Presentation endopthalmitis.pptx opthamo

Endopthalmotis eyes department and treatments

1. Endopthalmitis and panophthalmitis

2. In this presentation…. Introduction 11. Comparison and questions Classification Pathology Clinical features Signs Complications Differential diagnosis Investigation Treatment Panophthalmitis

3. Introduction Endophthalmitis is a severe, sight-threatening intraocular inflammation involving the vitreous and/or aqueous humor , usually due to infection (bacterial or fungal) but sometimes sterile (non-infective). It is considered an ocular emergency requiring immediate diagnosis and management to prevent blindness

4. Classification Based on Etiology Exogenous Endophthalmitis – infection enters from outside the eye: Post-surgical (most common, especially after cataract surgery, intravitreal injections, glaucoma surgery).Coagulase-negative staphylococci are the most common culprits. Post-traumatic (penetrating injury, intraocular foreign body).Bacillus cereus is a significant threat in this category. Keratitis-associated (extension of corneal ulcer).

5. Endogenous Endophthalmitis – spread via bloodstream from systemic infection (e.g., septicemia, endocarditis, liver abscess). Staphylococcus aureus, streptococci, and Gram-negative bacteria like Klebsiella pneumoniae are often implicated. Common organisms causing endophthalmitis A. Exogenous Acute onset Postsurgical
Gram positive: S. epidermidis, S. aureus, Streptococcus spp. Gram negative: Pseudomonas, Proteus,
H. influenzae , Klebsiella , E. coli, Enterobacter Delayed onset Postsurgical
Fungi: aspergillus , fusarium , candid, penicillum Bacteria: P. acnes S. epidermidis
Post-traumatic: Bacillus spp. S. epidermidis Streptococcus spp.
Fungi ( fusarium )
B. Endogenous Bacteria: B. cereus (IV abusers), Streptococcus spp.. S. aureus, Meningococci , H. influenzae Fungi: mucor , candida

6. Based on Onset Acute : Rapid onset within days of insult (pain, redness, decreased vision). Chronic/Delayed : Weeks to months after surgery or trauma (low-grade inflammation, insidious course, often fungal or Propionibacterium acnes).

7. Depending on the infecting organism, there is a correlation a between clinical presentation and microbiologic spectrum.
Gram-positive, coagulase-negative micrococci cause less severe infections compared with more virulent Gram-negative and “other” Gram-positive organisms.
Streptococcal endophthalmitis often results in earlier onset and notably worse outcomes than infections by staphylococcal species.
If more virulent pathogens are involved then signs and symptoms appear earlier, which is significantly correlated with a worse visual outcome.

8. Pathophysiology Entry of organisms → multiplication in vitreous cavity (avascular, poor host defense, antibiotic penetration difficult). Intense inflammatory response → pus, fibrin, necrosis → destruction of retina & other ocular structures → rapid vision loss.

9. Clinical Features Symptoms Sudden, severe loss of vision (may be partial to complete). Pain (moderate to severe, deep). Redness of eye. Swelling of lids. Photophobia. Floaters. Discharge (sometimes).

10. Signs Signs Anterior Segment Marked conjunctival congestion . Corneal edema (hazy cornea). Hypopyon (pus in anterior chamber). Aqueous flare and cells (+++). Fibrin in anterior chamber. Poor pupillary reaction. Posterior Segment Vitritis (hazy media, yellow reflex instead of red reflex). Retinal periphlebitis. Chorioretinitis patches. Loss of fundal glow (fundus not visible). Retinal detachment (late). Systemic (in endogenous type) Fever, systemic infection focus (e.g., liver abscess, urinary tract infection, IV drug use).

11. Complications Panophthalmitis (spread to all ocular coats). Phthisis bulbi (shrunken, non-functional eye). Total blindness. Secondary glaucoma. Retinal detachment. Extension to orbit, CNS (rare).

12. Differential Diagnosis Severe uveitis. Intraocular lymphoma. Sterile postoperative inflammation. Retinal detachment with hemorrhage.

