Preseptal Cellulitis & Orbital Cellulitis -Dr. Prabhat Devkota.pptx

Preseptal Cellulitis & Orbital Cellulitis -
Dr. Prabhat Kiran Devkota
MBBS(TU), MD(NAMS)

1. Infections of Orbit: Preseptal & Orbital Cellulitis Dr. PRABHAT DEVKOTA MBBS(TU), MD(NAMS) 1

2. Content Applied Anatomy Preseptal Cellulitis Bacterial Orbital Cellulitis Necrotizing Orbital Cellulitis Orbital Tuberculosis Fungal Orbital Cellulitis Orbital Parasitic Infections 2

3. Eyelid Anatomy Skin and Subcutaneous tissue Muscles of Protraction Orbital Septum Orbital Fat Muscles of Retraction Tarsus Conjunctiva 3

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5. Orbital Septum Thin, fibrous, multilayered membrane. Sup. orbital septum begins at the arcus marginalis along the orbital rim into the anterior surface of the levator aponeurosis inserted about 3-5 mm above the tarsal plate. Inf. orbital septum fuses with the capsulopalpebral fascia several millimeters below the tarsus. 5

6. Orbit Anatomy Roof: -Frontal bone -Lesser wing of the sphenoid bone Medial Wall: -Frontal process of the maxillary bone - Lacrimal bone - Ethmoid bone -Body of the sphenoid bone Floor: -Maxillary bone - Zygomatic bone -Palatine bone Lateral Wall: - Zygomatic bone -Greater wing of the sphenoid bone 6

7. Medial wall of Orbit Spread of infection occurs easily from the ethmoid sinuses to the medial Orbit:- Thin Lamina Papyracea Multiple foramina for passage of blood vessels and nerves. Valveless veins between the orbit and adjacent structures allowing for bidirectional passage of pathogens. Congenital bony defects ( Zuckerkandl dehiscences ) & acquired bony defects may be present. 7

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9. Orbital Spaces The four recti muscles arise from the annulus of Zinn at the orbital apex and course anteriorly to insert onto the sclera. The intermuscular septum between the recti form a cone that divides the orbit into: The Extraconal Space lies between the bony orbital walls and the annulus of Zinn . The Intraconal Space lies within the annulus, extending form the retrobulbar surface to the orbital apex. 9

10. The Subperiosteal Space: It is a potential space between the periorbita and the bony orbital walls. The periorbita is loosely attached to the orbital bones except at the suture lines & orbital margin. The Sub- Tenon's Space: It is a potential space between the globe and the Tenon's capsule. It is a fibroelastic membrane that extends from the dura of the optic nerve to the globe to fuse with it just behind the corneo-scleral limbus . 10

11. The Paranasal Sinuses Frontal sinuses : Begin pneumatization at 5-6 years of age. Maxillary sinuses : Begin pneumatization in utero ; the first sinuses to fully pneumatize . Ethmoid sinuses : Composed of three to four air cells by birth, continue to expand, and pneumatize till adulthood. Sphenoid sinuses : Start pneumatization at 3 months of age, and reach full size by 12 years 11

12. Inflammation : It is a protective response involving host cells, blood vessels, and proteins and other mediators that is intended to eliminate the initial cause of cell injury, as well as the necrotic cells and tissues resulting from the original insult, and to initiate the process of repair. Cardinal Signs of Inflammation: Calor : warmth Dolor: pain Rubor : redness Tumor: swelling Functio laesa : loss of function. 12

13. Orbital Inflammation caused by pathogenic organisms: Bacterial Virual Fungal Parasitic Infestations Potentially vision & life threatening 13

14. Chandler classification Stage I: Preseptal cellulitis with inflammatory edema anterior to the orbital septum Stage II: Orbital cellulitis with the extension of the inflammation and oedema beyond the orbital septum Stage III : Subperiosteal abscess (SPA) beneath the periosteum of lamina papyracea Stage IV: Orbital abscess within the intraconal space of orbit Stage V : Cavernous sinus thrombosis (CST) resulting after the extension of the infection through the superior ophthalmic veins 14

15. Jain and Rubin Classification Preseptal cellulitis 2. Orbital Cellulitis ( with or without intracranial complications) 3. Orbital abscess ( with or without intracranial complications) Intraorbital abscess , which may arise from collection of purulent material from orbital cellulitis . Subperiosteal abscess , which may lead to infection of orbital soft tissues. 15

