Rosen & Barkin's 5-Minute Emergency Medicine Consult (175 page)

TREATMENT

Rarely required in absence of concomitant pathology

General:

• Primarily symptomatic
  
• Wash area with mild soap and water
  
• Remove or avoid offending agent (including washing clothes)
  
• Cool, wet compresses; especially effective during acute blistering phase
  
• Antipruritic agents:
  
  • Topical:
    
    • Calamine lotion, corticosteroids (do not penetrate blisters); avoid benzocaine or hydrocortisone-containing products, which may further sensitize skin
      
  • Systemic: Antihistamines, corticosteroids
    
• Aluminum acetate (Burrows) solution: Weeping surfaces
  

Irritant dermatitis:

• Remove offending agent
  
• Wash well with soap and warm water
  
• Decrease wet/dry cycles (hand washing)
  
  • Alcohol-based cleansers decrease repetitive trauma
    
• Bland emollient
  
• Topical steroids for severe cases (ointment preferred), medium to high potency (hands), BID for several weeks
  

Allergic dermatitis:

• Topical steroids (ointment preferred) BID for 2–3 wk:
  
  • Face: Low potency
    
  • Arms, legs, and trunk: Medium potency
    
  • Hands and feet: High potency
    
• Oral steroids for severe cases
  

Rhus dermatitis:

• Follow general measures plus:
  
  • Wash all clothes and pets that have come in contact with the plant; oil persists and is contagious
    
  • Oatmeal baths can provide soothing relief
    
  • Aseptic aspiration of bullae may relieve discomfort
    
  • Severe reaction (>10% TBSA): Systemic corticosteroids for 2–3 wk with gradual taper:
    
    • Premature termination of corticosteroid therapy may result in rapid rebound of symptoms
      

Shoe dermatitis:

• Follow general measures plus:
  
  • Wear open-toe, canvas, or vinyl shoes.
    
  • Control perspiration: Change socks, use absorbent powder.
    

Diaper dermatitis:

• Follow general measures plus:
  
  • Topical zinc oxide, petrolatum ointment, or aquaphor
    
  • Change diapers after each soiling
    

Systemic:

• Antihistamine (H
  ₁
  -receptor antagonist, 1st and 2nd generation):
  
  • Cetirizine: Adults and children >6 yr, 5–10 mg PO daily (peds: Age 2–6 yr, 2.5 mg PO daily BID)
    
  • Diphenhydramine hydrochloride: 25–50 mg IV/IM/PO q6h PRN (peds: 5 mg/kg/24h div. q6h PRN)
    
  • Fexofenadine: 60 mg PO BID or 180 mg PO daily (peds: Age 6–12 yr, 30 mg PO BID)
    
  • Hydroxyzine hydrochloride: 25–50 mg PO IM up to QID PRN (peds: 2 mg/kg/24h PO div. q6h or 0.5 mg/kg IM q4–6h PRN
    
  • Loratadine: 10 mg PO BID
    
  • For refractory pruritus: Doxepin: 75 mg PO daily may be effective.
    
• Corticosteroid:
  
  • Prednisone: 40–60 mg PO daily (peds: 1–2 mg/kg/24h, max. 80 mg/24h) div. daily/BID
    
• For refractory pruritis:
  
  • Doxepin: 75 mg PO daily may be effective.
    

Topical:

• Aluminum acetate (Burrows) solution: Apply topically for 20 min TID until skin is dry.
  
• Calamine lotion: q6h PRN
  
• Topical corticosteroid: Triamcinolone ointment 0.025, 0.1%; cream 0.025, 0.1%; lotion 0.025, 0.1% TID or QID daily
  
  • Caution: Do not apply to face or eyelids
    

• Topical steroids
  
• Oral antihistamines
  

Oral steroids

FOLLOW-UP

Rarely indicated unless severe systemic reaction or significant secondary infection

• Symptomatic relief
  
• Adequate follow-up with primary care physician or dermatologic specialist
  

• Follow up with primary care physician in 2–3 days for recheck
  
• Return to ED for: Facial swelling, difficulty breathing, mucosal involvement causing decreased PO intake
  

• Remove offending agent
  
• Beware of progression to systemic anaphylaxis (e.g., latex allergy)
  
• Watch out for concurrent bacterial infections
  
• Rhus dermatitis wounds are no longer contagious after washed with soap and water:
  
  • Be sure to wash all clothes and animals that have come in contact with plant as oil remains contagious.
    

