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  • Drug overdoses can be accidental or intentional. They occur through the misuse of illicit drugs, used to get high, or when a person takes more than the medically recommended dose of a prescription or over-the-counter drug and cannot detoxify the drug fast enough to avoid dangerous side effects.
  • This may occur suddenly, when a large amount of the drug is taken at one time, or gradually, as a drug builds up in the body over a longer period of time. Prompt medical attention may save the life of someone who accidentally or deliberately takes an overdose. Drug overdose symptoms vary widely depending on the specific drug used. Knowing the signs and symptoms and the proper action to take can help you avoid a tragedy. While these are obvious signs of drug overdose, the list is certainly not all inclusive.
  • If you encounter a person who exhibits one or more of the signs and symptoms, do what you would do in any medical emergency:  Call 911 immediately. Depressant Overdose Opioids, benzodiazepines and alcohol are all depressants, which means they slow the central nervous system, including breathing and heart rate. Too much of any one of these substances on their own or in combination can kill...










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Regardless of the type of drug or poison ingested, the principles of initial supportive care are the same. Airway patency with adequate ventilation and oxygenation must be obtained. Unless otherwise contraindicated, oxygen therapy (100%) should be administered. Hypoventilation and obtunded airway reflexes require tracheal intubation and mechanical ventilation. Many clinicians routinely administer naloxone (up to 2 mg), dextrose 50% (50 mL), and thiamine (100 mg) intravenously to all obtunded or comatose patients until a diagnosis is established; this may help exclude or treat opioid overdose, hypoglycemia, and Wernicke-Korsakoff syndrome, respectively. The dextrose can be omitted if a glucose determination can be obtained by a fingerstick. In this case, intubation should be performed prior to naloxone because the respiratory depression is likely due to both the codeine and the diazepam.

Blood, urine, and gastric fluid specimens should be obtained and sent for drug screening. Blood is also sent for routine hematological and chemistry studies (including liver function). Urine is usually obtained by bladder catheterization, and gastric fluid can be aspirated from a nasogastric tube; the latter should be placed after intubation to avoid pulmonary aspiration. Alternatively, emesis material may be tested for drugs in conscious persons.

Hypotension should generally be treated with intravenous fluids unless the patient is obviously in pulmonary edema; an inotrope or vasopressor may be necessary in some instances. Seizure activity may be the result of hypoxia or a pharmacological action of a drug (tricyclic antidepressants) or poison. Seizure activity is unlikely in this patient because she ingested diazepam, a potent anticonvulsant.

Should flumazenil be administered?

Flumazenil should generally not be administered to patients who overdose on both a benzodiazepine and an antidepressant and those who have a history of seizures. Reversal of the benzodiazepine’s anticonvulsant action can precipitate seizure activity in such instances. Moreover, as is the case with naloxone and opioids, the half-life of flumazenil is shorter than that of benzodiazepines. Thus, it is often preferable to ventilate the patient until the benzodiazepine effect dissipates, the patient regains consciousness, and the respiratory depression resolves.

Should any other antidotes be given?

Because the patient also ingested an unknown quantity of acetaminophen (paracetamol) administration of N-acetylcysteine (NAC; Mucomyst) should be considered. Acetaminophen toxicity is due to depletion of hepatic glutathione, resulting in the accumulation of toxic metabolic intermediates. Hepatic toxicity is usually associated with ingestion of more than 140 mg/kg of acetaminophen. NAC prevents hepatic damage by acting as a sulfhydryl donor and restoring hepatic glutathione levels. If the patient is suspected of having ingested a toxic dose of acetaminophen, an initial dosage of NAC (140 mg/kg orally or by nasogastric tube) should be administered even before plasma acetaminophen levels are obtained; additional doses are given according to the measured plasma level. If the patient cannot tolerate oral or gastric administration of NAC, if the patient is pregnant, or if the risk of hepatotoxicity is high, NAC should be given intravenously.

What measures might limit drug toxicity?

