Rosen & Barkin's 5-Minute Emergency Medicine Consult (487 page)

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Authors: Jeffrey J. Schaider,Adam Z. Barkin,Roger M. Barkin,Philip Shayne,Richard E. Wolfe,Stephen R. Hayden,Peter Rosen

Tags: #Medical, #Emergency Medicine

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
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BASICS
DESCRIPTION
  • Inhibit cyclooxygenase (COX), thereby blocking the conversion of arachidonic acid to prostaglandin.
  • Typically morbidity is low when an NSAID is ingested
  • Most literature on nonselective NSAID toxicity involves ibuprofen exposure likely due to its OTC availability.
  • Fatalities have been reported with large ingestions.
  • Greater potential for toxicity with underlying CHF or renal failure:
    • NSAIDs cause sodium and water retention and decrease renal blood flow.
    • Little overdose experience with the COX-2 inhibitors (celecoxib); treatment should be the same as for the traditional NSAIDs.
    • Patients may ingest rofecoxib and valdecoxib from stored supplies even though both are no longer available in US
ETIOLOGY
  • Nonsteroidal medications are available by prescription and over-the-counter.
  • NSAIDs include:
    • Diclofenac
    • Diflunisal
    • Etodolac
    • Fenoprofen
    • Ibuprofen
    • Indomethacin
    • Ketoprofen
    • Ketorolac
    • Meclofenamate
    • Meloxicam
    • Nabumetone
    • Naproxen
    • Oxaprozin
    • Piroxicam
    • Sulindac
    • Tolmetin
DIAGNOSIS
SIGNS AND SYMPTOMS
  • GI:
    • Nausea
    • Vomiting
    • Epigastric pain
  • CNS:
    • Drowsiness
    • Dizziness
    • Lethargy
    • Aseptic meningitis
    • Seizures
  • Cardiovascular:
    • Hypotension
    • Tachycardia
  • Pulmonary:
    • Eosinophilic pneumonia
    • Apnea
    • Hyperventilation
  • Renal:
    • Acute renal failure, hyperkalemia
    • Acute tubular necrosis
    • Acute interstitial nephritis
  • Liver:
    • Hepatocellular injury
    • Cholestatic jaundice
  • Metabolic:
    • Mild, short-lived metabolic acidosis
  • Hypersensitivity:
    • Aseptic meningitis
    • Asthma exacerbation
    • Angioedema, urticaria
ESSENTIAL WORKUP
  • Generally, NSAID ingestion results in mild toxicity.
  • Exact identification of drug helpful:
    • Subtle toxicologic differences among the NSAIDs
    • Aseptic meningitis more common with ibuprofen exposure
    • Liver toxicity more common with diclofenac and sulindac exposure
DIAGNOSIS TESTS & NTERPRETATION
Lab
  • Electrolytes, BUN/creatinine, glucose:
    • Baseline renal function
    • Check for metabolic acidosis.
  • CBC
  • Arterial blood gas for large overdoses
  • PT/PTT:
    • False-positive bilirubin/ketone dipstick with etodolac ingestion
  • Acetaminophen and salicylate level—patients often confuse salicylate, acetaminophen, and NSAID products thinking they are all the same.
  • NSAID difficult to detect on toxicology screens and is not beneficial in management
DIFFERENTIAL DIAGNOSIS

Agents causing metabolic acidosis, altered mental status, and GI irritation:

  • Salicylates
  • Isoniazid
  • Ethylene glycol
  • Methanol
  • Isopropanol
TREATMENT
PRE HOSPITAL

Collect prescription bottles/medications for identification in the ED.

INITIAL STABILIZATION/THERAPY
  • ABCs
  • Naloxone, thiamine, dextrose (or Accu-Chek) for altered mental status
ED TREATMENT/PROCEDURES
  • Supportive care
  • Administer activated charcoal.
  • Extracorporeal methods to enhance elimination are not beneficial due to high degree of plasma protein binding.
MEDICATION
  • Activated charcoal slurry: 1–2 g/kg up to 90 g PO
  • Dextrose: D50W 1 amp (50 mL or 25 g; peds: D25W 2–4 mL/kg) IV
  • Naloxone (Narcan): 2 mg (peds: 0.1 mg/kg) IV or IM initial dose
  • Thiamine (vitamin B
    1
    ): 100 mg (peds: 50 mg) IV or IM
Pediatric Considerations

Piroxicam, naproxen, ketoprofen, and mefenamic acid have caused seizures in children.

FOLLOW-UP
DISPOSITION
Admission Criteria
  • Protracted vomiting, hematemesis
  • CNS depression, seizure activity
  • Metabolic acidosis
  • CHF, hypotension, hypertension
  • Renal failure
Discharge Criteria

Nontoxic ingestion in a patient who is asymptomatic 6–8 hr after ingestion

FOLLOW-UP RECOMMENDATIONS

Psychiatry follow-up/referral for intentional ingestion.

PEARLS AND PITFALLS
  • Investigate for coingestions for all NSAID overdoses.
  • Obtain acetaminophen and salicylate level on all patients who present with suspected NSAID ingestion.
  • NSAID poisoning is generally benign, except with massive overdoses; patients with underlying CHF, coronary artery disease may be at higher risk of toxicity
ADDITIONAL READING
  • Dajani EZ, Islam K. Cardiovascular and gastrointes-tinal toxicity of selective cyclo-oxygenase-2 inhibitors in man.
    J Physiol Pharmacol
    . 2008;59(suppl 2):117–133.
  • Frei MY, Nielsen S, Dobbin MD, et al. Serious morbidity associated with misuse of over-the-counter codeine-ibuprofen analgesics: A series of 27 cases.
    Med J Aust
    . 2010;193:294–296.
  • Halen PK, Murumkar PR, Giridhar R, et al. Prodrug designing of NSAIDs.
    Mini Rev Med Chem
    . 2009;9:124–139.
CODES
ICD9

976.0 Poisoning by local anti-infectives and anti-inflammatory drugs

ICD10
  • T39.391A Poisoning by other nonsteroidal anti-inflammatory drugs, accidental, init?
  • T39.392A Poisoning by other nonsteroidal anti-inflammatory drugs, self-harm, init?
  • T39.394A Poisoning by other nonsteroidal anti-inflammatory drugs, undet?, init?
NURSEMAID'S ELBOW
Neha P. Raukar

Daniel L. Savitt
BASICS
DESCRIPTION

The most common elbow injury in children <5 yr old.

ETIOLOGY
  • Sudden traction of the distal radius leads to a portion of the annular ligament slipping over the radial head and becoming trapped between the radius and the capitellum. Traction can occur by swinging the child, wrestling, and lifting the child by the arms.
  • By the time the child is 5 yr, the annular ligament is thick and strong and resists tearing and/or displacement.
DIAGNOSIS

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