#37 – Conjunctivitis





The conjunctiva is a mucous membrane that that lines the surface of the eyelids (palpebral) and globe up to the limbus (bulbar).


The conjunctiva itself is made up of non-keratinized squamous epithelium with goblet cells and substantia propria, which is highly vascularized.

The important thing to remember is that the conjunctiva is transparent, unless inflamed (which is termed “injected”).

Bacterial Conjunctivitis


  • Bacterial conjunctivitis is more common in children than adults (though viral is most common overall).
  • Transmission is spread from direct contact with infected drainage or contaminated objects
  • Pathogens
    • S. aureus, S. pneumoniae, H. influenza, M. catarrhalis
  • Signs and Symptoms
    • Redness and drainage in one eye
    • Matted shut in the morning
    • Drainage
      • Continues throughout the day
      • Thick and purulent
  • Special Concerns
    • Neisseria gonorrhoeae
      • Concurrent STI symptoms
      • Rapid onset of symptoms (< 12 hours)
      • More pain and tenderness with marked chemosis and lymphadenopathy
      • Admission with emergency ophthalmology evaluation
        • Keratitis and perforation may occur

Viral Conjunctivitis


  • Most common cause of acute conjunctivitis
  • Highly contagious and is spread through direct contact with drainage or contaminated objects
  • Pathogens
    • Adenovirus is the most common
  • Viral prodrome
    • Fever, adenopathy, pharyngitis, URI, conjunctivitis
  • Drainage
    • Watery, mucoserous drainage
    • Matted/thick in the morning with scant, watery drainage throughout the day
  • Corneal injection with burning/gritty sensation
  • Starts unilateral and spreads to contralateral eye within 48 hours of symptoms onset
  • Follicular pattern on palpebral conjunctiva
  • Self-limiting process
    • Worsens for 3-5 days with gradual resolution over the next 7-10 days

Allergic Conjunctivitis


  • Caused by airborne allergens that initiate an IgE-mediated local response with mast cell degranulation and release of histamine
  • Drainage
    • Watery and stringy
  • Signs and Symptoms
    • Bilateral eye involvement
    • Periorbital edema
    • Allergic symptoms
      • Sneezing, coughing, rash, sore throat
    • Profuse itching
    • Marked chemosis and injection
      • Bullous chemosis may occur in severe causes or as a result of itching

Non-Infectious/Non-Allergic Conjunctivitis


  • Causes
    • Mechanical or chemical insult
      • Patients with chronic dry eyes
      • Patients s/p irrigation from chemical splash
      • Transient foreign body
  • Self-limiting and spontaneously improve within 24 hours

Distinguishing Between The Types


Special Considerations for Contact Lens Wearers


These patients are at an increased risk for Pseudomonas infections and should be advised to refrain from wearing their contacts and to have a formal evaluation by an ophthalmologist to rule-out serious infection.  Any antibacterial treatment in these patients should also cover for Pseudomonas.



With the exception of gonococcal conjunctivitis, all types are self-limiting and will improve on their own.  Having said that, bacterial conjunctivitis will improve faster with topical antibiotics.



  • Erythromycin 5mg/gram ointment – 1cm ribbon 4x/day for 5-7 days
  • Trimethoprim-polymyxin B 0.1%-10,000 units/mL – 1-2 drops 4x/day for 5-7 days
  • Ciprofloxacin 0.3% – 1-2 drops 4x/day for 5-7 days


Viral and Allergic

  • Antihistamine/decongestant drops
    • Pheniramine/naphazoline – 1-2 drops 4x/day
    • Olopatadine 0.2% – 1 drop daily
    • Azelastine 0.05% – 1 drop 2x/day



  • Eye lubricants

Return to Work/School Issues


The safest recommendation is to be out until there is no longer any discharge, but this is not practical since it could last for up to 2 weeks.



