Time Pressure

quality of discussions between doctor and patient is not a function of time, but of the ability to understand the feelings of the other, as well as employing correct interview techniques. A good discussion certainly does not imply a long discussion, neither does a long conversation guarantee a successful interview. Many doctors will probably only be convinced than understanding discussion does not waste time, when they have had experience in this area.

Time pressure is infectious and can itself create further lack of time.

It is not possible to measure time pressure objectively, as it is the subjective experience of limited supplies of time. This also means that I can influence how I experience time pressure and cope with it. This in turns means that I can train myself to tolerate time pressure, instead of constantly feeling impotent under its influence. Whoever learns to tolerate shortness of time and time pressure will not mention his limited time again and again, thereby releasing the feeling of time pressure in the person he is talking to, and not disturb something very important that has just come up in the discussion.

It has become fashionable not to have much time; full diaries and overcrowded, loaded desks are supposed to be a status symbol; however they are certainly not evidence of an economical way of dealing with the time available. It is also not a sign of composure to brag about one’s lack of time and to wear time pressure like a badge of merit.

make an exact note of the number of times you glance at the time. Something is wrong if this is more than 5 times in half an hour: this can be either your attitude to time or your way of dealing with it.

The most important time-saving factors in discussion are those which, at the same time, are essential to a good discussion: active listening, empathy, an adequate interview technique and the ability to find a mutual reality.

Uncompleted tasks set off restlessness and stress. It is only a completely finished assignment which releases this burden. Because of this, it is advisable to complete one task after another, rather than to try to take on too many at one time. In fact, a completed task brings one much further on than 10 which are incomplete. A task which, in principle, will be repeated many times should be carried out the very first time in such a way (even if it takes longer) that the procedure can be used in similar tasks in the future, and then involve the use of less time.

Tasks should be put into blocks. It is an uneconomical use of time to telephone, to talk to a patient, to visit the laboratory, to chat to a colleague and then leaf through a journal in colourful succession. Putting these tasks into blocks of time means that continuous and effective work can be performed in each of these areas. Putting off a more difficult task by appearing busy (clearing up, reorganization etc) is only a substitute for work, and actually only puts off achievement of the major task.

make a clear offer of time, and stick to it whatever happens. This forces the other person to make his objectives and requirements clear without beating around the bush. If you have made it clear to your discussion partner that you have only 10 minutes available, it is not impolite to signal the dose of the discussion at the end of this time. It is much more difficult if you did not make this clear before the discussion commenced.

Most people are unwilling to delegate work, either because they do not trust those with whom they work or haven’t trained them well enough, or because they have the attitude that they are the only person would could do it all correctly. In fact new tasks can often motivate those that work for you and can be an incentive for a more responsible way of working. Not only the task, but also the responsibility for it should be delegated. The stress is removed when both are passed on.

Check list: to save time

Examine your own attitude to time

Learn to tolerate lack of time

Do not infect others with your time-pressure

Classify tasks into vital, important, and unimportant

It is better to complete one task than start ten

Work in blocks of tasks

Develop an efficient system of reading

Don’t put off tasks by substituting bustle

Match tasks to your own daily efficiency profile

Spring-clean your surroundings

Recognize “time thieves”

Be able to say “No”

Make clearly defined offers of time

Don’t let others interfere with your time plan

Learn how to delegate both a task and responsibility for it

Remember: The best time-saver is the successful discussion between doctor and patient

Tasks which are approached with less enthusiasm and motivation need an over-proportional amount of time. However pleasure in the work is the result of experiencing satisfaction with the results of one’s own work. This completes the circle: the discussion which is successful is the one which is understanding” therefore an understanding discussion is not one that steals time. In fact the successful discussion between doctor and patient represents the optimal economy of time.

The climate of the discussion

The bases for a fruitful climate of discussion are: a trusting atmosphere, openness and willingness to listen, as well as the ability to relate to the patient and to be on the “same wavelength”. No aggression arises in such a discussion, which is factual and not driven by emotions, allows recognition of resonance and does not create anxiety. Respect and appreciation characterize the relationship between the two people, and the discussion proceeds symmetrically.

Where the conversation is optimal, both partners are at the same level in discussion of the subject matter, and are communicating emotionally on the same level. Both sides profit from such a discussion: the patient because he feels that his problem has been accepted and the doctor, who finds it easier to obtain the necessary information.

disclosure & negotiation

• Does "full disclosure" really address conflicts of interest? – Barking up the wrong tree

  "Coming clean about conflicts of interest, they find, can promote less ethical behavior by advisers. People with a conflict gave biased advice to benefit themselves. disclosing the conflict of interest — far from being a solution — actually made advisers act in a more self-serving way." AND people were actually more likely to comply with the advice when the doctor’s bias was disclosed. people feel an increased pressure to take the advice to avoid insinuating that they distrust their doctor. People feel pressure to behave generously even if it’s not in their best interest

  tags: communication insight innocence influence

• Love and Negotiation | Psychology Today

  "When people feel valued, they tend to cooperate. When they don’t feel valued, they resist what feels to them like submission. If you want cooperation, you must show value. If you want resistance, all you have to do is devalue, criticize, demand, or otherwise show ill-will. But don’t think about showing value – that can smell of manipulation. Focus instead on feeling value for your partner. This will lower emotional intensity and shrink the subject under negotiation to manageable proportions. Regardless of your stance on any specific behavior, always remember that you are negotiating with someone you love, who is more important to you than whatever behavior request you want to make."

  tags: marriage starred communication collaboration

Posted from Diigo. The rest of my favorite links are here.

Art of questioning & mirroring

mirroring

advantages:

• allows Pt to get a grip on his internal experiences, feelings, attitudes, ways of behaviour, desires, objectives, & to manage them better.
• allows Dr to choose correct distancing or closeness to his Pt.
• most impressive way of signalling to the Pt that the Dr is listening to him actively.

procedure: not done mechanically by a facade or echo.
foremost to mirror are : all emotional statements, objectives & presumptions/biased judgements.
try to mirror:

• all imp statements as soon as possible, briefly, concretely, clearly.
• make the attempt to workout the meaning for the Pt
• use term ‘you’ not i, we or one
• interject to make sure you understood the Pt
• use synonymns/antonymns to replay/verbalise Pt’s emotions.

if the Pt doent feel undestood: either directly intervene with a verbal confirmation or indirectly imply by describing Pt’s experience.

ability for empathetic behaviour comes from

• ethical attitude & social involvement
• sensibility level & coping level
• perceiving the relation & influencing it

“If you can discover a person
who is peaceful,
without affectation
who, with presence of mind,
with true involvement,
can quietly listen to needs,
who does not interrupt, who does not pose two questions at the same time,
who waits for the answer and grasps it all,
who does not peer into the future or past,
who does not fix you with a studied look, and put you down,
who does not avoid your gaze, looking upwards or downwards,
who is as prudent as he is at ease, then -
then you will think that you have found treasure in a field,
then you will think that you have found a pearl”.

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art of questioning:

good questioning is like a zipper technique decreasing digressions from flow or contact & increases willingness & trust in communication. it shows that the Dr is interested & understands, so decreases Pt’s anxiety/anger/shame.

bad questioning is always with impricse wording & at an inappropriate timing which increases resistance of the Pt to answer.

open Q conveys interest & attention. Pt describes freely in his own words & attempts to make himself understood, this, increases confrontation with the conflicting matter leading to effective learning & better management. disadv – avoids unpleasant topics & is easier to digress.

closed Q is used only for extracting rapidly some precise info or to keep to the subject from excursions. it shouldnt be used at the onset since it decreases unravelling dimensions or building relations by preventing thinking & active listening.

inappropriate questioning arises from impatience & inexperience:

• multiple Qs overwhelms the Pt. so take time to ask one Q at a time.
• hold up Qs elicits irrelevant or aggressive Ans
• leading Qs have a backdrop of prejudice or wishful thinking of the Dr, exerting subconscious pressure on the Pt to avoid unpleasant topics
• ambush Qs suggest impoliteness or unawareness & makes the Pt defensive or aggressive. its easier to reply painful Qs if the A can be constructed on a preceeding fact.

forbidden Qs do not account for Pt’s autonomy:

• [epistaxis fingering]trap Qs trip up or over ride the A
• [potency, breastfeeding]curiosity satisfies the questioner but doesnt deepen relation & shames the Pt or evokes a climate of police interrogation
• [adi,nonlocalers]socratice Qs gives self-assurance to the questioner that others cannot answer & conveys to the Pt thatt he doesnt know what he believed he knew
• why instead of what reason]judgemental Qs puts Pt on defensive
• [esra doctors]aggressive Qs achieve the very opposite of the intended behaviour
• [status quo girls]flowery rhetorical Qs are hollow & insincere & maintain only superficial flow

questioning behavior of the Pt:

• need for info, contact, help, critism
• why is Pt asking at this time
• what is the overlying real Q
• why doe Pt repeat the same Q
• why doesnt Pt ask – out of anxiety, time pressure, speech barriers, different realities, insufficient stimulus

Peritonsillar abscess [quinsy]

Aetiology

often mixed infection : Strep pyogenes, Staph aureus, anaerobes
H/O denovo / acute tonsillitis
Infection & blockage of 1 crypt[C.magna] &larr intratonsillar abscess &larr bursts capsule causing peritonsillitis & abscess.

