Clinical Toxicology


By the end of this session the reader should be able to:

  • Describe the general treatment of drug overdose (gastric lavage, emesis, activated charcoal, charcoal/resin hemoperfusion, hemodialysis, peritoneal dialysis, cathartics, pressor agents, cardiac monitoring, support of airway)
  • Describe "zero-order pharmacokinetics"
  • Describe "first-order pharmacokinetics"
  • Define "serum half-life,"" first-pass effect," and "steady-state"
  • Describe the effect of renal function, hepatic function, and enzyme saturation on pharmacokinetics
  • Recognize the basic toxicologic features and treatment of poisoning with ethanol, methanol, isopropanol, ethylene glycol, aspirin, acetaminophen, tricyclic antidepressants, benzodiazepines, opiates, cocaine, amphetamines, barbiturates, phencyclidine, hallucinogens, designer drugs, digoxin, carbon monoxide, iron, lead, organophosphates, and carbamates
  • Describe the rationale for therapeutic drug monitoring and what advantages it offers
  • Discuss the therapeutic monitoring of phenytoin, theophylline, valproic acid, primidone, phenobarbital, carbamazepine, digoxin, aminoglycoside antibiotics (amikacin, gentamicin, tobramycin), cyclosporine, sirolimus, tacrolimus, and vancomycin


Clinical toxicology - the measurement and interpretation of concentrations of drugs and other toxic substances in human biological fluids for the purpose of patient care

Drug abuse screening - the identification of “street” drugs (e.g., opiates, phencyclidine, amphetamines) in urine of subjects suspected of abusing these compounds

Emergency toxicology - the laboratory diagnosis of the presence and severity of drug overdose, often in the comatose or obtunded patient

Forensic toxicology - the measurement of drugs and toxins in tissues for medicolegal purposes (e.g., determining cause of death)

Therapeutic drug monitoring (TDM) - the determination of whether plasma drug levels are therapeutic, subtherapeutic, or toxic so that dosages may be adjusted accordingly

Toxicology - the analysis and study of harmful compounds in biological materials.


There are over 2 million human exposures reported to poison control centers each year and 25% of these cases are seen in a health care setting. Many poisonings are accidental and the majority involve children. Most cases of poisoning require supportive therapy only, but in select cases effective antidotes are available and can be life-saving. Depending on the clinical setting, pharmacists often play a key role in treating patients after a toxic exposure.

Samples types to submit for the overdosed patient

  • Blood (whole blood or serum depending on analyte) is preferred whenever drug concentrations can be correlated with effects; quantitative analysis allows for interpretation of degree of toxicity for some compounds
  • Urine specimens are preferred when the concentration in blood is too low for detection due to extensive metabolism and clearance of the drug (e.g., many drugs of abuse); for most compounds only qualitative analysis is performed
  • Gastric fluid (available from lavage or emesis) is most useful for identifying the parent drug in overdose cases or if other fluids are not available or are not diagnostic; qualitative analysis often identifies parent drug
  • Pills, capsules, tablets, powders found with the patient
  • In overdose cases it is important to share with the toxicology laboratory the clinical history in order to allow a time-saving “directed” drug search

Drug screen

  • There is no universal drug screen
  • Important to communicate with the laboratory in order to understand what is covered in that particular lab’s “drug screen”
  • One out of every four drug screens detects at least one drug unsuspected from the clinical history
  • One out of every six drug screens detects only drugs unsuspected from the history
  • To identify drugs for which specific treatment protocol exists (e.g., acetaminophen, digoxin)
  • A “negative” toxicology report in overdose cases indicates the need to search for other causes of altered physical or mental status

General treatment of drug overdose

  • Comatose patients ABCD (Airway, Breathing, Circulation and Drugs)
  • Supportive care alone (emesis, lavage, intravenous fluids, activated charcoal, cathartics, pressor agents; cardiac monitoring)
  • Antidote if available and indicated
  • Rarely: peritoneal dialysis, hemodialysis, or hemoperfusion


Definition :

A mathematical description of the time course of a drug concentration in a patient

  • Provides a framework for interpreting quantitative drug concentrations

Important concepts for toxicologists

A) Zero-order kinetics : a constant amount of the drug is eliminated in a unit of time

  • Good example is ethanol
  • Can apply to drugs in an overdose situation when metabolic enzymes become saturated

B) First-order kinetics (see Figure 1) : a constant percent of the drug is eliminated in time

