The document provides a comprehensive overview of infections in the orbit, focusing on preseptal and orbital cellulitis, their anatomy, pathophysiology, and treatment options. It categorizes different stages of infections based on severity and outlines clinical symptoms, diagnostic criteria, and emergency management approaches. Various causative organisms are discussed, along with the necessary interventions for effective treatment and potential complications associated with these infections.

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

4. 4

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

8. 8

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
1. Preseptal cellulitis
2. Orbital Cellulitis (with or without intracranial complications)
3. Orbital abscess (with or without intracranial complications)
i. Intraorbital abscess, which may arise from collection of
purulent material from orbital cellulitis.
ii. 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
1. 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 (2nd
& 3rd 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

42. 42

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 Cellulitis
Fever Present Present
Lid oedema Moderate to severe Severe
Chemosis Absent or mild Moderate or marked
Proptosis Unusual Present
Pain on eye 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

57. 57

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

62. 62

63. 63

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. 69

69. 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

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

71. Clinical Features
Age: young Adults
Manifestations by 2 processes
(i) 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

72. 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

73. 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

74. 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

75. 82

76. • 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

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

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

79. Surgical Approaches
1. 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

80. 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

81. 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

82. 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

83. Predisposing Factors
1.Ulcerative/ Fungating Periorbital
Malignant Tumors
2.Contaminated traumatic wounds around
eyes
3. Previous eye surgery Eg: Evisceration
4.Poor hygiene, debilitation, mental or
physical disability.
91

84. Management
1. Maggots removal and control of infection
2. Surgical management:
• Limited orbital involvement – Reconstructive Surgery
• Globe invasion - Enucleation
• Extensive destruction of orbital tissues- Exenteration
92

85. Maggots Removal
• Firmly clamp onto tissues by hook-like
structure (use non-toothed forceps).
• To facilitate removal- Suffocating
agents- turpentine oil, petroleum jelly,
and liquid paraffin.
• Anesthetic agents- lignocaine and
cocaine paralyze the larvae and prevent
them from penetrating deeper.
93

86. Treatment of Severe Orbital Myiasis
Triple therapy:-
1. Tab. Ivermectin 12 mg PO OD for 3 days
2. Tab. Albendazole 400 mg PO BD for 5 days
3. Tab. Clindamycin 300 mg PO TDS for 5 days
• Terpentine oil dressing
• Oral Morphine a/c the pain score.
94

87. References
• Kanski Clinical ophthalmology, 9th edition
• Yanoff and Duker Ophthalmology, 6th Edition
• Albert and Jackobiec, Volume 4
• AAO Oculofacial Plastic & Orbital Surgery, 2022-2023
95

88. 96

89. Next Class: Friday (May 31 2024)
CASE PRESENTATION
97

90. 98