#46 – Heart Failure

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Definition of Heart Failure

  • Complex clinical syndrome resulting from conditions that affect the structure and/or function of the heart culminating in reduced systemic perfusion that is inadequate to meet the metabolic demands of the body
    • Main effect is decreased cardiac output
  • No more “congestive”

Epidemiology

  • 5.7 million adults in US
    • 550,000 new cases each year
    • 1.4 million are under 60 years of age
  • Annual incidence is 10 per 1,000 population AFTER 65 years of age
  • 287,000 deaths per year
    • 1 in 9 deaths included heart failure as contributing causes
    • Most common diagnosis in hospital patients over 65 years of age
  • Responsible for 11 million office visits each year in the US and more hospitalizations than all cancers COMBINED
  • 50% of adults who develop heart failure die within 5 years
  • Cost to US is ~$30 billion/year

Causes and Pathophysiology

Any condition that leads to alteration in left ventricular structure or function can cause heart failure and the specific causes depends on the preservation of ejection fraction.  There is considerable overlap between these with coronary artery disease and hypertension causes the majority of cases.

The problem is that the rest of the body feel the effects of the decreased cardiac output and activate the neurohormonal systems to compensate.  The issue is that this makes the heart failure worse and it is a vicious cycle until it can be broken.

Signs and Symptoms

  • History
    • Reduced cardiac output
      • Fatigue, weakness
    • Excessive fluid accumulation
      • Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, leg swelling, abdominal discomfort, palpitations
  • Physical Examination
    • Appearance and Vital Signs
      • Resting sinus tachycardia
      • Narrow pulse pressure
      • Cool, pale skin (peripheral vasoconstriction)
    • Volume Assessment
      • Pulmonary congestion
        • Rales on auscultation
        • AUDIO
      • Peripheral edema
        • Leg swelling, hepatic congestion, ascites, scrotal edema
      • Elevated jugular venous pressure
        • Hepatojugular reflux
  • Cardiac
    • S3 with gallop (if systolic failure)
    • S4 (if diastolic failure)
    • Displaced PMI past midclavicular line and below the 5th intercostal space
    • Pulsus alternans
      • Evenly spaced alternating strong and weak peripheral pulses
Pulsus Alternans

Framingham Clinical Criteria for Heart Failure

Clinical Decision Rule for Heart Failure

  • Age
    • < 60 = 0 points
    • 60-70 = 4 point
    • 71-80 = 7 points
    • > 80 = 10 points
  • History of coronary disease = 15 points
    • AMI, CABG, PCI
  • Loop diuretic = 10 points
  • Displaced PMI = 20 points
  • Rales = 14 points
  • Irregularly irregular pulse = 11 points
  • Heart murmur = 10 points
  • Pulse Rate = (HR-60)/3 points
  • Elevated jugular venous pressure = 12 points
  • NT-proBNP (pg/mL)
    • < 100 = 0 points
    • 100-200 = 8 points
    • 200-400 = 16 points
    • 400-800 = 24 points
    • 800-1600 = 32 points
    • 1600-3200 = 40 points
    • > 3200 = 48 points
  • Interpretation
    • < 13 points = < 10% probability of heart failure
    • > 54 points = > 70% probability of heart failure

Diagnostic Studies

  • Electrocardiogram
    • Not really diagnostic, but can evaluate for current ischemia, past infarction, low voltage, dysrhythmias
    • A normal EKG makes systolic dysfunction unlikely (98% NPV)
  • Laboratory studies
    • Brain natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP)
      • Released from ventricles  when stretched
      • < 100 pg/mL = very high NPV and rule out heart failure
    • Cardiac enzymes
    • CBC
    • CMP
  • Chest Radiography
    • Increased cardiothoracic ratio
    • Cephalization of pulmonary vessels
    • Kerley B-lines
    • Pleural effusions
  • Echocardiography
    • Recommended for all patient with dyspnea and suspicion of heart failure
    • Provides vital information on:
      • Ejection fraction
        • < 40% = reduced = systolic
        • > 50% = preserved = diastolic
      • Valvular disease
        • Aortic and mitral regurgitation/insufficiency
      • Atrial and Ventricular size and function
        • Enlarged left ventricle = systolic
        • Left atrial enlargement with normal/small left ventricle = diastolic
      • Left ventricular wall size
        • Thin = systolic
        • Thick = diastolic
  • Exercise/Stress Testing
    • Evaluate for underlying coronary disease, as well as potential candidates for transplantation
      • Patients with a peak oxygen uptake (VO2) < 14 mL/kg/min have better outcomes with transplanted
  • Coronary angiography
    • Not strongly recommended as part of the work-up, but can be useful to evaluate for underlying coronary disease and get an accurate ejection fraction

