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The Advanced and Difficult Airway Course

The Ultrasound Course

The Clinical Skills & Procedure Workshop

The Clinical Skills & Procedure Workshop + The Airway Course

The Clinical Skills & Procedure Workshop + The Ultrasound Course

Dermatology Overview

Dermatology Essentials

Definition

Cellulitis: infection of dermis and subcutaneous fat

Impetigo: superficial purulent lesions, esp. on face and extremities. Commonly with bullae and/or golden crust

Erysipelas: raised erythematous lesion with clear borders

Folliculitis: hair follicle inflammation. Superficial and limited to the epidermis.

Furunculosis: hair follicle infection that extend to dermis. Multiple = carbuncle

Necrotizing Infection: Deeper SSTI that involve fascial and/or muscle compartments

Etiology

Microbiology

  • Cellulitis: primarily Staph and Strep, incl. MRSA. In immunocomp./diabetics, GNRs also
    • Other etiologies: cat/dog bite P. moltocida; gardening Sporothrix; salt water Vibrio vulnificus; puncture wound → Pseudomonas
  • Impetigo: Strep or Staph
  • Erysipelas: group A Strep usu.
  • Folliculitis/furunculosis: S. aureus, Pseudomonas
  • Necrotizing Infections: Polymicrobial (eg strep and GNRs in Type I, Fournier’s), Group A Strep, S. aureus, Aeromonas hydrophila, Vibrio vulnificus

At risk: athletic teams, military, prison, MSM, communities with MRSA infxn, Diabetic

High risk for more aggressive infection: splenectomy, immunocompromised

Differential Diagnosis

  • Cellulitis
  • Impetigo
  • Erysipelas
  • Folliculitis
  • Furunculosis
  • Necrotizing fasciitis
  • Myonecrosis
  • Calciphylaxis
  • Cutaneous metastasis from neoplasms (especially adenocarcinoma)
  • Graft-versus-host disease (in appropriate population)
  • Sweet syndrome

Patient History

  • Recent trauma to the affected area?
  • Any recent surgeries (hip replacement is risk factor)?
  • Ask about the presence of HIV, diabetes, liver disease, or kidney disease.
  • History of IV drug abuse or subcutaneous injection.
  • Recurrent Cellulitis: Assess for predisposing conditions such as edema, obesity, eczema, venous stasis, and toe web abnormalities.
  • Recurrent Abscesses: Search for local causes such as pilonidal cyst, HS, or foreign body. Consider 5-day decolonization (intranasal mupirosin, daily chlorhexidine). Consider neutrophil disorder if abscesses began in childhood.

Physical Exam

  • Evaluate affected area for erythema, edema, warmth, and pain on palpation.
  • Look for lymphangiitis (erythematous tracks under the skin marking an inflamed lymphatic system), palpate for lymphadenopathy.
  • Assess for evidence of necrotizing infection: systemic toxicity with high temperature, hypotension, disorientation, lethargy, skin discoloration or bullous lesions, anesthesia, firm skin with wooden-hard induration, pain extending beyond cutaneous erythema, pain out of proportion to exam

Work Up

Note: Diagnosis is largely clinical

Laboratory:

  • CBC with diff, ESR/CRP if concern for osteo, CK if concern for necrotizing infection or pyomyositis.
  • Furuncle/pustule can be aspirated for gram stain and culture.
  • For cellulitis, blood cultures are generally low yield, but should be obtained in patients undergoing chemo, neutropenic patients, and those who suffered animal bites.

Imaging:

  • If concern for osteo, xray; consider MRI
  • If concern for necrotizing infection can look for gas in fascial planes on x-ray or CT, but this is highly insensitive

Triage

More serious presentations of skin and soft tissue infections:

  • Toxic shock syndrome: fever, HA, vomiting, myalgias, pharyngitis, diarrhea, diffuse rash with desquamation. Hypotension and shock.
  • Osteomyelitis: infection of bone due to hematogenous seeding or direct spread from overlying focus.
  • Necrotizing fasciitis: infection and necrosis of superficial fascia, subq fat, and deep fascia. Clues: rapidly spreading cellulitis, systemic toxicity (inc TSS), pain out of proportion to exam, bullae formation, gangrene, crepitus. Surgical and medical emergency.
  • Gas gangrene: Clostridial myonecrosis, a fulminant skeletal muscle infection. C. perfringins usually in the setting of trauma; C. septicum in setting of cancer. Surgical and medical emergency.

