UNIVERSIDAD DE ZAMBOANGA

PAGADIAN BRANCH, INC.

Name: Weliam Jhay P. Coyme

Clinical Toxicology Laboratory

Activity 7

Case Study

(No. 19-22)

Case Study #19: Isopropanol Poisoning

History:

A 19-year-old female presents to your emergency department after ingesting a large amount of rubbing
alcohol following a fight with her boyfriend. She appears very sleepy and complains of generalized
weakness. She now denies suicidal ideation and has no plan to injure herself. She denies any co-ingestion
and the paramedics found no other pills or substances in the house.

PMH: None.

SH: No previous suicide attempts or history of depression.

Physical Examination:

T: 99.4°F HR: 78 bpm RR: 18 breaths per minute BP: 90/60 mm Hg

General: Lethargic.

HEENT: Acetone odor on the breath, otherwise normal.

Pulmonary: Clear to auscultation.

CV: Regular rate and rhythm without murmur, capillary refill 4 seconds.

Neurologic: GCS 14. Cranial nerves II-XII intact. Ataxia is present. All deep tendon reflexes are depressed.

Strength is 3/5 all flexors and extensors of bilateral upper and lower extremities.

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 Questions

1. What substance did the patient ingest?

This patient ingested isopropyl alcohol. Rubbing alcohol contains approximately 70%
isopropanol. It is also found in solvents, antifreeze and disinfectants. The primary reason people ingest
this substance is to become intoxicated (for instance, as an inexpensive ethanol substitute in alcoholics)
or to harm themselves.

2. What are the usual signs of acute toxicity?

The major effects of acute isopropanol ingestion are on the central nervous system, mimicking
the inebriation caused by ethanol, and gastrointestinal systems. The usual signs and symptoms include
CNS depression, slurred speech, ataxia, lethargy, weakness, nausea and headache. Abdominal pain,
gastritis, hypotension and apnea can also occur. Uncommon adverse effects include hemolytic anemia,
hypothermia, renal tubular acidosis and rhabdomyolysis. Death from isopropyl alcohol use is rare but
can occur secondary to coma with untreated airway compromise, injury resultant from ataxia or stupor,
or rarely, hypotension caused by vasodilation and possible myocardial depression after massive
overdose. Some sources give an estimated lethal dose of 250 mL in adults; however, with treatment,
adults and children have survived much larger ingestions.

3. What initial therapy should be instituted?

Initial management should be focused on stabilizing the airway, breathing and circulation. It is
important to ensure that no methanol or ethylene glycol were coingested. Serum isopropanol levels are
mostly used to substantiate the diagnosis and treatment is supportive. Levels greater than 100 mg/dL
can cause a decreased level of consciousness. This patient requires intravenous access and volume
resuscitation. Hypoglycemia should be corrected. There is no role for gastrointestinal decontamination
due to rapid absorption and favorable outcomes with supportive care alone. Active charcoal can adsorb
isopropyl alcohol; however massive doses must be used and are impractical given the fact that most
patients will have CNS depression and recover with supportive care alone. Rarely, hemodialysis is needed
for massive ingestions. It effectively removes isopropyl alcohol and acetone from the circulation.
Indications for hemodialysis include isopropanol levels exceeding 400-500 mg/dL, renal failure,
hypotension and coma in patients unresponsive to supportive care (intravenous fluids or vasopressors).
Since the primary metabolite (acetone) is less toxic than the parent compound, there is no indication for
ADH inhibition with fomepizole or ethanol.

4. What are the characteristic laboratory findings?

Characteristic laboratory findings include euglycemia, ketosis, little or no acidosis and increased
osmolality. Isopropanol is metabolized by alcohol dehydrogenase to acetone, which can worsen CNS
depressant effects and accounts for the marked ketosis seen in these patients. Isopropanol can be
distinguished from methanol and ethylene glycol because it does not produce an elevated anion gap
metabolic acidosis.

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 Case Study #20: Methanol Poisoning

History:

A 17-year-old male presents to your emergency department after accidentally ingesting a large amount
of methanol because he thought it was Gatorade®. He is not suicidal. He denies any co-ingestion, and
the paramedics did not find any pills or substances in the house. The ingestion occurred approximately
four hours prior to the call to EMS. He is currently complaining of blurred vision and nausea.

PMH: None.

SH: No previous suicide attempts or history of depression.

Physical Examination:

T: 99.4°F HR: 120 bpm RR: 24 breaths per minute BP: 110/60mm Hg

General: He is awake and alert.

HEENT: Examination reveals dilated pupils with sluggishlight reaction and poor accommodation.