Classification and Grading

Current Nomenclature

Heart failure with reduced ejection fraction (HFrEF)

  • Systolic
  • < 40% EF

Heart failure with preserved ejection fraction (HFpEF)

  • Diastolic
  • > 50% EF

Management

  • Heart failure with reduced ejection fraction (HFrEF)
    • Lifestyle Modifications
      • Smoking cessation
      • Restrict sodium to < 3g/day
      • Restrict fluid to < 2L/day
    • Pharmacotherapy
      • Loop diuretic (if overload is present)
        • Furosemide, bumetanide, torsemide
      • ACE inhibitors
        • Lisinopril, enalapril
      • Angiotension receptor-neprilysin inhibitor (ARNI)
        • NYHA II or III and:
          • BNP > 150 ng/mL or hospitalized with last 12 months
          • SBP > 100 mmHg
          • GFR > 30 mL/min
          • No history of angioedema
      • ARB
        • Candesartan, valsartan
      • Beta blockers
        • Carvedilol, metoprolol, bisoprolol
      • Mineralcorticoid receptor antagonist (MRA)
        • Spironolactone, eplerenone
      • Selective sinus node inhibitor
        • Ivabradine
        • Need a resting HR > 70 bpm on maximum BB therapy
    • Ischemic heart disease
      • Increase coronary perfusion
      • Decrease myocardial demand
    • Hyperlipidemia
      • High-intensity statin
    • Cardiac rehabilitation
  • Heart failure with preserved ejection fraction (HFpEF)
    • Differences with HFrEF
      • ACEI/ARB not as useful
      • MRA used more often
      • Diuretics OK but be careful for volume depletion
      • Don’t use BB unless compelling indication

References

  1. Tan LB, Williams SG, Tan DK, Cohen-Solal A. So many definitions of heart failure: are they all universally valid? A critical appraisal. Expert review of cardiovascular therapy. 2010; 8(2):217-28. [pubmed]
  2. CDC Heart Failure Data Sheet. https://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_heart_failure.htm
  3. Emory Healthcare Heart Failure Statistics. https://www.emoryhealthcare.org/heart-vascular/wellness/heart-failure-statistics.html
  4. Mann DL, Chakinala M. Heart Failure: Pathophysiology and Diagnosis. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 20e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com.ezproxy.uthsc.edu/content.aspx?bookid=2129&sectionid=192028958
  5. Davie AP, Francis CM, Caruana L, Sutherland GR, McMurray JJ. Assessing diagnosis in heart failure: which features are any use? QJM : monthly journal of the Association of Physicians. 1997; 90(5):335-9. [pubmed]
  6. Kelder JC, Cramer MJ, van Wijngaarden J, et al. The diagnostic value of physical examination and additional testing in primary care patients with suspected heart failure. Circulation. 2011; 124(25):2865-73. [pubmed]
  7. Davie AP, Francis CM, Love MP, et al. Value of the electrocardiogram in identifying heart failure due to left ventricular systolic dysfunction. BMJ (Clinical research ed.). 1996; 312(7025):222. [pubmed]
  8. Maisel A. B-type natriuretic peptide levels: diagnostic and prognostic in congestive heart failure: what’s next? Circulation. 2002; 105(20):2328-31. [pubmed]
  9. Knudsen CW, Omland T, Clopton P, et al. Diagnostic value of B-Type natriuretic peptide and chest radiographic findings in patients with acute dyspnea. The American journal of medicine. 2004; 116(6):363-8. [pubmed]
  10. Badgett RG, Mulrow CD, Otto PM, Ramírez G. How well can the chest radiograph diagnose left ventricular dysfunction? Journal of general internal medicine. 1996; 11(10):625-34. [pubmed]
  11. Bart BA, Shaw LK, McCants CB, et al. Clinical determinants of mortality in patients with angiographically diagnosed ischemic or nonischemic cardiomyopathy. Journal of the American College of Cardiology. 1997; 30(4):1002-8. [pubmed]
  12. Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. Journal of the American College of Cardiology. 1993; 22(4 Suppl A):6A-13A. [pubmed]
  13. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2013; 128(16):1810-52. [pubmed]
  14. Yancy CW, Jessup M, et al. 2016 ACC/AHA/HFSA Focused Update on New Pharmacological Therapy for Heart Failure: An Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. Circulation. 2016; 134(13):e282-93. [pubmed]
  15. Ponikowski P, Voors AA, Anker SD, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC)Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. European heart journal. 2016; 37(27):2129-2200. [pubmed]
  16. Parch J, Powell C. No longer failing to treat heart failure: A guideline update review. JAAPA : official journal of the American Academy of Physician Assistants. 2019; 32(1):11-15. [pubmed]

