Transcript Assess the Danger

INITIAL EVALUATION OF THE
PATIENT WITH POISONING OR
DRUG OVERDOSE
Patients with drug overdoses or poisoning may initially
present with no symptoms or with varying degrees of overt
intoxication. The asymptomatic patient may have been
exposed to or may have ingested a lethal dose of a poison but
not yet have any manifestations of toxicity. It is always
important to
• (1) quickly assess the potential danger
• (2) perform gut decontamination to prevent
absorption, and
• (3) observe the patient for an appropriate
interval.
Assess the Danger
• If the toxin is known, the danger can be
assessed by consulting a text or
computerized information resource (eg,
POISINDEX) or by calling a regional
poison control center
• Assessment will usually take into account
the dose ingested (in milligrams per
kilogram of body weight), the time interval
since ingestion, the presence of any clinical
signs, preexisting cardiac, respiratory, renal,
or liver disease, and, occasionally, specific
serum drug or toxin levels. Be aware that
the history given by the patient or family
may be incomplete or unreliable.
Observation of the Patient
• Asymptomatic or mildly symptomatic patients should be
observed for at least 4–6 hours. Longer observation is
indicated if the ingested substance is a sustained-release
preparation or is known to slow gastrointestinal motility or
if there may have been exposure to a poison with delayed
onset of symptoms (such as acetaminophen, colchicine, or
hepatotoxic mushrooms). After that time, the patient may
be discharged if no symptoms have developed and
adequate gastric decontamination has been provided.
Before discharge, psychiatric evaluation should be
performed to assess suicidal risk. Intentional ingestions in
adolescents should raise the possibility of unwanted
pregnancy or sexual abuse.
THE SYMPTOMATIC PATIENT
• COMA
• Assessment & Complications
• Coma is commonly associated with
ingestion of large doses of antihistamines,
barbiturates, benzodiazepines, ethanol,
opioids, phenothiazines, or tricyclic
antidepressants
• The most common cause of death in comatose
patients is respiratory failure, which may occur
abruptly. Aspiration of gastric contents may also
occur, especially in victims who are deeply
obtunded or convulsing. Hypoxia and
hypoventilation may cause or aggravate
arrhythmias and seizures. Thus, protection of the
airway and assisted ventilation are the most
important treatment measures for any poisoned
patient.
Treatment
• A. Emergency Management: The initial
emergency management of coma can be
remembered by the mnemonic ABCD,for
Airway, Breathing, Circulation, and Drugs
(dextrose, thiamine, and naloxone or
flumazenil)
Airway
• Establish a patent airway by positioning, suction,
or insertion of an artificial nasal or oropharyngeal
airway. If the patient is deeply comatose or if there
is no gag or cough reflex, perform endotracheal
intubation. These airway interventions may not be
necessary if the patient is intoxicated by an opioid
or a benzodiazepine and responds rapidly to
intravenous naloxone or flumazenil
Breathing
• Clinically assess the quality and depth of respiration, and
provide assistance if necessary with a bag-valve-mask
device or mechanical ventilator. Provide supplemental
oxygen. The arterial blood CO2 tension is useful in
determining the adequacy of ventilation. The arterial blood
PO2 determination may reveal hypoxemia, which may be
caused by respiratory arrest, bronchospasm, pulmonary
aspiration, or noncardiogenic pulmonary edema. Pulse
oximetry is not reliable in patients with
methemoglobinemia or carbon monoxide poisoning.
Circulation
• Measure the pulse and blood pressure, and
estimate tissue perfusion (eg, by
measurement of urinary output, skin signs,
arterial blood pH). Insert an intravenous
line, and draw blood for complete blood
count, glucose, electrolytes, serum
creatinine and liver tests, and possible
toxicologic testing.
Drugs
• Dextrose and thiamine–Unless promptly treated,
severe hypoglycemia can cause irreversible brain
damage. Therefore, in all comatose or convulsing
patients, give 50% dextrose, 50–100 mL by
intravenous bolus, unless a rapid bedside blood
sugar test is available and rules out hypoglycemia.
In alcoholic or very malnourished patients who
may have marginal thiamine stores, give thiamine,
100 mg intramuscularly or over 2–3 minutes
intravenously.
Drugs
• Dextrose and thiamine–Unless promptly treated,
severe hypoglycemia can cause irreversible brain
damage. Therefore, in all comatose or convulsing
patients, give 50% dextrose, 50–100 mL by
intravenous bolus, unless a rapid bedside blood
sugar test is available and rules out hypoglycemia.
