorption is unpredicted but drowsiness and coma
develops rapidly . The coma depends on the type of
barbiturate , the dose and tolerance . Change of pupil
and reflexes vary .Withdrawal features such as restlessness
insomnia ,delirium and convulsion may occur .Ventilary
depression and hypotension is common. Bullous skin lesion
develops in 6% especially in short chain type
Management
1.General measures
2.Hemodialysis
3. Charcoal hem perfusion for short chain barbiturate
LEAD POISONING
Occur with lead level more than 600micro g per l
Common in children with accidental pica intake .
The features include abdominal pain .vomiting
Constipation encephalopathy , seizures delirium and
Coma . Encephalopathy more common in children than
Adult .Renal effect of reversible tubular dysfunction
Food drop due to peripheral neuropathy. Blood film
Shows sideroblastic anemia , hemolysis and punctuate
basophilia
Management
Use of chelating agent like SODIUM CALICUM
EDETATE 75mg per kg per day for 5 days which
is more effective in children than adult . other like
DMSA DIMERCAPTO SUCCNIC ACID but not
improve the neuropsychiatric manifestation and may
lead to zinc depletion
CORRESIVE POISONING
Stain, burn of lips , mouth buccal cavity sever abdominal
Pain, and shock
Management
1.General measures NO gastric lavage
2. Give alkaline or acid according to corrosive
3.Fluid s and sedation
IRON SALT TOXICITY
Clinical features
include epigastric pain , nausea vomiting
hematamesis, tachycardia tachypnea , melena acute circulatory
failure and if survive may develop hepatic or renal failure
Management
1 Desferoxamine iv infusion in dextrose not exceed 15mgperkg
2. 100 cc NAHCO3 5% through nasogastric tube
MUSHROM TOXICITY
Some toxic mushroom may cause serious poison , it is heat
Liable toxin with parasympathic over activity . Symptoms
Include gastro intestinal symptoms and hallucination
And excitation
Management – if no neurological problem then atropine 0.6-2
Mg atropine can be used and if neurological and excitation
then use of sedation with chlorpromazine injection
DIGOXIN TOXICITY
Occurring during chronic administration is common though
acute poisoning is infrequent.
Clinical features
These include nausea , vomiting , dizziness anorexia and
drowsiness .Rarely confusion ,visual disturbances and
hallucination occur .Sinus bradycardia is usually marked and
followed by supra ventricular tachy cardia with or without
block ,ventricular premature beats and ventricular tachycardia
Hyperkalamia occur owing to inhibition of NA-K ATPase
treatment
1.managment of arrhythmias
For bradycardia and block use atropine
For tachyarrhythmia use pheytoin
2. Specific antidote digoxin specific antibody fragment
6-8mg per kg should be administered
METHNOL POISONING
Used widely as solvent or antifreeze solutions metabolized
To formaldehyde and formate later cause metabolic acidosis
Clinical features
Drowsiness , blurred vision and decrease visual acuity
Then coma with dilated pupil unreactive to light and
Sever metabolic acidosis with hyperglycemia with
Elevated serum amylase If methanol concentration of
500mgper L confirm serious poisoning. Mortality is
Correlated with severity and duration of metabolic
Acidosis. Survivors show permanent blindness and
Parkinsonian –like sign
Management
1.Correction of metabolic acidosis
2.Ethanol administration
3.Hemodialysis to remove methanol and formate
4. Folic acid 30 mg I.v. protect against ocular toxicity
THEOPHYLLINE TOXICITY
Clinical features
Nausea ,vomiting, hyperventilation, hematamesis abdominal
Pain, diarrhea ,sinus tachycardia , supraventricular and
Ventricular arrhythmia ,hypotension, restlessness ,irritability
Headache ,hyperreflexia tremors and convulsions have been
Observed , Hyperkalamia ..Most patients have plasma level
In excess of 25 mg per l
Management
1.ondansetron 8 mg i.v. to suppress vomiting
2.charcoal to enhanced elimination of theophylline
3. correction of hypokalamia
4, Non selective beta adrenoceptor blocker
5.Diazepam 10-30 mg iv to treat convulsion
KEROSENE POISONING
Accidental poison in children especially in summer time
Clinical features
Include abdominal pain nausea , vomiting constipation
Cough , aspiration chemical pneumonitis with fever which
May be of high grade associate with shortness of breath
Management
1.Gastric lavage is contraindicated as it increases chance
For aspiration pneumonia
.2.Support patient and correct fluid and electrolyte imbalance
3.Liquid paraffin may help to open bowel
4.Treatment of aspiration pneumonia
INSECT BITES
Patients should observed for 2 hours for any signs of evolved
Urticaria , pruritus .,bronchospasm or oropharygeal edema
Treatment
1. treatment of anaphylaxis
2.prophylactic immune therapy
SCORPIONS STINGS
Scorpion venom stimulate release of acetylcholine and
catecholamine causing both adrenergic and cholinergic
symptoms
Clinical features
Sever pain at site of puncture then swelling . The systemic
symptoms include vomiting ,sweating, diarrhea , abdominal
colic, and in sever cases depend on species shock respiratory
and pulmonary edema may develop.