CFs : mostly in adults; usually unilateral pus in peritonsillar space [capsule &harr superior constrictor ms]

1. local :
   • unilateral severe throat pain
   • odynophagia [ ∴ no swallowing & dehydration]
   • ipsilateral earache [CN9 to tonsil & ear]
   • muffled thick voice
   • foul breath [sepsis]
   • trismus [pterygoid near sup constr]
2. general : septicaemia [104Ffever-chills-rigor, malaise, headache, bodyache, nausea, constipation

Signs:

• unilateral congested & swollen - tonsils, pillars, soft palate
• mucoid pus
• uvula pushed to opposite side
• torticollis - neck tilted towards abscess side
• jugulodigastric lymphadenopathy

Complications:

1. parapharyngeal abscess
2. laryngeal edema &rarr tracheostomy
3. septicaemia &rarr endocarditis, nephritis, brain abscess
4. aspirated pus &rarr pulmonitis, abscess
5. carotid artery & jugular venous thrombosis & spontaneous hmrrg

Rx : Hospitalization

• peritonsillitis -
  1. IV fluids &rarr dehydration
  2. IV antibiotics -high dose
  3. strong analgesics [pethidine] [not aspirin - bleeding]
  4. H2O2, saline, mouth washes &rarr oral hygiene
• abscess -
  1. incise[guarded knife, sinus forceps -drain] at max bulge at upper pole/lateral to junction of uvula base & ant pillar
     4-6wks later – interval tonsillectomy
  2. abscess tonsillectomy -less preferred since abscess rupture & bleeding.

Juvenile nasopharyngeal angiofibroma

Rare but commonest benign nasopharyngeal tumor.

Aetiology

probably testestorone appearance in an adolescent male [10-20 age] causes the hamartomatous nidus of vascular tissue in postnasal cavity near sphenopalatine foramen, to activate into angiofibroma which is fibrovascular pink-purple sessile firm locally-invasive mass without muscle coat, hence bleeding can’t be controlled by vasoconstrictors/adrenaline.

CFs :

1. nasal cavity obstruction [1 or both choana] -
   • recurrent profuse epistaxis [marked anaemia]
   • discharge
   • denasal speech
2. ET obstr – conductive deafness, serous otitis media
3. invasive destruction of PNS [max, sph, eth] – swelled cheek
4. pterygomax & infratemporal fossa – broad nasal bridge
5. enters inf/sup orbital fissure & destroys orbit apex – proptosis, frog face deformity
6. thr sphoid sinus into middle cranial cavity, thr ethmoid roof into anterior cranial cavity – involvement of CN 2,3,4,5

Δ : only from CFs, palpation should be done only during surgery since profuse bleeding[2l]

Biopsy [for D/D: teratoma, hemartoma, pleomorphic adenoma, chordoma, choristoma, paraganglioma] only under general anaesthesia with bleeding control arrangements & blood transfusion.

• Xray -
  • lateral nasopharynx – soft tissue mass
  • PNS – opaque sinuses, deviated nasal septum, anterior bowing/destruction of posterior max sinus wall.
  • Skull base – erosion of sphenoid Gwing & pterygoid plates, widenned lower lateral margin of superior orbital fissure
• CT scan – esp intracranial extensions
• Carotid angiography – extensions & feeding vessels

Rx : Surgical resection :
preoperative ↓ vascularity – stilbEsterol, radiation, cryotherapy, embolise feeding bv.

• transpalatal type – for nasopharyngeal tumor
• lateral rhinotomy type – for extended tumor

Nasopharyngeal cancer

Uncommon in India except in north-east[mongoloid origin]
Common in S.China, Indonesia, Taiwan.

Commonest origin : Rosenmuller fossa in lateral nasopharynx.
Metastases involves : nearly all Cranial nerves & Cervical lymph nodes.

Aetiology	genetic succeptibility in chineese Epstein-Barr virus environ - air pollution, smoking (tobacco, opium), dry salted fish(nitrosamines), incense & wood smoke
Pathological types
most common 85%	SqCC [variants: transitionalCC, lymphoepitheloima
10%	lymphomas
5%	rhabdomyosarcoma, malignant mixed salivary tumor, malignant chordoma
3 morphological types
proliferative	causes obstructive symptoms
ulcerative	epistaxis
infiltrative	invades sub-mucosa

CFs:

1. nasal obstruction:
   • discharge
   • denasal speech (rhinolalia clausa)
   • epistaxis
2. Eusthacian tube obstruction :
   • conductive deafness
   • unilateral serous/suppurative otitis media
3. Ophthalmo-neuralgic :
   • into orbit apex & CN2 - exophthalmos, blindness
   • 5 - facial pain, ↓ corneal reflex
   • CN6 - squint, diplopia
   • 3,4,6 - ophthalmoplegia
   • 9,10,11 - Jugular foramen syndrome
   • into hypoglossal canal - CN12
   • cervical sympathetic chain - Horner's syndrome
4. Cervical nodal metastases - in 75% , can be the only manifestation
5. Distant metastases to organs

Δ

• Ex postnasal space - NPmirror/nasopharyngoscope
• Xray,CTscan - extension, skull base erosion
• Biopsy - histology
• no lesion - histology by transpalatal approach for a strip of mucosa&submucosa from rosenmuller fossa

Rx

1. Irradiation for primary tumor - 6000rads
2. Radical neck dissection for persisting nodes
3. recurrent tumor -
   • external radiation
   • Brachytherapy [intracavitary implants]
   • Cryosurgery thr palatal fenestration
4. Palliative Systemic chemo – radiation failure, distant metastases

Diseases of Sclera

Sclera is posterior 5/6th outer opaque fibrous coat of eyeball with 3 layers:

1. vascular CT: episclera
2. avascular collagen: sclera porper
3. innermost brown: lamina fusca

Whole sclera has an outer tenon’s capsule & in addition covered anteriorly by bulbar conjunctiva.
Schlemm’s canal is the furrow near limbus.
It is thinner at extraocular ms insertions & is sieve-like lamina cribrosa at optic.N exit.
Apertures:

1. anterior limbal- anterior ciliary bv
2. middle- vortex veins
3. posterior- long&short ciliary N&bv

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Episcleritis:

benign recurrent inflmm of episclera & tenon+bulbar conjunctiva.
Etiology:

• usually in young adult [female]
• Associated with immune rxns:
  • rosacea, gout, psoriasis
  • TB, strep toxins

Pathogenesis:

1. episclera: localised lymphocytic infiltration
2. tenon+bulbar conj: edema & hyperaemia

CFs: red, gritty, [mild lacrimation & photophobia]

1. Diffuse: whole scleral inflmm but maximum confined to 1or2 quadrats
2. Nodular: firm, tender, pink-purple nodule 2-3mm form limbus with overlying mobile conjunctiva & surrounding injection

Rx:

• spontaneous regression after 10days-3wks
• protracted course of few days with topical steroids.
• recurrent disease- systemic NSAIDs

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Scleritis

seroius chronic inflmm of sclera proper.
Etiology:

• usually in elderly [40-70 female]
• Associated with:
  1. autoimmune collagen disorders- Rharthritis, PAN,SLE, ankylosing spondylitis, wegner’s granulomatis
  2. metabolic- gout, thyrotoxicosis
  3. scleral infections- Hzoster, staph, strep
  4. Granulomatous diseases- TB, syphilis, leprosy, sarcoidosis
  5. misc- rosacea, bechet’s, VHK syndrome, thermal/chemical burns

Pathogenesis: Granuloma-

1. fibrinoid necrosis
2. infiltration + collagen destruction
3. surrounded by epitheloid giant cells & bv

CFs:

• severe deep pain which radiates to jaw & temple
• local/diffuse redness
• mild to severe lacrimation & photophobia
• occasional visual impairment
• Types:
  

  Anterior non-necrotizing	DIFFUSE INFLMM [commonest]- pink/purple; ≥ 1quadrant NODULAR- 1or2 near limbus; hard elevated purple
  Anterior necrotizing	INFLAMM- localised acute severe; thin transparent ectatic vasculitic infarct; [associated uveitis] SCLEROMALACIA PERFORANS [non-inflmm due to obliteration of arterial supply]- initially yellow sequestrum → dead white → absorbed leaving a punched out sclearal peforation
  Posterior scleritis	CFs of inflmm of associated structures: exudative retinal detachment macular edema proptosis restricted ocular movts
  Complications	sclerosing keratitis, keratolysis complicated cataract secondary glaucoma

Diagnostic investigations:

• TLC, DLC, ESR
• immunological: C3, immune complexes, Rhfactor, LE cells, anti-nuclear antibodies
• syphilitic- VRDL
• gout- uric acid
• TB- mantoux test
• Xrays to rule out foreign body in chest, sacroiliac jt, PNS & orbit

Rx:

1. non-necritizing → topical steroids, systemic NSAIDs
2. necrotizing → oral+topical steroids [CI- subconj inj since scleral perforation], unresponsive cases – mtx,cyclophosphamide

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Blue sclera

Thinning due to

• osteogenesis imperfecta
• Marfan’s, Ehlers Danlos
• Buphthalmos
• high myopia
• healed scleritis

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Staphyloma

Types	localised bulge due to thinned outer fibrous coat	underneath shinning uvea is seen through
Anterior	pseudocornea [scar formed after total sloughing of cornea from organised exudate & eoithelial covering]	plastered prolapsed iris
Intercalary	limbal scar after perforating injury or peripheral corneal ulcer	iris root
Ciliary	thin sclera at 2-3mm from limbus due to perforating inj / scleritis / absolute glaucoma	ciliary body
Equatorial	at vortex vein perforations after scleritis / pathological myopia	choroid
Posterior	thinned sclera behind equatorial after perforating inj / pathological myopia / scleritis	excavation with dipping retinal bv

Glaucoma

ANATOMY:

Pathophysiology revolves around AqH dynamics:

Ciliary body:

AqH production.