Pulmonary: Clear to auscultation.

CV: Regular rate and rhythm without murmur, capillary refill slightly prolonged.

Neurologic: GCS = 14. Cranial nerves II-XII intact.

Questions

1. What are the usual signs of acute toxicity?

The initial effects of methanol are inebriation and gastrointestinal discomfort. Due to
metabolism of the parent alcohol to formic acid, a potent and specific neurotoxin, patients develop
edema of the optic nerve with resultant visual changes, and ultimately, permanent blindness. Ischemic
or hemorrhagic injury to the basal ganglia has been reported. Seizures, coma and death are possible. An
afferent papillary defect is an ominous sign in methanol poisoning. A funduscopic exam may reveal disc
hyperemia and papilledema.

2. Which initial therapies should be instituted?

Initial management should be focused on stabilizing the airway, breathing and circulation.
Methanol itself is of limited toxicity, but its metabolites produce toxicity. If methanol exposure is
suspected, a stat blood level should be obtained. In any patient who has ingested more than a sip, has a
metabolic acidosis and/or an osmolal gap, ADH inhibiting therapy with ethanol or fomepizole should be
started immediately. The agent of choice is generally institution specific but a knowledge of each is
important. Gastrointestinal decontamination is rarely indicated because of its rapid absorption and
limited binding to activated charcoal. Ethyl alcohol 1gm/kg followed by 0.5gm/kg/4 hours to maintain
blood ethanol at 100mg/dl. Ethanol, in sufficient concentrations, (greater than 100 mg/dL),
competitively inhibits the formation of the toxic metabolites, as it has a greater affinity for ADH than
methanol. This allows the unchanged parent alcohol (methanol) to be excreted by the pulmonary and
renal routes. The loading dose is 15 ml/kg of 5% ethanol followed by a maintenance infusion of 2-4

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 ml/kg/hr. Ideally, the blood ethanol level should be maintained between 100-150 mg/dL. Treatment can
be discontinued when methanol levels are below 20 mg/dL.

3. What are the characteristic laboratory findings?

Characteristic laboratory findings include an elevated anion gap metabolic acidosis and an osmolal gap.

Case Study #21: Marijuana Exposure

History:

A 13-year-old female presents to your emergency department with her parents. She returned home after
a party and has been complaining of dizziness, headache, palpitations and a feeling of chest tightness.
She claims to have taken no drugs, but says that she ate at the party. She vomited twice at home and
now feels very hungry.

PMH: None.

Physical Examination:

T: 99.4°F HR: 110 bpm RR: 19 breaths per minute BP: 153/86mm Hg

General: Pale, agitated and crying. She is very anxious.

HEENT: Examination is normal.

Pulmonary: Clear to auscultation.

CV: Tachycardic without murmur.

Abdomen: Soft and nontender.

Neurologic: GCS 15. Ccranial nerves II-XII intact.

Questions

1. What are the effects of marijuana?

The effects of marijuana are primarily due to delta-9-tetrahydrocannabinol, also known as THC.
Intoxication occurs within minutes if marijuana is inhaled and within hours if ingested and lasts 3-4
hours. THC intoxication includes both psychiatric and physical signs and symptoms. Although most
patients feel euphoric (“high”), first time users and susceptible individuals can experience paranoia,
anxiety and panic. Users may exhibit rapidly-changing emotions, irrelevant thought disturbed
association, increased awareness of stimuli, altered concepts of space and time (perceived time is faster
than clock time), impaired judgment, and speech changes (rapid, impaired, flighty). Other symptoms
include increased appetite and thirst, nausea, dizziness, dysesthesias, somnolence and restlessness.
Physical examination may show tachycardia, hypertension, tachypnea, ataxia, tremor, dry mucous
membranes, and injected conjunctivae.

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 2. How should this patient be managed?

Most patients do not require medical intervention. The patient should be placed in a calm,
supportive environment. In cases of severe agitation, benzodiazepines can be administered.

3. What other agents should be considered?

Marijuana intoxication can be distinguished from alcohol because these individuals often lack
the aggressive behavior, diminished appetite, nystagmus and ataxia seen in alcohol intoxication.
Differentiating marijuana from other drugs of abuse is more difficult and some individuals may combine
other drugs with marijuana. PCP typically presents with miosis, nystagmus (horizontal, vertical and
rotatory), hypertension, tachycardia, ataxia and CNS agitation. Cocaine and amphetamines produce a
more classic sympathomimetic presentation. Although anticholinergic agents can produce delirium, the
skin is dry and flushed with decreased GI motility and urinary retention.

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