  • Most drugs follow first-order kinetics

C) Serum half-life : time required for serum concentrations to decrease by one half

  • Only applies to first-order kinetics

D) First-pass effect : applies to drugs which are cleared by the liver before reaching systemic circulation

E) Steady-state : applies to repeated dosing and is reached in about 4 half-lives (94% of steady-state)

Factors which change pharmacokinetics

A) Renal function

  • Since many drugs are cleared by the kidneys it is often important to monitor creatinine clearance as an indicator of renal function

B) Hepatic function

  • Some drugs can induce liver enzymes (e.g., barbiturates) and decrease half-lives of other drugs
  • Some drugs competitively inhibit metabolism of other drugs (cimetidine and coumarins)

C) Saturation kinetics

  • In an overdose situation primary metabolic routes become overloaded, half-lives no longer apply and excretion becomes zero-order
  • Secondary metabolic routes can form toxic metabolites (e.g., acetaminophen)



  • Potent central nervous system depressant
  • Most frequently encountered and often most significant drug in toxicology cases
  • Effects vary with concentration; generally higher cortical functions (thought processes) are affected first followed by more basal functions (breathing)
  • Common cause of hyperosmolality in emergency room patients
  • Disulfiram (Antabuse) inhibits ALDH (Aldehyde dehydrogenase) causing a buildup of acetaldehyde which causes unpleasant effects (flushing, nausea, vomiting, etc.)
  • Ethanol metabolism follows zero-order kinetics and for normal people is from 0.01 to 0.02% w/v/hr but can be induced to 0.03% w/v/hr

Figure 2. Ethanol

Three metabolic pathways of ethanol
1) Alcohol dehydrogenase in cytosol
2) Microsomal ethanol oxidation (inducible)
3) Peroxidase-catalase (minor)


  • Toxicity is characterized by profound metabolic acidosis (uncouples oxidative phosphorylation and is metabolized to formic acid)
  • Metabolites also cause blindness
  • As little as 30 mL can be fatal

Figure 3. Methanol


  • Administer ethanol by drip until patients have ethanol concentrations of 100 to 150 mg/dL; ETOH competitively inhibits metabolism of methanol at ADH step
  • Methanol can then be removed by dialysis (if > 50 mg/dL)
  • Administer 4-methylpyrazole to inhibit alcohol dehydrogenase; hemodialysis may also be used


  • Generally considered to have twice the CNS depressant effect as an equivalent dose of ethanol
  • Metabolized to acetone
  • Upper GI bleeding
  • Belching (evaporates easily)

Figure 4. Isopropanol

Ethylene Glycol (Principle Antifreeze Ingredient)

  • Same CNS depressant effects as ethanol but has toxic metabolites
  • Progressively oxidized to glycolic acid and oxalic acid which causes myocardial depression and renal necrosis
  • Serious toxicity at concentrations just detected by osmolal gap
  • Hypocalcemia

Figure5:Ethylene Glycol Metabolism

A) Three stages of ethylene glycol intoxication

  • CNS depression (1-12 hours)
  • Cardiotoxic (12-24 hours)
  • Renal stage (24-72 hours)

B) Treatment of ethylene glycol intoxication

  • Ethanol to inhibit formation of toxic metabolites
  • Bicarbonate for metabolic acidosis
  • Ca++ replacement if necessary
  • 4-methylpyrazole to inhibit alcohol dehydrogenase; hemodialysis may also be used

Salicylate (Aspirin)

  • Analgesic, antipyretic and anti-inflammatory
  • Toxicity characterized by metabolic acidosis (see Figure 6)
  • Common symptoms include: tinnitus, hyperthermia, hyperventilation, CNS disturbances
  • Acute overdoses are generally suicidal
  • Chronic toxicity occurs at lower doses than acute overdose

Treatment for salicylate overdose

  • Hydration, glucose, K+ supplements, bicarbonate, hemodialysis

Figure 6: Salicylate Acid-Base Disruption

Acetaminophen (Tylenol)

  • Analgesic and antipyretic, not anti-inflammatory
  • Peak concentrations about 4 hours post-ingestion (for prediction of toxicity need to evaluate at this time, > 200 $\mu$g/mL, hepatotoxicity)
  • Normal half-life of 2-3 hours, if > 4 hours hepatic toxicity, if > l2 hours hepatic coma likely
  • Single acute threshold for liver damage in adults is in the range of 150 to 250 mg/kg; children under age of 10 are more resistant to toxicity than adults

Acetaminophen toxicity
The primary route of metabolism of acetaminophen is glucuronidation or sulfation, with some also being metabolized to imidoquinone, a toxic intermediate. Normally the imidoquinone is inactivated by conjugation with glutathione. In an overdose situation all the glutathione is used up and the imidoquinone reacts with surrounding hepatocytes causing liver failure. N-acetylcysteine (Mucomyst) is the antidote and functions by supplying a substrate which replenishes glutathione stores.