13. Investigations Clinical diagnosis is primary. Vitreous/aqueous tap → Gram stain, KOH mount, culture & sensitivity. B-scan ultrasonography if fundus not visible → shows vitreous opacities, membranes, retinal detachment. Blood culture in endogenous cases. Systemic work-up for infection source (urine, blood, chest X-ray, abdominal USG).

14. Treatment (Outline) ⚠️ Emergency – treatment must be started immediately. Intravitreal antibiotics (mainstay): Vancomycin (1 mg/0.1 ml) → gram-positive. Ceftazidime (2.25 mg/0.1 ml) → gram-negative. Amphotericin B or Voriconazole → for fungal cases. Vitrectomy (Pars plana vitrectomy) Removes infective load & exudates. Indicated in severe/end-stage cases with no fundal view or hand movements vision.

15. Systemic antibiotics Useful in endogenous cases. Topical therapy Intensive fortified antibiotics, cycloplegics, steroids (after control of infection). Enucleation/evisceration Last resort in panophthalmitis or painful blind eye.

16. Panophthalmitis Definition Panophthalmitis is a severe, purulent inflammation of all coats of the eyeball (cornea, sclera, uvea, retina, choroid) along with involvement of intraocular structures (aqueous, vitreous) and orbital tissues . Essentially, it is an advanced form of endophthalmitis where infection spreads beyond the globe. It is a sight- and globe-threatening ocular emergency .

17. Etiology Exogenous (most common) Extension of untreated endophthalmitis . Penetrating ocular trauma with contamination. Post-surgical (esp. cataract, IOL surgery, keratoplasty). Severe corneal ulcer perforation (infective keratitis). Endogenous (rare) Hematogenous spread from systemic infections (septicemia, pneumonia, liver abscess).

18. Pathophysiology Infective organisms enter → multiply in aqueous & vitreous → spread to retina, choroid, sclera . Infection breaches the sclera → extends to orbital tissue . Results in necrosis, abscess formation, orbital cellulitis, and destruction of ocular contents . Eye becomes irreversibly damaged and painful.

19. Symptoms Severe, excruciating ocular pain . Rapid, complete loss of vision (no light perception). Marked redness, swelling of lids . Purulent discharge. Systemic fever, malaise (in endogenous

20. Signs External / Anterior Segment Marked chemosis , lid edema . Corneal haze or ulcer , perforation may be seen. Hypopyon or pus filling anterior chamber. Scleral abscess, yellowish patches. Severe proptosis (due to orbital involvement). Posterior Segment Vitreous full of pus → no fundal glow.
B-scan: vitreous opacities, thick membranes, scleral thickening, orbital involvement. Systemic Fever, septicemia signs if endogenous.

21. Complications Orbital cellulitis → orbital abscess. Cavernous sinus thrombosis (life-threatening). Meningitis, brain abscess (rare but fatal). Phthisis bulbi (shrunken, non-functional eye). Septicemia, systemic death if untreated

22. Differential Diagnosis Severe orbital cellulitis (but globe is not destroyed in cellulitis). Severe pan-uveitis. Malignant intraocular tumor with necrosis.

23. Investigations Clinical diagnosis (classical severe pain, swelling, pus, no light perception). B-scan ultrasonography → vitreous echoes, scleral thickening, orbital extension. CT/MRI orbit if needed → differentiate from orbital cellulitis, abscess. Culture : from pus, vitreous/aqueous tap. Systemic work-up for infection source.

24. Treatment ⚠️ Emergency, but visual prognosis is NIL (eye usually unsalvageable). Goal = life-saving & pain relief. Medical (Supportive) Broad-spectrum systemic antibiotics (IV). Analgesics, anti-inflammatories. IV fluids, systemic stabilization. Local Topical antibiotics and cycloplegics for comfort. Not effective in controlling infection

25. Surgical Evisceration (removal of ocular contents leaving scleral shell) → preferred if orbital spread not severe. Enucleation (removal of entire globe) if sclera severely involved or suspicion of tumor. Done to relieve pain and prevent orbital/CNS spread. Systemic Support Identify & treat systemic focus of infection (esp. endogenous cases)

26. Prognosis Visual prognosis : Hopeless (no vision recovery) . Life prognosis : guarded, depends on early systemic management.