In alcoholic or very malnourished patients who
may have marginal thiamine stores, give thiamine,
100 mg intramuscularly or over 2–3 minutes
intravenously.
Drugs
• Dextrose and thiamine–Unless promptly treated,
severe hypoglycemia can cause irreversible brain
damage. Therefore, in all comatose or convulsing
patients, give 50% dextrose, 50–100 mL by
intravenous bolus, unless a rapid bedside blood
sugar test is available and rules out hypoglycemia.
In alcoholic or very malnourished patients who
may have marginal thiamine stores, give thiamine,
100 mg intramuscularly or over 2–3 minutes
intravenously.
Drugs
• Dextrose and thiamine–Unless promptly treated,
severe hypoglycemia can cause irreversible brain
damage. Therefore, in all comatose or convulsing
patients, give 50% dextrose, 50–100 mL by
intravenous bolus, unless a rapid bedside blood
sugar test is available and rules out hypoglycemia.
In alcoholic or very malnourished patients who
may have marginal thiamine stores, give thiamine,
100 mg intramuscularly or over 2–3 minutes
intravenously.
Drugs
• Dextrose and thiamine–Unless promptly treated,
severe hypoglycemia can cause irreversible brain
damage. Therefore, in all comatose or convulsing
patients, give 50% dextrose, 50–100 mL by
intravenous bolus, unless a rapid bedside blood
sugar test is available and rules out hypoglycemia.
In alcoholic or very malnourished patients who
may have marginal thiamine stores, give thiamine,
100 mg intramuscularly or over 2–3 minutes
intravenously.
Drugs
• Dextrose and thiamine–Unless promptly treated,
severe hypoglycemia can cause irreversible brain
damage. Therefore, in all comatose or convulsing
patients, give 50% dextrose, 50–100 mL by
intravenous bolus, unless a rapid bedside blood
sugar test is available and rules out hypoglycemia.
In alcoholic or very malnourished patients who
may have marginal thiamine stores, give thiamine,
100 mg intramuscularly or over 2–3 minutes
intravenously.
• Narcotic antagonists–Naloxone, 0.4–2 mg
intravenously, may reverse opioid-induced
respiratory depression and coma. If opioid
overdose is strongly suspected, give additional
doses of naloxone (up to 5–10 mg may be required
to reverse potent opioids). Caution: Naloxone has
a much shorter duration of action (2–3 hours) than
most common opioids; repeated doses may be
required, and continuous observation for at least
3–4 hours after the last dose is mandatory
• Flumazenil–Flumazenil, 0.2–0.5 mg
intravenously, repeated every 30 seconds as
needed up to a maximum of 3 mg, may reverse
benzodiazepine-induced coma. Caution:
Flumazenil has a short duration of effect (2–3
hours), and resedation requiring additional doses
is common. Furthermore, flumazenil should not be
given if the patient has co-ingested a tricyclic
antidepressant or has a seizure disorder.
HYPOTHERMIA
• Assessment & Complications
• Hypothermia commonly accompanies coma due to
opioids, ethanol, hypoglycemic agents,
phenothiazines, barbiturates, benzodiazepines, and
other sedative-hypnotics and depressants.
Hypothermic patients may have a barely
perceptible pulse and blood pressure and often
appear to be dead. Hypothermia may cause or
aggravate hypotension, which will not reverse
until the temperature is normalized
HYPOTENSION
• Assessment & Complications
• Hypotension may be due to poisoning by many
different drugs and poisons. The most common
drugs causing hypotension are antihypertensive
drugs, beta-blockers, calcium channel blocking
agents, iron, theophylline, phenothiazines,
barbiturates, and tricyclic antidepressants.
• Poisons causing hypotension include cyanide,
carbon monoxide, hydrogen sulfide, arsenic, and
certain mushrooms.
Treatment
• Most patients respond to empiric treatment
(200 mL intravenous boluses of 0.9% saline
or other isotonic crystalloid up to total of 1–
2 L). If fluid therapy is not successful, give
dopamine, 5–15 mg/kg/min by intravenous
infusion in a large peripheral or central line.
Consider pulmonary artery catheterization if
hypotension persists.
• Hypotension caused by certain toxins may respond
to specific treatment. For hypotension caused by
overdoses of tricyclic antidepressants or related
drugs, administer sodium bicarbonate, 1–2 meq/kg
by intravenous bolus injection. For beta-blocker
overdose, glucagon intravenously may be of value.
For calcium antagonist overdose, administer
calcium chloride, 15–20 mg/kg intravenously
(repeated doses may be necessary).
