GLAUCOMA

Glaucoma: group of diseases in which increased IOP (intraocular pressure) in an eye produces optic disc cupping and visual field defects.

Normal IOP: 10-21 mm Hg
- Usually slightly high in the morning and slightly deceased at night.


PRODUCTION OF AQUEOUS HUMOR:
(a) Active Secretion: 80% ultrafiltration & 20% diffusion
(b) Drainage: 90% through the Trabecular pathway & 10% through the Uveo-scleral pathway
(c) Level o episcleral venous pressure


CLASSIFICATION:
A. Developmental aka. Congenital: Children present with BUPTHALMOS (increased corneal diameter)
- Primary
- Rubella
- Secondary to other ocular causes such as aniridia
B. Acquired
1. Open angle
- Primary – chronic open angle
- Secondary
2. Closed angle
- Primary – Acute and Chronic closed angle
- Secondary – Due to trauma, raised episcleral venous pressure, steroid induced, associatd with other ocular disease such as uveitis


TONOMETRY (measurement of tension or pressure, particularly IOP)
1. Goldmann tonometer
2. Schiotz tonometer
3. Perkin’s tonometer
4. Air Puff tonometer
5. Tono pen

EYE EXAM:
1. Check IOP
2. Look for optic disc cupping
3. Test field of vision

GONIOSCOPY (examination of anterior chamber of the eye to demonstrate ocular motility and rotation)
- Done to identify structures in the irideo-corneal angle.
- Use a triple-mirror GONIOLENS to visualize the angle and the periphery of the retina
- Opening of the angle is graded (Grades 0-4)
Grade 0: Closed angle
Grade 1:Narrow angle
Grade 2: Moderately narrow angle
Grade 3: Open angle
Grade 4: Widest angle


OPTIC NERVE HEAD CHANGES SEEN IN GLAUCOMA:
1. Retinal nerve fiber changes
2. Concentric expansion of optic disc cup
3. Localized expansion of optic disc cup (notching at inferior or superior pole)
4. Narrowing of neuro-retinal rim
5. Pallor
6. Splinter hemorrhages on disc margin
7. Deepening of optic cup
8. Nasalization of vessels
Note: Papillomacular area is spared and tunnel vision is preserved!!


PERIMETRY:
Visual field: an island of vision surrounded by a sea of darkness.
Normal visual field:
- Superiorly 50 degrees
- Inferiorly 70 degrees
- Nasally 60 degrees
- Temporally 90 degrees

VISUAL FIELD DEFECTS SEEN IN GLAUCOMA:
1. Arcuate Scotomas
2. Isolated paracentral scotoma
3. Nasal step
4. Temporal wedge
5. Ring scotoma


PRIMARY OPEN ANGLE GLAUCOMA:
1. Adult onseT
2. IOP > 21mm Hg at some point in the course of the disease
3. An open angle of normal appearance
4. Glaucomatous optic nerve damage
5. Visual field defect


RISK FACTORS for the development of glaucoma:
1. Age > 40 years
2. Race (higher incidence in Black people)
3. Family history
4. Diabetes
5. Hypertension
6. Myopia
7. Prolonged use corticosteriods (oral or topical)


SYMPTOMS: Usually symptomless & diagnosed on routine eye examination!!
- Patient with Acute closed angle Glaucoma may present with : photophobia, and painful eye, loss of vision, watering of the eye

SIGNS:
1. Increased IOP
2. Fluctuating IOP
3. Optic disc changes
4. Glaucomatous field change


TREATMENT:
1. Medical :
- Alpha-2 agonists eg. Apraclonidine
- Beta Blockers eg. Timolol, Carteolol
- Carbonic anhydrase inhibitors eg. Brinzolamide, Dorzolamide
- Prostaglandins eg. Latanoprost, Travaprost
- Sympathomimetic and Parasympahtomimetic agents eg. Adrenaline, Pilocarpine

2. Laser cyclophotocoagulation

3. Surgery (has a lot of complications and is therefore the last resort of treatment!)
- Argon Laser trabeculoplasty
- Trabeculectomy (a fistula is created between the angle of the anterior chamber and sub Tenon’s space to allow drainage of the fluid)
- Cryotherapy of ciliary body