Treatment

Purulent (furuncle/carbuncle/abscess):

  • Mild: I & D
  • Moderate: I & D, send for culture and sensitives
    • Empiric treatment: Bactrim 1-2 DS tab BID or Doxycycline 100mg BID
    • Defined treatment: MRSA: Bactrim 1-2 DS tab BID, MSSA: Dicloxacillin 250 Q6H or Cephalexin 500 Q6H or Cefadroxil 500mg po q12.
  • Severe: I & D, send for culture and sensitiivies
    • Empiric treatment: Vancomycin or Daptomycin or Linezolid or Ceftaroline
    • Defined treatment: MRSA: similar to empiric, MSSA: Nafcillin or Cefazolin or Clindamycin (if Susceptible)

Nonpurulent (necrotizing infection/cellulitis/erysipelas):

  • Mild: impetigo: topical mupirocin; oral treatment: Penicillin VK or Cephalosporin (eg Cephalexin 500mg PO Q6H) or Dicloxacillin 500mg PO Q6H or Clindamycin 300mg PO Q8H
  • Moderate: IV therapy: penicillin or Cefriaxone or Cefazolin or Clindamycin 300mg PO Q8H or 600mg IV Q8H
  • Severe: emergency surgical evaluation/debridement to rule out necrotizing process
    • Empiric treatment: Vancomycin PLUS Piperacillin/Tazobactam
    • Defined treatment for necrotizing infections:
      • Strep. pyogenes:Penicillin PLUS Clindamycin
      • Vibrio vulnificus:Doxycycline PLUS Ceftazidime
      • Aeromonas hydrophila:Doxycycline PLUS Ciprofloxacin
      • Polymicrobial: Vancomycin PLUS Piperacillin/Tazobactam

Duration of Therapy: 5-7 Days

Treatment Notes:

Erythema may initially worsen with antibiotics 2/2 local bacterial killing.

– For cellulitis, elevation of the affected extremity is essential to treatment.

– For Staph aureus infections (eg suppurative cellulitis) in 2014 at Hopkins susceptibilities were: TMP-SMX 87-88%, Tetracycline 89-91%, and Clindamycin 46-60%.

– For Beta-hemolytic Strep infections (eg non-suppurative cellulitis) all strains are susceptible to penicillin. At Hopkins there are high rates of resistance to TMP-SMX and tetracyclines and variable rates of resistance to Clindamycin.

– If you are concerned for a necrotizing infection, CONSULT SURGERY. Empiric antibiotic treatment with vancomycin (or linezolid) PLUS zosyn (or carbapenem) should be initiated. Clindamycin can be added to inhibit toxin production.

References

  1. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10-52. [PMID:24973422]
  2. Swartz MN. Clinical practice. Cellulitis. N Engl J Med. 2004;350(9):904-12. [PMID:14985488]

Resources

Heart Failure

Cardiology Essentials

Definition

Syndrome characterized by impaired myocardial performance and progressive maladaptive neurohormonal activation of the cardiovascular system leading to circulatory insufficiency to meet the body’s demands.

Systolic heart failure or heart failure with reduced ejection fraction (HFrEF): Clinical diagnosis of heart failure and an EF of less than 50%.

Diastolic heart failure or heart failure with preserved ejection fraction (HFpEF): Clinical signs and symptoms of heart failure with evidence of normal or preserved EF and evidence of abnormal LV diastolic function by Doppler echocardiography or cardiac catheterization

Right heart failure: Majority of cases are a result of left heart failure, although isolated pulmonary diseases can also cause this syndrome.