HYPERTENSION
• Assessment & Complications
• Hypertension may be due to poisoning with
amphetamines, anticholinergics, cocaine,
phenylpropanolamine, or monoamine
oxidase inhibitors (mainly as a result of a
concomitantly administered drug).
• Severe hypertension (eg, diastolic blood
pressure > 105–110 mm Hg in a person who
does not have chronic hypertension) can
result in acute intracranial hemorrhage,
myocardial infarction, or aortic dissection.
Patients often present with headache, chest
pain, or encephalopathy
Treatment
• Treat hypertension (see Chapter 11) if the patient
is symptomatic or if the diastolic pressure is
greater than 105–110 mm Hg—especially if there
is no prior history of hypertension.
• Administer phentolamine, 2–5 mg intravenously,
or nitroprusside sodium, 0.25–8 mg/kg/min
intravenously. If excessive tachycardia is present,
add propranolol, 1–5 mg intravenously, or esmolol
25–100 mg/kg/min intravenously. Caution: Do not
give beta-blockers alone, since doing so may
paradoxically worsen hypertension.
ARRHYTHMIAS
• Assessment & Complications
• Arrhythmias may occur with a variety of
drugs or toxins
• They may also occur as a result of hypoxia,
metabolic acidosis, or electrolyte imbalance
(eg, hyper- or hypokalemia, hypocalcemia),
or following exposure to chlorinated
solvents or chloral hydrate overdose.
Common toxins or drugs causing
arrhythmias.
Arrhythmia
• Sinus bradycardia
Common Causes
• Beta-blockers,
verapamil,
organophosphates,
digitalis glycosides,
opioids, clonidine,
sedative-hypnotics.
• Atrioventricular block
• Beta-blockers, digitalis
glycosides, calcium antagonists,
tricyclic antidepressants,
lithium.
• Sinus tachycardia
• Theophylline, caffeine, cocaine,
amphetamines, phencyclidine,
beta-agonists (eg, albuterol),
iron, anticholinergics,
tricyclicantidepressants,
antihistamines
• Wide QRS complex
• Tricyclic antidepressants,
quinidine and class 1a
antiarrhythmics,class 1c antiarrhythmics, phenothiazines,
Treatment
• Arrhythmias are often caused by hypoxia or electrolyte
imbalance, and these conditions should be sought and
treated. If ventricular arrhythmias persist, administer
lidocaine at usual antiarrhythmic doses. Caution: Avoid
class Ia agents (quinidine, procainamide,
disopyramide), which may aggravate arrhythmias
caused by tricyclic antidepressants, calcium
antagonists, or beta-blockers.Wide QRS complex
tachycardia in the setting of tricyclic antidepressant
overdose (or quinidine and other class Ia drugs) should
be treated with sodium bicarbonate, 50–100 meq
intravenously by bolus injection. For tachyarrhythmias
induced by chlorinated solvents, chloral hydrate, or
sympathomimetic agents, use propranolol or esmolol.
CONVULSIONS
• Assessment & Complications
• Convulsions may be due to poisoning with many
drugs and poisons, including amphetamines,
antihistamines, camphor, cocaine, isoniazid,
lindane, phencyclidine (PCP), phenothiazines,,
theophylline, and tricyclic antidepressants.
• Convulsions may also be caused by hypoxia,
hypoglycemia, hypocalcemia, hyponatremia,
withdrawal from alcohol or sedative-hypnotics,
head trauma, central nervous system infection, or
idiopathic epilepsy
Treatment
• Administer diazepam, 5–10 mg intravenously over
2–3 minutes, or lorazepam, 2–3 mg intravenously,
or—if intravenous access is not immediately
available—midazolam, 5–10 mg intramuscularly.
If convulsions continue, administer phenobarbital,
15–20 mg/kg slowly intravenously over no less
than 30 minutes; or phenytoin, 15 mg/kg
intravenously over no less than 30 minutes
(maximum infusion rate, 50 mg/min). The drugs
may be used together if necessary
HYPERTHERMIA
• Assessment & Complications
• Hyperthermia may be associated with poisoning
by amphetamines, atropine and other
anticholinergic drugs, cocaine, dinitrophenol and
pentachlorophenol, phencyclidine (PCP),
salicylates, strychnine, tricyclic antidepressants,
and various other medications
• Hyperthermia is a rapidly life-threatening
complication. Severe hyperthermia (temperature >
40–41 °C) may rapidly cause brain damage and
multiorgan failure, including rhabdomyolysis,
renal failure, and coagulopathy
Treatment
• Treat hyperthermia aggressively by removing all
clothing, spraying with tepid water, and fanning
the patient. If this is not rapidly effective, as
shown by a normal rectal temperature within 30–
60 minutes, or if there is significant muscle
rigidity or hyperactivity, induce neuromuscular
paralysis with pancuronium, 0.1 mg/kg
intravenously, or another nondepolarizing
neuromuscular blocker
DECONTAMINATION OF THE SKIN
• Corrosive agents rapidly injure the skin and eyes and
must be removed immediately. In addition, many toxins
are readily absorbed through the skin, and systemic
absorption can be prevented only by rapid action.