PAINE #PANCE Pearl – Cardiovascular

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Question

Hypercholesterolemia is most commonly a laboratory diagnosis, but there are some class physical examination findings that can be seen. What are they?

Answer

There are five (5) classic physical exam findings associated with hypercholesterolemia and are more common in familial, genetic hyperlipoprotenemias.

  • Tendon xanthomas (most commonly at the achilles tendon and hands)
  • Planar xanthomas on hands and feet
  • Xanthelasmas (soft, cholesterol filled, yellow plaques on the upper eyelids)
  • Corneal arcus (white/grey ring around cornea)
  • Lipemia retinalis (white colored retinal vessels associated with hypertriglyceridemia)
  • Planar xanthomas on hands and feet
  • Xanthelasmas (soft, cholesterol filled, yellow plaques on the upper eyelids)
  • Corneal arcus (white/grey ring around cornea)
  • Lipemia retinalis (white colored retinal vessels associated with hypertriglyceridemia)
  • Xanthelasmas (soft, cholesterol filled, yellow plaques on the upper eyelids)
  • Corneal arcus (white/grey/yellow ring around cornea)
  • Lipemia retinalis (white colored retinal vessels associated with hypertriglyceridemia)

Ep-PAINE-nym

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Bundle of Kent

Other known aliases – atrioventricular bypass tract

Definition – As discussed in the WPW eponym, the Bundle of Kent is an accessory conduction pathway between the atrium and ventricle on either the right or left side of the heart.

Clinical Significance – this pathway occurs in up to 0.3% of patients and the cause of Wolff-Parkinson-White syndrome. It bypasses the traditional conduction system and allows for pre-excitation tachydysrthymias.

History – Named after Albert Frank Stanley Kent (1863-1958), an English physiologist who received his degree in 1886 from the Magdalen College of Oxford. He first described lateral atrioventricular connections in a monkey heart in 1893 and erroneously believed these were part of the normal specialized conduction system. These findings generated a lot of controversy at the time and were actually rejected by several notable anatomists and physiologists. In fact, in 1955, Lev and Learner dissected 33 neonatal hearts and found no evidence of “normal” lateral conduction systems.

References

  • Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  • Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  • Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  • Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  • Up To Date. www.uptodate.com
  • Kent AF. Researches on the Structure and Function of the Mammalian Heart. The Journal of physiology. 1893; 14(4-5):i2-254. [pubmed]
  • LEV M, LERNER R. The theory of Kent; a histologic study of the normal atrioventricular communications of the human heart. Circulation. 1955; 12(2):176-84. [pubmed]

Ep-PAINE-nym

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Wolff-Parkinson-White Syndrome

Other known aliases – ventricular pre-excitation with arrhythmia, auriculoventricular accessory pathway syndrome

Definition – paroxysmal supraventricular tachycardia caused by conduction through an abnormal accessory bypass tract between the atria and ventricles known as the Bundle of Kent. There are two types depending on the side of the heart it effects; Type A is between the right atrium and ventricle and Type B is between the left atrium and ventricle.