  • I tell patients that you treat it like the common cold and practice good hand hygiene to limit the spread of any infectious drainage


  • Most schools require 24 hours of therapy before children are allowed to return to school

Cottage Physician



  1. Friedlaender MH. A review of the causes and treatment of bacterial and allergic conjunctivitis. Clinical therapeutics. 1995;17(5):800-10; discussion 779. [pubmed]
  2. Ullman S, Roussel TJ, Culbertson WW. Neisseria gonorrhoeae keratoconjunctivitis. Ophthalmology. 1987; 94(5):525-31. [pubmed]
  3. Wan WL, Farkas GC, May WN, Robin JB. The clinical characteristics and course of adult gonococcal conjunctivitis. American journal of ophthalmology. 1986; 102(5):575-83. [pubmed]
  4. Azar MJ, Dhaliwal DK, Bower KS, Kowalski RP, Gordon YJ. Possible consequences of shaking hands with your patients with epidemic keratoconjunctivitis. American journal of ophthalmology. 1996; 121(6):711-2. [pubmed]
  5. Roba LA, Kowalski RP, Gordon AT, Romanowski EG, Gordon YJ. Adenoviral ocular isolates demonstrate serotype-dependent differences in in vitro infectivity titers and clinical course. Cornea. 1995; 14(4):388-93. [pubmed]
  6. Sheikh A, Hurwitz B, van Schayck CP, McLean S, Nurmatov U. Antibiotics versus placebo for acute bacterial conjunctivitis. The Cochrane database of systematic reviews. 2012; [pubmed]
  7. Rose PW, Harnden A, Brueggemann AB. Chloramphenicol treatment for acute infective conjunctivitis in children in primary care: a randomised double-blind placebo-controlled trial. Lancet (London, England). ; 366(9479):37-43. [pubmed]


Ishihara Test


Other Known AliasesPseudo-isochromatic plates

DefinitionTest for detecting color blindness using different color dots to outline numbers

Ishihara 9.png

Clinical SignificanceAllows for quick assessment of color blindness using different styles plates (a full test is 38 plates) and even differentiate between different types of color blindness.  Research has proven that a score of 12 out of 14 red/green plates indicates normal color vision with a sensitivity of 97% and a specificity of 100%.

History – Named after Shinobu Ishihara (1879-1963), who developed these while working as a military surgeon for the Japanese army during World War I as a better way of assessing color blindness in troops.  He first published these findings in 1917 in Japan and it was first translated and reviewed in the American Journal of Ophthalmology in June 1918 extolling its usefulness.



  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Ishihara S.  Tests for Color Blindness.  AJO. 1918;1(6):457 [article]
  6. Ishihara S.  Tests for Color Blindness.  1972 [book]
  7. http://www.eyemagazine.com/feature/article/ishihara




What do you expect to find on Weber and Rinne tests in sensorineural hearing loss (SSNHL)?




Both of these tests are easy bedside maneuvers to perform in the early evaluation of hearing loss and only require a 256 Hz tuning fork.  The main thing to remember is that in the Rinne test, air conduction is supposed to be greater than bone conduction….but because the problem with SSNHL is the conversion of sound waves to neural impulses, AC will still be greater than BC because the sound waves can still travel through the canal uninhibited.  So AC>BC can be both normal and abnormal, which is why it always done in tandem with the Weber to help figure out which side is affected.


Epstein’s Pearls


Other Known Aliasesnone

DefinitionSmall, fluid filled cysts on the hard palate of newborns that are most commonly found along the median palatal raphae.

Image result for epstein's pearls


Clinical SignificanceNone.  These are completely normal and occur in 65-80% of newborns.  The are formed by epithelium that becomes trapped during palatal development.

Image result for epstein's pearls


History – Named after Alois Epstein (1849-1918), who was a Czechoslovakian pediatrician, graduating from the University of Prague in 1873.  His career was highlighted by becoming the first physician-in-chief for the University of Prague hospital in 1873 and being appointed to professor at the University of Prague in 1884.  He first described these findings in 1880.


  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Lewis DM. Bohn’s nodules, Epstein’s pearls, and gingival cysts of the newborn: a new etiology and classification. Journal – Oklahoma Dental Association. ; 101(3):32-3. [pubmed]
  6. Singh RK, Kumar R, Pandey RK, Singh K. Dental lamina cysts in a newborn infant. BMJ case reports. 2012; 2012:. [pubmed]
  7. Epstein A. Ueber die Gelbsucht bei Neugeborenen Kindern. Leipsic. 1880. [book]


Tullio’s Phenomenon


Other Known AliasesSound-induced vestibular activation.