Management of TRABECUECTOMY FAILURE:
1. Adjunctive Antimetabolites- such as 5-FU and Mitomycin
2. Artificial drainage shunts
3. Cyclodestructive procedure using Lasers OR Cryotherapy


LOW-TENSION GLAUCOMA:
- Also known as Normotensive Glaucoma
- The intraocular pressure is normal but optic disc cupping and field defects are present


OCULAR HYPERTENSION: IOP > 21 mm Hg but there’s no cupping and visual field defects

Cataract

Any congenital or acquired opacity in the lens capsule or substance, irrespective of the effect on vision, is a cataract. Cataract is the commonest cause of treatable blindness in the world.


Lens: The lens is biconvex and transparent. It is held in place behind the iris by the suspensory ligament whose zonular fibers are composed of protein fibrillin which attach its equator to the ciliary body. Disease may affect structure, shape and position.

Normal lens: 4-5mm thick and approx. 10 mm in diameter.
Outer: cortex.
Inner: Nucleus


Classification:
I. According to Age
- Congenital
- Infantile
- Juvenile
- Pre-senile
- Senile

II. According to Morphology
- Capsular
- Sub-capsular
- Cortical
- Nuclear

III. According to Etiology
- Age related: example senile cataract
- Traumatic cataract
- Metabolic cataract: due to diabetes mellitus, hypoparathyroidism
- Toxic cataract: due to use of steroids, and other medications
- Complicated cataract: secondary to some other eye disease such as chronic anterior uveitis, acute angle closure glaucoma, pathological myopia

IV. According to Maturity
- Immature cataract
- Mature cataract
- Hypermature cataract: Proteins are liquefied and the permeability of the capsule is increased. This results in leakage of proteins and deposition of calcium.

Example: MORGAGNIAN CATARACT (Cortex liquefies and the nucleus sinks down)

Intumescent cataract: Lens is swollen due to water retention. Maybe immature, mature or hypermature.


Symptoms:
1. Blurred vision (most important symptom)
2. Glare
3. Monocular diplopia
4. Haloes around light
5. Improvement in near vision


Signs:
Depend on the state of maturity of the cataract
1. Decreased visual acuity
2. Change in the colour of the pupil
3. Iris shadow
4. Abnormal red reflex


Management:
(There is no medical treatment for cataract!)
1. Surgery (Goal of cataract surgery: to leave the patient emmetropic)
2. Glasses


Indications for Cataract Surgery:
1. Visual improvement
2. Medical indication eg. The patient develops glaucoma or diabetic retinopathy,r etinal detachment
3. Cosmetic indication


Pre-operative Assessment:
1. Complete ocular exam
2. Macular function test
3. Optic nerve function test
4. Biometry
5. Investigations:
- CP & ESR (complete blood picture and erythrocyte sedimentation rate)
- FBS (fasting blood sugar)
- UDR (urine detailed report)
- Hep B and C virology


Anaesthesia:
1. Facial Block
2. Retrobulbar block


Surgical Techniques:
1. ECCE (Extra Capsular Cataract Extraction)
2. ICCE (Intra Capsular Cataract Extraction)- not used anymore
3. Phacoemulsification – the newest method


Disadvantages of ICCE (Intra Capsular Cataract Extraction):
1. Large incision
2. Posterior capsule is removed and so the vitreous gel may come out
3. Posterior capsule is removed and therefore, there is no support for the IOL (intraocular lens)


Advantages of Phacoemulsiication:
1. Small tunnel incision
2. Quick recovery
3. Early visual rehabilitation
4. Useful for the removal of soft cataract (nucleus is soft)


Complications of Cataract Surgery:
1. Operative complications
- Rupture of posterior capsule
- Vitreous loss
2. Post-op complications
- Iris prolapse
- Corneal edema
- Uveitis
- Endopthalmitis
- Post-op Astigmatism
- Cystoid macular edema
- Retinal detachment
- Posterior capsule opacification

Congenital Cataract
- Opthalmological emergency!!!!
- Bilateral congenital cataract results in a significant effect on visual acuity and results in nystagmus and amblyopia.
Nystagmus: involuntary rapid movement (horizontal, vertical, rotatory or mixed i.e. of two types) of the eyeball.
Amblyopia: dimness of vision without detectable organic lesion of eye.

