TOXICITY FOR

ASPIRIN AND OTHER SALICYLATES

CARBON MONOXIDE
THEOPHYLLINE

EDITED
BY MR MOMPATI LETSWELETSE
(CPhT) SECOND YEAR STUDENT

ASPIRIN AND OTHER

SALICYLATES

MECHANISM OF TOXICITY
Salicylates impair cellular respiration by
uncoupling oxidative phosphorylation.
They stimulate respiratory centers in the
medulla, causing primary respiratory
alkalosis.
Salicylates simultaneously and
independently cause primary metabolic
acidosis
Salicylates alter platelet function and may
also prolong the prothrombin time.

SIGNS AND SYMPTOMS

Altered mental status (coma)
Sweating
Because fluid overload can result in pulmonary
edema,
Increased vital signs (HTN, inc RR, inc T)
hyperventilation resulting from direct respiratory
center stimulation
Irritable
Seriousdehydrationmayoccurfromhyperventilation,
vomiting,andfever.

DIAGNOSIS
Serum salicylate level
Every 2-4 hours until clearly decreasing
Then q 4-6 until <30 mg/dL

Bedside tests
Trinders reagent 10% ferric chloride
Ames phenistix

chest x-ray
prothrombin time
serum creatinine

MECHANISM OF TOXICITY
There is no specific antidote for
salicylates
Sodium bicarbonate is often used to
increase the excretion of the
Salicylates .Treat metabolic acidosis
with intravenous sodium bicarbonate
Activated charcoal
Hemodialysis if severe

MECHANISM OF TOXICITY
Drugs which are weak acids (e.g. salicylates) exist in a
state of equilibrium between their ionised and unionised form
By increasing the systemic pH with sodium
bicarbonate more of the salicylate is trapped in its
ionized form in the extra-cellular fluid resulting in
enhanced renal excretion.
Therefore sodium bicarbonate should be
administered to correct any acidosis
(arterial pH should not rise above 7.6) and
to alkalinise the urine (optimum pH 7.5-8.5)

SAFETY PROFILE
It is very difficult to produce an alkaline pH if
the patient is hypokalaemic as hydrogen ions
tend to be excreted with the bicarbonate
instead of potassium. Therefore the potassium
should be kept at the upper end of normal

CARBON MONOXIDE

Carbon monoxide (CO) is a

deadly, colorless, odorless,
poisonous gas. It is
produced by the incomplete
burning of various fuels,
including coal, wood,
charcoal, oil, kerosene,
propane, and natural gas.

MECHANISM OF TOXICITY
CO combines with oxygen binding sites on
hemoglobin
CO has higher affinity for hemoglobin than
Oxygen.
It forms carboxyhemoglobin
(Carboxyhemoglobin is a stable complex of carbon
monoxide and hemoglobin that forms in red blood cells
upon contact with carbon monoxide. Large quantities
of CO hinders the ability of Hb to deliver oxygen to the
body. which cannot transport oxygen). Thus

decreasing the transfer of oxygen to tissues.

MOT Cont
second mechanism -CO also has a high
affinity for myoglobin(a red protein
containing haem, which carries and stores
oxygen in muscle cells) and effects on the
mitocondrial A respiratory enzyme chain
which is responsible for effective tissue
utilization of oxygen. After acute CO
poisoning the organs most sensitive to
hypoxia(deficiency in the amount of oxygen
reaching the tissues.) will be most affected;
i.e. the brain and the heart

SIGNS AND SYMPTOMS

Mental confusion
Shortness of breath due to oxygen depletion
Loss of muscular coordination due to low
energy
Loss of consciousness
Coma
Shock
respiratory failure
Ultimately death

DIAGNOSIS
Obtain history of potential CO exposure
e.g. being exposed to a residential fire
Measuring the levels of CO in the blood by
measuring the amount of carboxyhemoglobin
compared to the amount of hemoglobin in the
blood. A CO-oximeter is used determine
carboxyhemoglobin levels.
Measuring the concentration of CO in exhaled
sample(ppm) by using a device called Breath
CO monitor., the CO concentration correlates
with the levels of carboxyhemoglobin.

TREATMENT/ANTIDOTE
Administration of 100% oxygen.
Provide 100% oxygen by tightfitting mask or via endotracheal
tube
Oxygen increases the removal of CO
from hemoglobin in turn providing
the body with normal levels of
oxygen.

SAFETY PROFILE(ANTIDOTE)
Oxygen is a flammable gas therefore
should be handled accordingly.
Keep backup tanks on hand.
Secure extra tubing and cords so that
you don't trip over them

THEOPHYLLINE

MECHANISM OF TOXICITY
is an antagonist of adenosine
receptors, and it inhibits
phosphodiesterase at high levels,
increasing intracellular cyclic
adenosine monophosphate (cAMP)

SIGNS AND SYMPTOMS

cardiotoxicity:
cardiac dysrhythmias, supraventricular
tachycardia, atrial fibrillation and flutter,
ventricular tachycardia, refractory
hypotension.
metabolic abnormalities:
hypokalaemia (severe, refractory),
hypophosphataemia, hypomagnaesemia,
hyperglycaemia, metabolic acidosis
(lactate), respiratory alkalosis.

DIAGNOSIS
Serum theophylline levels are
essential for diagnosis and
determination of emergency
treatment
electrolytes, glucose, BUN,
creatinine, hepatic function tests,
and ECG monitoring.

antidote
ACTIVATED CHARCOAL

MECHANISM OF ACTION
It binds to the poison to prevent stomach and
intestinal absorption. Binding is reversible so a
cathartic such as sorbitol may be added as well.
It is important to aggresively control nausea and
vomiting in order to perform MDAC treatment. It is
also important that the patient is able to protect
his/her airway in order to prevent aspiration of
activated charcoal which can be detrimental.
Haemoperfusion is effective in theophylline
overdose, and is the elimination procedure of choice

 Haemoperfusion is effective in
theophylline overdose,
and is the elimination procedure of
choice

SAFETY PROFILE
Activated charcoal is safe for most adults
when used short-term. Side effects of
activated charcoal include constipation
and black stools. Most serious, but rare
side effects are a slowing or blockage of
the intestinal tract, regurgitation into the
lungs, and dehydration.