Toxicology

1. Approach to the poisoned patient
Domina Petric, MD

2. Death causes in poisoning
• Many toxins depress the central nervous system.
• Comatose patients lose their airway protective
reflexes and their respiratory drive.
These patients may die as a result of airway
obstruction by:
• flaccid tongue
• aspiration of gastric contents into the
tracheobronchial tree
• respiratory arrest
These are the most common causes of death due to
overdoses of narcotics and sedative-hypnotic drugs
(for example barbiturates combined with alcohol).

3. Death causes in poisoning
• Cardiovascular toxicity is also common in
poisoning.
• Hypotension may be due to depression of
cardiac contractility.
• Hypovolemia may be result of vomiting,
diarrhea or fluid sequestration.
• Peripheral vascular collapse may be due to
blockade of α-adrenoreceptor-mediated
vascular tone.
• Hypothermia or hyperthermia, due to exposure
to temperature-dysregulating effects of many
drugs, can produce hypotension.

4. Death causes in poisoning
Lethal arrhythmias (ventricular
tachycardia, ventricular fibrillation) can
occur as a result of overdose with:
• ephedrine
• amphetamines
• cocaine
• digitalis
• theophylline
• tricyclic antidepressants
• antihistamines
• some opioid analogs

5. Death causes in poisoning
Cellular hypoxia, in spite of
adequate ventilation and oxygen
administration, may occur in case of
poisoning with:
• cyanide
• hydrogen sulfide
• carbon monoxide
• other poisons that interfere with
transport of utilization of oxygen

6. Death causes in poisoning
Cellular hypoxia is evident by the
development of:
• tachycardia
• hypotension
• severe lactic acidosis
• signs of ischemia on the
ECG
These patients may not be cyanotic.

7. Death causes in poisoning
Seizures, muscular hyperactivity and
rigidity may cause death in patients
poisoned with:
• antidepressants
• isoniazid (INH)
• diphenhydramine
• cocaine
• amphetamines

8. Death causes in poisoning
• Seizures may cause pulmonary
aspiration, hypoxia and brain
damage.
• Hyperthermia may result from
sustained muscular hyperactivity
and can lead to muscle
breakdown, myoglobinuria, renal
failure, lactic acidosis and
hyperkalemia.

9. Death causes in poisoning
Paraquat attacks lung tissue,
resulting in pulmonary
fibrosis that begins several
days after ingestion.
Massive hepatic necrosis due to
poisoning by acetaminophen or
certain mushrooms results in hepatic
encephalopathy and death 48-72
hours or longer after ingestion.

10. Death causes in poisoning
Intoxication with alcohol and
other sedative-hypnotic drugs
is common contributing factor
to motor vehicle accidents.
Patients under the influence
of hallucinogens (PCP, LSD)
may suffer trauma in state of
good or bad trip (for example,
fall from a height).

11. INITIAL MANAGEMENT OF THE
POISONED PATIENT

12. ABCD in toxicology
Airway
Breathing
Circulation
Dextrose
Unconscious and
intoxicated patient!

13. ABCD
• Airway should be cleared of
vomitus or any other obstruction.
• An oral airway or endotracheal
tube should be inserted if not
breathing spontaneously.
• For many patients, simple
positioning in the lateral, left-side-
down position is sufficient
(breathing spontaneously).

14. ABCD
Breathing: observation, pulse
oximetry and arterial blood
gases.
Patients with respiratory
insufficiency should be
intubated and mechanically
ventilated.

15. ABCD
Circulation: continous monitoring
of pulse rate, blood pressure,
urinary output and evaluation of
peripheral perfusion.
An intravenous line, quick
blood test for serum glucose
and other determinations.

16. ABCD
• Every patient with altered mental
status should receive concentrated
dextrose, unless a rapid blood
glucose test demonstrates that the
patient is not hypoglycemic.
• Adults: 50 mL of 40-50% dextrose
solution iv.
• Children: 5 mL/kg of 10% glucose
or 2 mL/kg of 25% dextrose iv.

17. ABCD
Alcoholic or malnourished
patients should receive
100 mg of thiamine im. or in the
iv. infusion solution together
with glucose/dextrose to
prevent Wernicke´s syndrome.

18. ABCD
• The opioid antagonist is
naloxone, dose is 0,4-2 mg iv.
• Naloxone reverses respiratory and
CNS depression.
• Larger doses of naloxone may be
needed for patients with overdose
involving propoxyphene, codeine
and some other opioids.