Anterior chamber angle

Formed by [ICSTL] iris root, ciliary body anterior, scleral spur, trabecular mesh, Schwalbe’s line[corneal descemet]

Width varies in different individuals

Visualised by Gonioscopic examination [diverts light to angle]

Shaffer’s system of angle width grading:

• 0 0degrees Closed, no structures visible
• 1 10degree chances of closure high [ICSTL]
• 2 20degree possible chances of closure [ICSTL]
• 3 20-35degrees Open angle [ICSTL]
• 4 Wide open [ICSTL]

AqH outflow system:

Trabecular mesh: sieve through which AqH leaves eye

1. UVEAL meshwork – innermost
2. CORNEOSCLERAL meshwork – middle larger portion with elliptical & smaller than uveal openings
3. JUXTACANALICULAR / ENDOTHELIAL meshwork – outermost connecting with Schlemm’s canal & narrowest offerring normal resistance to AqH outflow

Schlemm’s canal:

• oval circumferential channel in scleral sulcus
• inner endothelial cells have giant vacuoles
• Collector channels opn into outer cells

Collector channels / Intrascleral aqueous vessles:

terminate into episcleral veins

2 systems – larger ones terminate directly; smaller ones form intrascleral plexus before terminating

PHYSIOLOGY:

Aq production:

clear watery fluid whicxh maintains IOP & provides substrates & removes metabolites from avascular cornea & lens.

water [99.9], proteins [0.04], Na[144], K[4.5], Cl[110], glucose[6], lactic acid[7.4], aa[5], inositol[0.1

derived from cilliary processes at 2.3 microl/min filling anterior & posterior chambers. Mechanisms: [fluctuates diurnally; passive mechanisms altered by capillary BP, osmotic pressure, IOP; active secretion altered by vasopressin & adenylcyclase]

1. Ultrafiltration of ciliary processes’ stromal capillary plasma & accumulation behind non-pigment epithelium [BaqB].
2. Active secretion of some ions,aa, ascorbic across BaqB into posterior chamber by Na-K-ATPase pump & Carbonic anhydrase.
3. this in-turn causes osmotic diffusion of other plasma constituents into posterior chamber.

Through pupil, AqH flows from posterior to anterior chamber.

AqH drainage from anterior chamber: 2 routes

CONVENTIONAL TRABECULAR OUTFLOW [90%]-

1. giant vacuoles in inner endothelium of Schlemm’s canal trasport AqH from juxtacanalicular to collecting channels by forming intracellular transport channel.
2. 10mm pressure gradient is responsible for unidirectional flow from intraocular trabeculae to intrascleral episcleral veins

Unconventional UVEOSCLERAL outflow:[10%] from ciliary body to suprachoroidal space then into veins of choroid, sclera, ciliary body.

Maintenance of IOP: [10-21 mm]

Local factors:

1. AfH production depends on capillary permeability, osmotic pressure, IOP.
2. resistance offerred at juxtacanalicular /endothelial trabular meshwork.
3. episcleral pressure increases during valsalva & inturn rises IOP
4. in narrow anterior chamber, relative obstruction by iris during pupil dilation rises IOP.

General factors:

1. hereditary, age >40 & greater in females
2. cortisol diurnal fluctuation of 8mm]
3. postural variation & HTN
4. indirectly proportional to plasma osmotic pressure which ris high with mannitol, glycerol, uraemia & low with drinking water provacation tests.
5. general anaesthetics, anti-glaucoma drugs varyIOP. steroids, caffeine, smoking rise IOP & alcohol lowers.

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Glaucoma

gorup of disorders where IOP is raised. above tolerance limit damaging optic.N head leading to irreversible visual defects

Ocular HTN

constantly raised IOP without visual field defects.

Normal/low tension glaucoma

disc cupping +/- visual field defects

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Primary developmental glaucoma

abnormally high IOP due to congenital trabeculodysgenesis causing abscence of angle from flat/concave iris insertion to trabeculum obstructing drainage.

True congenital – if it manifests prior to birth

Infantile – if it manifetss prior to age 3

Juvenile – if it manifests between 3-16 age.

BUPHTHALMOS / Hydrophthalmos – prior to age 3, high IOP even enlarges eyeball.

75% bilateral.

CFs:

1. Lacrimation + photophobia + blepharospasm + eyerubbing – from raised IOP irritating corneal nerves.
2. corneal signs -
   • Corneal edema is frequently the first sign & opacities may occur.
   • Corneal enlargement >13mm with deep anterior chamber [if prior to age 3 , buphthalmos also]
   • Haab’s striae in descemet since it is less elastic than stroma.
3. thin sclera with underlying blue uveal color
4. Iridodonesis
5. flat/subluxated lens due to stretched zonules
6. cupped optic disc
7. moderately high IOP measured with PERKIN’s applanation tonometer [instead of Schiotz since low scleral rigidity in children]

D/D

• corneal trauma/interstitial keratitis/endothelial dystrophy causing corneal edema
• megalocornea
• blocked nasolacrimal duct causing lacrimation
• uveitis, keratitis causing photophobia.
• high IOP from retinoblastoma, prematuruty retinopathy, hyperplastic vitreous, other types of glaucoma.

Rx:

Primarily surgical with prior lowering of IOP with acetazolamide,mannitol, glycerol, beta-blockers.

1. GONIOTOMY
2. Trabeculotomy + trabeculectomy – when corneal clouding prevents gonioscopic examination.

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DEVELOPMENTAL GLAUCOMAS ASSOCIATED WITH SYSTEMIC/OCULAR ANOMALIES

• Iridocorneal dysgenesis – Axenfeld anomaly, Peter’s anomaly, Rieger anomaly.
• Aniridia
• Displaced lens in Marfan, homocystenuria,
• phakomatosis in sturge-weber syndrome, Von recklinghausen’s neurofibromatosis
• Lowe syndrome [oculo-cerebro-renal], microcornea, rubella syndrome.

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Primary open angle glaucoma / Chronic simple [commonest]

↑ IOP due to sclerosed thickenned trabeculae & abscence of giant vacuoles.

Predisposing factors

1. heriditary
2. old age >40yr
3. myopic
4. diabetis, smoking, HTN, thyrotoxicosis

Symptoms:

1. insidious, bilateral, asymtomatic [mild headache/eyeache]
2. after 40% visual field loss – tunnel vision which is progressive & irreversilble.
3. accommodative failure due to pressure on ciliary muscle & nerve.
4. delayed dark adaptation

Signs:

1. Anterior segment [late stage]:sluggish pupillary reflex & corneal haze.
2. IOP [tonometry]:initially exagerrated diurnal variation >8mm. contrary to closed angle glaucoma, falls during evening. In late stages, permanently >21mm.
3. Optic disc: assymetric, progressive changes so recorded [most accurate method: confocal scanning laser topography]. PATHOPHYSIOLOGY: high IOP pushes back lamina cribrosa, mechanically squeezing nerve fibres’ axoplasma + causing vascular ischaemia [no increase in glia = Cavernous optic atrophy]
   • EARLY-
     • vertical oval cup due to superior& inferior loss of neural rim.
     • bilateral assymetry >0.2
     • cup:disc >0.5 [normal=0.3-0.4]
     • splinter hmmrhges at disc margin & pallor areas on disc.
     • atrophied retinal nerve fibre layer [ganglion cells] with red free light.
   • LATE-
     • markedly enlarged cup 0.7-0.9
     • crescentic margin due to notch created from thinning of neural rim.
     • nasal shift in retinal vessels & Bayonetting sign[broken at disc margin; hidden if margin overhangs]
     • Pathognomic: arteriolar pulsations at disc margin when IOP is very high.
     • Lamellar dot sign: slit pores of lamina cribrosa at disc margin.
   • Optic atrophy- head appears white & deeply excavated.
4. Visual field defects:[confrontation test]
   • temporal sup&inf arcuate fibres are most sensitive & macular horizontal fibres are most resistant to glaucomatous damage, hence central vision lost at the end. [central optic fibres are in superficial retina while peripheral fibres in deeper retina.]
   • Natural history of progression:
     1. ISOPTER CONTRACTION- mild total field constriction.
     2. BARING OF BLIND SPOT from central field.
     3. PARACENTRAL SCOTOMA in Bjerrum’s area [above&below blind spot]- earliest clinically significant sign.
     4. SIEDEL’S SCOTOMA- sickel shaped due to joining of blind spot & paracentral.
     5. ARCUATE BJERRUM’S SCOTOMA- extension of siedel’s above&below to reach horizontal line.
     6. RING/DOUBLT ARCUATE SCOTOMA- due to joining of similar arcs.
     7. ROENNE’S CENTRAL NASAL STEP- joining of different arcs forming a right angled defect
     8. PERIPHERAL FIELD DEFECTS- may appear early or late.
     9. ADVANCED DEFECTS- tunnel vision sparing small central & temporal islands. temporal is ultimately left before total blindness.