• Wash the affected areas with copious quantities of
lukewarm water or saline. Wash carefully behind the
ears, under the nails, and in skin folds. For oily
substances (eg, pesticides), wash the skin at least twice
with plain soap and shampoo the hair. Specific
decontaminating solutions or solvents (eg, alcohol) are
rarely indicated and in some cases may enhance
absorption.
DECONTAMINATION OF THE
EYES
• Act quickly to prevent serious damage. Flush the eyes
with copious amounts of saline (preferred) or water. (If
available, instill local anesthetic drops in the eye before
beginning irrigation.) Remove contact lenses if present.
Direct the irrigating stream so that it will flow across
both eyes after running off the nasal bridge. Lift the
tarsal conjunctiva to look for undissolved particles and
to facilitate irrigation. Continue irrigation for 15
minutes by the clock or until each eye has been
irrigated with at least 1 L of solution. If the toxin is an
acid or a base, check the pH of the tears after
irrigation, and continue irrigation until the pH is
between 6.5 and 7.5.
GASTROINTESTINAL
DECONTAMINATION
• Removal of ingested poisons is an essential
part of emergency treatment. However,
studies indicate that if more than 60 minutes
has passed, induced emesis and gastric
lavage are relatively ineffective
• For small or moderate ingestions of most
substances, toxicologists generally
recommend activated charcoal alone
without prior gastric emptying. Exceptions
are large ingestions of anticholinergic
compounds and salicylates, which often
delay gastric emptying, and ingestion of
sustained-release or enteric-coated tablets,
which may remain intact for several hours.
• Gastric emptying is not generally used for
ingestion of corrosive agents or petroleum
distillates, because further esophageal injury
or pulmonary aspiration may result.
However, in certain cases, removal of the
toxin may be more important than concern
over possible complications. Consult a
medical toxicologist or regional poison
control center for advices.
Emesis
• Emesis using syrup of ipecac is a
convenient and fairly effective way to
evacuate gastric contents if given very soon
after ingestion (eg, at work or at home).
However, it may delay or prevent use of
oral activated charcoal and is not generally
used in the hospital management of
ingestions
• A. Indications: For removal of poison in conscious,
cooperative patients and for promptness, ipecac can be
given in the home or at work in the first few minutes
after poisoning.
• B. Contraindications: Induced emesis is
contraindicated for drowsy, unconscious, or convulsing
patients and for patients who have ingested kerosene or
other hydrocarbons (danger of aspiration of stomach
contents), corrosive poisons, or rapidly acting
convulsants (eg, tricyclic antidepressants, strychnine,
nicotine, camphor).
• C. Technique: Give syrup of ipecac, 30 mL (15 mL in
children), followed by an 8-oz glass of water. Repeat in
20 minutes if necessary
Gastric Lavage
• Gastric lavage is more effective for liquid
poisons or small pill fragments than for
intact tablets or pieces of mushroom. It is
most effective when started within 60
minutes after ingestion. The lavage
procedure may delay administration of
activated charcoal and may hasten passage
of pills and other toxic material into the
small intestine.
Indications
• Gastric lavage is indicated for removal of
ingested poisons when emesis is refused,
contraindicated, or unsuccessful; for
collection and examination of gastric
contents for identification of poison; and for
convenient administration of charcoal and
antidotes.
Contraindications
• Do not use lavage for stuporous or
comatose patients with absent gag reflexes
unless they are endotracheally intubated
beforehand. Some authorities advise against
lavage when caustic material has been
ingested; others regard it as essential to
remove liquid corrosives from the stomach.
Technique
• In obtunded or comatose patients, the danger of
aspiration pneumonia is reduced by placing the
patient in a head down, left lateral decubitus
position and, if necessary, protecting the airway
with endotracheal intubation. Gently insert a
lubricated, soft but noncollapsible stomach tube
(at least 37–40F) through the mouth or nose into
the stomach. Aspirate and save the contents, and
then lavage repeatedly with 50–100 mL of fluid
until the return fluid is clear. Use lukewarm tap
water or saline
Activated Charcoal
• Activated charcoal effectively adsorbs
almost all drugs and poisons. Poorly
absorbed substances include iron, lithium,
potassium, sodium, cyanide, mineral acids,
and alcohols.