Age-Related Macular Degeneration

• It is the leading cause of irreversible blindness in developed countries.
• Complex multifactoral progressive disease with genetic and environmental influences.

PATHOGENESIS:
Not well understood but it is believed that oxidative stress is the key component of retinal pigment epithelial (RPE) degeneration. Progressive diffuse thickening of the Bruch's membrane (retinal layer that provides nourishment and oxygen to the RPE and the outer layers of retina, including the rod and cone cells) causes hypoxia----> choroidal neovascularisation---->weak new vessels leak serous fluid/blood---->distort central vision and reduce clarity of central vision.
Alternatively death and atrophy of RPE also occurs.

DRUSEN BODIES: visualized clinically as yellow deposits situated within Bruch's membrane. Vary in size and shape/maybe discrete or confluent. Either collagen-based or granular lipid rich.


ESSENTIALS OF DIAGNOSIS:
Older age group (>55year)
Gradual progressive simultaneous or sudden sequential deterioration of central vision in both eyes affecting reading and recognising faces.
Distortion or abnormal size of images (demonstrated by Amsler chart)
No pain or redness.
Macular abnormalities seen by ophthalmoscope.

Suggested Associated Risk Factors:
famale sex
smoking history
family history
hypertension
hypercholestrolemia
history of exposure to UV light
hypermetropia
cataract surgery

Dry ARMD/ Atrophic Degeneration 85%:
Gradual progressive bilateral visual loss of moderate severity.
Atrophy and degeneration of outer retina and RPE.
Variable and may result in severe visual impairment over a span of 5-10 years.
In advanced stages it is possible to see underlying choroidal vessels.

Treatment: No specific treatment but patients benefit from visual rehabilitation (refraction and low vision assessment). Peripheral fields and hence navigational vision are always maintained.

Wet ARMD/ Exudative Degeneration 15%:
Aggressive form of the disease.
Rapid clinical course and 75% of the patients have marked reduction in vision over 3 years.
Disease characterized by choroidal neovascularisation----> fluid leakage and bleeding in the macular region.

Treatment: is aimed at closing off blood flow through the area of choroidal neovascularisation to allow resolution of exudative changes. It is based on which of the following categories (as seen in Fundus Fuorescien Angiography) the disease falls in:
Classic only- neovascularisation fully delineated
Predominantly classic with little occult- ≥50% classic with some occult
Minimally classic- ≤ 50% but >0% classic
Occult only- full extent of neovascularisation not visible

Laser Photocoagulation: occludes neovascular regions of retina
Done for classic-extrafovealand juxtafoveal conditions but also causes considerable to adjacent retina.

Photodynamic Therapy: light activated agent, verteporfin, is given IV. Laser is then used at a particular wavelength to activate the photosensitizer which causes local vessel occlusion without damage to nearby retina. Needs to be repeated every 12 weeks.
This too is used for the subfoveal type of the classic lesion.

Antiangiogenic Agents:
Inhibitors of vascular endothelial growth factor(eg synthetic steriods) which would reverse neovascularisation.
Have to be administered every 4-6 weeks with risks of intraocular infection, inflammation and retinal detachment.
These can be used for both classic and occult.

Submacular Surgery:
Microsurgical viterectomy + retinal incision and then removal of vessels.
Suitable for selected cases.

Macular Rotation:
Macular region of retina is physically moved to overlie another place where the RPE is healthy followed by strabismus surgery. The procedure is complicated and carried significant risk.

Pathology- GIT MCQ's

1) A 60 year old man presents to his physician because of progressive dysphagia, first for solids, then for liquids. Endoscopy reveals a large fungating mass 2 cm above the gastroesophageal junction. Biopsy of the mass demonstrates glands, extending into the muscular layer, containing cells with large hyperchromatic nuclei. Which one of the following conditions is most likely associated with the development of this mass?