Ocular associations:

high myopia, fuch’s ED, retinitis pigmentosa, CRVO, retinal detachment.

Diagnosis:

1. Established POAG: cupping/visual field defects with IOP>21mm.
2. Glaucoma suspect / Ocular HTN: IOP>21mm.
   A suspect must be categorised as established case if :
   • IOP>30mm
   • diurnal variation>8mm
   • +Provocation test
   • assymmetry of cups>0.2mm
   • splinter hmrrges near disc.
   • family history
   • DM
   • high myopia
   • Anterior chamber pigment changes
3. NT glaucoma: normal IOP but with cupping+/-visual field defects.
   Etiology- chronic low perfusion makes OPitc.N succeptible to even normal IOP.
   Rx- frustrating

Rx:

1. Good baseline examination – for periodic supervision to prevent further vision loss while lowering IOP.
   • visual acuity, fundus photography, perimetry
   • applanation tonometry, diuranl variation, provocation test
   • slit lamp ex of anterior chamber, goniscopy
   • Nerve fibre layed analyzer – early detection before cup/field changes.
2. Medical therapy to lower IOP- 1st choice topical drug, if ineffective/intolerable shift to 2nd choice drug, if insufficient combination therapy.
   1. beta blockers [↓ AqH secretion]- 1st choice
      Systemic ADRs by absorption through higly vascular nasal mucosa from NLD ∴ CI: asthma, bradycardia
      • timolol, levobunolol [longest action]
      • betaxolol [beta1 selective] – cardiopulmonary case
      • cartiolol – hyperlipidemic
   2. CAinhibitors [dorzolamide - ↓ AqH secretion] – 2nd choice
   3. PG [latanoprost - ↓ uveal outflow] – most used adjuvant but expensive
      low ADRs – ↑ eyelash growth& iris melanin
   4. short-term adjuvants :
      1. acetazolamide [CAinh]
      2. pilocarpine [ciliary spasm opens trabeculae] – CI- older pt with axial lenticular opacities & chronic use in young since myopia&headache.
   5. alpha2 adrenergic [brimonidine- ↓ Aq production] – last resort adjuvant since allergic rxn & tachyphylaxis.
3. Laser trabeculoplasty – shrinking collagen in trab mesh ↑ outflow.
   Indications- noncompliance or failure of medical Rx.
   Complications-
   • transient ↑ IOP if no pretreatment with acetazolamide/pilocarpine
   • inflamm – treat with steroids
   • hmmrg
   • synechiae
   • ↓ accommodation
4. Fistulizing filtration surgery [trabeculectomy]- creates a new ouflow channel from anterior chamber to subconjunctival space.
   Indications- advanced disease or uncontrolled IOP or unavailability of laser trabeculoplasty
   Complications- visual risks

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Primary angle closure glaucoma

↑ IOP due to narrow angle blocking AqH outflow.
Mid-dilated pupil → pupil block → iris bombe [from built up AqH in posterior chamber] → iridocorneal angle closure → transient ↑ IOP → peripheral anterior synechiae causes a chronic ↑ IOP.

Predisposers:

1. Anatomical:
   • hypermetropia, antrerioly placed lens, plateau iris configuration
   • small cornea, small eyeball
   • large lens, large ciliary body
2. General: 50age female, anxiety, familiar, rainy season, SEasian
3. Ppt: dim light, emotional or physical stress, mydriatrics.

Clinical course	CFs	Diagnosis	Rx
Latent Glaucoma / Prodromal phase transient(seconds) ↑ IOP due to ppt factors	blurred vision, colored halos, mild headache corneal edema, shallow anterior chamber, narrow angle	colored halos around bright lights due to corneal edema [D/D: acute purulent conjunctivitis [discharge] & immature cataract [Fincham's test segmented halos when viewed thr stenopic slit] Gonioscopy -grade 1or 2 Slit-lamp grading against conreal thickness Provocation tests – darkroom [1hr & awake for dilated pupil], mydriatric test + → succeptible to spontaneous closure - → doesn’t rule out closure so warn for symptoms	pre-operative pilocarpine + both eyes : iridectomy / laser iridotomy
Intermittent Glaucoma / Constant instabaility phase recurrent (min-hrs) regular ↑ IOP followed by bright light/sleep induced miosis	impaired vision, colored halos, eyeache/ frontal headache dilated pupil corneal edema, shallow anterior chamber, narrow angle	similar to above	similar to above
Acute congestive/angle closure Glaucoma sudden total angle closure causing high ↑ IOP for days	sudden severe pain [with vomiting, prostration] rapid progressive vision impairment redness lacrimation, photophobia edema of lids, conj, cornea very shallow anterior chamber, total angle closure pupil is mid-dilated : vertically oval, fixed optic disc : edema, hyperaemia fellow eye : shallow anterior chamber, narrow angle	D/D: acute red eye: conjunctivitis, iridocyclitis secondary acute congestive glaucomas: neovascular, phacomorphic, glaucomatocyclitic	temporary emergency medical therapy: stat analgesic [pethidine] injection topical drugs to lower IOP: initially [mild drugs since iris is ischaemic]- hyperosmotics[mannitol, glycerol], acetazolamide later- pilocarpine, beta blockers inflmm- steroid drops synechiae causing <50%angle closure- iridectomy / laser iridotomy to bypass pupil block >50% synechiae or uncontrolled IOP- fistualization filtration surgery [trabeculectomy] prophylactic surgery on fellow eye
Chronic closed angle Glaucoma constant ↑ IOP due to extensive peripheral anterior synechiae formed from intermittent or gradual[creeping] angle closure	permanently red & painful except in creeping[white, painless] visual field defects similar to POAG ↓ visual acuity gonioscopy: angle closure due to peripheral anterior synechiae optic disc cupping	D/D of creeping synechiae: POAG	for synechiae: ↓ IOP with medical therapy + filtration surgery prohylactic surgery in fellow eye
Absolute Glaucoma due to untreated chronic phase	completely blind painful eye perilimbal red-blue zone due to dilated anterior ciliary veins; later caput medusae initial corneal insensitivity → later hazy, bullous keratopathy / filamentous keratitis very shallow anterior chamber atrophic iris pupil : dilated, fixed, green disc atrophy stony hard eyeball due to high IOP	-	for pain- destroy ciliary ganglion with retrobulbar alcohol inj lower IOP- destroy secretory ciliary epithelium with cyclocryotherapy / diathermy/ photocoagulation failed conservativeRx / malignant progression- enucleation
Complications	corneal ulcer staphyloma from bulged out atrophic sclera from high IOP atrophic bulbi from ciliary body degeneration	-	-

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Scondary glaucomas

Phacogenic glaucomas	MOA	Rx
Phacomorphic [angle/pupil block]	altered lens morphology intumescent [swollen] anterior subluxated / dislocated spherophakia	medical to ↓ IOP & lens extraction surgery
Phacolytic	morgagnian hypermature cataractous lens leaks fine white protein thr lens capsule → phagocytosed by macrophages → clog trabe mesh	medical therapy to ↓ IOP & lens extraction surgery
Lens particle	disloged lens particles after trauma → clog trabe mesh	medical therapy to ↓ IOP & apsirate lens particle
Phacogenic uveitis	lens induced uveitis → lens particles & inflm cells clog trabe mesh	medical therapy to ↓ IOP uveitis- steroids & cycloplegics aspirate lens particles
Phacoanaphylaxis	fulminating inflm from antibody attacks to lens protein	medical to ↓ IOP steroids

Inflammatory glaucomas Glaucomas associated with uveitis	MOA & CFs	Rx
Acute anterior uveitis	clogged trabe mesh from inflm cells exudate turbid AqH edema ↑ IOP	steroids, cycloplegics & ↓ IOP with medical therapy
Post-inflmmatory	pupil block from annular synechiae or iris bombe angle closure from organization of inflmm debris	synechiae prophylaxis – steroids&cycloplegics &darrIOP with medical therapy [CI-miotics] pupil block – iridectomy angle closure – trabeculectomy
Specific HTNisve uveitis syndromes	Fuch’s uveitis syndrome Glaucomatocyclitic crisis	-

Pigmentary glaucoma [young myopic male]	pigment shedding from mechanical rubbing of iris & zonules → clog trabe mesh krukenberg’s spindle on posterior cornea zonules lens SAMPAOLESI’s line [inferior schwalbe's line] Pathognomic: iris shows radial slits in mid-periphery on trans-illumination	Rx: similar to POAG

Neovascular intractable glaucoma 3 stgaes: rubeosis iridis pretrabecular neovascular membrane → open angle glaucoma goniosynechiae [contacture of neovasc membrane] → zipper angle closure glaucoma	Etiology: retinal ischaemia in D.retinopathy CRVO, CRAO Sickle cell retinopathy Eale’s disease Intraocular – chronic inflm, tumor R.detachment	Rx: curb neovasc → Pan-retinal photocoagulation ↓ intractableIOP with Artificial drainage shunt [seton valve implant]

Intraocular tumors [MalignantMelanoma (iris, choroid, ciliary body) Retinoblastoma]	tumor cell invasion or clogging of trabe mesh neovasculariztn of angle vortex venous stasis from obstruction anterior subluxation of iris	Rx: enucleation

Pseudo-exfoliative / Glaucoma capsulare	amorphous grey dandruff like material deposition on: anterior lens posterior iris zonules ciliary processes	Rx: similar to POAG