• Goldner R, Tuchinda P (2012). Irritant Contact Dermatitis in Adults,
  Up To Date
  , retrieved Jan 13, 2013 from
  http://www.uptodate.com/contents/irritant-contact-dermatitis-in-adults
  .
  
• Hogan DJ, ed. (2011). Allergic Contact Dermatitis,
  Medscape
  . Retrieved Dec 12, 2012 from
  http://emedicine.medscape.com/article/1049216-overview
  .
  
• Hogan DJ, ed. (2011). Irritant Contact Dermatitis,
  Medscape
  . Retrieved Dec 12, 2012 from
  http:emedicine.medscape.com/article/1049353-overview
  .
  
• Marx JA, Hockberger RS, Walls RM, et al., eds.
  Rosen’s Emergency Medicine: Concepts and Clinical Practice
  . 7th ed. St. Louis, MO: Mosby; 2009.
  
• Rietschel RL, Fowler JF, eds.
  Fisher’s Contact Dermatitis
  . 6th ed. Ontario, ON: BC Decker; 2008.
  

CODES

• 692.2 Contact dermatitis and other eczema due to solvents
  
• 692.9 Contact dermatitis and other eczema, unspecified cause
  
• 692.81 Dermatitis due to cosmetics
  

BASICS

Right ventricular hypertrophy (RVH) or dilation caused by elevated pulmonary artery pressure. RVH due to a
systemic
defect or congenital heart disease is not classified as cor pulmonale.

• Acute cor pulmonale:
  
  • Right ventricle is dilated and muscle wall stretched thin
    
  • Overload due to acute pulmonary hypertension (HTN)
    
  • Most often caused by massive pulmonary embolism
    
• Chronic cor pulmonale:
  
  • RVH with eventual dilation and right-sided heart failure
    
  • Caused by an adaptive response to chronic pulmonary HTN
    
  • Predominately occurs as a result of alveolar hypoxia
    
• The pulmonary circulation is a low-resistance, low-pressure system:
  
  • The pulmonary arteries are thin walled and distensible
    
  • Mean pulmonary arterial pressure is usually 12–15 mm Hg
    
  • Normal left arterial pressure is 6–10 mm Hg
    
  • The resulting pressure difference driving the pulmonary circulation is only 6–9 mm Hg
    
• 3 factors affect pulmonary arterial pressure:
  
  • Cardiac output
    
  • Pulmonary venous pressure
    
  • Pulmonary vascular resistance
    
• Pulmonary HTN can arise through a number of mechanisms:
  
  • A marked increase in cardiac output
    
  • Left-to-right shunt secondary to congenital heart disease
    
  • Hypoxia:
    
    • The most common cause of increased pulmonary vascular resistance
      
    • Hypoxic pulmonary vasoconstriction is an adaptive vasomotor response to alveolar hypoxia
      
    • A compensatory rise in pressure is seen in the pulmonary arterial system, so flow is maintained across the pulmonary vascular bed.
      
  • Pulmonary embolus causes a similar change by increasing resistance to pulmonary blood flow
    
  • Dramatic rises in blood viscosity or intrathoracic pressure also impede blood flow
    
• Pulmonary HTN is classified into 5 groups
  
  • Group 1: Pulmonary arterial HTN
    
  • Group 2: Pulmonary HTN owing to left heart disease
    
    • RV dysfunction in this category is not considered cor pulmonale
      
  • Group 3: Pulmonary HTN owing to lung diseases and/or hypoxia
    
  • Group 4: Chronic thromboembolic pulmonary HTN
    
  • Group 5: Pulmonary HTN with unclear multifactorial mechanisms
    

• ∼86,000 patients die from COPD each yr:
  
  • Associated RV failure is a significant factor in many of these cases, and accounts for 10–30% of heart failure admissions in US.
    
• In patients >50 yr with COPD, 50% develop pulmonary HTN and are at risk of developing cor pulmonale.
  
• The course of cor pulmonale is generally related to the progression of the underlying disease process.
  
• Once cor pulmonale develops, patients have a 30% chance of surviving 5 yr.