Clinical Significance – Patients with WPW can numerous cardiac dysfunction symptoms including tachydysrhythmias, palpitations, dyspnea, presyncope, syncope, and sudden cardiac arrest. It is characterized by the triad of abnormalities on EKG of widened QRS, shortened PR interval, and slurring of the initial part of the QRS (called a delta wave).

History – Named after Louis Wolff (1898-1972), Sir John Parkinson (1885-1976), and Paul Dudley White (1886-1973). Dr. Wolff was an American cardiologist who received his medical doctorate from Harvard Medical School in 1922. Dr. Parkinson was an English cardiologist who received his medical doctorate from University of Freiburg in 1910 and was also knighted by King George in 1948. Dr. White was an American cardiologist who received his medical doctorate from Harvard Medical School in 1911 and one of the founding presidents for the American Heart Association. He was a prominent advocate for preventive medicine receiving many national and international awards for his efforts to advance the importance of diet, exercise, and weight control in the prevention of cardiovascular disease. They collaborated to publish a series of 11 cases entitled “Bundle‐Branch Block with Short P‐R Interval in Healthy Young People Prone to Paroxysmal Tachycardia” in the American Heart Journal in 1930. It should be noted that Dr. Frank Norman Wilson and Dr. Alfred Wedd both described and published these findings in 1915 and 1921.

  • Wolff
  • Parkinson
  • White

References

  • Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  • Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  • Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  • Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  • Up To Date. www.uptodate.com
  • Wolff L, Parkinson J, White PD. Bundle‐Branch Block with Short P‐R Interval in Healthy Young People Prone to Paroxysmal Tachycardia. American Heart Journal. 1930;5(6):985-704 [article]

PAINE #PANCE Pearl – Dermatology

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Question

Vitiligo and tinea versicolor are both hypomelanocytic dermatologic afflications. What are some ways to differentiate these two conditions?

Answer

  • Location
    • Tinea versicolor – trunk and proximal extremities
    • Vitiligo – can occur anywhere, but most common on hands and face
  • Color
    • Tinea versicolor – hypopigmented, more prominent with sun exposure
    • Vitiligo – milk or chalk-white, no change with sun exposure
  • Wood’s lamp
    • Tinea versicolor – fluoresce yellow/green
    • Vitiligo – fluoresce blue/white

Ep-PAINE-nym

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Langer’s Lines

Other known aliases – Langer’s lines of skin tension, cleavage lines

Definition – topographical lines on the human body that correspond to the natural orientation of the collagen fibers of the dermis and are parallel to the orientation of the underlying muscle fibers

Clinical Significance – Incisions made on the skin that run parallel with these lines produce much less tension on the wound, heal better with less scarring, and have a much better cosmetic appearance.  This is important in cosmetic surgery applications, as well as elective surgical procedures when you can select where to make your incision.

History – Named after Karl Langer (1819-1887), an Austrian anatomist, who received his medical doctorate from the Universities of Vienna and Prague.  He worked under Joseph Hyrtl as a prosector for the University of Vienna and later becoming the director in 1874.  In his famous procedure discovering these tension lines, he punctured circular holes on the skin of cadavers and noticed that they would result in ellipisoidal wounds.  By following the direction of these ellipses, he was able to topographically map these lines on the entire body.  He did give credit to Baron Dupuytren as being the first to observe this phenomenon and published his findings in 1861 entitled “Zur Anatomie und Physiologie der Haut. Über die Spaltbarkeit der Cutis”

Karl Langer

References

Ep-PAINE-nym

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Dix-Hallpike Manuever

Other known aliases – Nylen-Barany test

Definition – Starting supine, the patient’s head is rotated to one side and then quickly lowered to supine with the neck extended over the exam table.  Patient is observed for nystagmus for 30 seconds and then returned to supine and observed for another 30 seconds.  This is then repeated for the other side.