Glaucomas-in-aphakia	conditions: poat-operative ↑ IOP due to hyphaema, inflm, chymotrypsin, vitreous in anterior chamber angle closure due to flat anterior chamber pupil block from anterior synechiae / vitreous herniation pre-existing POAG steroids for post-operative cataract post-operative epithelial ingrowth into trabe mesh aphakic malignant glaucoma

Steroid induced glaucoma [topical/systemic]	inn a genetically determined[40%] patient may cause mucopolysaccharides deposition in trabe mesh	Rx: monitoring IOP while steroid use discontinue steroids & treat glaucoma with timolol filtration surgery if glaucoma is intractable after 1mos

Traumatic glaucoma	blunt/perforating injury causes the following conditions which ↑ IOP: uveitis hmmrg ruptured lens anterior synechiae adherent leucoma epithelial/fibrous ingrowth trabe disruption & fibrosis causing angle recession	Rx: ↓ IOP with medical therapy treat the causative conditions

Malignant glaucoma / Ciliary block glaucoma [rare early post-operative complication of any intraocular surgery esp PACG - peripheral iredectomy / trabeculectomy]	Ciliary block of AqH flow at: cilio-lenticular in phakic cilio-vitreal in aphakic which causes AqH to collect posteriorly as vitreous pockets & ↑ IOP: persistent flat anterior chamber negative Seidel’s test unresponsive to miotics	Rx: atropine to dilate ciliary ring acetazolamide & timolol to ↓ AqH production i.v mannitol to shrink vitreous posterior sclerotomy if unresponsive to medical Rx for 5days aspirate fluid from vitreous inject air into anterior chamber

Intraocular hmmrges [hyphaema, vitreous]

types of glaucoma: Red cell glaucoma – trabe clogged by RBCs in fresh massive traumatic hyphaema [after few days corneal blood staining occurs] Hemolytic glaucoma – trabe clogged by macrophages with lysed RBC Ghost cell glaucoma [vitreous hmmrg in aphakia]- after 2wks RBCs turn khaki colored ghost cells which clog trabe Hemosiderin glaucoma [rare]- sclerosis induced by iron from trabe’s endothelial cells’ phagocytosed Hb.

Iridocorneal endothelial syndromes progressive iris atrophy [iris hole] chandler’s syndrome [corneal edema] cogan reese syndrome [iris pigmented lesions]	usually seen in a middle aged female with abnormal corneal endothelium → proliferates forming a membrane in angle → contraction causes synechiael angle closure glaucoma

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Surgical procedures for glaucoma:

1. Peripheral Iridectomy- Rx+prophylaxis for PACG
2. Fistulization guarded filtering surgery – trabeculectomy [partial thickness fistula] – [post-operative complications: hyphaema, iritis, endophthalmitis, cataract]
   1. POAG
   2. >50% synechiae in PACG
   3. congenital&dev glaucomas where trabeculotomy&goniotomy fail
   4. secondary glaucoma
3. Antimetabolites[fluprpuracil,mitomycinC] + trabeculectomy:
   1. previous failed fistula
   2. glaucoma in aphakia
   3. some secondary glaucomas [inflmm,trauma]
   4. >3yr medical Rx for glaucoma
4. Artificial drainage shunt [seton's valve implant] – neovascular glaucoma, glaucoma with aniridia, intractable primary/secondary glaucomas
5. Cyclocryotherapy – destroy secretory ciliary epithelium in Absolute glaucomas.

Diseases of Conjunctiva

DISEASES OF CONJUNCTIVA

ANATOMY

CONJUCTIVA:

translucent mucous membrane posterior to eyelids & anterior to eyeballs.

3 parts:

PALPEBRAL

Marginal- from lid margin to sulcus subtarsalis

Tarsal- firmly adherent & highly vascular; whole upper tarsal plate & half of lower tarsal; yellow streaks of tarsal glands.

Orbital- loosely between tarsal plate and fornix.

BULBAR

loose over epislera & tenon’s capsule (anterior to sclera)

limbal conjunctiva- 3mm ridge around cornea firmly adherent to episclera & tenon.

FORNIX

circular cul-de-sac joining bulbar & palpebral, broken at the medial caruncle & plica semilunaris.

structure: 3 layers

EPITHELIUM

Marginal & Limbal have 5layered str sq.

Tarsal has 2layered cylindrical & flat.

Fornix & Bulbar have 3layered cylindrical, polyhedral & cuboidal.

ADENOID/LYMPHOID

fine CTreticulum with lymphocytes

most dev at fornix

dev after 3mos of birth, so no follicular rxn in infants.

FIBROUS

thick with c&e fibres, bv & nerves; blends with tenon’s in bulbar region.

thin in tarsal region.

Glands: 2types

MUCIN SECRETORY GLANDS:

epithelial goblet

tarsal henle crypts

limbal manz

ACCESSORY LACRIMAL GLANDS:

Krause (fornix: upper 42 & lower 8),

Wolfring (upper superior tarsus & lower inferior tarsus)

PLICA SEMILUNARIS in medial canthus: pink crescent conjunctival fold with concave lateral border.[atavistic nictitating membrane].
CARUNCLE medial to plica: small oval pink mass covered with str sq & contains sweat glands, sebaceous gl & hair follicles.

ARTERIES:

Marginal palpebral arcade

Peripheral palpebral arcade

Anterior ciliary artery

Palpebra & fornix by peripheral & marginal arcades

Bulbar & pericorneal plexus by posterior conj[peripheral arcade] & ant conj[ant ciliary]

LYMPHATICS

Preauricular -lateral

Submandibular -medial

NERVES

Long ciliary nerve supplies cornea

rest supplied by lacrimal, infra & supra trochlear, supraorbital, frontal.

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INFLAMMATORY DISEASES

= hyperaemia + discharge.

INFECTIVE commonest [inspite protection from low temp due to air exposure, lids, tears flush, lysozymes, Igs.]

BACTERIAL CONJUNCTIVITIS

common in developing countries & epidemics during monsoon.
PREDISPOSERS- hot dry, unhygienic, flies.
CAUSE-

1. Staph aureus most common
2. Staph epidermidis [innocuous]
3. Strep pneum [acute with subconjunctival petechiae]
4. Strep pyo(hemolyticus) [virulent- pseudomembranous]
5. Pseudomonas pyocyanea [virulent- invades cornea]
6. H.inf [mucopurul red eye epidemics in tropics]
7. Neiseria mening [mucopurul conj]
8. Moraxella lacunate [angular conj]

MODE

EXOGENOUS air,water, flies, fingers, towels.

LOCAL from lids, lacrimal sac, nasopharynx; innocuous organism

ENDOGENOUS[rare] blood e.g. neisseria

PATHOLOGY [more marked in purulent than in mucopurulent]

Vasodilation- congestion of conj bv

Cellular exudation of macrophages into substansia propria & conj sac

Edematous epithelium- superficial desq, basal prolifertn, increased goblet cells

Discharge- tears, mucus, infl cells, fibrin, bacteria [severe infection even causes RBC diapedesis

CLINICAL TYPES

Acute- catarrhal/mucopurul, purul, membranous, pseudomembranous

Chronic- catarrhal, angular

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Acute mucopurulent/catarrhal conj most common acute bacterial conj; generally accompanies measles & scarlet fever.

Cause

Staph

Strep

H.inf

Signs & Symptoms

Conjunctival congestion other than circumcorneal zone[fiery red eye]& chemosis -Foreign body sensation due to vasodil.

Flakes in fornices, canthi, lid margins & matted cilia with yellow crusts -mucopurulent discharge, sticking lid margins after sleep, colored halos due to prismatic effect on cornea.

[Petechiae if Strep.pneum.]

Course – 10-15 days or passes to less intense Chr catarrhal conj.

Rx

Topical broad spectrum antibiotics : chloramphenicol, gentamycin, framycetin [unresponsive cases cipro]

1-2/day Irrigation with sterile warm saline [CI: but freq eyewash removes lysozyme]

Dark goggles for photophobia [CI: bandaging rises temp promoting bacteria]

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Acute purulent/ Hyperacute conjunctivitis predominat in adult males.

acute purulent conj of adults

ophthalmia neonatorum in newborn

Acute purulent conj of adults

CAUSE

Gonococci – commonest & usually associated with urethritis/arthritis.

Staph aureus

Strep pneum

COURSE

3 stages

INFILTRATION: initial 5 days of painful bright red velvety chemosed conj, swollen lids, watery discharge, enlarged preauricular LN.

BLENORRHOEA: purulent copiuos trickling discharge,lids swelling incr.

SLOW HEALING: all symptoms decrease except conj remain chemosed.

Rx:

imp to give systemic antibiotics for 5days[norfloxacin/cefoxitim], followed by 7days of doxycycline/erythromycin.

topical bacitracin/erythro every 2hrs for 3days then 5times/day for 7days

irrigation with sterile saline every hr to remove debris.

[if cornea involved - topical atropine]

Ophthalmia neonatorum:

bilateral conj inflm in less than 30day infant.

MODE

BEFORE BIRTH – infected liquor amnii with ruptured membranes.

DURING BIRTH(common) – face presentation / with forceps.

AFTER BIRTH – contamination from lochia or during first bath.