Toxicity might be reduced by decreasing drug absorption or enhancing elimination. Gastrointestinal absorption of an ingested substance can be reduced by emptying stomach contents and administering activated charcoal. Both methods can be effective up to 12 h following ingestion. If the patient is intubated, the stomach is lavaged carefully to avoid pulmonary aspiration. Emesis may be induced in conscious patients with syrup of ipecac 30 mL (15 mL in a child). Gastric lavage and induced emesis are generally contraindicated for patients who ingest caustic substances or hydrocarbons because of a high risk of aspiration and worsening mucosal injury.

Activated charcoal 1-2 g/kg is administered orally or by nasogastric tube with a diluent. The charcoal irreversibly binds most drugs and poisons in the gut, allowing them to be eliminated in stools. In fact, charcoal can create a negative diffusion gradient between the gut and the circulation, allowing the drug or poison to be effectively removed from the body.

Alkalinization of the serum with sodium bicarbonate for tricyclic antidepressant overdose is beneficial because, by increasing pH, protein binding is enhanced; if seizures occur the alkalinization prevents acidosis-induced cardiotoxicity.

What other methods can enhance drug elimination?

The easiest method of increasing drug elimination is forced diuresis. Unfortunately, this method is of limited use for drugs that are highly protein bound or have large volumes of distribution. Mannitol or furosemide with saline may be used. Concomitant administration of alkali (sodium bicarbonate) enhances the elimination of weakly acidic drugs such as salicylates and barbiturates; alkalization of the urine traps the ionized form of these drugs in the renal tubules and enhances urinary elimination. Hemodialysis is usually reserved for patients with severe toxicity who continue to deteriorate despite aggressive supportive therapy.


Treatment with Intralipd of overdose of a lipophilic drug.


Complications of Injecting Drug Use

  • Local problems—Abscess (Figures 240-2 
    Image not available.

    A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of ­Richard P. Usatine, MD.)

    and 240-3; Abscess), cellulitis, septic thrombophlebitis, local induration, necrotizing fasciitis, gas gangrene, pyomyositis, mycotic aneurysm, compartmental syndromes, and foreign bodies (e.g., broken needle parts) in local areas.2
    • IDUs are at higher risk of getting methicillin-resistant Staphylococcus aureus(MRSA) skin infections that the patient may think are spider bites (Figure 240-4).
    • Some IDUs give up trying to inject into their veins and put the cocaine directly into the skin. This causes local skin necrosis that produces round atrophic scars (Figure 240-5).
  • IDUs are at risk for contracting systemic infections, including HIV and hepatitis B or hepatitis C.
    • Injecting drug users are at risk of endocarditis, osteomyelitis (Figures 240-6and 240-7), and an abscess of the epidural region. These infections can lead to long hospitalizations for intravenous antibiotics. The endocarditis that occurs in IDUs involves the right-sided heart valves (see Chapter 50, Bacterial Endocarditis).2 They are also at risk of septic emboli to the lungs, group A β-hemolytic streptococcal septicemia, septic arthritis, and candidal and other fungal infections.


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A 45-year-old healthy businessman just returned from a trip to Vietnam where he was traveling on vacation. Five days after his return, he developed fever and a headache followed 12 hours later by diarrhea and abdominal pain. The next day, he had >10 bowel movements in 12 hours, the final two with gross blood in the stool, prompting his presentation to the emergency department. His vital signs are as follows: temperature 37.8°C, HR 90 bpm, RR 14 breaths/min, and oxygen saturation 98% on room air. Gram stain of a stool specimen identifies a small curved helical-shaped gram-negative rod. You suspect a Campylobacter spp. Which of the following statements regarding his most likely infection is true?

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The correct answer is A. You answered C.