16. Preseptal Cellulitis Cellulitis : Latin; cellula (cell)+ itis (inflammation), misnomer Cellulitis is a diffuse acute inflammatory infectious process that involves the dermal and subcutaneous layers of the skin. Preseptal cellulitis refers to infection of the subcutaneous tissues anterior to the orbital septum. The facial veins are valveless and preseptal cellulitis may spread posteriorly to produce orbital cellulitis . Etiology: -Staphylococcus aureus -Streptococcus pyogenes and - Haemophilus influenzae . 16

17. Modes of Infection The organisms may invade the preseptal tissue by any of the following modes:- 1. Exogenous infection : may result following skin lacerations, insect bites and eyelid surgery. 2. Extension from adjacent infections: such as from an acute hordeolum , dacryocystitis , conjunctivitis, sinusitis. 3. Endogenous infection : may occur by haematogenous spread from remote infection of the middle ear or upper respiratory tract infection(URTI). 17

18. Clinical Features Painful acute periorbital swelling, Erythema and hyperaemia of the lids, Fever and leukocytosis may be present, Proptosis is absent, Ocular movements are normal, Conjunctiva is usually not congested, and Visual acuity is normal. 18

19. Treatment 1 . Systemic antibiotics : • Mild-to-moderate cases may be treated by oral Amoxicillin + Clavulanate (500+125mg) TDS or Flucloxacillin 500 mg QID for about 10 days. • Severe cases need hospitalization for intravenous Ceftriaxone , 1-2g/day in divided doses for 5 days . Then treat as mild cases. 2. Systemic analgesics and anti-inflammatory drugs 3 . Warm compresses , 2-3 times a day 4. Surgical exploration and debridement is required in the presence of a fluctuant mass or abscess, or when retained foreign body is suspected. 19

20. Bacterial Orbital Cellulitis Orbital cellulitis refers to serious infection of the soft tissues of the orbit behind the orbital septum. medical emergency: sight/life threatening most common cause of unilateral proptosis in children may progress to a subperiosteal or, orbital abscess. team effort required between Ophthalmologist + Physician + ENT surgeon+ Neurosurgeon 20

21. Etiology 1. Exogenous infection : Penetrating injury with intraorbital foreign body and following surgeries like evisceration, enucleation , dacryocystectomy and orbitotomy . 2. Extension of infection from adjacent structures : Paranasal sinuses, teeth, face, lids, intracranial cavity and intraorbital structures . It is the commonest mode of orbital infections. 3. Endogenous infection : may rarely develop as metastatic infection from breast abscess, puerperal sepsis, thrombo -phlebitis of legs and septicaemia . 21

22. Pathophysiology Sequelae to paranasal sinusitis (m/c ethmoid sinusitis.) Inflammatory mediators released by sinus mucosa d/t infection Causing the blockage of osteum - sinus drainage block Conducive environment for prolifaeration of microorganism Gains orbit to through the Lamina papyracea Intraorbital pressure rise Inflammatory reaction 22

23. Polymicrobial infection - adults Aerobes and anaerobes have synergistic effects. The aerobes create hypoxia, which helps the anaerobes to proliferate, The anaerobes produce beta- lactamases , which protect the aerobes against beta- lactam antibiotics. 23

24. Causative organisms: Staph. aureus including MRSA , Strep. epidermidis , Strep. pneumoniae , H. influenzae , Diphtheroids , Anaerobes, Pseudomonas & Fungal (Diabetic & Immunocompromised ) Pathology: special features: Infection establishes early due to absence of lymphatics in the orbit. Rapid spread with extensive necrosis is common since in most cases infection spreads as thrombophlebitis from the surrounding structures. Damage produced is rapid and extensive as orbital infection is associated with raised intraorbital pressure due to the tight compartment. 24

25. Bacteriology- Children In children <9 years - single organism Streptococcus species, Staphylococcus aureus , and Haemophilus influenzae . Since the early 2000s, the Streptococcus anginosus group has been an emerging pathogen in pediatric orbital infections. Haemophilus influenzae was the m/c pathogen before the introduction of H. influenzae type B ( HiB ) vaccine. 25

