2d:I[856015,["/_next/static/immutable/chunks/1xzisbplk9czp.js","/_next/static/immutable/chunks/3j2i1faptc_-9.js","/_next/static/immutable/chunks/0fma7nlq6immz.js","/_next/static/immutable/chunks/08tq8rmv423j5.js","/_next/static/immutable/chunks/1chr5wkk3j58k.js","/_next/static/immutable/chunks/37kmmh_zm4dov.js","/_next/static/immutable/chunks/311zvdjfxff-f.js","/_next/static/immutable/chunks/1a_hqhrsle_n_.js"],"default"] 2e:T5da5,

Summary Table

Category	Details
Risk Factors	Penetrating ocular trauma (especially soil or vegetable matter contamination), recent intraocular surgery (cataract, vitrectomy), perforated corneal ulcer, untreated endophthalmitis, sepsis or bacteremia, intravenous drug use, immunocompromised state (diabetes, malignancy, HIV)
Etiology	Severe purulent infection. Common bacteria include Staphylococcus aureus, Streptococcus species, Bacillus cereus (post-traumatic, fulminant), Pseudomonas aeruginosa, and gram-negative rods. Fungal causes (Candida, Aspergillus) seen in immunocompromised hosts and IV drug users
Patient Presentation	Sudden severe ocular pain, complete or near-complete vision loss, redness, swelling around the eye, fever, malaise, headache, history of penetrating trauma or recent eye surgery
Classic Physical Exam	Marked lid edema, conjunctival chemosis, proptosis, restricted extraocular movements (ophthalmoplegia), corneal haze, hypopyon, absent red reflex, no view of the fundus, tender globe, often no light perception (NLP)
Key Diagnostic Results	Clinical diagnosis. B-scan ultrasound shows vitreous opacities and scleral thickening. CT orbit shows diffuse intraocular and orbital inflammation. Vitreous tap and aqueous tap for Gram stain and culture. Blood cultures if endogenous source is suspected
Management	Ophthalmologic emergency. Admit. Empirical broad-spectrum intravenous antibiotics plus intravitreal antibiotics (vancomycin plus ceftazidime). Topical fortified antibiotics. Cycloplegics for pain. Evisceration or enucleation often required when vision is irrecoverable and infection threatens intracranial spread
Keywords	"Inflammation of all coats of the eye", "proptosis with hypopyon", "no light perception following penetrating trauma", "frozen globe", "purulent panuveitis with orbital signs", "post-traumatic Bacillus cereus infection", "fulminant globe destruction"

1. Pathophysiology

Panophthalmitis represents the most severe end of the intraocular infection spectrum. Unlike endophthalmitis, which is confined to the intraocular cavities (vitreous and aqueous humor), panophthalmitis describes purulent inflammation involving all three coats of the eye (sclera, uvea, retina) along with extension into the orbital tissues. This distinction matters because the presence of orbital signs (proptosis, ophthalmoplegia, lid edema) on the vignette is the cardinal feature that separates panophthalmitis from endophthalmitis on examinations.

The infection reaches the eye through two main routes. The exogenous route accounts for most cases and follows direct inoculation of organisms after penetrating trauma, intraocular surgery, or perforation of an infected corneal ulcer. The endogenous route occurs through hematogenous seeding in patients with bacteremia, fungemia, infective endocarditis, urinary tract infection, liver abscess (classically Klebsiella pneumoniae in diabetics), or in intravenous drug users.

Once organisms enter the eye, they multiply rapidly in the avascular vitreous, which lacks robust immune surveillance. Bacterial toxins and host inflammatory response cause liquefaction of intraocular tissues. As the infection breaches the sclera, it extends into Tenon's capsule and orbital fat, producing the orbital inflammatory signs that define this condition. Bacillus cereus infection following soil-contaminated penetrating trauma is the most aggressive form and can destroy the eye within 24 to 48 hours.

The patient's complaints map directly onto these mechanisms. Severe pain results from stretching of pain fibers in the sclera and uvea by suppurative material under pressure. Vision loss is due to clouding of ocular media by inflammatory cells and toxic damage to the retina and optic nerve. Proptosis and limited eye movements arise from orbital fat involvement and inflammation around the extraocular muscles. Systemic features such as fever and malaise reflect either the underlying bacteremia (in endogenous cases) or absorption of bacterial toxins.