Clinical Significance – The Dix-Hallpike maneuver is the diagnostic maneuver to induce vertigo and nystagmus in patients with benign paroxysmal positional vertigo by relocating canaliths to the posterior semicircular canals.

History – Named after Margaret Ruth Dix (1902-1991), a British neuro-otologist, and Charles Skinner Hallpike (1900-1979), an English otologist.  Dr. Dix earned her medical doctorate in 1937 from the Royal Free Hospital School of Medicine and Dr. Hallpike earned his from the University of London in 1926.  Dr. Dix was training to become a surgeon when she was injured during the World War II air raids of London and suffered facial and ocular injuries which forced her to change her medical career path.  It was during this time she was hired by Dr. Hallpike to pursue the field of neuro-otology.  Their work resulted in a landmark series in the Proceedings of the Royal Society of Medicine and Annals of Otology, Rhinology, and Laryngology.  It was this series in 1952 where one of the papers describing their eponymous finding  entitled “The Pathology, Symptomatology, and Diagnosis of Certain Common Disorders of the Vestibular System” was published.

References

  • Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  • Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  • Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  • Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  • Up To Date. www.uptodate.com
  • DIX MR, HALLPIKE CS. The pathology symptomatology and diagnosis of certain common disorders of the vestibular system. Proceedings of the Royal Society of Medicine. 1952; 45(6):341-54. [pubmed]
  • Margaret Ruth Dix – Royal College of Surgeons [link]

#45 – Preseptal vs Orbital Cellulitis

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Definitions

  • Orbital Septum
    • Membranous structure that extends from orbit to the tarsal plate and is the anterior boundary of the orbital compartment
  • Preseptal Cellulitis
    • Infection of the soft tissues ANTERIOR to the orbital septum
  • Orbital Cellulitis
    • Infections of the soft tissues POSTERIOR to the orbital septum

Numbers

  • Preseptal cellulitis is much more common than orbital (>90%)
  • Both conditions are more common in children than adults

Pathogenesis

  • Preseptal
    • Usually due to superficial dermatologic infections (though the data has wide variability in reported causes)
  • Orbital
    • Bacterial rhinosinusitis
      • Due to perforations in the lamina papyracea
    • Other causes:
      • Ophthalmologic surgery
      • Dacrocystitis
      • Orbital trauma
      • Dental infections

Microbiology

  • Preseptal
    • Staphylococcus aureus (skin causes)
      • Increasing incidence of MRSA
    • Streptococcus pneumoniae (sinus/nasopharynx causes)
  • Orbital
    • Same as preseptal, but include:
      • Fungal (mucormycosis and Aspergillus spp.)

Signs and Symptoms

  • Both present with unilateral eyepain, erythema, and edema, but:
  • Preseptal
    • No pain with eye movement
    • Sclera is white
Preseptal Cellulitis (sclera is white and quiet)

    • Orbital
      • Painful eye movement
      • Vision changes (acuity, diplopia)
      • Proptosis
      • Sclera injection and chemosis
      • Decreased pupillary response
Orbital cellulitis (notice sclera is red and angry with chemosis)

Complications

  • Complications of preseptal cellulitis are rare, but orbital cellulitis can lead to:
    • Vision loss (3-11%)
    • Subperiosteal abscess
    • Orbital abscess
    • Cavernous sinus thrombosis

Diagnostic Studies

  • CBC with differential may be helpful in risk stratification or atypical presentation
  • Preseptal
    • None! –> Clinical diagnosis
  • Orbital
    • Indications for CT scan
      • Inability to assess vision or deteriorating vision
      • Double vision
      • Inability to examine due to age
      • Proptosis
      • Restricted, limited, and/or painfuleye movement
      • Edema extending beyond eyelid margin
      • Lack of improvement in 24 hours on antibiotics
      • Cyclical fevers
      • Signs of CNS involvement
      • ANC > 10,000 cell/microL
a. proptosis, b. soft tissue inflammation, c. choroidal detachment, d. retrobulbar inflammation, e. optic nerve sheet enhancement
medial orbital subperiosteal abscess with left sided ethmoid sinusitis
  • Blood cultures are not routinely recommended but should be entertained in ill appearing children prior to antibiotic administration