Figure 7: Nomogram for Prediction of Acetaminophen Hepatoxicity.


Figure 8

A) Stages of acetaminophen toxicity which develop over several days

  • GI distress (0 to 8 hours post dose): nausea, vomiting, malaise
  • General well being (0 to 24 hours post ingestion)
  • Liver toxicity (8 to 36 hours post ingestion): severe overdose leads to fulminant hepatic failure
  • Recovery (days to weeks post dose): liver transaminases return to normal in 5-7 days, complete resolution takes weeks

B) Treatment for acetaminophen overdose

  • Activated charcoal (if patient presents early)
  • N-acetylcysteine is the antidote
  • Functions by binding the toxic metabolic intermediate
  • N-acetylcysteine, if given early can completely prevent liver failure and death
  • N-acetylcysteine administration is indicated in patients with acetaminophen concentrations above the nomogram treatment line, or with elevated AST, prolonged serum acetaminophen half-life, and history suggestive of significant acetaminophen overdose; patients with concentrations above the Rumack-Matthew line are at increased risk of hepatic toxicity

Tricyclcic Antidepressants

  • Overdoses are monitored by EKG (better than blood concentrations, which do not correlate well with myocardial toxicity), prolonged QTc, widened QRS, arrhythmias
  • Death due to cardiac arrest
  • Effects include muscarinic blockade, block reuptake of norepinephrine, alpha adrenergic blockade, and membrane stabilization, all combine to give arrhythmias
  • Selective Serotonin Reuptake Inhibitors (SSRI) have greatly decreased use of this class of drugs, but they are used if patients fail to respond to SSRI


  • Anxiolytic/sedative/hypnotic depending on dose
  • Frequently encountered, almost never fatal unless combined with other CNS depressants (if coma is present look for other drugs as well, especially ethanol)
  • Antidote is flumazenil, which is a competitive antagonist, rarely used due to lack of overt toxicity
  • Flumazenil is contraindicated when patients co-ingest tricyclic antidepressants due to potential for precipation of seizures


  • Triad of coma, decreased respiration and pinpoint pupils suggests opiate overdose
  • Naloxone is competitive antagonist, administer 0.4 to 2 mg iv every 2-3 min until improvement (up to 10 mg); if no improvement is observed consider alternate diagnosis; important to remember that naloxone has a shorter half-life than other opiates; patients can improve dramatically and want to be discharged, but should be evaluated after 24-48 hours
  • This class of drugs includes: morphine, codeine, hydrocodone, hydromorphone, as well as others


  • Routes of administration: insufflated (snorted), smoked (free base), intravenous and oral (buccal mucosal)
  • Mechanism of action is blockade of norepinephrine reuptake and blockade of fast sodium channels, a local anesthetic effect
  • Toxicity is due to excessive norepinephrine, beta-1 receptor activation (increase in heart rate, contractility and conduction velocity) and alpha-1 receptor activation (vasoconstriction, increase in blood pressure and ischemia), leading to: unidirectional heart block and reentry, coronary artery disease and myocardial infarctions
  • Can become tolerant to stimulant effects, but not local anesthetic effects which can cause complete heart block
  • Usually detected as inactive metabolite benzoylecgonine in urine specimens
  • Active metabolite ethylbenzoylecgonine (cocaethylene) formed by transesterification with ethanol, if present; longer serum half-life than parent drug

Treatment for cocaine overdose

  • Stabilize the patient; if the patient reaches the hospital alive, prognosis is good due to rapid metabolism
  • IV diazepam for agitation and seizures
  • Ice baths for hyperthermia


  • Methamphetamine (crystal) very prevalent in San Diego (“Meth Capital of the World”)
  • Routes of administration include: smoking (free base form), intravenous and oral
  • Mechanism of action is to release catecholamines from synaptic vesicles, block reuptake and some direct effects on CNS receptors
  • Toxicity includes: hypertension, arrhythmias, agitation, hyperthermia, paranoia
  • Street grade often contaminated with adulterants (ephedrine, phenylpropanolamine, etc.)
  • Death usually not immediate but several hours after administration
  • Treatment is supportive