Management
1. Local infiltrate with anesthesia
2.Use specific anti venom if available
SPIDER BITE
The black widow spider{Lacrodectus mactans} is found in
North America and in tropic and some times in Middle East
Clinical features
The bite is painful . patient feels generalized muscle pain
sweating, headache and shock
Management
Specific anti venom should be given if available
VENOMOUS SNAKES
About 15% out of 3000 species are dangerous to human
Being, There are 3 main groups of danger snake
1.Viperidae with 2 subgroups. ,Viperinae-European adders and
Russell s vipers and Crotalinae-American rattlesnake
lanceheade vipers and Asian pit viper
2.Elapidae cobra ,,mambas, ,kraits. .coral snake
3.Hydropidae Sea snake
Clinical features
In viperidae
local tissue necrosis ,,evidence of systemic
involvement occur within 30 minutes including vomiting, shock
hypotension hemorrhages due to DIC
In Elapidae There is usually NO swelling at the site except
cobra in whom there is local tissue necrosis, Vomiting which
is followed by shock and neurological paralysis muscle
weakness ,,respiratory muscle paralysis
In Hydrophidae myalgia and myoglobinuria which lead to
Renal failure ..cardiac and respiratory paralysis .
Management
1.;Local measures bandage pressure ,,clean area ,antibiotic
If there is necrosis .NO arterial pressure NO incision ,skin
Grafting may be needed later . The type of snake should be
identified
2.General measures
which include iv fluid ,diazepam and
treatment for cardiac respiratory and renal failure
3. Antivenom use with much care and allergic reaction need
adrenalin {1 in 1000 solution} in sever cases
Antivenom is given with s c adrenalin
4.Neostigmin and atropine use in some form of neurotoxicity
HYPOTHERMIA
Core body temperature<35 may pass unnoticed because classic
Thermometer may not detected it. .Temperature is controlled by
Preoptic hypothalamus. Skin is key organ for heat exchange
Which depend on blood flow and environment ..Shivering can
increase body temperature 8 folds . At T 20 there is 50%
reduction in BMR this cause hypotension and irritability of
Myocardium with atrial fibrillation and in more sever condition
Ventricular fibrillation may occur .J wave is specific wave and
seen follow QRS complex ..Decrease respiratory rate and
cerebral blood flow decreases about 6% for every 1degree
drop in temperature .At the same time oxy hemoglobin
Shift to left. Lactic acidosis occurs and there is leucopenia and
Thrombocytopenia due to collection of these cells in the organs.
Pancreatic necrosis that cause elevation of amylase and
renal failure may take place
Causes of hypothermia
1.Envormintal
2. Metabolic disorders
Hypothyroidism
Hypopituitrism
Hypoglycemia
3. Neurological disorders
Hypothalamic disorders
Wernick encelopathy
Brain tumor
Head trauma
4.Dermatological disorders
Burn
Erythroderma
5.Drugs
Ethanol
Barbiturate
Phenothiazine
Anasthetic agents
6.Sepsis
7.Miscellenous
Anorexia nervosa
Malnutrition
Uremia
‫ا‬Sever liver disease
Shock
Acidosis
Management
Once diagnosed direction should be to know the cause. More
with invasive approach ,especially when more cardiovascular
problems develop. Peritoneal dialysis cardiovascular bypass
with extracorporeal warming and irrigation of medistanium
with warm normal saline have all used with good results
The choice of either active or pass rewarming depends on the
Condition of the patient ..The patient able to shiver or not .