A point that often appears as a distractor: in panophthalmitis, the inflammation has already crossed beyond the globe, so visual prognosis is poor and the immediate threat is spread to the cavernous sinus and brain through emissary veins. Recognizing this danger drives the aggressive management approach.

2. Classification and Clinical Manifestation

Classification	Subtype	Clinical Features
By route of entry	Exogenous	Penetrating trauma, recent intraocular surgery, or corneal perforation. Unilateral. Most common form
By route of entry	Endogenous	Hematogenous spread from a distant infection. May be bilateral. Often in diabetics, IV drug users, or immunocompromised patients
By onset (post-surgical)	Acute	Within 6 weeks of surgery. Usually virulent organisms (Staph, Strep, gram-negative rods)
By onset (post-surgical)	Delayed/chronic	Beyond 6 weeks. Indolent organisms (Propionibacterium acnes, fungi)
By causative organism	Bacterial	Most common. Gram-positive cocci predominate post-surgically. Bacillus cereus in trauma. Pseudomonas in contact lens-related cases
By causative organism	Fungal	Candida (endogenous, IV drug users), Aspergillus (post-traumatic with vegetable matter)

3. Diagnostic Workup

Test	Role	Findings
Visual acuity	Initial assessment	Markedly reduced, often light perception or worse
B-scan ultrasonography	Best initial imaging when fundus view is obscured	Vitreous opacities, membranes, retinal/choroidal thickening, scleral thickening, extension into orbit
CT scan of orbit	Confirms orbital involvement	Diffuse orbital inflammation, scleral thickening, intraocular gas in some cases, rules out retained foreign body
Vitreous tap and aqueous tap	Gold standard for microbiologic diagnosis	Gram stain, culture, sensitivity. Performed before or at the time of intravitreal antibiotic injection
Blood cultures	When endogenous source is suspected	Identify primary source organism
Complete blood count, blood glucose, HIV, ESR, CRP	Workup for systemic infection and risk factors	Leukocytosis, raised inflammatory markers, hyperglycemia

The diagnostic approach to suspected panophthalmitis begins at the bedside. Panophthalmitis is fundamentally a clinical diagnosis, and treatment must not be delayed while awaiting investigations. Once the typical features (severe pain, proptosis, hypopyon, ophthalmoplegia, near-total vision loss) are identified in a patient with the appropriate risk profile, the immediate priority shifts to obtaining material for culture and starting antibiotics.

The best initial diagnostic test after clinical examination is B-scan ultrasonography, particularly when corneal opacity, hypopyon, or vitreous haze prevent direct visualization of the posterior segment. B-scan demonstrates the extent of vitreous involvement and can detect retinal detachment, choroidal thickening, and posterior scleral inflammation that hint at extension beyond the globe.

A CT scan of the orbit is ordered when there are clinical signs of orbital extension or when a retained intraocular foreign body is suspected after trauma. CT helps distinguish endophthalmitis from true panophthalmitis by showing inflammatory changes in orbital fat and around the extraocular muscles. MRI is reserved for evaluating suspected cavernous sinus or intracranial extension.

The most accurate test (gold standard) for microbiological confirmation is a vitreous tap with culture and Gram stain. Vitreous yields a higher diagnostic rate than aqueous because it harbors a larger bacterial load. The tap is performed in the operating room under sterile conditions, and intravitreal antibiotics are injected at the same sitting. In endogenous cases, blood cultures are required to identify the primary source, and additional workup looks for endocarditis (echocardiography), urinary tract infection, or liver abscess.

Routine workup also includes a complete blood count, blood glucose (diabetes is a major risk factor for endogenous infection), HIV testing where appropriate, and inflammatory markers to monitor response to therapy.