27. Endopthalmitis vs panophthalmitis Feature Endopthalmitis Panophthalmitis Definition Severe purulent inflammation of intraocular fluids (aqueous & vitreous), usually due to infection. Severe purulent inflammation of all coats of eyeball (cornea, sclera, uvea, retina, choroid) + orbital tissue involvement. Extent of involvement Limited to intraocular cavities (aqueous, vitreous, retina, choroid). Involves whole eyeball and orbit (extension beyond sclera). Etiology Post-operative (cataract surgery, IOL, intravitreal injections), post-traumatic, endogenous (bloodstream). Untreated endophthalmitis , severe trauma, corneal ulcer perforation, systemic sepsis.

28. Onset Acute (hours–days) or chronic (weeks–months) Acute, rapidly progressive. Symptoms Pain (moderate to severe), sudden ↓ vision, redness, photophobia, floaters Excruciating pain, rapid total vision loss (no light perception), swelling, systemic fever. Signs – Anterior segment Conjunctival congestion, corneal edema, hypopyon , fibrin in AC. Severe chemosis , lid edema, corneal ulcer/perforation, pus filling AC, scleral abscess Signs – Posterior segment Vitritis , hazy media, loss of fundal glow, retinal detachment. Vitreous full of pus, no fundal glow, orbital cellulitis, proptosis . Systemic involvement Seen in endogenous type. Common (fever, septicemia, CNS spread possible) Investigations Vitreous/aqueous tap for Gram stain, culture; B-scan USG. B-scan, CT/MRI orbit; pus culture; systemic sepsis work-up.

29. Complications Panophthalmitis , retinal detachment, phthisis bulbi , blindness. Orbital cellulitis, cavernous sinus thrombosis, meningitis, phthisis bulbi , death (rare). Treatment Goal = salvage vision. Intravitreal antibiotics ( vancomycin + ceftazidime ), vitrectomy , systemic antibiotics (endogenous), topical therapy. Goal = relieve pain, save life (eye unsalvageable). Evisceration/ enucleation + systemic antibiotics + supportive care. Prognosis Guarded but vision may be salvaged if treated early. Hopeless for vision; life-threatening if untreated.

30. Q1. The most common cause of postoperative endophthalmitis after cataract surgery is: A. Staphylococcus epidermidis B. Staphylococcus aureus C. Pseudomonas aeruginosa D. Candida albicans Q2. The hallmark clinical feature of endophthalmitis is:
A. Severe ocular pain with proptosis B. Sudden painless loss of vision
C. Hypopyon with severe intraocular inflammation
D. Cherry red spot at macula

31. Q3. Which of the following is NOT true about panophthalmitis ? A. Involves all coats of the eye including sclera B. Usually associated with orbital cellulitis C. Always follows trauma only D. Vision is irreversibly lost Q4. The drug of choice for fungal endophthalmitis is:
A. Vancomycin intravitreal B. Amphotericin B intravitreal C. Ciprofloxacin systemic
D. Acyclovir IV

32. . Which of the following is the most important investigation for diagnosis of endophthalmitis? A. Fundus fluorescein angiography B. Ultrasound B-scan C. CT orbit D. Visual field charting

33. Q1. Most common cause of postoperative endophthalmitis after cataract surgery Answer: A. Staphylococcus epidermidis ✔ Normal conjunctival flora, most common in postoperative cases. Q2. Hallmark feature of endophthalmitis Answer: C. Hypopyon with severe intraocular inflammation
✔ Hypopyon (pus in anterior chamber) + vitreous involvement are typical Q3. Which is NOT true about panophthalmitis Answer: C. Always follows trauma only
✔ Panophthalmitis can occur post-surgery, systemic sepsis, or trauma—not only trauma. Q4. Drug of choice for fungal endophthalmitis Answer: B. Amphotericin B intravitreal ✔ Voriconazole is also used, but amphotericin B is the classic answer for fungal endophthalmitis . Q5. Important investigation for endophthalmitis Answer: B. Ultrasound B-scan
✔ Especially useful when fundus is not visible due to hazy media (corneal edema, hypopyon , vitreous exudates).