Rosen & Barkin's 5-Minute Emergency Medicine Consult (120 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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ED TREATMENT/PROCEDURES
  • Nonseptic bursitis:
    • Rest and removal of aggravating factors (e.g., avoid direct pressure and repetitive use; protective padding where necessary)
    • Ice affected areas for 10 min, 4 times a day until improved; may alternate with heat.
    • NSAIDs for at least 7 days; best if continued for 5 days after improvement to help prevent recurrence
    • If fluctuant, then aspirate and place compression dressing
    • If no improvement within 5–7 days and infection has been ruled out (by culture), injection of lidocaine and corticosteroids may be considered:
      • Mix 2 mL of 2% lidocaine with appropriate depo-corticosteroid (see below) and inject 1–3 mL of this mixture into the bursa using sterile technique.
      • Steroid injections should not be repeated until 4 wk have passed, and no >2 injections per bursa should be performed without consultation.
  • Septic bursitis:
    • Superficial bursae: Aspiration and antibiotics may be sufficient with close follow-up.
    • Other major bursae: Antibiotics and drainage of bursae (leaving in perforated drainage catheter can reduce period of treatment and avoid eventual bursectomy)
    • Febrile patients may need IV antibiotics.
    • Base antibiotic choice on the Gram stain when available or empiric coverage based on local susceptibilities:
      • Penicillinase-resistant penicillins may be used if Gram stain shows gram-positive cocci in chains but should be broadened for MRSA coverage if cocci in clusters are seen
      • If gram-negative organisms are found, blood cultures should be done and another primary source for the infection should be sought.
  • Antibiotics should be continued for 5–7 days beyond resolution of signs of infection (thus may require follow-up)
  • Treat associated diseases as needed (e.g., gout).
MEDICATION
  • NSAIDs (many choices; a few are listed here):
    • Naprosyn: 500 mg PO q12h
    • Ibuprofen: 600 mg PO q6h (peds: 5–10 mg/kg PO q6h)
    • Ketorolac: 30 mg IV/IM q6h or 10 mg PO q4h–q6h
    • Meloxicam: 7.5 mg PO q12h or 15 mg PO daily
  • Corticosteroids for intrabursal injection:
    • Triamcinolone acetonide: 20–40 mg (1st choice)
    • Methylprednisolone acetate: 20–40 mg
    • Dexamethasone acetate/sodium: 8 mg
FOLLOW-UP
DISPOSITION
  • Most patients may be treated as outpatients.
  • Most patients respond to therapy in 3–4 days and may follow-up within 1 wk or PRN.
  • Septic bursitis requires repeated bursal aspiration every 3–5 days until sterile.
Admission Criteria
  • Patients with systemic inflammatory response syndrome (SIRS), large surrounding cellulitis, unable to take PO antibiotics, failed outpatient therapy, or immunosuppressed
  • Unusual organisms, extrabursal primary site, or deep bursal involvement
Discharge Criteria
  • Able to tolerate pain
  • Septic bursitis are safe to discharge if appropriately treated and close follow-up is secure
Issues for Referral

Rheumatology or orthopedic referral is recommended for patients who do not respond to intrabursal steroids or recurrent bursitis or need operative management.