26. Bacteriology- Adults Mixed aerobes and anaerobes ( Bacteroides , Peptostreptococcus , Fusobacterium ) Gram positive Organism > Gram negative Organism ( Gram-positive bacteria especially Staphylococcus & Streptococcus are the m/c organisms in adults.) Polymicrobial infection (d/t well-developed frontal sinuses which is heavily colonized by aerobes & anaerobes.) Orbital cellulitis resulting from infection of the maxillary sinus secondary to dental infections can be caused by microorganisms indigenous to the mouth including anaerobes commonly Bacteroides . 26

27. Clinical Features Symptoms: • Swelling and severe pain (increased by movements of the eyeball or pressure) • Constitutional Symptoms: Fever, nausea, vomiting and prostrations. • Vision loss and/or diplopia (moderate to advanced disease) 27

28. Signs: Swelling, woody hardness and erythema of lids Conjunctival chemosis , Proptosis , Mechanical ptosis , Diplopia , Painful Ophthalmoplegia , Diminution of VA ±impaired color vision, RAPD may occur due to optic neuropathy or CRAO, Fundus may show congestion of retinal veins and signs of papillitis . (Disc swelling, Choroidal Fold) 28

29. Warning Signs of Orbital Cellulitis Painful restriction of extraocular movement Proptosis Reduced visual acuity Abnormal color vision Relative afferent pupillary defect or fixed nonreacting pupil Fever & Toxic appearance 29

30. CNS Involvement Fever, malaise, associated nasal discharge and cough Throbbing headache, nausea, vomiting and altered sensorium Associated systemic comorbidities : -Diabetes mellitus, immunosuppression , HIV infections, -Fungal orbital cellulitis . 30

31. Investigations Bacterial cultures from nasal/ conjunctival swabs & blood culture. 2. Complete Blood Count 3. X-ray PNS to identify associated sinusitis. 4. Orbital ultrasonography to detect intraorbital abscess. 5. NCCT scan and MRI 31

32. Indication of Imaging To differentiate preseptal and postseptal cellulitis , To know the extent of the disease Subperiosteal /Intra Orbital Abscess To identify the origin Differentiate Infective/Inflammatory To detect intracranial extension, Cavernous Sinus Thrombosis Presence of Foreign Body Plan for Drainage of abscess To differentiate Fungal from Bacterial Condition worsening despite treatment 32

33. CT Scan Periorbital cellulitis :- Diffuse soft tissue thickening with patchy enhancement anterior to septum. Orbital cellulitis :- Diffuse Inflammatory stranding of intraconal fat with oedema of the EOM. 33

34. MRI Diffuse inflammatory stranding in the intraconal fat with oedema of the EOM . Abscess shows a high signal in T2 with diffusion restriction and thin peripheral rim enhancement. Tenting of the globe due to severe inflammatory edema of the orbit on imaging has an unfavorable prognosis. Identifying complications Sup.Ophthalmic Vein Thrombosis, Cavernous Sinus Thrombosis, Brain Abscess. 34

35. Treatment Indications of medical therapy:- Preseptal cellulitis Empirical therapy in orbital cellulitis Subperiosteal abscess in young children(<9yr) Indications of surgical therapy:- Subperiosteal /orbital abscess in older children and adults Orbital abscess a/w frontal sinusitis Worsening of vision/ proptosis / ophthalmoplegia Presence of a retained foreign body An identified dental source of the infection Intracranial complications No response to medical therapy 35

36. Treatment It is an emergency so the patient should be hospitalised for aggressive management. 1.Intensive antibiotic therapy: After obtaining nasal, conjunctival and blood culture samples, intravenous antibiotics should be administered. Antibiotics are commenced on an empirical basis and then altered based on bacteriology results. Usually a 48-hour window period is used to assess improvement before considering a change in regimen. If no response is noted, or if there is worsening of visual function, surgical intervention must be considered. 36

37. Broad-spectrum antibiotics commonly used: Gram-positive coverage : Amoxicillin + Potassium Clavulanate Gram-positive + gram-negative coverage : Cephalosporins (2 nd & 3 rd generation) MRSA : Vancomycin Vancomycin -resistant S. aureus (VRSA ) : Linezolid Gram-negative coverage : Aminoglycosides Broad-spectrum combinations : Piperacillin+Tazobactam ; Ticarcillin+Clavulanate Anaerobic coverage : Metronidazole . 37