Etiology

  • Non-ischemic dilated cardiomyopathy (familial or idiopathic)
  • Hypertrophic cardiomyopathy
  • Restrictive cardiomyopathy
  • Cardiomyopathy as a result of fibroelastosis
  • Mitochondrial disease
  • Left ventricular non-compaction
  • Ischemic cardiomyopathy
  • Stress induced cardiomyopathy
  • Valvular obstruction or insufficiency
  • Hypertensive cardiomyopathy
  • Inflammatory (lymphocytic, eosinophilic, giant cell myocarditis)
  • Infectious (Chagas, Lyme disease, HIV, viral, bacterial, or fungal infections)
  • Endocrine disorders (thyroid disease, adrenal insufficiency, pheochromocytoma, acromegaly)
  • Familial storage disease (hemochromatosis, glycogen storage disease, Hurler syndrome, Anderson-Fabry disease)
  • Amyloidosis
  • Connective tissue disease (SLE, polyarteritis nodosa, scleroderma, myositis, sarcoidosis)
  • Muscular dystrophies
  • Neuromuscular disease (Friedreich ataxia, Noonan disease)
  • Toxins (alcohol, anthracyclines, radiation)
  • Tachyarrhythmia

Pathophysiology

Progressive disorder initiated by a form of myocardial injury either sudden (MI or myocarditis) or chronic insults (familial, metabolic, HTN, valve disease, shunting) that result in maladaptive compensatory mechanisms.

These mechanisms include activation of the sympathetic nervous system and activation of the RAS system which overtime lead to pump dysfunction and circulatory collapse.

Differential Diagnosis

Other entities that may look like acute decompensated heart failure:

  • Acute coronary syndrome
  • Interstitial lung disease
  • Pneumonia
  • ARDS
  • Other sources of volume overload such as CKD/ESRD vs cirrhosis, pulmonary hypertension, PE, cardiac tamponade, constrictive or restrictive pericarditis

Patient History

Ask about the signs and symptoms:

  • Worsening dyspnea at rest or exertion?
  • Fatigue?
  • Orthopnea?
  • PND?
  • Weight gain?
  • Increased edema?
  • Lightheadedness?
  • indigestion?
  • Chest heaviness?
  • Fever?
  • Chest pain?
  • Timing of symptom onset?

Ask about triggers of acute decompensation:

  • dietary indiscretion? foods high in Na like lunch meats, chips, canned foods, fast foods?
  • missed medication doses (diuretic)?
  • are they weighing themself daily? adjusting diuretics?
  • any signs or symptoms that an ischemic event has occurred?
  • do they consume alcohol excessively?

Physical Exam

  • Weight gain (if possible look at previous discharge weights)
  • Elevated jugular venous pulsations (Key!), hepatojugular reflux
  • Orthopnea
  • Pulmonary rales
  • Third and/or fourth heart sound
  • Pedal edema
  • Sacral edema in patients who are mostly in bed

Work Up

Laboratory

  • Renal function panel, liver function panel (CMP): Patients who are volume overloaded due to acute decompensated heart failure often have an acute kidney injury and hepatic congestion.
  • Potassium, calcium (CMP), magnesium. May need to check more frequently (e.g. bid) especially if pt will be diuresed.
  • CBC: Anemia is present in up to 40% of patient with heart failure.
  • Consider pro-BNP if volume exam not helpful; compare to prior.
  • If patient is presenting newly with HF and/or etiology is unclear:
    • troponin and lipid profile, especially if HFrEF the pt may need further work up for ischemic disease
    • TSH
    • in the right patient, consider iron studies (hemochromatosis), serum ceruloplasmin (Wilson’s), trypanosoma cruzi IgG (chagas), blood alcohol level or CDT etc.

Imaging

  • ECG, chest x-ray, echocardiography

Other imaging and diagnostic modalities that can be considered based on the patient’s history:

  • Cardiac MR
  • Nuclear imaging
  • Right heart catheterization
  • Left heart catheterization
  • CT angiogram.
  • Endomyocardial biopsy

 

Triage

Strongly consider step-down or ICU if evidence of decompensation with hypoperfusion (cold and wet):

Altered mental status, Cold extremities, evidence of organ hypoperfusion: increasing lactate or rising creatine, narrow pulse pressures

Risk Stratification