Indications
• Activated charcoal should be used for
prompt adsorption of drugs or toxins in the
stomach and intestine. Studies show that
activated charcoal given alone may be as
effective as or more effective than ipecacinduced emesis or gastric lavage.
Contraindications
• Activated charcoal should not be used for
stuporous, comatose, or convulsing patients
unless it can be given by gastric tube and
the airway is first protected by cuffed
endotracheal tube. This substance is
contraindicated also for patients with ileus
or intestinal obstruction or those who have
ingested corrosives for whom endoscopy is
planned.
Technique
• Administer activated charcoal, 60–100 g
orally or via gastric tube, mixed in aqueous
slurry. Repeated doses may be given to
ensure gastrointestinal adsorption or to
enhance elimination of some drugs
Catharsis
• A. Indications: For stimulation of peristalsis to hasten
the elimination of unabsorbed drugs and poisons and
the activated charcoal slurry.
• B. Contraindications and Cautions: Do not use mineral
oil or other oil-based cathartics. Avoid sodium-based
cathartics in patients with hypertension, renal failure,
and congestive heart failure and magnesium-based
cathartics in those with renal failure.
• C. Technique: Magnesium sulfate 10%, 2–3 mL/kg; or
sorbitol 70%, 1–2 mL/kg. Sorbitol is commonly used in
prepackaged charcoal slurry products.
Whole Bowel Irrigation
• Whole bowel irrigation utilizes large
volumes of balanced polyethylene glycolelectrolyte solution to mechanically cleanse
the entire intestinal tract. There is no net
gain or loss of systemic fluids or
electrolytes.
• Indications: Whole bowel irrigation is particularly
effective for massive iron ingestion in which intact
tablets are visible on abdominal x-ray. It has also
been used for ingestions of sustained-release and
enteric-coated tablets as well as drug-filled
packets.
• B. Contraindications: Same as for cathartics.
• C. Technique: Administer the balanced
polyethylene glycol-electrolyte solution (CoLyte,
GoLYTELY) into the stomach via gastric tube at a
rate of 1–2 L/h until the rectal effluent is clear
Increased Drug Removal
• Forced Diuresis
• Dialysis (Hemodialysis or Hemoperfusion)
• Repeat-Dose Charcoal
DIAGNOSIS OF POISONING
•
•
•
•
Sympathomimetic Syndrome
Sympatholytic Syndrome
Cholinergic Syndrome
Anticholinergic Syndrome
Sympathomimetic Syndrome
• The blood pressure and pulse rate are elevated,
though with severe hypertension reflex
bradycardia may occur. The temperature is often
elevated, pupils are dilated, and the skin is sweaty,
though mucous membranes are dry. Patients are
usually agitated, anxious, or frankly psychotic.
• Examples: Amphetamines, cocaine, ephedrine and
pseudoephedrine, phencyclidine (pupils normal or
small), phenylpropanolamine (bradycardia
common)
Sympatholytic Syndrome
• The blood pressure and pulse rate are
decreased and body temperature is low. The
pupils are small or even pinpoint. Peristalsis
is usually decreased. Patients are usually
obtunded or comatose.
• Examples: Barbiturates, benzodiazepines
and other sedative hypnotics, clonidine and
related antihypertensives, ethanol, opioids.
Cholinergic Syndrome
• Stimulation of muscarinic receptors causes
bradycardia, miosis, sweating, and hyperperistalsis
as well as bronchorrhea, wheezing, excessive
salivation, and urinary incontinence. Nicotinic
receptor stimulation may produce initial
hypertension and tachycardia as well as
fasciculations and muscle weakness. Patients are
usually agitated and anxious.
• Examples: Carbamates, nicotine,
organophosphates, physostigmine
Anticholinergic Syndrome
• Tachycardia with mild hypertension is common, and
the body temperature is often elevated. Pupils are
widely dilated. The skin is flushed, hot and dry.
Peristalsis is decreased, and urinary retention is
common. Patients may have myoclonic jerking or
choreoathetoid movements. Agitated delirium is
frequently seen, and severe hyperthermia may occur.
• Examples: Atropine, scopolamine, other naturally
occurring and pharmaceutical anticholinergics,
amantadine, antihistamines, phenothiazines
(hypotension, small pupils), tricyclic antidepressants.