38. 2. Analgesic and anti-inflammatory drugs are helpful in controlling pain and fever. 3. Topical antibiotic eye ointment QID for corneal exposure and chemosis when there is severe proptosis . 4. Nasal decongestant drops should be started. 5. Revaluation, at least twice to thrice daily in the hospital, is required to monitor the response and modify the treatment accordingly. 38

39. 6. Surgical intervention:- Indications : unresponsiveness to antibiotics, decrease in vision and presence of an orbital or subperiosteal abscess. Principles : drainage of pus & ventilation to the sinus Immediate lateral canthotomy / cantholysis may be needed, if the orbit is tight, an optic neuropathy is present, or the IOP is severely elevated. Incision and drainage of the abscess: Subperiosteal abscess is drained by a 2-3 cm curved incision made in the upper medial aspect of the orbit. In most cases, it is necessary to drain both the orbit as well as the infected paranasal sinuses. 39

40. Indication of Urgent Surgical Drainage Large orbital abscess (superior or inferior) Presence of frontal sinusitis. Intracranial Complications Inadequate response on medical therapy Aanaerobic Infection(abscess with gas) Any abscess compressing on the optic nerve cause visual dysfunction Orbital abscess- orbital apex or intracranial extension. An SPA size of more than 1250ml, regardless of patient age. Infection of dental origin (anaerobic) 40

41. Role of Steroids! Reduces tissue damage and toxic effects of inflammatory mediators. Reduces hospital stay and duration of IV antibiotics Insufficient evidence to conclude the use of corticosteroids Must be administered only after visible clinical improvement starts with IV antibiotics Avoided in immunocompromised , uncontrolled diabetics and fungal orbital cellulitis 41

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43. Complications Corneal involvement : Exposure keratopathy , Neurotrophic keratitis Intraocular involvement : Endophthalmitis , septic uveitis , elevated IOP Posterior orbital changes : Orbital abscess, Subperiosteal abscess, Optic Neuritis, Compressive Optic Neuropathy, CRAO, CRVO, Extraocular Motility Deficits, Intracranial complications : Cavernous Sinus Thrombosis, Meningitis, Intracranial Abscess 43

44. Differential Diagnosis 44

45. Necrotizing Orbital Cellulitis Form of Gangrene- Extensive Soft tissue Necrosis Polymicrobial infection- Aerobic, Anerobic , Clostridia Crepitant (Gas forming) or Non Crepitant Streptococcus anginosus /Streptococcus milleri group polysaccharide capsule hinders phagocytosis , The production of hydrolytic enzymes or the presence of capsular proteins that suppress lymphocyte and fibroblast proliferation but do not affect leucocyte migration. 45

46. Rapid progression of orbital signs Severe systemic toxicity Poor response to appropriate antibiotics Orbital abscesses must be assumed Aggressive surgical drainage of the orbit is an absolute requirement Failure to improve despite surgery mandates repeated surgery Aggressive multidisciplinary surgical management High risk of loss of sight and possibly loss of life. 46

47. Preseptal vs Orbital Cellulitis Finding Preseptal Cellulitis Orbital C ellulitis Fever Present Present Lid oedema Moderate to severe Severe Chemosis Absent or mild Moderate or marked Proptosis Unusual Present Pain on e ye movement Absent Present Ocular mobility Normal Decreased Vision Normal Diminished +/- Diplopia RAPD Absent May be seen Leucocytosis Mild to moderate Marked Adenopathy Absent May be seen ESR Normal/ elevated Markedly elevated Additional findings Skin infection Sinusitis, Dental abscess 47

48. Orbital Tuberculosis m/c seen in developing countries, in developed countries usually a/w HIV coinfection . Most commonly from hematogenous spread from a pulmonary focus, which is often subclinical. Less often, spread occurs from an adjacent tuberculous sinusitis. 48

49. Clinical Presentation Proptosis Motility dysfunction Bone destruction Chronic draining fistulas 49

50. Unilateral usually HPE : caseating necrosis, epithelioid cells, and Langhans giant cells . Skin testing and FNAC with culture may help establish the diagnosis . Treatment : Antituberculosis therapy 50