Definition – Vertigo, dizziness, nausea, and nystagmus caused by a load noise.

Clinical Significance This pathology is due to a communication between the middle and inner ear classically associated with congenital syphilis.  Recently, it has been associated with superior canal dehiscence syndrome (SCDS).  This can also be elicited with nose-blowing, valsalva, and heavy lifting.

History – Named after Italian biologist Pietro Tullio, Ph.D. (1881-1941), who originally studied this finding in pigeons and published it in 1929. 

Tullio blowing a whistle in the ear of rabbit test subject


  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com/
  5. Tullio, Pietro: Das Ohr und die Entstehung der Sprache und Schrift. Berlin, Germany: Urban & Schwarzenberg; 1929.
  6. Kaski D, Davies R, Luxon L, Bronstein AM, Rudge P. The Tullio phenomenon: a neurologically neglected presentation. Journal of Neurology. 2012; 259(1):4-21. [pubmed]
  7. Halmagyi GM, Curthoys IS, Colebatch JG, Aw ST. Vestibular responses to sound. Annals of the New York Academy of Sciences. 2005; 1039:54-67. [pubmed]


Argyll Robertson Pupils


Other Known Aliases – Prostitute’s Pupil

Definition – Small, bilateral pupils with an absence of miotic reaction to light, both direct and consensual, with preservation of miotic reaction to near stimulus.  In other words, they accommodate, but do not react light (light-near dissociation).

Clinical Significance Classically associated with tabes dorsalis of neurosyphylis, but can also be seen in diabetic neuropathy.  Rare now due to the widespread of antibiotics and treating early syphilis infections

History – Named after Douglas Moray Cooper Lamb Argyll Robertson (1837-1909), who was a Scottish surgeon and ophthalmologist and one of the first to specialize in the eye.  He published his findings of several case reports in two articles in the “Edinburgh Medical Journal” in 1869.  Previous to this however, he was also the first to discover and use the extract of the Calabar bean (otherwise known as physostigmine) for treatment of various eye disorders.

“Dougie”, as his friends called him****


  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com/
  5. Robertson DA. On an interesting series of eye symptoms in a case of spinal disease, with remarks on the action of belladonna on the iris. Edinb Med J. 1869;14:696–708.
  6. Robertson DA. Four cases of spinal myosis with remarks on the action of light on the pupil. Edinb Med J. 1869;15:487–493
  7. Robertson, D. A.:  On the Calabar Bean as a New Agent in Ophthalmic Medicine.  Edinb Med J. 1863;93:815-820.

****I have no source for this but he looks like a Dougie….plus with a name like Douglas Moray Cooper Lamb Argyll Robertson, you have to have a nickname, right?



6-year-old boy is brought in my his mother to the office for evaluation of a 3-day history of irritability, fever, and ear pain.  She also says that his older sister has had a cold the past week, but it doesn’t seem to be that bad.  He is up to date on his immunizations.  She also report she has had an intermittent, non-productive cough, but denies any decrease in eating/drinking, diarrhea, or vomiting.


Vital signs show a BP-117/72, HR-94, RR-16, O2-100%, and T-99.2.  Physical exam reveals:

  • General – Non-toxic appearing, NAD, WN/WD
  • Skin – no rash
  • Eye – sclera white, conjunctiva clear
  • Ear – (below)


  • Throat – OP clear, no erythema or tonsillar swelling
  • Neck – no LAD
  • Heart – RRR without M/G/R
  • Lung – CTA without adventitial sounds
  • Abdomen – S/NT/ND
  • PV – 2+ pulses throughout, BCR < 2s
  • Neuro – No focal deficits


Mother is wanting an antibiotic because the holiday season is here and she can’t afford to have him sick.

