KC + Orbital Inflammations PDF

Keratoconus Ectatic dystrophy Ectasia- thinning and bulging of the sclera and center of the cornea is thinned out Diagnosed b/w 10-30 years age ○ You don’t get KC when you’re 40 Progresses for 7-8 years, then stabilizes Bilateral and asymmetric (one eye worse than...

Keratoconus Ectatic dystrophy Ectasia- thinning and bulging of the sclera and center of the cornea is thinned out Diagnosed b/w 10-30 years age ○ You don’t get KC when you’re 40 Progresses for 7-8 years, then stabilizes Bilateral and asymmetric (one eye worse than the other) Histopathology: fragmentations/interruption on Bowman’s defective collagen?? ○ Dystrophy or degeneration? Rubbing eyes because of itchiness?? Hard cl?? Symptoms ○ Slow, progressive refractive changes w/ reduced VA over months to years ○ Frequent hx of bronchial asthma, allergies, atopias, chronic eye rubbing (eczema can be cause of the eye rubbing), also Down’s syndrome ○ Glare, mild photophobia, painless, diplopia, or polyopia may be reported ○ May have family hx Signs ○ Usually bilateral, but asymmetric ○ Progressive irregular astigmatism secondary to paracentral thinning Regular astigmatism: 90 degrees apart vs. irregular is not 90 apart ○ Maximal thinning near the apex of the protrusion Think of a car and its tires; more milage and used the tires are getting cracks - same thing w/ cornea ○ Vogt’s striae (vertical lines of tension in the posterior cornea) Eye pressure is not sustained in the cornea ○ Irregular retinoscopy reflex (irregular motion) ○ Egg-shaped K’s (if mires are round in keratometer, pt does not have KC) ○ Fleischer’s ring (epithelial iron deposits at the base of the cone)  ○ Munson’s sign ○ Superficial corneal scarring (too much thinning) ○ If Descemet ruptures: Corneal hydrops (stromal edema in cone area) Water gets into cornea and in KC due to Na/K pump imbalance, water creates water pockets called hydrops and burst Pain is unbearable ○ Prominent corneal nerves (“die off” and becomes more prominent)  ○ Corneal topography Blue = flatter, red = steeper Complications ○ Ecstatic KC; refer to remove that bulged fluid  ○ Treatment ○ Correct refractive error w/ glasses or RGP RGPs do not stop the progression of the cone ○ F/U depending on signs and symptoms 3-12 mo ○ Severe thinning/recurrent episodes of Hydrops INTACTS Intrastromal corneal rings PMMA rings inserted in the peripheral stroma to flatten the cornea— shortens cornea arc length Rings can be removed or exchanged Placed centrally cornea to help with the steepness; initially used as myopia management but didn’t work so Corneal transplant ○ Corneal hydrops protocol Cycloplegia, hypertonic ointment to get water out (Glycerin, Muro 128 might not even be enough for it) Rupture of hydrops need steroid and refer to ophthalmologist ^ prophylactic ab and CL if necessary Remove c/l in 24 hours, NaCl 5% sol/oint BID-QID until resolved F/U q 5-7 days until resolved INFECTIOUS ORBITAL INFLAMMATIONS Orbital septum ○ Thin, fibrous membrane that serves as a barrier b/w the superficial lids and the orbit ○ Arises from the orbital periosteum at the orbital rim and extends to the tarsal plates of the eyelids Chandler Classification for Infections Involving orbit and adnexa  ○ ○ Group I – Preseptal cellulitis ○ Group II – Orbital cellulitis edema and inflammation of orbital contents without abscess formation ○ Group III – Subperiosteal abscess between the bone and periosteum ○ Group IV – Orbital abscess collection of purulent material within the orbital contents ○ Group V – Cavernous sinus thrombosis = septic emboli At the CS- extension posterior to orbit Infections Preseptal cellulitis ○ Group I ○ NOT an orbital disease but it can progress into an orbital disease It is an EYELID disease but can turn into an orbital disease ○ Infection of the soft tissue of eyelids anterior to the orbital septum ○ The glove and orbit are NOT involved ○ Most common causes: From eyelid lesions: internal hordeolum, dacryocystitis From spread from sinus: sinusitis From trauma, bites ○ Etiology Contiguous infectious spread: facial/eyelid injuries, insect/or animal