51. Fungal Orbital Cellulitis Rare aggressive, fatal infection caused by fungi of the family Mucoraceae . Life threatening and invasive Fungus : Mucorales : ( Rhizopus , Mucor , Lichtheimia ) Aspergillus 51

52. Risk Factors Aspergillosis :- Prolonged neutropenia AIDS Organ transplantation/ hematopoietic stem cell transplantation Advancing age Diabetes mellitus Mucormycosis :- Diabetes mellitus with ketoacidosis Hematological malignancies Renal disease 52

53. Clinical Features Symptoms: • Periocular pain and swelling • Headache • Blurring of vision/ vision loss • Diplopia • Droopy eyelid • Nasal discharge/bleed 53

54. Signs: • Ptosis • Proptosis (minimal) • Ophthalmoplegia • Facial discoloration • CRAO • Nasal or Palatal eschar Ophthalmoplegia Sinusitis CRAO TRIAD 54

55. When to Investigate?? 55

56. Investigation CT /MRI Diagnostic Endoscopy Microbiology: Nasal swab, KOH, CFW, RTPCR Histopathology: Nasal eschar , FESS debrided tissue 56

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58. Clinical Suspician Ophthalmoplegia Sinusitis CRAO IV Amphotericin (Liposomal) Confirm Diagnosis Microbiology/ Histopathology Medical (Non Exenteration ): Systemic antifungal FESS/ Sinus irrigation TRAMB Surgical ( Exenteration ) Total Extended Treatment Protocol: 58

59. Treatment Principle Early diagnosis Reversal of predisposing factors ( glycemic control) Correction of underlying metabolic defect Wide local debridement of necrotic tissue Establishing adequate sinus drainage Systemic Antifungals . 59

60. Medical Treatment Liposomal Amphotericin -B : 5-10mg/kg/day X 2 weeks Posaconazole : 300mg BD X 2-4 week Transcutaneous Retrobulbar Amphotericin B (TRAMB): 1ml of 3.5mg/ml Amphotericin +1:1 ratio 2% Lidocaine , 0.5% Bupivacaine ADR: Neurotoxicity Hyperbaric oxygen may be helpful. 60

61. Surgical Treatment Early surgical debridement of Sinuses Orbital Exenteration Indication: • Diffuse orbital involvement • Unilateral • Non-seeing eye with progressive disease • No or minimal extension to cavernous sinus • Worsening of the orbital component or no improvement in 72 hours after FESS and Amphotericin B • Panophthalmitis Partial vision, responding to Treatment – Avoid Exenteration 61

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64. 64 DOI: 10.4103/ijo.IJO_1165_21

65. Conclusion: Survival Rate 3% untreated, 61% with Amphotericin - B, 57% with surgery alone & 70% with both 65

66. Orbital Parasitic Infections Orbital Cysticercosis Orbital Echinococcosis Orbital Myiasis 66

67. Cysticercosis Cysticercosis is a parasitic infestation by Cysticercus cellulosae , which is the larval form of Taenia solium (Tape worm) Through the blood stream, cysts get located mostly in CNS, eye & striated muscles. The high glucose or glycogen content of these tissues explains their tropism for Cysticerci . The most common form of systemic involvement is neurocysticercosis . 67

68. Taeniasis Humans are the definitive hosts and the adult parasites live in the small intestine. The pig is the intermediate host and harbours the larval stage of T. solium 68

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70. Ocular Cysticercosis Ocular and adnexal cysticercosis represents 13% to 46% of systemic disease. Localization of Cysticercus larva in the orbit is facilitated by the blood circulation, as the ophthalmic artery is the first and single collateral branch of the internal carotid artery . The larval form enter the eye through the choroidal circulation and migrate into the subretinal space/ vitreous cavity/ anterior chamber. 70

71. Orbital Cysticercosis Extraocular muscles Optic Nerve Subconjunctival Lacrimal gland Eyelid 71

72. Stages of Cysticercus cyst Cysticercus cellulosae can be seen in various stages of evolution Live cyst- Vesicular stage Dying cyst- Colloidal vesicular stage Dead cyst- Granular/ Calcified nodular stage 72