CAUSE

chemicals [Incubation period 5hrs]-silver nitrate, prophylactic antibiotics.

genital gonococcal infection [Incubation period 2-3 days]

Staph aureus, Strep pneum, Strep hemolyticus.[Incubation period 4-5 days]

D to K Chlamydia trachomatis [neonatal inclusion conj][Incubation period 5-14 dys]

Herpes simplex2 (rare)[Incubation period 5-7 days]

SIGNS & SYMPTOMS:

pain [hyperaemia, chemosis]

discharge- purulent in gonococci, others mucoid/mucopurulent.

swollen lids

[herpes simplx - corneal superficial punctate keratitis, mild papillary]

Rx:

PROPHYLAXIS:

1. antenatal- genital inf in mother.
2. natal most common so imp]- aseptic delivery, throrough cleansing & drying of neonatal’s closed lids.
3. postnatal- immediately after birth topical tetracyline/erythr/silver nitrate; if mother has gonococcal inf: single inj of ceftriaxone

CURE:

1. chemical cause – self limiting condition.
2. gonococcal inf – topical [saline irrigation, bacitracin 4times/day, cornea involv needs atropine]; systemic [7days of cipro/ceftriaxone/cefotaxime]
3. other bacterial inf with topical broad spectrum antibiotics for 2wks
4. neonatal inclusion conj with topical tetracyline/erythr for 3wks 7 the implied chlamydia colonization of upper resp tract with systemic erythr qid 3wks
5. herpes simplex is self-limiting & topical anti-virals prevent recurrences.

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Acute membranous conjunctivitis rare in unimmunised 2-8yr chidren [violent inflm of conj; membrane=fibrinous exudate in palpebral conj[surface as well in substance] which undergoes coag necrosis & sloughing & granulation]

CAUSE

Corynebact diphth [typically]

virulent Strp hemolyticus

Course

febrile; 3 stages.

INFILTRATION: pain, red chemosed & firmly adherent grey-yellow membrane on conj, enlarged preauricular LN.

SUPPURATION:symptoms decr with sloughing of membrane & copious purulent discharge.

CICATRISATION: healing by epithelialisation which may cause triciasis & xerosis[symblepharon].

Rx:

TOPICAL

1. pencillin drops every 1/2hr.
2. antidpth serum every 1hr.
3. broad spectrum antibiotic before bedtime.
4. [corna invlv -atropine]

SYSTEMIC

1. stat antidpth serum i.m.inj
2. i.m. inj of crystalline Pn 2times daily for 10days.

Symblepharon prevention-

apply contact shell or sweeping fornices with a oint smeared glass rod.

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Acute Pseudo membranous conjunctivitis ~mucopurulent conj + fornices&palpebral conj has thin yellow white pseudomembrane can be easily peeled off leaving intact conjunctiva.

Cause

Bacteria: low virulent C.dipth, staph, strep, H.inf.

viral: H.simplex, adenovirus.

chemicals: acids, NH3, lime, silver nitrate, coppur sulfate.

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Chronic catarrhal conjunctivitis:mild catarrhal inflm.

Cause

Predisposing: chronic exposure to dust/smoke/chemicals, local trichiasis/concretions/foreign body/seborrhoeic scales, eye strain[refractive errors/phorias/convergence insufficiency], insomnia, alcohol, metabolic disorders.

Staph aureus is commonest cause, Gm- bacteria: Proteus mirabilis, K.pneum, E.coli, Moraxella lacunata.

contact/air/contamination, untreated acute mucopurulent conj, from chronic dacryocystitis/rhinitis/Upper RT inf.

Signs & symptoms:

mild

burning & grittiness[paillary hypertrophy in palpebral] esp in evening, red[posterior conj bv] sticky conj, mucoid discharge esp in canthi, intermittent lacrimation, hot dry congested lid margins, tired & sleepy eyes.

Rx:

TOPICAL- chloramphenicol/gentamycin 3/day for 2wks.

symtomatic relief – zinc boric acid drops.

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Angular conjunctivitis / Diplobacillary conj -type of chr conj mild inflm confined to angles of lids & conj + macerated skin.

Cause

Predisposing: chronic exposure to dust/smoke/chemicals, local trichiasis/concretions/foreign body/seborrhoeic scales, eye strain[refractive errors/phorias/convergence insufficiency], insomnia, alcohol, metabolic disorders

Moraxella axenfeld is commonest cause- spread from nasal cavity to eyes by contaminated fingers; its proteolytic enzyme collects in angles & macerates epithelium of conj.lids,skin followed by vascular & cellular responses of mild chronic inflm

Signs & symptoms

angles [conj,lids,excoriated skin]- redness, dirty white foamy mucopurulent discharge, irritation.

Rx

prophylactic therapy for nasal infs.

cure: topical oxytetracycline 3times daily for 14 days, zincoxide for maceration.

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CHLAMYDIAL CONJUNCTIVITIS

intracellular, sensitive to antibiotics; PLT group

Trachoma chr keratoconj with mixed follicular 7 papillary response; leading cause of preventable blindness after cataract.

Etiology:

Chlamydia trachomatis – epitheliotropic, HP intracytoplasmic inclusion bodies, 11serotypes-

• A-C cause hyperendemic/blinding trachoma with secondary bacterial infection, hypoendemic trachoma without secondary infection.
• D-K cause paratrachoma/oculogenital trachoma which is predominantly seen in urban areas & spreads from genitals. it includes adult inclusion conjunctivitis & ophthalmia neonatorum.

Predisposers: early childhood, females, jews, dry dusty weather [common in outdoor workers], unhygenic,flies.

superimposed bacterial inf discharge intensifies spread; modes- air, water, contamination from flies/fingers/fomites.

Course-

Insidious[subacute] onset [incubation 5-21 days]; in endemic regions acute infection in first decade of life & becomes inactive in second decade & sequelae start in 4th/5th decade.

pure disease is symptomless [mild foreign body sensation & occassional lacrimation, scant mucoid discharge & slight sticky lids.

typical acute mucopurulent conjunctivitis symptoms only with secondary bacterial inf which in early stages is indistinguishable [trachoma dubium]

1. upper palpebral conjunctival signs – esp at tarsus & fornix shows hyperaemia [Incipient stage], follicles & papillae [Florid stage], scarring [Cicatrization stage], concretions [Sequelae due to mucus&epithelial debris in henle glands].
   sometimes follicles are seen even in lower fornix, caruncle, & pathognomically on bulabr conjunctiva.
   Follicles are scattered lymphocyte aggregations in adenoid layer. histiocytes& multinucleated leber cells are seen centrally while proliferating lymphocytes, bv are in the periphery. Differentiated from other follicular conjunctivitis by presence of Leber cells & necrosis.
   Papillae are red, flat topped raised areas giving a velvety appearance with central dilated blood vessels & surrounding lymphocytes covered by epithelial hypertrophy.
2. Corneal signs – upper part shows superficial epithelial keratitis & pannus, limbus shows herbert follicles & healed herbert pits, end stage shows corneal opacity which may encroach pupil area causing visual impairment.
3. Sequelae -
   lids- trichiasis, entropion, tylosis, ptosis, madarosis, ankyloblepahron.
   conjunctiva- concretions, pseudocyst, xerosis, symblepharon.
   cornea- opacity, ectasia, xerosis, total pannus [blindness]
   chronic dacryocystitis
   secondary glaucoma
4. the only complication – corneal ulcer from concretions / trichiasis + secondary bacterial infection.

WHO classification-

1. Trachomatous inflammation follicular – ≥ 5 follicles on upper tarsal conjunctiva; visible deep tarsal bv thr follicles&papillae.
2. Trachomatous inflammation intense – thickenned upper tarsal conjunctiva
3. Trachomatous scarring – white sheets in tarsal conjunctiva
4. Trachomatous trichiasis – atleast 1 eyelash rubs eyeball
5. Corneal opacity – atleast encroaching the pupil margin

Diagnosis-

• giemsa smear shows lymphocytes, leber cells, inclusion bodies.
• isolation by yolksac inoculation & tissue culture.
• serotyping for TRIC agents[A-K].

D/D:

adenoviral epidemic KC [follicles on lower conj , unlike trachoma no papillae or panus]
spring catarrh [large cobblestone papillae, ropy discharge, but unlike trachoma no acidic tears / papillae / pannus]

Rx:

topical or systemic antibiotics in mild cases

• tetracycline / erythromycin / sulfacetamide drops 3/day fro 6wks.
• tetracycline / erythromycin doxycycline tabs for 4wks or single dose arithromycin.
• cimbined topical 7 systemic in severe cases.

Sequalae-

• concretions – reomove with hypodermic needle
• trichiasis – remove with epilation / electrolysis / cryolysis
• entropion – surgical
• xerosis – artificial tears

Adult inclusion conjunctivitis

Cuase – genital contamination [male urethritis, female cervicitis] from D-K chlamydia
CFs-

• mucopurulent discharge, foreign body sensation, mild photophobia.
• conjunctival hyperaemia esp fornices.
• follicles in lower conjunctiva.
• superficial keratitis in upper cornea.
• pre-auricular lymphadenopathy.

Rx: systemic + topical antibiotics [since asymptomatic venereal disease]

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Viral KC- serous, hmmrg, follicular

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Follicular conjunctivitis-

1. Acute catarrhal [lower conjunctiva]
   • adult inclusion
   • adenoviral epidemic KC
   • pharygoconjunctival fever
   • newcastle conjunctivitis
   • acute herpetic conjunctivits
2. mild Chronic catarrhal [lower conjunctiva]
3. specific conjunctivitis with follicles like trachoma.