19. ABCD
• The benzodiazepine
antagonist is flumazenil.
• It should not be used if there is
a history of tricyclic
antidepressant overdose or a
seizure disorder because it can
induce convulsions in such
patients.

20. HISTORY AND PHYSICAL
EXAMINATION

21. History
syringes
empty bottles
household products
over-the-counter medications
Found in the
immediate vicinity
of the possibly
poisoned patient.

22. Physical examination
Brief examination with emphasizing
important areas for the toxicologic
diagnosis:
• vital signs
• eyes
• mouth
• skin
• abdomen
• nervous system

23. Vital signs
• Blood pressure, pulse,
respiration and temperature!
• Hypertension and
tachycardia are typical with
amphetamines, cocaine and
antimuscarinic
(anticholinergic) drugs.

24. Vital signs
Hypotension and
bradycardia: overdose
with calcium channel
blockers, β blockers,
clonidine and sedative
hypnotics.

25. Vital signs
Hypotension with
tachycardia: tricyclic
antidepressants, trazodone,
quetiapine, vasodilators and
β agonists.

26. Vital signs
Rapid respirations:
salicylates, carbon monoxide
and other toxins that produce
metabolic acidosis or cellular
asphyxia.

27. Vital signs
Hyperthermia:
sympathomimetics,
anticholinergics, salicylates
and drugs producing seizures
or muscular rigidity.
Hypothermia: CNS-
depressant drugs, especially
when accompanied by
exposure to a cold
environment.

28. Eyes
Constriction of the pupils (miosis):
• opioids
• clonidine
• phenothiazines
• cholinesterase inhibitors
(organophosphate insecticides)
• deep coma due to sedative drugs

29. Eyes
Dilation of the pupils (mydriasis):
• amphetamines
• cocaine
• LSD
• atropine and other
anticholinergic drugs

30. Eyes
Horizontal nystagmus is
characteristic of intoxication
with:
• phenytoin
• alcohol
• barbiturates
• other sedative drugs

31. Eyes
Both vertical and
horizontal
nystagmus is
strongly suggestive
of phencyclidine
poisoning.

32. Eyes
Ptosis and
ophthalmoplegia
are characteristic
features of botulism.

33. https://www.eyedoctorophthalmologistnyc.com

34. Mouth
Signs of burns due to corrosive
substances.
Soot from smoke inhalation.
Typical odors of alcohol,
hydrocarbon solvents or ammonia.
Cyanide: odor like bitter almonds.

35. Caustic burns of tongue
Medscape.com

36. Skin
• Poisoning with atropine and
other antimuscarinics:
flushed, hot and dry skin.
• Excessive sweating:
organophosphates, nicotine
and sympathomimetics.

37. Skin
• Cyanosis may be caused by
hypoxemia or by
methemoglobinemia.
• Icterus may suggest hepatic
necrosis due to
acetaminophen or Amanita
phalloides mushroom
poisoning.

38. Abdomen
Ileus
Typical of
poisoning with
antimuscarinic,
opioid and
sedative drugs.
Hyperactive bowel sounds,
abdominal cramping and diarrhea
Common in
poisoning with
organophosphates,
iron, arsenic,
theophylline,
A. phalloides and
A. muscaria.

39. Nervous system
Focal seizures or motor
deficits suggest a structural
lesion (intracranial
hemorrhage due to trauma)
rather than toxic or
metabolic encephalopathy.

40. Nervous system

41. Nervous system
Twiching and
muscular
hyperactivity are
common with
atropine and other
anticholinergic
agents, also with
cocaine and other
sympathomimetic
drugs.

42. Nervous system

43. Nervous system
Serotonin syndrome:
generalized hypertonicity of
muscles and lower
extremity clonus.

44. Nervous system
Seizures are often caused by overdose
with:
• antidepressants (especially tricyclic
antidepressants and bupropion)
• cocaine
• amphetamines
• theopylline
• isoniazid
• diphenhydramine

45. Nervous system
• Flaccid coma with absent
reflexes and even an
isoelectric
electroencephalogram may be
seen with deep coma due to
sedative-hypnotic or other
CNS depressant intoxication.
• This should not be mistaken
for brain death!

46. LABORATORY AND IMAGING
PROCEDURES

47. Arterial blood gases
• Hypoventilation results in
hypercapnia (elevated pCO2) and
hypoxia (low pO2).
• Hypoxia may be present in a patient
with aspiration pneumonia or drug-
induced pulmonary edema.
• Poor tissue oxygenation due to
hypoxia, hypotension or cyanide
poisoning results in metabolic
acidosis.