A. Barrett's esophagus
B. Esophageal rings
C. Esophageal webs
D. Scleroderma
E. Sliding hernia


The correct answer is A. Biopsy is consistant with esophageal adenocarcinoma which usually arises in aread of gastric or intestinal metaplasia (Barrett's esophagus) in the lower or middle one third of the esophagus. The prognosis for adenocarcinoma is poor, unless caught very early.

Esophageal rings (choice B) are rims of fibrovascular tissue found in the lower esophagus.

Esophgeal webs (choice C) are mucosal ledges in the upper esophagus.

Scleroderma (choice D) can cause fibrosis and impaired motility of the esophagus.

In sliding hiatal hernias (choice E), part of the stomach protrudes above the diaphragm.



2) A 30 year old man with a 15-year history of ulcerative colitis develops intermittent cholestatic jaundice. Ultrasonographic examination fails to reveal gallstones. Liver biopsy demonstrates a large bile duct obstruction. Which of the following would most likely be seen on endoscopic retrograde cholangiopancreatography (ERCP)?

A. Beading of transhepatic bile ducts
B. Markedly dialted common bile duct containing irregular radioluscent masses
C. Mass at the ampulla of Vater
D. Moderately dilated intrahepatic bile ducts and stricture in the bile duct at the lower end of the common bile duct


The correct answer is A. The most likely diagnoses is primary sclerosing cholangitis, a disorder with a probable autoimmune component that is associated with ulcerative colitis (66% correlation). The disease is characterized by inflammation and fibrosis of the intrahepatic and extrahepatic bile ducts, producing alternating strictures and dilatation of the structures. These changes are seen as "beading" on ERCP.

Gallstones in the biliary tree produce irregular radiolucent masses (choice B).

Choice C describes the findings associated with carcinoma of the ampulla of Vater.

Choice D describes the findings associated with carcinoma of the extrahepatic bile ducts.

Choice E describes the findings associated with carcinoma of the pancreas.



3) A patient has had years of intermittent diarrhea and abdominal pain, but has never consulted a physician. Eventually he begins to pass fecal material in his urine and he seeks medical attention. Which one of the following diseases is most likely to cause this complication?

A. Celiac disease
B. Crohn's diease
C. Diverticulitis
D. Ulcerative colitis
E. Whipple disease


The correct answer is B. Passing fecal material in urine strongly suggests the possibility of a fistula between the bowel and bladder. Of the diseases listed, only Crohn's disease commpnly produces fistulas. Fistulas are produced in Crohn's disease because the disease affects the entire thickness of the bowel wall, rathar than being restricted to the mucosa (e.g., ulceratice colitis).

Celiac disease (choice A) is a mucosal disorder of the small intestine caused by intolerance to certain components of gluten from wheat and other grains.

Diverticulitis (choice C) can cause bowel perforation with peritonitis but does not usually cause fistula formation.

Ulcerative colitis (choice D) is much less commonly associated with fistula formation than is Crohn's disease.

Whipple's disease (choice E) is a small intestinal disorder caused by infection with Tropheryma whippelii.



4) A 40 year old man complains of increasing difficulty in swallowing in the past 3 years. He reports a feeling of pressure in the chest occurring 2-3 seconds after swallowing a solid bolus. He also experiences regurgitation of undigested food eaten hours previously. A radiograph taken after swallowing barium shows a distended esophageal body with a smooth tapering at the lower esophageal sphincter. Manometry shows the absence of esophageal peristalsis and a lower esophageal sphincter that fails to relax. What is the most likely diagnosis?