  1. What is your diagnosis?
  2. What is your treatment?
  3. What do you tell the mother?


  1. Diagnosis
    1. Viral Otitis Media
      1. Based on the 2013 consensus guidelines from Pediatrics, the following findings suggests a viral etiology:
        1. Non-toxic appearance
        2. Non-bulging tympanic membrane
        3. > 48hr onset of symptoms
        4. Temperature < 39°C (102.2°F)
        5. No middle ear effusion
  2. Treatment
    1. Given the patient’s age (6yo), there are 2 acceptable options:
      1. Observation
        1. This is the ideal patient for close observation as it is most likely viral, immunocompetant, no ottorhea, no severe symptoms, and non-toxic appearing.  Treatment should be directed towards pain control and recommendations should be given to the parents on how to treat:
          1. Ibuprofen – 10mg/kg TID
          2. Acetaminophen – 10mg/kg TID
          3. Topic antipyrine/benzocaine – no longer available
          4. Topical lidocaine – off label, but can be used
      2. Antibiotic Therapy
        1. If the patient fails to improve in 48-72hr, then antibiotics are warranted. Duration of therapy for children > 2yo is 5-7 days.


Case Resolution

After examination of the patient and discussion with the mother, you recommend a course of MICOS:

Masterful Inactivity with Catlike Observations

You explain that his symptoms are likely viral and self-limiting and the best thing for him now is to control his pain.  You give the dosing guidelines for ibuprofen and acetaminophen and offer a prescription of topical lidocaine.  You encourage the mother to call back to the clinic in 3 days time if he is not improving, at which time you will call in a prescription for antibiotics.



  1. Lieberthal AS, Carroll AE, Chonmaitree T. The diagnosis and management of acute otitis media. Pediatrics. 2013;131(3):e964-99. [pubmed]
  2. Bolt P, Barnett P, Babl FE, Sharwood LN. Topical lignocaine for pain relief in acute otitis media: results of a double-blind placebo-controlled randomised trial. Archives of Disease in Childhood. 2008;93(1):40-4.  [pubmed]

#24 – Retinal Detachment



A retinal detachment is defined as a separation of the multilayer neurosensory retina from the underlying retinal pigment epithelium and choroid.



Retinal detachments have been reported to occur in 6-20 per 100,000 population worldwide, but there is wide variability in incidence between the types.  Risk factors include:

  • Myopia (most common)
  • Age (50-75yr)
  • Previous eye surgery or injury
  • Use of fluoroquinolones
  • History of glaucoma
  • Family history of retinal detachment
  • Diabetes
  • Hypertension

Pathophysiology and Types

There are 2 main types of retinal types and the pathophysiology is slightly different.

  • Rhegmatogenous (most common)
    • Full-thickness tear caused by vitreous traction on the retina
      • Not to be confused with tractional detachment
        • RRD à tear 1st, then vitreous traction forces fluid in
        • TRD à traction pulls the layers away, but no tear
      • Most common site is a posterior vitreous detachment
        • Typically take weeks to months to fully develop
      • Traumatic retinal detachment can occur from surgery or injury
  • Nonrhegmatogenous
    • Tractional
      • Vitreous traction separates the layers and neovascularization from DM, HTN, sickle cell causes fluid to accumulate
    • Exudative
      • Fluid accumulation from inflammatory states or ocular malignancies causes the separation of layers


Signs and Symptoms

  • Mostly slow onset (weeks to months), but can be acute if traumatic
  • Increase, or worsening of floaters
    • Multiple, cob-web like
    • Single, large
      • Romans called this “mosca volante” –> large housefly
  • Gradual loss of peripheral vision (“curtain pulled over eye”)
  • Decrease in visual acuity once the macula is involved

Physical Exam

All patients with any eye complaint should have visual acuity checked and documented.  If you suspect a detachment from the history, visual fields should be assessed.  Fundoscopic exam should be performed to look for any gross retinal defects.  All patients with a suspected retinal detachment should be referred for urgent evaluation by an ophthalmologist for dilated retinal exam with slitlamp.  The test of choice is a 360o scleral depressed examination using an indirect ophthalmoscope.


Rhegmatogenous Retinal Detachment

Rhegmatogenous Retinal Detachment


Tractional Retinal Detachment


Exudative Retinal Detachment


Ultrasound technology is getting better and better and ocular scanning can see detachments at the bedside in the hands of a competent provider.