48. Arterial blood gases
• The pO2 measures only oxygen
dissolved in the plasma and not
total blood oxygen content or
oxyhemoglobin saturation.
• It may appear normal in patients
with severe CO poisoning.
• Pulse oximetry may also give
falsely normal results in CO
intoxication.

49. Electrolytes
• Sodium, potassium, chloride
and bicarbonate are measured
and anion gap is then
calculated.
Anion gap=(Na++K+)-(HCO3
- +Cl-)
• Normally, the sum of the cations
exceeds the sum of the anions
by no more than 12-16 mmol/L.

50. Electrolytes
Elevated anion gap is caused by the
presence of unmeasured anions
(lactate…) accompanying metabolic
acidosis:
• diabetic ketoacidosis
• renal failure
• shock-induced lactic acidosis
• aspirin, metformin, methanol,
ethylene glycol, isoniazid, iron

51. Anion gap
Type of elevation
of the anion gap
Agents
Organic acid
metabolites
Methanol, ethylene glycol,
diethylene glycol
Lactic acidosis Cyanide, CO, ibuprofen,
isoniazid, metformin,
salicylates, valproic acid…
Any drug-induced seizures,
hypoxia or hypotension

52. Electrolytes
Drugs that may cause
hyperkalemia, despite normal
renal function, are:
• potassium
• β blockers
• digitalis glycosides
• potassium-sparing diuretics
• fluoride

53. Electrolytes
Drugs that may cause
hypokalemia are:
• barium
• β agonists
• caffeine
• theophylline
• thiazide
• loop diuretics

54. Renal function tests
• Some toxins have direct
nephrotoxic effects.
• In other cases, renal failure is
due to shock or
myoglobinuria.
• Blood urea nitrogen and
creatinine levels!
• Urinalysis!

55. Renal function tests
• Elevated serum creatine
kinase (CK) and myoglobin in
the urine suggest muscle
necrosis due to seizures or
muscular rigidity.
• Oxalate crystals in large
numbers in the urine suggest
ethylene glycol poisoning.

56. Serum osmolality
2xNa+(mmol/L) +
𝑔𝑙𝑢𝑐𝑜𝑠𝑒 (
𝑚𝑔
𝑑𝑙
)
18
+
𝐵𝑈𝑁 (
𝑚𝑔
𝑑𝑙
)
3
Normally, value is 280-290 mOsm/L.

57. Serum osmolality
• Ethanol and other alcohols may
contribute significantly to the
measured serum osmolality and
cause osmol gap.
Osmolar gap=Measured osmolality-Calculated osmolality.

58. Osmol gap
Substance Serum level
(mg/dL)
Corresponding
Osmol Gap
(mOsm/kg)
Ethanol 350 75
Methanol 80 25
Ethylene
glycol
200 35
Isopropranol 350 60

59. ECG
• Widening of the QRS complex
duration (more than 100 ms) is
typical of tricyclic antidepressant
and quinidine overdoses.
• The QTc interval prolongation
(more than 440 ms) may be due to
quinidine, antidepressants,
antipsychotics, lithium and arsenic
poisoning.

60. ECG
• Variable atrioventricular (AV)
block and variety of atrial and
ventricular arrhythmias are
common with poisoning by
digoxin and other cardiac
glycosides.
• Hypoxemia due to CO
poisoning may result in
ischemic changes on ECG.

61. Imaging findings
• Some tablets, particularly iron and
potassium, may be radiopaque
and can be seen on plain film of
the abdomen.
• Chest radiography may reveal
aspiration pneumonia,
hydrocarbon pneumonia or
pulmonary edema.
• CT is indicated when head trauma is
suspected.

62. Toxicology screening tests
When a specific
antidote or other
treatment is under
consideration,
quantitative laboratory
testing may be
indicated.

63. Hemodialysis
Hemodialysis may be indicated
depending on the severity of
poisoning or the blood
concentration:
• carbamazepine, ethylene glycol
• lithium, methanol, metformin
• phenobarbital, salicylate
• theophylline, valproic acid

64. Hemodialysis
Hemodialysis is ineffective or is not
useful:
• amphetamines, antidepressants
• antipsychotic drugs
• benzodiazepines
• calcium channel blockers
• digoxin, metoprolol, propranolol
• opioids

65. Literature
• Katzung, Masters, Trevor. Basic
and clinical pharmacology.
• Medscape.com
• Healthtap.com
• Eyedoctorophthalmologistnyc.com
• WebMD.com
• LabCE.com