A. Diffuse esophageal spasm
B. Incompetent lower esophageal sphincter
C. Oropharyngeal dysphagia
D. Scleroderma
E. Achalasia


The correct answer is E. Achalasia is an acquired esophageal motility disorder that slowly develops. The motility is abnormal due to the loss of inhibitory enteric neurons of the esophageal body and lower esophageal sphincter. Both vasoactive intestinal peptide and nitric oxide function as inhibitory neurotransmitters here, and the presence of both is decreased in achalasia. Radiographs typically show a dilated esohpagus that tapers at the lower esophageal sphincter, producing the so called "bird's beak". Because of the poor motility, ingested food is regurgitated and can lead to aspiration symptoms. Manometric demonstration of absent peristalsis in the esophageal body and poor relaxation of the lower esophageal sphincter with a swallow confirm the diagnosis.

The primary complaint with diffuse esophageal spasm (choice A) is mid-sternal pain that can be misdiagnosed as cardiac pain. The pain is caused by prolonged contraction of the entire esophageal body. Symptoms can be brought on by eating certain hot or cold meals. A manometric study may show poor peristalsis in the smooth muscle portion of the esophageal body, but lower esophageal sphincter function is unaffected.

The primary complaint with incompetant lower esophageal sphincter (choice B) is heart burn and regurgitation due to gastroesophageal reflux. Endoscopic examination of the esophagus may reveal inflammation, erosions, and even ulcers. A manometric study would show lower than normal resting tone in the lower esophageal sphincter.

The fact that the patient's symptoms do not occur until 2-3 seconds after a swallow suggests that oropharyngeal dysphagia (choice C) is not the diagnosis. The presence of cogh, Hoarseness, or nasal regurgitation commonly occurs with this disorder. Oropharyngeal dysphagia is often due to neurological or muscle disorders like stroke, amyotrophic lateral sclerosis, muscular dystrophy, or myasthenia gravis.

Scleroderma (choice D) is a connective tissue disease in which esophageal smooth muscle is gradually replaced by dense collagenous material. Manometry woud show poor esophageal peristalsis and decreased lower esophageal sphincter tone. Significant acid reflux with resultant esophagitis is almost universal.


More questions to come soon...

Diabetic Retinopathy

Diabetic Retinopathy is one of the commonest cause of blindness in the world. Diabetics are at 25% more risk to be blind than normal people. Also, almost half of the diabetics at some stage develop eye disease. Hence, diabetes is a major predisposing factors to ophthalmic pathology.


Ocular diseases that are associated with Diabetes include:

a- Diabetic Retinopathy
b- Cataract
c- Glaucoma
d- Infections

(Delayed healing is also a result of diabetes)


Pathogenesis:

The major factor in the pathogenesis of Retinopathy in diabetics is a microangiopathy of vessels supplying the retina )or a part of it(.

The main vascular damage can be divided into two parts: a) Leakage; b) occlusion

a) Endothelial cells rely exclusively on glucose for nutrition and insulin helps in the transport of glucose into them. Thus, when there is absence of insulin or a resistance to it, the cells start becoming undernourished. And overtime they suffer injury (and most likely cell death). The dead cells result in a leaky and weakened vessel wall. The leaky vessel wall leads to edema of the retina, followed by hemorrhage and finally WBC infiltration - thus resulting in damage to the retina.

b) As the vessel continues to weaken, microaneurysms form in the vasculature which over time can get occluded and thus lead to infarction of the retina supplied distally to the occlusion.
As the retina is denourished due to thrombosis of the vessel supplying it, there is release of Vascular Angiogenesis Factor (VAF). Under the influence of VAF, new blood vessels are formed to keep the retina nourished but that is to no avail as the new vessels leaky and weak and thus more hemorrhage and edema occurs, resulting in further loss of vision.


Risk Factors:

a) Duration of diabetes
b) Control of Diabetes
c) Pregnancy and other diabetogenic conditions
d) Anemia
e) Hypertension - DM and HTN go hand in hand
f) Smoking
g) Obesity and Hyperlipidemia


Symptoms:

This form of retinopathy is asymptomatic initially. Although some people might complain of dark areas in their vision.


Signs:

On Ophthalmic examination, red (hemorrhagic) and white (exudative) dots are seen. Exudates are of two types: hard and soft. Hard exudates contain protein, have marked edges and are small and discrete. the soft exudates on the other hand are of a lighter colour. They appear softer and have less marked edges with fuzzy borders.