  • Detachment without tear
    • Reassurance that floaters with resolve over 3-12 months
  • Tear without detachment
    • Risk of detachment is around 30% if left untreated
    • 2 options
      • Laser Retinopexy
      • picture1

      • Cryoretinopexy
        • (see below scleral buckling video)
      • Both take approximately 2 weeks to form strong adhesions
    • Tear with detachment
      • Without treatment, will progress to complete vision loss
      • Small tears
        • Laser or cryoretinoplexy
      • Large tears
        • Pneumatic retinopexy (office)
          • Cryoretinopexy with injection of gas bubble and head position to tamponade the tear
          • 24-48hr for fluid reabsorption and retinal re-attachment
          • 70-80% 1st time success
        • Scleral buckle (OR)
          • Cryoretinopexy with suturing of an exoplant to the outside of the sclera, which causes an indentation in the wall of the eye
          • picture1
          • 80-90% 1st time success
        • Vitrectomy
          • Removal of central and peripheral vitreous humor with gas or liquid injection
          • 80-90% 1st time success


  1. Mitry D, Charteris DG, Fleck BW, Campbell H, Singh J. The epidemiology of rhegmatogenous retinal detachment: geographical variation and clinical associations. The British Journal of Ophthalmology. 2010;94(6):678-84. [pubmed]
  2. Wilkes SR, Beard CM, Kurland LT, Robertson DM, O’Fallon WM. The incidence of retinal detachment in Rochester, Minnesota, 1970-1978. American Journal of Ophthalmology. 1982;94(5):670-3. [pubmed]
  3. Haimann MH, Burton TC, Brown CK. Epidemiology of retinal detachment. Archives of Ophthalmology (Chicago, Ill. : 1960). 1982; 100(2):289-92. [pubmed]
  4. Risk factors for idiopathic rhegmatogenous retinal detachment. The Eye Disease Case-Control Study Group. American Journal of Epidemiology. 1993;137(7):749-57. [pubmed]
  5. Pasternak B, Svanström H, Melbye M, Hviid A. Association between oral fluoroquinolone use and retinal detachment. JAMA. 2013;310(20):2184-90. [pubmed]
  6. Go SL, Hoyng CB, Klaver CC. Genetic risk of rhegmatogenous retinal detachment: a familial aggregation study. Archives of Ophthalmology (Chicago, Ill. : 1960). 2005;123(9):1237-41. [pubmed]
  7. Hikichi T, Trempe CL, Schepens CL. Posterior vitreous detachment as a risk factor for retinal detachment. Ophthalmology. 1995;102(4):527-8. [pubmed]
  8. Wolfensberger TJ, Tufail A. Systemic disorders associated with detachment of the neurosensory retina and retinal pigment epithelium. Current Opinion in Ophthalmology. 2000;11(6):455-61. [pubmed]
  9. Hollands H, Johnson D, Brox AC, Almeida D, Simel DL, Sharma S. Acute-onset floaters and flashes: is this patient at risk for retinal detachment? JAMA. 2009;302(20):2243-9. [pubmed]
  10. Byer NE. Natural history of posterior vitreous detachment with early management as the premier line of defense against retinal detachment. Ophthalmology. 1994;101(9):1503-13. [pubmed]
  11. Coffee RE, Westfall AC, Davis GH, Mieler WF, Holz ER. Symptomatic posterior vitreous detachment and the incidence of delayed retinal breaks: case series and meta-analysis. American Journal of Ophthalmology. 2007;144(3):409-413. [pubmed]
  12. D’Amico DJ. Clinical practice. Primary retinal detachment. The New England Journal of Medicine. 2008;359(22):2346-54. [pubmed]
  13. Hilton GF, Tornambe PE. Pneumatic retinopexy. An analysis of intraoperative and postoperative complications. The Retinal Detachment Study Group. Retina (Philadelphia, Pa.). 1991;11(3):285-94. [pubmed]
  14. Tornambe PE, Hilton GF. Pneumatic retinopexy. A multicenter randomized controlled clinical trial comparing pneumatic retinopexy with scleral buckling. The Retinal Detachment Study Group. Ophthalmology. 1989;96(6):772-83. [pubmed]