73. Clinical Features Age : young Adults Manifestations by 2 processes The mass effect of the space-occupying lesions (live cyst) (ii) The local inflammatory response (dying cyst) Signs and symptoms: 1. Periocular swelling (± pain) 2. Ptosis 3. Diplopia 4. Restriction of ocular motility 5. Proptosis 6. Decreased vision 7. Spontaneous extrusion* 73

74. Treatment Based on clinico -radiological diagnosis Medical management : Mainstay DOC - Oral Albendazole as 15 mg/kg per day in two divided doses for 4 weeks Mechanism of Action- Blocks glucose uptake of the parasite & leads to death of the larva that results in release of toxins and hence severe inflammation. Oral Steroids to suppress the inflammatory reaction a/w death of the larva 1mg/kg per day for 4 weeks, thereafter tapered over next 4 weeks. 74

75. Response to treatment: Serial USG Guides the duration of cysticidal therapy Cysticidal drugs are discontinued once the previously imaged scolex is lost and corticosteroids are continued until active myositis persists. 1-2 weeks • Reduction cyst size • Loss of the scolex 3-4 weeks • Collapse of the cyst wall • Persistent echoes from the surrounding tissues 6-8 weeks • Reduction in echogenicity within the muscle Albendazole Prednisolone 75

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78. Role of Fundus Examination Rule out Intraocular ( subretinal / intravitreal / anterior chamber) cyst before starting cysticidal therapy. 78

79. Miliary Neurocysticercosis • "Starry sky" appearance • Vision loss may occur d/t: 1. Secondary optic atrophy 2. Chiasmal compression 3. Occipital lobe involvement 4. ON cyst 79

80. Hydatid cyst • Echinococcus granulosus (dog tapeworm) • Prevalent in Mediterranean, Middle East, South America, New Zealand, Australia, and Southeast Asia. • Echinococcus parasite live in the intestines of dogs ( definitive host ) • Eggs are shed in dog faeces , ingested by intermediate host via contaminated grass /food ( sheep/ human ), leading to hydatid disease in the intermediate host . 80

81. Echinococcosis variants Within the genus Echinococcus , four species are recognized: 1 . E. granulosus that causes cystic echinococcosis (CE), {displacement and pressure atrophy} 2. E. multilocularis that causes alveolar echinococcosis (AE) {infiltrative growth} 3. E. oligarthrus and 4. E. vogeli cause polycystic echinococcosis • Orbital echinococcosis is caused by E. granulosus , which typically manifests as a unilocular cyst 81

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83. 3 layers Grows an average of 1.5 cm each year Daughter cysts are formed as part of the aging process by endogenic vesiculation within the mother cyst 83

84. USG Characteristics:- Double wall sign Hydatid Sand : Localized condensation in the cyst wall corresponding to the area of collection of scolices . 84

85. Why it is important to diagnose early ? Progressive expansion 1. ON compression - Threatens vision 2. Risk of spontaneous rupture 85

86. Surgical Approaches Conventional en-bloc removal Challenges: • Thin walled, large cyst • Restricted access/ exposure in orbit for en-bloc removal 2. Aspiration of the cyst fluid - collapse of inner laminated layer - dissection of outer fibrous layer - Cryo assisted extraction of the inner cyst. 86

87. Role of Perioperative Cysticidal Treatment Oral Albendazole (15mg/kg) in two 4-week courses with a 2-week interval. • Non-orbital cysts : Decrease cyst size before surgery (complete resolution in 30%). • Orbital hydatid cysts:( no added benefit) ➤short course of treatment ➤urgent necessity for early surgery. 87

88. Role of PAIR Puncture (P), Aspiration (A), Instillation (I) and Reaspiration (R) Percutaneous aspiration of cyst contents with 21-G needle under USG guidance. Injection of 15% hypertonic saline solution Reaspiration 10 minutes later 88

89. Ophthalmomyiasis Classified as:- Ophthalmomyiasis externa (superficial, larvae attack the conjunctiva) Ophthalmomyiasis interna (invade the globe, and anterior and posterior segments of the eyeball, cause uveitis ). Orbital myiasis ( Ophthalmomyiasis profunda ) - A severe clinical variant, invades into the periorbita and orbit 89

90. Orbital Myiasis Infection with the larval stage (maggots) of flies is called myiasis . Infestation of human tissue by botfly larvae, typically the sheep botfly Oestru ovis and the human botfly Diptera hominis . 90