bites, conjunctivitis, internal hordeolum (comes from meibomiam glands), dacryo, or sinusitis: MC- S. Aureus, Strep. Pyogenes, Strep. Pneumoniae Human/animal bite wound: suspect anaerobic bacteria like Peptostreptococcus and Bacteroides Skin trauma: laceration or insect bites: S. aureus, S. pyogenes Spread of local infection: from acute hordeolum or dacryocystitis, sinusitis- Strep. pneumonia/ H. influenza From remote infection: of the upper respiratory tract or middle ear by hematogenous spread ○ Signs and symptoms Unilateral eyelid erythema, edema, warmth, tenderness  No proptosis or EOMs restriction Might not be able to open the eye VA’s are not affected (no color vision loss either) Red-purplish coloration in children signals CT scan: opacification anterior to the orbital septum Symptoms: Mild fever Redness and lid tenderness Irritability in children ○ Differentials Orbital cellulitis: proptosis, pain upon EOM test, decreased VA, fever, chemosis Other orbital disorders (proptosis) Chalazion: focal inflammation, palpable mass, pointing meibomian gland Difference b/w internal hordeolum to chalazion: chalazion is a “non-tender lipid bump/cyst” that sometimes precedes a meibomian gland infection which is an internal hordeolum Allergic eyelid swelling: sudden onset, bright red, prominent itching, no tenderness, no pain, hx of allergies, new medication for eye or skin Viral conjunctivitis- has all signs of conjunctivitis Cavernous sinus thrombosis: proptosis, paresis of III, IV, VI CNs typically bilateral Decreased sensation of the 1st and 2nd division of CN V Others: insect bite, angioedema, maxillary osteomyelitis, etc Dental ○ Work-up: focused on R/O of orbital cellulitis History: cause, pain w/ EOM, trauma? Cancer? Fever? Malaise? Sinus? Lid lesions (retrobulbar tumor)? Exam VA loss EOMs Pain on movement Proptosis RAPD Order CT scan: significant trauma or suspect IOFB; brain and orbit axial and coronal view; shows opacification anterior to the orbit septum, *CANNOT open eye Order gram stain and culture in open wounds or drainage Palpate periorbital area, head, and neck lymph nodes for mass Retropulsion test also CBC and blood cultures: if systemic is suspected Suspect anaerobes: animal or human bites ○ Treatment Mild, older than 5, afebrile Children ○ Amoxicillin/Clavulanate (Augmentin) 20-40 mg/kg/day in 3 doses OR commonly used 2nd generation cephalosporin: Ceclor (Cefaclor) same dose (max 1 g/day) for 10 days Adults ○ Augmentin 250-500 mg q 8hr 7-10 days Other ABs Penicillins ○ Flucloxacillin, Dicloxacillin, Cloxacillin 250-500 mg BID-QID ○ Resistant to penicillinase Cephalosporins ○ Cephalexin (Keflex), Cefadroxil, Cephradine 250-500 mg BID-QID Macrolides (not TOC according to DJ) ○ Azithromycin Zpack (as directed), Clarithromycin 500 mg BID Fluoroquinolones (such a harsh medication) ○ Ciprofloxacin, Levofloxacini 500 mg BID-QID Sulfamethoxazole-trimethoprim (SMX-TMP)- BID ○ Unless we’re suspecting MRSA ^ Maintained for 7-10 days IF allergic to penicillin Bactrim (Trimethoprim/Sulfamethoxazole): ○ Peds: 8 mg/kg/day Trimethoprim and 40 mg/kg/day sulfamethoxazole PO in 2 divided doses  ○ Adults: 160 mg Trimethoprim and 800 mg Sulfamethoxazole PO BID for 10 days IF allergic to penicillin and sulfa drugs Erythromycin ○ Children 30-50 mg/kg/day in 3-4 doses ○ Adults: 250-500 mg q 6 hr for 10 days Cross reaction of cephalosporin w/ PCN Based on the side chain Keflex, Keflin, Ultracef, Cefazolin have same side chain as PCN! DO NOT USE! Ceftin, Cefopodoxime, Cefzil, Omincef ○ Do not have the same side chain as PCN ○ Possible to use based on previous PCN reaction using w/ caution but just don’t Bite wounds (anaerob. mouth): suspecting streptococcus or pyogenes PenicillinG IV, Ampicillin/Sulbactam, Cefoxitin, Metronidazole, and Clindamycin (TID)- DJ’s choice, all cover anaerobes. Palliative Warm compresses reduce swelling and provide comfort Hydration can help support the immune system Rests aids to aid recovery and alleviate fatigue Hospitalization for IV antibiotics < 5 y/o H. influenza No response w/ oral tx Non-compliance The patient appears toxic IV antibiotics ○ Ceftrizone: Child: 100 mg/kg/day IV in 2 doses Adult: 1-2 g IV q 12 hr and ○ Vancomycin (if you suspect MRSA) Child: 40 mg/kg/day IV 3-4 doses Adults: 0.5 to 1 g IV q 12 hr x 2 weeks, then can be changed to oral AB once there is improvement Orbital cellulitis ○ Group II ○ Bacterial orbital cellulitis is LIFE THREATENING INFECTION that affects the soft tissue behind the orbital septum ○ ○ ○ Typical precipitating factors Penetrating lid trauma Orbital medial wall blow-out fracture (big risk for boxers) Severe lid infectious disease (dacryoadenitis- inflammation of lacrimal gland, cancer, or severe internal hordeolum) Bite wounds from insects, human, or animal, meningitis Sinus* and dental infection Most common routes of infection: adjacent sinuses or teeth, and direct inoculation through penetrating lid injury Dental work, ethmoid sinus infection is common ○ Microbes Staphylococcus aureus and Streptococcus pyogenes predominate when infection arises from local trauma Streptococcus pneumoniae: most common pathogen associated w/ sinus infection H. influenzae type B (HIB), once a common cause, is now less common b/c of widespread vaccination (ask if has vaccines) Mucormycosis/fungus- uncommon; causes orbital cellulitis in diabetic or immunosuppressed patients ○ Signs and symptoms Prominent lid edema and redness, distention, proptosis, and significant pain upon palpation  Diplopia from EOM limitations and pain (pain on movement) Loss of VA/APD may often be present CT scan shows preseptal and orbital opacification Transverse section ○ What is the most ventral (anterior) aspect? Nose Symptoms: pain, reduced vision, redness, diplopia, fever, malaise Fever and malaise are not present in pre-septal because there is inflammation of the sinuses ○ Work-up History: trauma? ENT or systemic infection? Stiff neck- meningitis (Kerning and Brudzinski test are positive to confirm meningitis)? Mental status? DM? Immunosuppressive illness? (for these 2 suspect mucormycosis) Complete ophthalmic evaluation VA Diplopia work-up ○ CN 3, 4, 6 are involved in motor. Although there are 5 in the orbit but they’re not all motor. Exophthalmomoeter Pupils (may have afferent pupil) ONH (papilledema may present) Skin sensation around!! Test CN V Vital signs, mental status, neck flexibility CT orbits and sinuses (axial and coronal, w/o contrast) and R/O FB, orbital or periosteal abscess and sinus disease.. MRI contraindicated in metallic foreign bodies* CBC w/ differential Blood cultures Gram stain and culture if wound is present Lumbar puncture if meningitis is suspected ○ Management True emergency and treated in the hospital  Refer hospital emergency room for hospitalization w/ intravenous antibiotics IV AB for G(+), G(-), and anaerobic for 2-3 weeks or until it improves Unasyn (Ampicillin-sulbactam) 1.5-3 g IV q6h For MRSA coverage (if suspected MRSA) Vancomycin (a glycopeptide drug) ○ Children: 40 to 60 mg/kg per day IV divided into 3 or 4 doses; maximum daily dose 4 g ○ Adults: 2 g IV per day (2 g IV q 12 hours if an intracranial extension is suspected) Have to check Vancomycin levels after 4th dose to avoid toxicity Vancomycin trough A greater risk of nephrotoxicity occurs when doses exceed 4 grams per day and trough levels are higher than 15mcg/mL Plus one of the following: ○ Ceftriaxone ○ Cefotaxime ○ Ampicillin-sulbactam ○ Piperacillin-tazobactam ○ Other tx considerations If an anaerobic infection is suspected or is an adult w/ chronic orbital cellulitis, then consider adding Metronidazole 15 mg/kg IV load, then 7.5 mg kg IV q 6 hr Allergic to PCN/Cephalosporin W/ Vancomycin: ○ Ciprofloxacin ○ Levofloxacin For uncomplicated orbital cellulitis w/ good response to IV ab’s, it is reasonable to switch to oral therapy If afebrile and the eyelid and orbital findings have begun to resolve substantially, then switching to oral antibiotics is warranted ○ Oral antibiotics and additional management (If someone has been on IV treatment, can rx oral antibiotic. No diplopia and EOM restriction) Clindamycin Trimethoprim-sulfamethoxazole (Bactrim) Ocular TRUST (Tracking Resistance in the US Today) & MRSA  ○ MMSA: All (Fluoroquinolones) except penicillin were effective ○ MRSA: Trimethoprim is the only one truly effective Plus 1 of the following: Amoxicillin Amoxicillin-clavulanic Cefpodoxime Cefdinir Monitor ON function ENT consultation for sinuses drainage Nasal decongestant Erythromycin ung QID if exposure keratopathy secondary to proptosis ○ Invasive treatment Orbital decompression because if not decompressed, optic nerve will have severe damage, drain an abscess, open infected sinuses or a combination of both Circumstances Vision is compromised if nothing is done (warning sign) Excessive suppuration or FB is suspected ○ Guy got into a bar fight and the guy that punched him had a knuckle brass. Oh Really??? Imaging shows orbital or large subperiosteal abscess that could be associated w/ a condition The infection does not resolve w/ antibiotics Obtain culture material, like in patients with suspected fungal or mycobacterial infection of the orbit ^^^ All these things mean more invasive treatment if the initial treatment is not resolved  Rhino-orbital mucormycosis ○ Aggressive opportunistic fungal infection, aka phycomycosis and zygomycosis ○ Can affect other parts of the body such as the lungs and GI tract ○ The fungus is found in soil and on decaying vegetation. ○ B/c the fungus is so widespread, humans are exposed to it regularly ○ The spores of the fungus are inhaled through the mouth and nose, but infection rarely occurs in a person with an intact immune system b/c macrophages phagocytize the spores Candida ○ Immunocompromised occur, germination of spores and hyphae formation may occur, and infection develops, most commonly in the sinuses and lungs ○ Invasion to the paranasal sinus mucosa (ethmoid sinus is an important route of infection, since mucormycosis may invade through the thin lamina papyracea), it may spread directly to the orbital apex and, from there, gain intracerebral access ○ Difficult to diagnose early, as patients often present with nonspecific symptoms Can present with a minor infection but be aware of these predisposing factors for diabetics, obese, etc. ○ By the time signs of orbital apex involvement develop, it is often too late to save the patient’s vision, or even the patient’s eye or life ○ The presentation is typically a rapidly progressive infection, and the disease is associated with a high mortality rate ○ Predilection for distinct patient populations diabetes mellitus (especially those with diabetic ketoacidosis) persons who have received multiple blood transfusions immunocompromised patients as those with transplants or hematopoietic malignancies those on chronic steroids or immunosuppressants ○ Fungal hyphae directly invade blood vessels, producing tissue infarction and massive necrosis w/ bone destruction  ○ Signs Proptosis Examination of the nose and palate reveals necrotic mucosa A smear will show septate hyphae (fingerlike projections) and the white around it is the septate Gradual onset of facial and periorbital swelling, diplopia and visual loss Ischemic infarction w/ septic necrosis, black eschar (dead tissue that falls off (sheds) from healthy skin)) may develop on the palate, turbinates, nasal septum, skin and eyelids Ophthalmoplegia has a slower progression compared to orbital cellulitis Symptoms: patient is quite ill, pain, proptosis ○ Some dx clues Nasal congestion Postnasal drip Dark blood-tinged or purulent rhinorrhea Sinus tenderness HA, fever, and malaise  A black necrotic eschar on the nasal turbinates or hard palate is characteristic of maxillary sinus involvement ○ Treatment Hospitalize: needs treatment of underlying condition Infectious disease specialist, ENT or both IV Amphotericin B 0.25-0.30 mg/kg IV slowly over 3-6 hrs the 1st day 0.5 mg/kg IV the 2nd day Then 45-50 mg IV daily Duration of tx depends on the clinical condition Blood urea nitrogen (BUN) and creatinine levels are obtained every day: watch renal compromise Daily irrigation w/ amphotericin to the affected areas Excision of devitalized and necrotic tissues Adjunctive hyperbaric oxygen Exenteration… in severe responsive cases Removal of the whole orbital content is gone.