  • Sedative/hypnotic
  • Different kinetics for individual barbiturates are important; short-acting (pentobarbital, secobarbital) are more potent than long-acting (phenobarbital)
  • Necessary to identify type to interpret blood concentrations
  • Not seen very often anymore (used to be a major concern), as benzodiazepines have replaced them as the first line drug
  • Death due to respiratory arrest

Phenyclidine (PCP)

  • Localized to certain region of the country (Washington DC)
  • A dissociative veterinary anesthetic
  • Patients can be very combative (treat with major tranquilizer such as haloperidol)
  • Positive drug screen results should be confirmed by gas chromatography/mass spectrometry due to the low prevalence of this drug

Hallucinagoens (LSD, Mescaline, Marijuana, etc.)

  • Not detected by most routine toxicology screens
  • Generally not frankly toxic, behavioral toxicity more common (e.g., dangerous behavior)
  • Analysis of powders, drug-impregnated papers, pills sometimes useful in helping determining type of exposure

Designer Drugs (fentanyl, analogs, MDA, MDMA etc.)

  • Originally synthesized to bypass DEA regulations
  • Fentanyl analogs caused several deaths due to potency (e.g., “China White,” alpha-methylfentanyl); can be treated with naloxone
  • MDA and MDMA (“Ecstasy,” XTC) are amphetamine analogs with similar toxicity, yet cause a long term toxicity to serotonin containing neurons
  • Designer meperidine drug caused severe Parkinson’s disease (MPTP)

Digitalis (digoxin)

  • Cardiac drug with narrow therapeutic index, used to treat congestive heart failure (not a first line drug)
  • Inhibits sodium/potassium ATPase and increases force of contraction
  • Toxicity is characterized by A/V block, nausea/vomiting
  • Overdose treated with digoxin FAB antibody fragments (Digibind) which inactivate digoxin
  • FAB fragments can crossreact with immunoassays designed to detect digoxin, so interpretation of laboratory values when giving Digibind can be confusing
  • Monitor digoxin and serum K+ concentration (K+ increases with toxicity) in an overdose situation

Carbon monoxide (for concentration effect see table 1)

  • The most common cause of fatal chemical poisoning (primarily due to smoke inhalation)
  • Colorless, odorless, tasteless gas
  • Has 240 times the affinity for hemoglobin than oxygen (yields carboxyhemoglobin, COHb)
  • Normal nonsmokers 1-2% COHb, smokers 5-6% COHb
  • Treatment is fresh air, 100% O2 and possibly hyperbaric oxygen
Table 1 : Blood Carbon Monoxide -Concentrations and Effects
% COHb Effect*
10 Shortness of breath with vigorous exercise, dilation of cutaneous vessels
20 Shortness of breath, headache
30 Irritability, dizziness, nausea
40-50 Confusion, collapse
50-70 Syncope, coma
70-80 Death
* Greatly dependent on degree of activity


  • Most cases are due to children ingesting vitamin preparations with iron
  • Causes metabolic acidosis by a complex mechanism involving uncoupling of oxidative phosphoralation, renal failure, and formation of unbuffered hydrogen ions when iron is hydrated

A) Iron toxicity often has 4 phases

  • Stage I (immediate effects): may include: vomiting, diarrhea, abdominal pain, metabolic acidosis, hyperglycemia
  • Stage II (6 and 24 hours post ingestion): hypovolemia, hypotension, metabolic acidosis, serum concentrations may not have peaked yet
  • Stage III (12 to 24 hours post ingestion): multiple organ failure (GI, CNS, hepatorenal, coagulopathies, hypoglycemia); fulminant hepatic failure is commonly fatal
  • Stage IV (4-6 weeks post ingestion): gastric scarring and pyloric obstruction
  • Overdoses cause gastrointestinal corrosion

B) Treatment for iron poisoning

  • Serial monitoring of serum iron; maximum concentrations can occur up to 24 hours post-ingestion
  • Obtain creatinine, electrolytes, hemoglobin, prothrombin time, liver function tests and arterial blood gases; a positive radiograph confirms diagnosis, but a negative radiograph does not exclude overdose
  • Calculate elemental iron dose ingested; between 20 and 60 mg Fe/kg poses moderate risk, > 60 mg/kg has high risk for toxicity
  • < 350 $\mu$g/dl and no symptoms, no deferoxamine; use supportive care
  • > 300 $\mu$g/dl and symptomatic, give deferoxamine (15 mg/kg/hr) by continuous intravenous infusion
  • Deferoxamine chelates iron into a form that is rapidly excreted unchanged in urine (half-life of 6 hours), imparting a “vin rose” color to the urine