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Allergic conjunctivitis

conjunctiva is 10 more sensitive than skin to allergens.
It is either delayed CMI or immediate HMI.

Simple allergic conjunctivitis:

Etiology:

non-specific

1. hay fever- due to pollen & fur; associated allergic rhinitis.
2. seasonal [common] – due to pollen.
3. perennial [uncommon] – due to dust mites.

Pathogenesis:

• vascular response – sudden extreme vasodilation, exudation.
• cellular response – eosinophils, plasma cells, histamine releasing mast cells.
• conjunctival tissue response – mild papillae, boggy due to ↑ CT

CFs: acute / subacute

• intense itch & burn
• watery discharge
• mild photophobia
• conj – hyperaemia, chemosis, mild papillae
• swollen lids

Diagnosis:

eosinophils in conj tissue & no infection

Rx:

• avoid allergen
• vasoconstr- adr, eohedrine, naphazoline
• recurrent cases – cromoglycate
• severe / nonresponsive – steroids

Vernal KC / Spring catarrh:

Etiology:

due to external allergens; family history of other atopic diseases [hay, asthma, eczema]
Predisposers:

• 4-20 age boys
• periodically in summer in warm humid tropics

Pathology:

• papillae in upper tarsal conjunctiva due to epithelial hyperplasia; subepithelial projections from papillae
• adenoid infiltration
• vascular – dilation, exudation, proliferation

CFs: bilateral

• intense itch & burn
• ropy discharge
• mild photophobia
• heavy lids
• upper tarsal conjunctiva – cobblestone papillae; cauliflower like giant papillae in severe cases
• bulbar conjunctiva – dusky red trinagular hyperaemia on either side, gelatinous limbal membrane + white tranta’s spots
• Keratopathy -
  • upper cornea shows punctate keratitis or shallow transverse ulcer.
  • plaques due to deposition of altered exudates on macroerosions
  • subepithelial ring scar
  • cupid bow pseudogerontoxon

Rx: recurrent but self-limiting; regresses after 5-10yrs

• dark goggles, cold compresses / climate
• topical steroids [medrysone; + monitor IOP for induced glaucoma], naphazoline, cormoglycate, acetic acid [neutralize alkaline tears], cyclosporine in severe/nonresponsive cases
• systemic aspirin[anitPG] & anti-H; seveere/nonresponsive case-steroids
• giant papillae – supratarsal inj of long acting steroid /cryo/ beta-radiation /surgery
• keratopahty- high dose steroids, keratectomy

Atopic KC:

History:

young adult male + atopic dermatitis

CFs:

• itch, sore, dry
• mucoid discharge
• photophobia / blurring
• chronically inflamed lid margins
• tarsal conj – fine papillae, milky, hypaeraemia, scar
• lower cornea – punctate, vascularztn, thinning, plaques
• [keratoconus, atopic cataract]

Rx: recurrent diseae, regresses after age 50

frustrating [cromoglycate, steroids, artificail tears] ; treat dermatitis & lids.

Giant papillary conjnctivitis:

Etiology:

due to tears leaching the rough surface of a foreign body [lens,sutures]

CFs:

• itch
• stringy discharge
• ↓ wearing of lens
• 1mm papillae with hyperaemia in upper tarsus

Rx:

resolves after 1mos of foreign body removal; cromoglycate to hasten resolution.

Phlyctenular KC: [D/D for bulabr conjunctival nodule: episcleritis, scleritis, FBgranuloma]

Etiology:

delayed CMI to endogenous microbial proteins [TB, staph, moraxella, parasites]

Predisposers- 3-15 age female, malnourishment, poor hygiene

Pathological stages:

• nodule – due to exudative infiltrate into deep conjunctiva; [neutrophylls at centre, peripheral lymphocytes, surrounded by bv dilation+proliferation
• ulceration - at apex, mast cells & plasma cells
• granulation of floor
• healing with minimal scarring

CFs: few, mild

discomfort, watering

secondary mucopurulent conjunctivitis

bulbar conjunctival nodule near limbus

• simple [common] – 1or2 pink-white nodules + hyperaemia + apex ulcerates&epithelializes
• necrotizing – pustular conj due to very large nodule+ulcer
• miliary – multiple nodules

Keratitis

• ulcerative-
  1. sacrofulous – shallow marginal perpendicular to limbus, heals without scarring
  2. fascicular – with parallel leash of bv; heals with band opacity
  3. miliary – multiple small ulcers
• diffuse infiltrative – central infiltration & rich vasculrztn around limbus

Rx: recurrent; self-limiting in 10days

• topical steroids, antibiotics for secondary inf
• corneal lesion – atropine 1% ointment OD
• treat the cause – TB, sepsis, parasite
• high protein diet

Contact dermoconjunctivits:

Etiology:

delayed CMI to drugs [atropine, penicillin, neomycin/genta/sofra]

CFs:

conj esp lower- hyperaemia, papillae
cutaneous eczema of lids & face

Diagnosis:

eosinophylls in conjunctiva

+skin test for allergen

Rx:

discontinue the drug

topical steroids – eyedrops & skin oint

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Degenerative conditions: due to exposure to sun,dust,wind

Pinguecula:

on bulbar conj near limbus – avascular yellow-white triangular patch due to collagen degeneration&hyaline deposition.

Pterygium:

Etiology:

• usually seen in elderly male
• subconjunctival degeneration & hyperplasia as vascular granulation triangular fold encroaching & destroying cornea in interpalpebral area often nasal.
  1. Progressive- fleshy with cap
  2. Regressive- atrophic, less vascular, without cap

Complications- infection, cystic degenertion, neoplasia

D/D: pseudopterygium from chemical burns = chemosed bulbar conjunctiva adherent to corneal ulcer.

Rx:

• surgery – cosmetic, progressive from, hindered ocular movts causing diploplia
• recurrent cases
  1. transplant to lower fornix
  2. beta-radiation
  3. anti-mitotic drugs
  4. excise with sclera or mm graft
  5. recalcitrant cases – excise + lamellar keratectomy/plasty

Concretions:

• seen in elders or scarring trachoma
• upper conj – yellow-white hard raised areas due to mucus-epithelial debris in henle loops
• may cause corneal abrasion
• Rx: removal with hypodermic needle

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Conjunctival symptoms:

simple Hyperaemia: [not associated with disease]

1. Transient -
   1. irritation from cilia, dust, fumes, wind, light, cold/heat, rubbing
   2. reflex from eyestrain, inflm in neighbouring structures
   3. acute febrile conditions
2. chronic – smokers, alcoholics, dusty ill-ventilated rooms, prolonged exposure to heat, rosacea, insomnia

CFs:

gritty, heavy, tired eyes

mild watering & mucus

hyperaemic fornix

Rx:

topical decongestant[adr] & astringent[Zn-Boric acid]

Chemosis/ conj edema causes:

1. Inflm – conjunctivitis, corneal ulcer, fulminant iridocyclitis, end/pan ophthalmitis, stye, dacrocystitis, meibomitis, cellulitis, tenonitis
2. obstruction to blood/lymph by tumor, cyst, exophthalmos, CSthrombosis, acute glaucoma, surgical damage
3. systemic – severe anaemia, nephrotic syndrome, CHF, angioneurotic edema, urticaria

Ecchymosis:

• defined bright-red flat small/extensive hmrrg
• causes;
  ‘
  1. trauma
  2. inflm – pneumococcal, leptospirus, picorna virus
  3. sudden venous congestion of head causes capillary rupture – whooping cough, epilepsy, jugular vein strangulation, crush inj to thorax/abdomen
  4. spontaneous rupture dut to ATH, HTN, DM, anomalies like aneurysm, varicosity, telangectasia, blood disorders
  5. acute febrile conditions
  6. rare vicarious due to menstruation
• Rx: assurance since absorbed within 21days [severe cases some pigmentation may be left] ; cold compress in early stages & later hot

Xerosis: dry lustreless conjunctiva

1. Parenchymatous – after cicatrization
   • interstitial conjnctivitis – trachoma, diphtheria, pemphygoid, SJsyndrome, thermal, chemical, radiation
   • prollonged exposure to air – proptosis, facial palsy, ectropion, coma, lagophthalmos due to symblepharon
2. Epithelial – usually in children due to ↓ vitA = XEROPHTHALMIA where conj is thick, wrinkled,pigmented.

Rx:artificial tears.

Diseases of Lacrimal apparatus

Anatomy:

Main Lacrimal gland: [serous acinus glands like salivary]

1. ORBITAL part:
   • superior surface is in contact with outer orbital plate of frontal bone.
   • inferior surface is separated from Palpebral part by levator palpebrae superioris.
2. PALPEBRAL part: smaller part continous posteriorly with the larger Orbital part.
3. Ducts of lacrimal gland [10-12] pass downwards to open in lateral part of superior fornix [1or2 in inferior fornix]

Nerve supply:

1. Sensory: trigeminal-ophth-lacrimal.N
2. Sympathetic: cervical carotid plexus.
3. Secretomotor [parasympathetic]: superior salivary nucleus.

Accessory Lacrimal gland:

1. KRAUSE -beneath superior[42] & inferior[6-8] palpebral conjunctiva.
2. WOLFRING -extremes of superior&inferior tarsus.