4. Management and Treatment

Phase	Intervention	Details
Immediate	Hospital admission	Ophthalmologic emergency. Surgical consultation
Empirical antibiotics (intravitreal)	Vancomycin 1 mg in 0.1 mL plus Ceftazidime 2.25 mg in 0.1 mL	Covers gram-positive and gram-negative organisms. Repeated every 48 to 72 hours if needed
Empirical antibiotics (systemic)	IV vancomycin 15 to 20 mg/kg every 8 to 12 hours plus IV ceftazidime 1 to 2 g every 8 hours	Continue 10 to 14 days. Mandatory in panophthalmitis given orbital and systemic involvement
Topical therapy	Fortified vancomycin (50 mg/mL) and fortified ceftazidime (50 mg/mL) hourly	Adjunct to penetrate the anterior segment
Adjunctive	Cycloplegic (atropine 1% three times daily). Topical steroid started 48 hours after antibiotics, only if bacterial cause is confirmed	Reduces pain, prevents posterior synechiae
Antifungal therapy	Intravitreal voriconazole 100 mcg in 0.1 mL plus systemic voriconazole	Reserved for confirmed fungal etiology. Steroids contraindicated
Surgical	Pars plana vitrectomy	Considered when vision is light perception or worse, or in fulminant cases
Definitive	Evisceration or enucleation	Indicated when the eye is blind, painful, and infection threatens intracranial spread. Evisceration preferred unless an intraocular tumor is suspected
Long-term	Prosthetic rehabilitation	After healing of the socket, usually 6 to 8 weeks postoperatively

The cornerstone of acute management is immediate intravitreal antibiotic injection combined with systemic antibiotics. Empirical intravitreal therapy uses vancomycin 1 mg in 0.1 mL to cover gram-positive organisms (including methicillin-resistant Staphylococcus) plus ceftazidime 2.25 mg in 0.1 mL to cover gram-negative organisms including Pseudomonas. An alternative for ceftazidime in penicillin-allergic patients is amikacin 0.4 mg in 0.1 mL, although aminoglycoside retinal toxicity limits its use. Injections may be repeated every 48 to 72 hours based on clinical response.

Unlike isolated endophthalmitis, where systemic antibiotics are sometimes deferred, panophthalmitis always requires intravenous antibiotics because orbital and systemic involvement places the patient at risk for cavernous sinus thrombosis and meningitis. Standard regimens use IV vancomycin (15 to 20 mg/kg every 8 to 12 hours) plus IV ceftazidime (1 to 2 g every 8 hours), continued for 10 to 14 days and adjusted based on culture results.

Adjunctive measures include topical fortified antibiotics applied hourly, cycloplegic drops (atropine 1% three times daily) to relieve ciliary spasm and prevent posterior synechiae, and analgesia. Topical and oral corticosteroids may be added 48 hours after starting antibiotics in confirmed bacterial cases to reduce inflammation, but they are contraindicated until fungal etiology has been excluded.

When fungal panophthalmitis is confirmed (Candida or Aspergillus), treatment shifts to intravitreal voriconazole 100 mcg in 0.1 mL plus systemic voriconazole or amphotericin B. Steroids must be avoided in this setting.

The "next best step" question on examinations often asks what to do when vision deteriorates to no light perception despite optimal antibiotic therapy, or when the globe is clearly destroyed. The answer is evisceration (removal of intraocular contents leaving the scleral shell intact) or enucleation (removal of the entire globe). Evisceration is generally preferred because it preserves orbital anatomy for a better prosthetic outcome, but enucleation is mandatory when an underlying intraocular tumor (such as retinoblastoma) is suspected, since evisceration risks tumor seeding.

In pregnancy, both vancomycin and ceftazidime are acceptable. Aminoglycosides should be avoided due to fetal ototoxicity. Voriconazole is contraindicated in pregnancy because of teratogenicity, and amphotericin B is the preferred antifungal. In renal failure, vancomycin and ceftazidime doses must be adjusted based on creatinine clearance.