Treatment

  • Preseptal
    • Outpatient
      • > 1 year old and no signs of systemic toxicity
      • Treatment duration typically 5-7days, but treatment should continue until eyelid erythema and swelling have resolved
    • Inpatient
      • < 1 year old, children who can’t cooperate with exam, toxic appearance, or outpatient treatment failing to improve in 24-48 hours
      • Follow orbital cellulitis treatment
  • Orbital
    • Medical
      • Staphylococcal coverage
        • Vancomycin
      • Streptococcal coverage
        • Ceftriaxone
        • Cefotaxime
      • Anaerobic coverage
        • Metronidazole
      • Improvement should occur within24-48 hours
      • Transition to oral therapy when:
        • Afebrile and periorbital signs are resolving
        • Typically 3-5 days
        • Follow culture data (if obtained) or follow outpatient preseptal cellulitis regimen
      • Treat for a total of 2-3 weeks
    • Surgical indications
      • Radiographically identified abscess
        • Typically > 10mm, though small abscesses respond to antibiotics well
      • Intracranial extension
      • Failure to respond to antibiotic treatment
      • Threat to vision

References

  1. Hauser A, Fogarasi S. Periorbital and orbital cellulitis. Pediatrics in review. 2010; 31(6):242-9. [pubmed]
  2. Botting AM, McIntosh D, Mahadevan M. Paediatric pre- and post-septal peri-orbital infections are different diseases. A retrospective review of 262 cases. International journal of pediatric otorhinolaryngology. 2008; 72(3):377-83. [pubmed]
  3. Horton JC. Disorders of the Eye. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 20e New York, NY: McGraw-Hill; http://accessmedicine.mhmedical.com/content.aspx?bookid=2129&sectionid=192011900
  4. Chaudhry IA, Shamsi FA, Elzaridi E, Al-Rashed W, Al-Amri A, Arat YO. Inpatient preseptal cellulitis: experience from a tertiary eye care centre. The British journal of ophthalmology. 2008; 92(10):1337-41. [pubmed]
  5. Moran GJ, Krishnadasan A, Gorwitz RJ, et al. Methicillin-resistant S. aureus infections among patients in the emergency department. The New England journal of medicine. 2006; 355(7):666-74. [pubmed]
  6. Brook I, Frazier EH. Microbiology of subperiosteal orbital abscess and associated maxillary sinusitis. The Laryngoscope. 1996; 106(8):1010-3. [pubmed]
  7. Erickson BP, Lee WW. Orbital Cellulitis and Subperiosteal Abscess: A 5-year Outcomes Analysis. Orbit (Amsterdam, Netherlands). 2015; 34(3):115-20. [pubmed]
  8. Howe L, Jones NS. Guidelines for the management of periorbital cellulitis/abscess. Clinical otolaryngology and allied sciences. 2004; 29(6):725-8. [pubmed]
  9. Rudloe TF, Harper MB, Prabhu SP, Rahbar R, Vanderveen D, Kimia AA. Acute periorbital infections: who needs emergent imaging? Pediatrics. 2010; 125(4):e719-26. [pubmed]
  10. Tanna N, Preciado DA, Clary MS, Choi SS. Surgical treatment of subperiosteal orbital abscess. Archives of otolaryngology–head & neck surgery. 2008; 134(7):764-7. [pubmed]
  11. Greenberg MF, Pollard ZF. Medical treatment of pediatric subperiosteal orbital abscess secondary to sinusitis. Journal of AAPOS : the official publication of the American Association for Pediatric Ophthalmology and Strabismus. 1998; 2(6):351-5. [pubmed]