Lead (for concentration effect level see figure 9)

Essentials (from Ford, M.D. et al., Clinical Toxicology, 1st edition, Philadelphia: Saunders, 2001)

  • Multisystemic signs and symptoms include headache (in severe cases encephalopathy), abdominal pain, anemia, and, less commonly, gout, motor neuropathy, and renal insufficiency
  • Subclinical effects in children include neurocognitive deficits, growth retardation, and developmental delay
  • Laboratory tests may show anemia and basophilic stippling; definitive diagnosis is made by elevated blood lead concentration

Lead summary

  • One of the most common devastating environmental diseases of young children
  • Demyelinates nerve fibers causing peripheral neuropathy (wrist drop) and encephalopathy
  • Causes decreased IQ and developmental disturbances in children
  • Inhibits Fe incorporation into heme, and thus increases free erythrocyte protoporphyrin (FEP) which has been used to measure exposure; however, FEP generally is not as sensitive as blood lead levels
  • Complex cellular toxicity of lead due to interaction with calcium in cellular signaling leading to neuropathies as well as hypertension
  • Chronic lead poisoning causes hypochromic anemia, with basophilic stippling
  • Whole blood lead concentrations are used to triage patients, as 99% of circulating lead is in the red cells
  • 90% of adult body burden of lead is stored in bones
  • Most common form of treatment is EDTA (versenate), which chelates lead; the chelation product is excreted into the urine

Treatment for lead poisoning

  • Optimal treatment of lead intoxication combines decontamination, supportive care, and judicious use of chelating agents
  • CDC recommends children with blood lead >45 ug/dL get chelation therapy; Adults with elevated blood lead and symptoms of lead toxicity should receive chelation therapy
  • Chelation therapy includes CaNa2-EDTA intravenous
  • Some clinicians advise including dimercaprol (BAL) 3-5 mg/kg IM with EDTA therapy
  • Monitor blood lead 24-48 hours after chelation to monitor for rebound lead concentrations
  • Multiple rounds of chelation therapy are often necessary

Organophsophate or carbamate overdose

  • Used as insecticides
  • Patients present with SLUD (salivation, lacrimation, urination, and defecation) due to excessive cholinergic stimulation
  • Treat with atropine until drying of pulmonary secretions
  • Pralidoxime can be used with atropine for severe organophosphate poisonings (functions by reactivating cholinesterases; best if given within 24 hours)

Figure 9: Effects of lead in children correlated with blood lead concentrations


Case 1

A 23-year-old male patient presented to the emergency department smelling of alcohol and in an incoherent state with significant ataxia. His initial laboratory findings included:

Lab Result Reference Range
Arterial blood gas (pH) 6.85 (7.35-7.45)
pCO2 (mmHg) 14 (35-45)
Lactic acid (mmol/L) 30.3 (0.7-2.1)
Plasma ethanol (mg/dL) 217 Negative
Glucose (mg/dL) 63 (70-110)
Sodium (mmol/L) 129 (139-145)
SUN (mg/dL) 30 (8-23)
Osmolality (mOsm/kg) 376 (270-310)
Calcium (mg/dL) 8.2 (8.4-10.2)
Potassium (mmol/L) 4.3 (3.4-4.8)
Chloride (mmol/L) 78 (95-107)
HCO3 (mmol/L) 5 (22-28)

1. Calculate this patient’s osmol gap.
2. How much osmolality does the ethanol account for?
3. What are common causes of elevated osmolality?
4. Calculate this patient’s anion gap.
5. What potential toxin could explain these results?
6. What additional laboratory tests would you like to order?
7. What therapeutic options would you suggest?