5. Differential Diagnosis and Distractors

Differential	Why it's similar	Key Discriminator
Endophthalmitis	Both follow trauma or surgery and present with pain, hypopyon, vitritis, vision loss	No proptosis, no lid swelling, no ophthalmoplegia in endophthalmitis. Globe and orbit examination is the dividing line
Orbital cellulitis	Proptosis, lid edema, ophthalmoplegia, fever	Vision is initially preserved. No hypopyon and no vitritis. Origin is usually ethmoid sinusitis. Sinus opacification on CT
Cavernous sinus thrombosis	Proptosis, ophthalmoplegia, pain, fever	Bilateral involvement, multiple cranial nerve palsies (III, IV, V1, V2, VI), papilledema. MRI/MRV shows thrombus in the cavernous sinus
Acute angle-closure glaucoma	Severe ocular pain, vision loss, red eye, mid-dilated pupil, nausea, vomiting	No hypopyon, no vitritis, IOP markedly raised (above 40 mmHg), shallow anterior chamber. No history of trauma or surgery
Severe non-infectious uveitis (HLA-B27, Behcet)	Anterior chamber inflammation, hypopyon, photophobia	No fever, no proptosis, no orbital signs, vitreous tap is sterile. Recurrent episodes, systemic features of underlying disease
Carotid-cavernous fistula	Proptosis, chemosis, dilated episcleral vessels	Pulsatile proptosis with bruit, history of trauma, dilated tortuous corkscrew vessels. MRA confirms
Intraocular tumor with necrosis (retinoblastoma in children)	Vision loss, leukocoria, secondary inflammation can mimic infection	Age younger than 5 years, calcifications on B-scan/CT. Enucleation rather than evisceration is the procedure of choice. Biopsy is contraindicated

The most common pitfall is failing to separate endophthalmitis from panophthalmitis. The vignette will provide a clue: if proptosis, lid swelling, restricted motility, or systemic signs (fever, leukocytosis) are mentioned, the answer is panophthalmitis. If the inflammation is confined to the eye with no orbital involvement, the answer is endophthalmitis.

Another classic distractor is orbital cellulitis. The discriminator is that vision is preserved early in orbital cellulitis (until optic nerve compression develops) and there is no hypopyon or vitritis. In panophthalmitis, intraocular signs (hypopyon, absent red reflex) coexist with orbital signs.

6. Traps and High-Yield Pearls

The most frequent trap in panophthalmitis questions is treating the diagnosis as if it were ordinary endophthalmitis. Test writers exploit this by giving a patient with a recent penetrating injury who initially had endophthalmitis but now presents with proptosis, ophthalmoplegia, lid edema, and fever. Students who answer "intravitreal vancomycin and ceftazidime alone" miss the point that systemic involvement now mandates intravenous antibiotics and consideration of evisceration.

A second high-yield trap involves the eviscerate versus enucleate decision. If the question describes a child with leukocoria and a painful, opaque eye, the answer is enucleation, not evisceration, because of the risk of seeding an underlying retinoblastoma. In adults with no suspicion of tumor and a blind, painful eye after fulminant infection, evisceration is the correct procedure.

A third common pitfall is the organism-trauma association. Penetrating trauma with vegetable or soil contamination strongly suggests Bacillus cereus, an organism notorious for fulminant globe destruction within 24 to 48 hours. Recognizing this scenario should prompt immediate surgical and antibiotic intervention rather than observation.

A fourth pearl concerns the endogenous case. When panophthalmitis develops without trauma or surgery, the question is testing whether you remember to look for a systemic source. Diabetic patients with liver abscess (Klebsiella pneumoniae), patients with infective endocarditis, and intravenous drug users are the typical scenarios. The workup must include blood cultures, echocardiography, and abdominal imaging.

Finally, the underlying competency being tested is prompt recognition of an orbital and intraocular emergency that threatens both the eye and the brain. The exam wants you to recognize the constellation of intraocular suppuration plus orbital signs, initiate intravitreal and intravenous antibiotics without delay, and identify the threshold for surgical removal of the globe to prevent intracranial spread.

1e:["$","$L2d",null,{"article":{"id":"f160243f-e4b3-4df6-abe7-50d07f794087","title":"Panoftalmitis","content":"$2e","category":"Oftalmologi","created_at":"2026-05-01T18:31:19.768463+00:00","status":"published","subcategory":null},"questionCount":1,"sections":[{"id":"section-pathophysiology","num":"01","title":"Pathophysiology"},{"id":"section-classification-and-clinical-manifestation","num":"02","title":"Classification and Clinical Manifestation"},{"id":"section-diagnostic-workup","num":"03","title":"Diagnostic Workup"},{"id":"section-management-and-treatment","num":"04","title":"Management and Treatment"},{"id":"section-differential-diagnosis-and-distractors","num":"05","title":"Differential Diagnosis and Distractors"},{"id":"section-traps-and-high-yield-pearls","num":"06","title":"Traps and High-Yield Pearls"}],"hasSummaryTable":true}]