Classification:

Diabetic Retinopathy are classified in two types depending on vascular proliferation. They are as follows:

a) Non-proliferative: they don't grow from the initial lesion and there is no neovascularization, or only minimal.

b) Proliferative: there is dangerous level of neovascularization and they appear as fronds. These vessels might bleed into the Vitreous and give rise to opaque membranous plaques which can then result in retinal detachment.
If all the above is present along with glaucoma, the condition is called Advanced Diabetic Eye DIsease (ADED).


Diagnosis:

It is based on positive history of Diabetes and Ophthalmoscopic examination.


Complications:

a) Vitreous hemorrhage
b) Retinal detachment
c) Formation of opaque membranes
d) Burnt-out stage


Treatment:

Specific: is to get rid of the new vessels being formed and removing the occlusion
Non-specific: control Diabetes and Hypertension; avoid ischemia


Screening:

Screening is an important tool in preventing the development of Retinopathy in cases with high index of suspicion. Diabetics should be examined at least once a year and the frequency should increase with every decade.

Common Nose Emergencies - Their Management.

• Foreign Body in the Nose? Outline your management.

History/examination

Plain X ray of the nose in lateral and anteroposterior view (when necessary)

Removal of the foreign body (depending on the type):

*Flattened FB (eg piece of paper) -----> Removal by pair of Crocodile forceps

*Ireggular rounded FB ------>Removal by a rounded Hook or Probe (do NOT attempt by Crocodile forceps as it may cause the fb to be lodged deeper in the nose).

Treating Epistaxis?

Pinching ---->if unresponsive-----> Anterioir Nasal Packing ---->if unresponsive--- >Posterior Nasal Packing ----->if unresponsive-----> Cautery by Silver Nitrate.

*the patients presenting with severe epistaxis must be immediately made hemodynamically stable by:

maintaining ABGs, Vitals, Topical Decongestants and Normal Saline.

Sedation of the patient is necessary in most cases.

Blood should be arranged for trasnfusion.

If a patient is a known case of HTN, it must be controlled immediately to prevent further blood loss and plasma expanders to be infused.

*patients with posterior nasal packing are usually admitted in the ICU because the PNP may cause oxygen desaturation.

• Simplest method for Posterior Nasal Packing?

14 FR Foley's Catheter

• Management of Complicated Sinusitis (usually involving the eye and sometimes, the brain also)?

(In order of importance):

1. History/Examination


2. Call for assistance from Opthalmology/Neurology


3. IV antibiotics infusion (Ceftriaxone works best)


4. Observe for 24 hours, if sympotoms persist then proceed with surgery (Functional Endoscopic Sinus Surgery or External Ethmoidectomy) after a CT scan.

• Trauma leading to fracture of the nose, outline the treatment?

History/Examination

X- ray (it has great medicolegal importance)

Analgesics.

Reduction of the fracture ---> ONLY if the patient is brought in within 2 hours of the trama.

*If, however, the patients comes to you 2 hours after the trauma and edema is present then do NOT reduce the fracture then. Give analgesics and send the patient home, call after 7 days (aftet the edema has settled) to reduce the fracture.

• Treatment of Septal Hematoma?

Make an incision on one side

Drain the blood

Leave a small drain (to prevent re accumulation)

Pack the nose on both sides (remove after 48 hours)

Start prophylactic Systemic Antobiotics.

• Management of post Septoplasty (or any other nasal surgery) Septal Hematoma?

Re-open the already present surgical incision.

Drainage ----> leave the drain in for 1 day ----> Pack the nose

Give an Anti biotic cover.

• Treating Septal Abscess?

Incision on the most dependent part of the abcess

Evacuate the pus

(any necrosed cartilage will also be removed)

Place a small drain

Do nasal cavity packing

Send the pus was C/S and till the report comes in keep the patient on broad spectrum antibiotics.

*nasal pack should be removed daily and any pus accumulated should be drained for a few days till the condition subsides.

-Sources: Udairpuwala, Dr. K.I - HOD ENT department ZMUH KDLB, Dr. K.M - Professor of ENT department ZMUH KDLB.