FOLLOW-UP RECOMMENDATIONS
  • Close follow-up for septic bursitis
  • PRN to the emergency department for worsening symptoms but otherwise follow-up with primary care physician.
PEARLS AND PITFALLS
  • Exam alone may be unreliable in distinguishing between traumatic and septic bursitis:
    • Aspiration and fluid analysis may be the only method of distinguishing.
  • Beware of risk for GI hemorrhage associated with PO NSAIDs and for nephrotoxicity with ketorolac
  • If presents with the 4 signs of infection—
    humor, dolor, rubor,
    and
    calor
    —then it is likely septic but still needs an aspiration and culture
  • Beware of the potential of seeding organisms to adjacent joints when aspirating septic bursae.
ADDITIONAL READING
  • DeLee JC, Drez D, Miller MD, ed.
    DeLee & Drez’s Orthopaedic Sports Medicine: Principles and Practice
    . 3rd ed. Philadelphia, PA: Saunders Elsevier; 2010:889–891, 1209–1212, 1246–1249, 1455–1458, 2030–2041.
  • Fayad LM, Carrino JA, Fishman EK. Musculoskeletal infection: Role of CT in the emergency department.
    Radiographics
    . 2007;27(6):1723–1736.
  • Larsson L, Baum J. The syndromes of bursitis.
    Bull Rheum Dis
    . 1986;36(1):1–8.
  • Stephens MB, Beutler Al, O’Connor FG. Musculoskeletal injections: A review of the evidence.
    Am Fam Physician
    . 2008;78(8):971–976.
  • Baumbach SF, Wyen H, Perez C, et al. Evaluation of current treatment regimens for prepatellar and olecranon bursitis in Switzerland.
    Europ J Trauma Emerg Surg.
    2013;39(1):65–72.
CODES
ICD9
  • 726.10 Disorders of bursae and tendons in shoulder region, unspecified
  • 726.33 Olecranon bursitis
  • 727.3 Other bursitis
ICD10
  • M70.20 Olecranon bursitis, unspecified elbow
  • M71.9 Bursopathy, unspecified
  • M75.50 Bursitis of unspecified shoulder
CALCIUM CHANNEL BLOCKER POISONING
Christopher S. Lim

Steven E. Aks
BASICS
DESCRIPTION
  • 3 classes of calcium channel blockers (CCBs):
    • Phenylalkylamines (verapamil):
      • Vasodilation resulting in a decrease in BP
      • Negative chronotropic and inotropic effects: Reflex tachycardia not seen with a drop in BP.
    • Dihydropyridine (nifedipine):
      • Decreased vascular resistance resulting in a drop in BP
      • Little negative inotropic effect: Reflex tachycardia occurs
    • Benzothiazepine (diltiazem):
      • Decreased peripheral vascular resistance leading to a decrease in BP
      • Heart rate (HR) and cardiac output initially increased
      • Direct negative chronotropic effect, which leads to a fall in HR
  • Effects of calcium channel blockade
    • Calcium plays key role in cardiac and smooth muscle contractility
    • CCBs prevent
      • the entry of calcium, resulting in a lack of muscle contraction
      • the normal release of insulin from pancreatic islet cells, resulting in hyperglycemia
DIAGNOSIS
SIGNS AND SYMPTOMS
  • Cardiovascular:
    • Hypotension
    • Bradycardia
    • Reflex tachycardia (dihydropyridine)
    • Conduction abnormalities/heart blocks
  • Neurologic:
    • CNS depression
    • Coma
    • Seizures
    • Agitation
    • Confusion
  • Metabolic:
    • Hyperglycemia
History
  • Inquire about risk of medication error.
  • Inquire about risk of suicidal ideation with intent.
  • Inquire about possible exposure to medications with a pediatric patient.
Physical-Exam
  • Hypotension
  • Bradycardia
  • Skin may be warm instead of cool and clammy.
ESSENTIAL WORKUP

ECG:

  • Bradycardia (reflex tachycardia with nifedipine)
  • Conduction delays: QRS complex prolongation
  • Heart blocks
DIAGNOSIS TESTS & NTERPRETATION
Lab
  • Ionized calcium level when administering calcium
  • Digoxin level if patient taking digoxin (dictate safety of calcium administration)
  • CBC
  • Electrolytes, BUN, creatinine, glucose
    • Strongly consider CCB overdose in the setting of bradycardia, hypotension, and hyperglycemia
    • Degree of hyperglycemia may correlate with severity of CCB poisoning in nondiabetics
  • Toxicology screen if coingestants suspected
DIFFERENTIAL DIAGNOSIS
  • β-Blocker toxicity
  • Clonidine toxicity
  • Digitalis toxicity
  • Acute myocardial infarction with heart block
TREATMENT

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