The answer is A. (Chap. 192) This patient is suffering from classic traveler’s diarrhea (of which, Campylobacter is a common cause). A prodrome of fever, headache, myalgia, and/or malaise often occurs 12–48 hours before the onset of diarrheal symptoms. The most common signs and symptoms of the intestinal phase are diarrhea, abdominal pain, and fever. The degree of diarrhea varies from several loose stools to grossly bloody stools; most patients presenting for medical attention have ≥10 bowel movements on the worst day of illness. Abdominal pain usually consists of cramping and may be the most prominent symptom. Pain is usually generalized but may become localized; Campylobacter jejuni infection may cause pseudoappendicitis. Fever may be the only initial manifestation of C jejuni infection, a situation mimicking the early stages of typhoid fever. Even among patients presenting for medical attention with Campylobacter enteritis, not all clearly benefit from specific antimicrobial therapy. Indications for therapy include high fever, bloody diarrhea, severe diarrhea, persistence for >1 week, and worsening of symptoms. Macrolides are generally the empirical treatment of choice with <10% of isolates demonstrating resistance. A single dose of azithromycin 500 mg is effective and is the regimen of choice; a 5- to 7-day course of erythromycin (250 mg orally four times daily or—for children—30–50 mg/kg/d in divided doses) is also effective. Resistance to quinolones as well as to tetracyclines is substantial; approximately 22% of U.S. isolates in 2010 were resistant to ciprofloxacin. Except in infection with Campylobacter fetus, bacteremia is uncommon, developing most often in immunocompromised hosts and at the extremes of age. Due to its proclivity to cause bacteremia and distant organ involvement, C fetus has a far worse prognosis than other subtypes. Systemic infection with C fetus is much more often fatal than that due to related species; this higher mortality rate reflects in part the population affected.


A 75-year-old triathlete complains of gradually worsening vision over the past year. It seems to be involving near and far vision. The patient has never required corrective lenses and has no significant medical history other than diet-controlled hypertension. He takes no regular medications. Physical examination is normal except for bilateral visual acuity of 20/100. There are no focal visual field defects and no redness of the eyes or eyelids. Which of the following is the most likely diagnosis?

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The correct answer is A. You answered A.

Age-related macular degeneration is a major cause of painless, gradual bilateral central visual loss. It occurs as nonexudative (dry) or exudative (wet) forms. Recent genetic data have shown an association with the alternative complement pathway gene for complement factor H. The mechanism link for that association is unknown. The nonexudative form is associated with retinal drusen that leads to retinal atrophy. Treatment with vitamin C, vitamin E, beta-carotene, and zinc may retard the visual loss. Exudative macular degeneration, which is less common, is caused by neovascular proliferation and leakage of choroidal blood vessels. Acute visual loss may occur because of bleeding. Exudative macular degeneration may be treated with intraocular injection of a vascular endothelial growth factor antagonist (bevacizumab or ranibizumab). Blepharitis is inflammation of the eyelids usually related to acne rosacea, seborrheic dermatitis, or staphylococcal infection. Diabetic retinopathy, now a leading cause of blindness in the United States, causes gradual bilateral visual loss in patients with long-standing diabetes. Retinal detachment is usually unilateral and causes visual loss and an afferent pupillary defect.


Mr. Jenson is a 40-year-old man with a congenital bicuspid aortic valve who you have been seeing for more than a decade. You obtain an echocardiogram every other year to follow the progression of his disease knowing that bicuspid valves often develop stenosis or regurgitation requiring replacement in middle age. Given his specific congenital abnormality, what other anatomic structure is important to follow on his biannual echocardiograms?

Next Question
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The correct answer is A. You answered A.

The answer is A. (Chap. 282) Bicuspid aortic valve is among the most common of congenital heart cardiac abnormalities. Valvular function is often normal in early life and thus may escape detection. Due to abnormal flow dynamics through the bicuspid aortic valve, the valve leaflets can become rigid and fibrosed, leading to either stenosis or regurgitation. However, pathology in patients with bicuspid aortic valve is not limited to the valve alone. The ascending aorta is often dilated, misnamed “poststenotic” dilatation; this is due to histologic abnormalities of the aortic media and may result in aortic dissection. It is important to screen specifically for aortopathy because dissection is a common cause of sudden death in these patients.



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