#37 – Conjunctivitis



***LISTEN TO THE PODCAST HERE***

 



Pathophysiology

 

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.


Treatment

 

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.

 

Bacterial

  • 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

 

Non-Infectious/Non-Allergic

  • 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.

 

Viral

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

Bacterial

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

Cottage Physician

 


References

  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]

Ep-PAINE-nym



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.


 


References

  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

PAINE #PANCE Pearl – HEENT



Question

 

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

 



Answer

 

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.

Ep-PAINE-nym



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.


References

  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]

#36 – Basics of the Ventilator with Wes Johnson, PA-C



***LISTEN TO THE PODCAST HERE***

 



Guest Information

 

Wes Johnson, MSPAS, PA-C, (soon to be), DHSc was a former student of mine at UAB and was a respiratory therapist prior to PA school.  He is the Regional Director of Clinical Education for Island Medical Management Emergency group in North Alabama.  He won the Preceptor of The Year award from UAB in 2016 and currently finishing up his doctorate degree from A.T. Still University.

Twitter – @wesj2288



Disclaimer

 

For the purposes of this podcast and post, we will be using the Puritan Bennett 840 ventilator (pictured below).  All the term we use are synonymous with all vents, but the screens will be different.

Puritan Bennett 840


Big Concepts of The Ventilator

 

  1. Mode
    1. Assist Control (AC)
      1. Every breath is either a machine driven (set by rate) or fully assisted (initiated by the patient)
        1. Uses either pressure (ACPC) or volume (ACVC)
    2. Synchronized Intermittent Mechanical Ventilation (SIMV)
      1. Set number of machine driven breaths, and patient intitated breaths are partially assisted
    3. Pressure Support (PS)
      1. No machine driven breaths and all breaths are initiated by the patient and partially assisted
  2. Delivery
    1. Pressure
      1. Static Controls
        1. Pressure
        2. Time (inspiratory)
        3. Peak flow
      2. Variable Factors
        1. Volume
        2. Total flow
    2. Volume
      1. Static Controls
        1. Tidal volume (cc)
        2. Flow (L/min)
      2. Variable Factors
        1. Pressure
  3. Positive End Expiratory Pressure (PEEP)
    1. The pressure left in the circuit at the end of expiration
    2. Prevents alveolar collapse and improves oxygenation
    3. Can cause barotrauma and affect hemodynamics

Static Controls

 

(For this section, refer back to the vent picture above)

  1. Fraction of Inspired Oxygen (FiO2)
    1. Start at 100% and titrate down to 21%
  2. f (machine breath rate)
  3. Control
    1. Pressure Control (PC)
      1. Inspiratory pressure (Pi)
        1. Peak pressure in circuit
        2. Initial setting = < 20 cm H20
      2. Inspiratory time (I-time)
        1. Initial setting = 1.25 seconds
    2. Volume Control (VC)
      1. Vt (tidal volume of each breath)
        1. Initial setting = 6-8 cc/kg IBW
      2. Vmax (flow rate)
  4. Spontaneous Support
    1. Trigger for spontaneous support
      1. Volume = V-trig
      2. Pressure = P-trig
    2. Pressure Support (PS)
      1. I was always taught at least 5 cm H20 to overcome circuit resistance

Real-Time Controls

 

  1. Flashing “C” and “S”
    1. Lets you know what breaths are controlled (machine) or spontaneous (patient)
  2. Airway Pressure
    1. Ppeak (max airway pressure)
      1. A marker of resistance
    2. Pmean (average airway pressure)
      1. A measure of alveolar pressure
    3. Pplat (small airway and alveoli pressure)
      1. A measure of compliance
  3. fTotal (machine + spontaneous breaths)
  4. I:E (inspiratory:expiratory ratio)
    1. Normal = 1:2 (at rest)
    2. Inverse ratio (2:1) can improve oxygen due to intention auto-PEEP

Wes Johnson’s Approach to Setting Up a Ventilator (after RSI)

 

Mode: AC

Vt: 6-8 mL/kg based on pt’s IBW

Rate: 12-16 bpm

FiO2: 100%

PEEP: 5.0

At the 5-minute mark:

  • Check an ABG
    • Titrate FiO2 off of PaO2 and pulse oximeter
    • Adjust minute ventilation off of PaCO2 and/or ETCO2


References

  1. Respiratory Review YouTube Channel https://www.youtube.com/channel/UCtaRF58UDVthvH36YYCttng
  2. Deranged Physiology.  Mechanical Ventilation. http://www.derangedphysiology.com/main/core-topics-intensive-care/mechanical-ventilation-0
  3. Weingart SD – “Spinning Dials – How to Dominate the Ventilator” – https://emcrit.org/wp-content/uploads/vent-handout.pdf
  4. Weingart SD. Managing Initial Mechanical Ventilation in the Emergency Department. Annals of emergency medicine. 2016; 68(5):614-617. [pubmed]
  5. Air Link Regional West – “Initial Adult Ventilator Settings” – https://www.rwhs.org/sites/default/files/airlink-factsheet-ventsettings.pdf
  6. Open Anesthesia. Modes of Mechanical Ventilation. https://www.openanesthesia.org/modes_of_mechanical_ventilation/
  7. Modern Medicine Network.  A Quick Guide to Vent Essentials. http://www.modernmedicine.com/modern-medicine/content/tags/copd/quick-guide-vent-essentials
  8. Tobin MJ. Extubation and the myth of “minimal ventilator settings”. American journal of respiratory and critical care medicine. 2012; 185(4):349-50. [pubmed]

PAINE #PANCE Pearl – Emergency Medicine



Question

 

What are the 5 main life-threatening causes of chest pain?


Answer

 

The 5 main life-threatening causes of chest pain you should ALWAYS think of are:

  1. Acute Myocardial Infarction
  2. Pulmonary Thromboembolism
  3. Pneumothorax (risk of tension)
  4. Pericarditis (risk of tamponade)
  5. Aortic Dissection

There are a few others that should also cross your mind:

  1. Esophageal Rupture (Boerhaave’s Syndrome)
  2. Acute Chest Syndrome in Sickle Cell patients
  3. Unstable angina

 


References

  1. The Five Deadly Causes of Chest Pain Other than Myocardial Infarction. JEMS. 2017
  2. Chest Pain.  Life in The Fastlane.
  3. Woods WA, Young JS, Just JS. Emergency Medicine Recall.  2000.