LACRIMAL PASSAGES:

1. Puncta: opening on papilla of each lid near inner canthus, dipping into lacus lacrimalis [tear collection]
2. Canaliculi: from each puncta a short vertical part right angles with long horz part to converge to open into lacrimal sac.
3. Lacrimal sac: [fundus, body, neck] in lacrimal fossa of medial orbital wall [lacrimal bone, maxilla frontal process]
4. Nasolacrimal duct: [15-18mm] laterally down&backwards in the bony canal formed by maxilla & inferior turbinate, upper part is narrowest; one of its important valve is HASNER which prevents reflux from lower nose.

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Tear film

apart from washing away debris/noxious irritants & providing oxygen to cornea, has 3 layers:

1. outer lipid layer- Meibomian, Zeis, Moll secretion; air-tear interface that lubricates [facilitating movts] eyelids, retains shape & retards evaporation of tears.
2. bulky Aqueous layer- Lacrimal glands’ antibacterial [lysozyme,betalysin,lactoferrin] alkaline/saltish[solutes] watery secretion.
3. thin inner Mucus layer- conjunctival mucin secretory glands’ [goblet, henle, manz] secretion which by its hydrophilic nature keeps cornea & conjunctiva moist.

Tears are continously secreted by lacrimal glands. Basal secretion from accessory glands; Reflex secretion due to sensations[dry epithelium,broken tears] from cornea&conj from Main lacrimal glands; Hyperlacrimation due to irritants.

Elimination of tears by downward&medial flow towards lacus lacrimalis is due to:

1. orbicularis pump mechanism due to its insertion on lacrimal sac creates a negative syphoning pressure due to fundus distension & lower part compression.
2. orbicularis relaxation refills lower part from the fundus.
3. Hence, despite patency, atonia of lacrimal sac causes EPIPHORA.

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DRY EYE: deficiency / abnormality of tear film.

Etiology:

KCS [&darr water]	congenital alacrimia paralytic hyposecretion Sjorgen, RileyDay syndromes
&darr mucin	xerophthalmia [&darr vitA] conjunctival scarring – StevensJohnson, trachoma, pemphigoid, chemicals, radiation.
&darr lipids [rare]	congenital anhydrotic ectodermal dysplasia meibomian abscence – chronic meibomitis, chr blepharitis
&darr blinking	Bell’s plasy, nocturnal lagophthalmos, pterygium, ectropion, exposure keratitis, dellen, symblepharon
Corneal epeithelial abnormality affects tear film stability.

CFs:

• sandy sensation, itch, sore
• unresponsive to eyedrops
• particulate matter, stringy mucus
• lustreless
  • conjunctiva – xerosis, bitot spots, absent marginal tear strip.
  • cornea – punctate epithelial erosions & filaments

TEAR FILM tests:

Break up time	fluorescein is introduced & examined under cobalt blue slit-lamp while the patient is asked to keep blinking	corneal dry spot appearance normal=15-35sec, in unstable tear film <10sec
Schirmer 1	whatman41 filter paper in lower fornix & patient is asked to look up for 5min	[>15mm normal] in severe KCS <5mm.
Rosebengal staining		A pattern = confluent [severe KCS] B pattern = extensive staining [moderate KCS] C pattern = fine punctate stains in interpalpebral area [mild KCS]

Rx:

• artificial tears – cellulose, polyvinyl alcohol.
• &darr evaporation – cool temp, high humidity, glasses, bandage contact lens
• &darr drainage – punctal occlusion with collagen implants, cyanacrylate tissue adherent, electrocautrztn, argon laser, surgery
• &darr viscosity – mucolytic acetylcysteine
• retinoids, NSAIDs, steroids

Sjogren’s syndrome

autoimmune multi-sysytem chronic inflm [focal infiltrate + destruction of lacrimal gland = KCS]

• primary +xerostomia
• secondary +Rharthritis

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Watering eye:

Etiology:

1. Hyperlacrimation -
   1. Primary – direct stimulation, early Lgland tumor/cyst, parasympathomimetics
   2. Reflex – irritation to sensory br of trigeminal.N
      • eyelids – meibomitis, stye, entropion
      • conjunctivitis
      • corneal abrasion, ulcer, keratitis
      • scleritis, episcleritis
      • uveitis
      • acute glaucomas
      • end, pan ophthalmitis
      • orbital cellulitis
   3. Central – emotional, hysterical, voluntary
2. Epiphora -
   1. atonia causing lacrimal pump failure [weak orbicularis]
   2. mechanical obstruction to lacrimal passages
      • punctal obstruction – senile lax eversion, chr conj/blepharitis, ectropion, congenital abscence, foreign body/cicatrial closure, prolonged Rx with idoxuridine pilocarpine causes stenosis.
      • canalicular obstruction – foreign body, strictures from inflm[actinomyces] / trauma.
      • lacrimal sac – congenital folds, traumatic strictures, tumor, stones, atonia, dacryocystitis, TB, syphilis.
      • NLD obstruction – congenital non-canalization, imperforated valves, inflm/traumatic strictures, tumor, bone disease.

Evaluation:

diffuse illumination under magnification	reflex hypersecretion causes, punctal obstruction, Lsac swelling
Regurgitation test [press over Lsac]	mucopurulent discharge thr punctum in chr dacryocystitis
Flourescein dye disappearance	retention of dye in conjsacs is due to obstruction to passages
Lacrimal syringing with N.saline into lower punctum under topical anaesthesia 4%xylocain	partial obstruction requires more pressure while syringing for free passage into nose reflux from the same lower punctum indicates lower canalicular obstruction if on repeating the syringing thr upper punctum also causes reflux from opposite lower punctum, then it indicates common canalicular obstruction reflux thr opposite upper punctum indicates NLD/ Lsac obstruction.
Jones dye [flourescein into conjsac, 5min & cotton bud at NLD end]	positive dye stain indicates primary hyperlacrimation negative unstaining indicates epiphora on syringing gives positive stain, then it indicates partial obstruction causing the retained dye in Lsac. still negative unstaining indicates pump failure.
Dacryocystography [Xrays after radioopaque dianosil.condray280 into Lsac]	obstruction extent, fistulae, diverticulae, stone, tumor
Non-invasive Scintillography with radioactive tracer [sulphur, technitium] to visualize passages with gamma camera

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Dacryocystitis: [Lsac inflm]

Congenital dacryocystitis:

etiology:	symptoms:	complications:
NLD obstruction [membranous(mostly at hasner), epithelial debris, non-canlization, bony occlusion] + infection [staph, strep, pneum]	mild chronic inflm epiphora after 7days copious mucopurulent discharge positive regurgitation test [swelling]	recurrent conjunctivitis chronic dacryocystitis abscess, fistulae

Rx:

1. age <8wks : antibiotic drops + massage[hydrostaticP] to open membranous occlusion
2. >2mos: irrigation &uarr HydraulicP
3. >4mos: bowmann’s probe, if unsuccessful silicone intubation of NLD for 6mos.
4. >4yrs: DCR surgery

Adult dacryocystitis:

Chronic [more common]	Acute
Etiology: chronic NLD obstruction &darr mild infection of conjunctiva, nose, sinuses.	acute exacerbation of chronic disesa or direct extension of infection from neighbouring structures
predisposers: 40-60 age, narrow NLD [females, heriditary], poor hygiene. stasis causes- narrow bony canal, partial canalization, mem folds foreign body, polyp, hypertrophied concha, tumor, DNS hyperlacrimation inflmmatory epithelial debris & mucus plugs stenosis from atrophic rhinitis organisms – staph, strep, pneum, pseudomonas, [granulomatous]
Stages:	Stages:
chronic catarrhal - mild inflm of Lsac [red inner canthus] NLD obstruction epiphora- regurgitation test shows clear fluid [few mucoid flakes]	cellulitis- red hot painful firm swelling epiphora constitutional – fever, malaise
mucocoele- swelling just below inner canthus epiphora – regurgitation test shows mucoid discharge [negative regurgitation test is seen in ENCYSTED mucocoele(large fluctuant swelling) due to obstruction of opening of canaliculi into Lsac. Rx: conjunctivocystorhinostomy.	Abscess- canalicular obstruction causes pus to burst Lsac's ant wall forming a fluctuant PERICYSTIC swelling which due to gravity&ligament opens below&out.
Pyocoele- red swelling, epiphora, conjunctivitis regurgitation test shows purulent discharge.	fistula discharging spontaneously.
chronic fibrotic sac- thickenned mucosa from repeated infection [dacryocystography shows a small sac with mucosal folds]
complications: chronic intractable conjunctivitis lower lid ectropion, skin maceration, eczaema corneal abrasions, hypoyon ulcer surgery on unresolved infection causes endophthalmitis, ∴ prior syringing is essentisl.	complications: conjunctivitis lid abscess corneal ulcer facial cellulitis, osteomyelitis, ethmoiditis cavernous sinus thrombosis septecaemia
Rx: recent cases require SYRINGING + topical antibiotics later DCR is essential [DCT indications: aga60, fibrotic Lsac, granulomatous infection, tumor, atrophic rhinitis	Rx: topical&systemic antibiotics for cellulitis abscess requires draining & later DCT/DCR end stage requires fistulectomy with DCT/DCR

DCR:

• general anaesthesia
• skin incision medial to canthus
• expose MPligament & antLcrest
• dissect Lsac
• expose thick oink nasal mucosa
• prepare lacrimal & nasal H-flaps
• suture nasal with lacrimal flaps.

DCT – Lsac is removed & infected NLD parts are curettaged.