If the patient is shivering bands able to generate heat ,,he may
be a candidate for passive rewarming provided that hypothermia
is not extreme and thermoregulation is still active .Passive
Rewarming include
1.Rewarm gradually with spaced blanket or iv normal saline
2.Correct metabolic abnormalities
3.Anticipate and correct arrhythmias
4,Search and treat hypothyroid
FROSTBITE
When the extremities exposed to cold it becomes pale ,grayish
And initially it will be felt as doughy ,,later it freeze hard when
look like meat out of freeze . When temp -5 sensation will be
Lost. Possible necrosis and blistering occurs .Treatment by
rapidly rewarming the whole body with good insulation and hot
drink and by warming the affected part in water with
temperature 40 degree
Acclimatization to heat and heat injury
In cool climate heat production in the body is balanced by loss
from the surface chiefly by radiation and conviction .When
atmospheric temperature is above that of the body.. Evaporation
of the sweat is all important in maintenance of a stable body
temperature
. Acclimatization to heat is an essential
preparation for workers exposed to excessive heat in certain
industries and people who are going to work in tropic{excersis
in hot climate for 10-14 days}Acclimatization will cause;
1.Expand vascular bed
2.increase circulatory volume
3.Decrea se pulse rate
4.Increase cardiac out put
5 .Decrease salt excretion in urine and sweat
6. Sweat glands become more active and respond to elevation
of body temperature ,provided person good intake of salt and
water
Heat syncope –occurs when the person who is not well
Acclimatized to heat is doing unusual exercise or heavy clothes
Or stand for long time.
Sunburn -- This is occurs when person expose to ultraviolet
light.. fair, ,red hair ,green eyes people more susptable to burn
If short period exposure lead to erythema and itching ,pain,
edema and even bullae .Prolong exposure lead to symptoms
Like malaise . headache , nausea ,prostration and acute
circulatory failure if large area of skin affected this may
Interfere with sweating and lead to heat hyperpyrexia
HEAT HYPERPYREXIA
This occurs when person expose for long time to high degree of
temperature unacclimitized ,peoples are more suspitable but
still even acclimatized person when exposed for long period.
This condition is associated with cessation of sweating with
rectal temperature 42-43 ,other co factors include unsuitable
clothes poor ventilation old age , congenital absence of sweat
glands .cystic fibrosis and skin disorders
CNS pathological changes include
1.Congestion of brain
2. Increase CSF pressure
Complication s
1.acute circulatory failure
2.hypokalamia
3.acute renal failure
4.hepatic failure
5.Hemorrhage
Clinical features Usually no warning . the patient look dry and
hot loss of consciousness or signs of CNS irritation
Management
1.Remove clothes and move to shade
2.Fan with water temperature 15 degree
3Stop cooling when rectal temperature fall to 39
4.correct hypokalamia
5.Control hemorrhage circulatory failure .renal failure
6. Give antimalarial drugs in endemic area
SOLAR KERATOSIS
If person stay for long time in hot climate this leads to atrophic
Skin changes
that end with hyperkeratosis which is a
premalignant condition . Treatment include use of 5% fluorinate
cream for a week
PRICKLY HEAT
When person exposes to humidity environment sweat ducts
block within prickly layer of the skin so the sweat escapes to the
epidermis causes irritation to skin producing papule and
Then pustule with sterile pus. Management include reduce sweat
To the miniminal and over come the block of sweat gland by
Cool place and calamine lotion . The obese person should
reduce their weight.
HIGH ALTITUDE ACCLIMITIZATION AND
DETERIORATION
O2 atmospheric pressure decrease with altitude Physiological
acclimatization start at 7000ft and most people feel the need of
acclimatization 12000ft. Pulmonary ventilation and perfusion
increase . Plasma volume decreases and renal excretion of
HCO3 increases. These with other changes try to maintain
arterial O2 tension normal till RBC production raise HB . Above
14000 ft PR increase and CO increase with pulmonary
hypertension
Young people acclimatized best than old
.Lack of
acclimatization show by increase in RR CHYNE STOCK
respiration .,mild headache and irritability ,easy fatiqubilty and
sleeplessness . Exercise may induce lactic acidosis Prolong
residency in high altitude cause anorexia . weight loss decrease
mental and physiological capacity and suspitabilty to infection
.
ACUTE MOUNTAIN SICKNESS
To high and to rapid ascend causes headache nausea and
vomiting followed by lassitude muscle weakness and
breathlessness dizziness rapid pulse insomnia retinal
hemorrhage may occur The symptoms may be related to
intracellular edema which may herald the onset of 2 sever fatal
complications 1. P edema 2. Cerebral edema
These complications are prevented by ascending gradually and
By use of acetozolamide which induce metabolic acidosis and
increase derive of ventilation . Management is to descend
rapidly and give O2 treatment of P edema by frusamide 40-120
.morphine 15mg . If patient develops cerebral edema use of
dexamethasone . VENOUS THROMBOSTIS MANAGE by
Good hydration
CHRONIC MOUNTAIN SICKNESS
Occur due to alveolar hypoventilation and chronic hypoxia
May affect high Lander .This may cause cyanosis cardiac failure
Pulmonary hypertension with neuropsychiatric symptoms
treatment is to take patient to sea level