Clinical Toxicology

CLINICAL STRATEGY FOR TREATMENT

OF THE POISONED PATIENT
The following general steps represent important components
of the initial clinical encounter with a poisoned patient:
1. Stabilization of the patient
2. Clinical evaluation (history, physical , laboratory, and
radiology)
3. Prevention of further toxin absorption
4. Enhancement of toxin elimination
5. Administration of antidote (if available)
6. Supportive care and clinical follow-up

Clinical Stabilization
1- to stabilize the patient.:
-Assessment of the patients airway (ability to move air into and
out of the lungs),
- breathing (the presence of spontaneous respirations), and
- circulation (adequate blood pressure and perfusion of vital
organs)
In critically ill patients, sometimes treatment interventions must be
initiated before a patient is truly stable.
Clinical History in the Poisoned Patient
substance the patient was exposed to and the extent and timing
of exposure.
sometimes not available because either the patient is
unresponsive and unable to provide the history or the history
provided is unreliable.

additional resources sometimes employed to obtain an

informative clinical history include:
interviewing family members,
emergency medical technicians who were at the scene,
a pharmacist who can sometimes provide a listing of
prescriptions recently filled, or
an employer who can provide a list of chemicals found in
the work environment for an occupational exposure.

Taking an accurate history in the poisoned patient can be

challenging and in some cases unsuccessful:
In this setting, the treatment proceeds empirically
as an unknown ingestion poisoning.

 Physical Examination

Categorization of the patients

presentation into toxic syndromes
allows for the initiation of rational
treatment based on the most likely
category of toxin responsible, even if
the exact nature of the toxin is
unknown

Generally Physical examination should include

Vital signs
Evaluation of specific parts of the body

Laboratory Evaluation
Because of the limited clinical availability of diagnostic
laboratory tests or poisons, toxicologists utilize specific,
routinely obtained clinical laboratory data
especially the anion gap and the osmol gapto
determine what poisons may have been ingested
The anion gap is calculated as the difference between the
serum Na ion concentration and the sum of the serum Cl
and HCO3 ion concentrations.
A normal anion gap is < 12. When there is laboratory
evidence of metabolic acidosis,

the osmol gap is calculated as the numerical difference between

the measured serum osmolality and the serum osmolality
calculated from the cl inical chemistry measurements o the serum
sodium ion, glucose, and blood urea nitrogen (BUN)
concentrations. The normal osmol gap is < 10 mOsm.

determinations must be interpreted

cautiously in certain clinical settings

Radiographic Examination
The use of clinical radiographs to visualize drug overdose or poison ingestions
is relatively limited due to lack of radiopacity.
Generally, plain radiographs can detect a significant amount of ingested oral
medication containing ferrous or potassium salts. In addition, certain
formulations that have an enteric coating or certain types o sustained release
products are radiopaque as well .
The most useful radiographs ordered in a case of overdose or poisoning
include the chest and abdominal radiographs
and the computed tomography (CT ) study of the head.
The abdominal radiograph has been used to detect recent lead paint
ingestion in children, and ingestion of halogenated hydrocarbons, such as
carbon tetrachloride or chloroform, that may be visualized as a radiopaque
liquid in the gut lumen.

Prevention o Further Poison Absorption

The our primary methods to prevent continued absorption
of an oral poison are:
induction of emesis with syrup of ipecac(cardio- and neurotoxicity )
gastric lavage,
oral administration of activated charcoal , and
whole bowel irrigation(very imited )

Enhancement of Poison Elimination

The primary methods employed for this use today
include alkalinization of the urine, hemodialysis,
hemoperfusion, hemofiltration, plasma exchange or
exchange transfusion, and serial oral activated
charcoal .

The dialysis technique, either

peritoneal dialysis or hemodia
lysis, relies on passage of the toxic
agent through a semipermeable
dialysis membrane so that it can
subsequent y be removed.

Hemodialysis incorporates a blood

pump to pass blood next to a dialysis
membrane, which allows agents
permeable to the membrane to pass
through and reach equilibrium.
Some drugs are bound to plasma
proteins and so cannot pass through
the dialysis membrane; others are
distributed mainly to the tissues and
so are not concentrated in the blood,
making dialysis impractical .

Hemoperfusion is similar to hemodialysis except there is no dialysis

membrane or dialysate involved in
the procedure. The patients blood is pumped through a perfusion
cartridge, where it is in direct contact with adsorptive
material (usually activated charcoal ).
Protein binding does not significantly interfere with removal by
hemoperfusion. Because of the more direct contact of the patients
blood with the adsorptive material ,
the medical risks of this procedure include thrombocytopenia,
hypocalcemia, and leukopenia.
Hemofiltration, the patients blood is delivered through hollow fiber
tubes and an ultra filtrate of plasma is removed by hydrostatic
pressure from the blood side of the membrane.
The perfusion pressure or the technique is generated either by the
patients blood pressure ( or arteriovenous hemofiltration) or by a
blood pump ( or venovenous hemofiltration).
Needed fluid and electrolytes removed in the ultrafiltrate are replaced
intravenously with sterile solutions.

The use of either plasma exchange or exchange

transfusions has been relatively limited in the field of
clinical toxicology.
risks and complications (allergic-type reactions,
infectious complications, and hypotension).
Exchange transfusion involves replacement of a
patients blood volume with donor blood.

Use of Antidotes in Poisoning

A relatively small number of specific antidotes are available or clinical use in
the treatment of poisoning
The mechanism of action of various antidotes is quite different:
For example, a chelating agent or Fab fragments specific to digoxin will
work by physically binding the toxin, preventing the toxin from exerting a
deleterious effect in vivo, and, in some cases, facilitating body clearance
for the toxin.
Other antidotes pharmacologically antagonize the effects of the toxin:
Atropine, an antimuscarinic, anticholinergic agent (organophosphate
insecticides that produce lethal cholinergic, muscarinic effects).
Certain agents exert their antidote effects by chemically reacting with
biologic systems to increase detoxifying capacity for the toxin: sodium
nitrite is given to patients poisoned with cyanide to cause formation of
methemoglobin, which serves as an alternative binding site for the
cyanide ion, thereby making it less toxic to the body.