Case 2

A 32-year-old male with history of depression, alcoholism, hepatitis C, and a past suicide attempt presented at 20:30 to the emergency department with acute Tylenol/Benadryl overdose. The patient reported taking 100 pills of Tylenol PM (acetaminophen 500 mg and Benadryl 25mg) at about 20:00. The admission laboratory findings included:

WBC 19.2 x 103 cells/mL with 60% segs, few bands, Hgb 14.1 g/dL, Hct 41.4 %

Na 141 mEq/L, K 3.9 mEq/L, Cl 106 mEq/L, total CO2 25 mmol/L, SUN 4 mg/dL, Creatinine 0.7 mg/dL, glucose 95 mg/dL, and Ca 8.7 mg/dL. Liver function tests were within normal limits as were coagulation studies

The admission serum acetaminophen concentration was 40 ug/mL.
1. How should this patient be treated?
2. Does this patient’s past medical history have any impact on his therapy?

After being in the emergency department for 3 hours his acetaminophen concentration rises to 175 ug/mL.

3. How do you interpret this concentration using the Rumack diagram and what does this tell you about potential toxicity?

After being in the emergency department for 5 hours his acetaminophen concentration rises to 192 ug/mL, and after 10 hours the acetaminophen concentration is 105 ug/mL.

4. What do the excretion kinetics demonstrate with regards to potential acetaminophen toxicity?
5. What other laboratory tests would be monitored in this case?

Case 3

South. Med. J. 98(2):241-244, 2005

An 18-year-old woman who weighed 61 kg was admitted to a community hospital, 4 to 5 hours after a one-time ingestion of approximately 100 ferrous sulfate pills (200 mg of FeS04 per pill). The patient had had an altercation with a friend, and the overdose was with suicidal intent. Shortly thereafter, she had nausea and one episode of scant hematemesis with epigastric pain and one episode of watery diarrhea. The emergency medical service personnel brought her to the hospital after being called by the patient.
At admission, the patient vomited visible pill fragments.

Laboratory Parameters Day 1 Day 2 Day 3 Day 4
Serum creatinine (normal range: 0.5-1.5 mg/dL) 0.7 0.7 0.6 0.4
Serum bicarbonate (normal range: 23-27 mmol/L) 20 19 19 22
Serum albumin (normal range: 3.5-4.5 g/dL) 3.9 3.0 3.0 2.7
Total bilirubin (normal range: 0.0-1.0 mg/dL) 0.3 3.1 2.3 2.3
Conjugated bilirubin (normal range: 0.0-0.3 mg/dL) 0.1 1.6 1.2 1.5
Alkaline phosphatase (normal range: 35-129 U/L) 59 87 84 85
Serum alanine aminotransferase (normal range: 4-41 U/L) 14 4,048 3,618 2,642
Serum AST (normal range: 4-37 U/L) 17 2,417 1,993 630
PTT (normal range: 24.7-35.8 seconds) 34.4 35.3 39.5 33.8
Prothrombin time (normal range: 12.8-14.8 seconds) 14.5 46.3 51.5 38.8
International normalized ratio 1.0 5.0 5.8 4.0
Platelets (normal range: 150-400 k/mm3) 225 166 165 164
White blood cell count (normal range: 3.5-10.5 k/mm3) 8.4 7.8 6.9 9.3
Iron (normal range: 37.158 ug/dL) 240 136 219 207
  1. How much elemental iron did this patient ingest?
  2. Is this a potentially toxic dose of iron?
  3. How should this patient be treated?
  4. How do you interpret her laboratory values on day 2?
  5. How would you expect her serum to appear on day 2?
  6. What other laboratory studies would be indicated?
  7. Is this a typical presentation for an iron overdose?

Case 4

A middle-aged man is brought to the Emergency Department ataxic and dysarthric with the strong odor of alcohol on his breath. The blood ethanol concentration is reported to be 130 mg/dL (0.13%), and the serum osmolality is found to be 320 mOsm/kg (nl 275 - 298). The man is monitored until he is ambulatory and is then discharged.

  1. How do you interpret the blood ethanol concentration?
  2. Does the blood ethanol concentration explain the ataxia and dysarthria?
  3. Why is the serum osmolality elevated?
  4. How long will it take for the patient's blood ethanol to decline to less than 100 mg/dL (0.10%)?

Case 5

A 17-year-old heroin addict lapses into coma shortly after "shooting up." After arrival at the Emergency Department he suffers a respiratory arrest. Following successful resuscitation of the patient, his pupils are noted to be miotic, and he has shallow respirations. After administration of four ampules of naloxone, the patient wakes up. His pupils and respirations return to normal, and he quickly becomes ambulatory. He objects to staying in the hospital.

  1. Is it safe to discharge the patient at this point?
  2. What laboratory tests should be ordered?
  3. Can naloxone be given routinely to the comatose patient?

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