Showing posts with label Ophthalmology. Show all posts
Showing posts with label Ophthalmology. Show all posts

Friday, July 26, 2019

Effector blockade in the eye.

This is a mechanism by which the eye wards off the secondary effector phase of the immune response arc.
Thus, the cell mediated immunity appears to function less effectively in the uvea compared to the rest of the body.
Possible mechanisms include-

1. Immunomodulatory cytokines produced by the ocular tissues.

2. Immunomodulatory neuropeptides produced by ocular nerves

3. Functionally unique APCs.

4. Compliment inhibitors

..and some other factors.

-Sushrut

Choroid and fungi

The large spaces of choroid act as a sort of trap to organisms, especially fungi. Therefore most fungal lessons of the posterior segment begin as choroiditis.

Tuesday, July 23, 2019

Efferent optic nerve fibres

It's interesting to note that the optic nerve, which is considered to be a purely sensory nerve has some efferent fibres, that is, fibres from the brain to the optic disc. The presumed role of these fibres is in dreams, where the brain sends impulses to the retina, image is generated and it is carried back to the brain via the afferent fibres.

-Sushrut

Monday, July 22, 2019

Anterior chamber associated immune deviation

Some specific antigens when placed in the anterior chamber of the eye result in a suppression of cell mediated immunity, with a normal humoral component.

There is something known as the ' oculo splenic axis' , whereby the antigens travel via the trabecular meshwork and reach the spleen. In the spleen, they secrete MIP 2 which attracts the NK cells. The NK cells in turn secrete IL10 and TGF beta. The T cells in this environment become regulatory cells and suppress the cell mediated immunity. Production of IL2 is suppressed.

The eye is an immuno privileged organ, as it needs to be structurally maintained pristine to preserve it's light carrying capability. ACAID is a mechanism by which Nature attempts to limit unwanted inflammatory responses in the anterior chamber.

It has implications in intraocular tumors, autoimmune, and infectious immune responses.

-Sushrut

PS- The failure of ACAID in the mechanism of lens induced uveitis still remains unexplained!

Monday, May 6, 2019

Diabetic Retinopathy

Here is Upasanas video on Diabetic Retinopathy.



I edited the slides so you can see better :)

Slides are available for download here:

Sunday, May 5, 2019

Oblique muscle mnemonic

It can be hard to remember which oblique does what. Remember this. 'Extortion' as we all know is forcing money out of someone. People from the 'inferior' strata of the society extort money. See where am I  going?!

So! Inferior oblique causes extorsion( 'extortion' is a bit different- c'mon, be a grammar Nazi!)
What remains? Superior oblique. So..it then is responsible for intorsion.

Similar is the case for superior and inferior recti.

Hope I saved you from ophthalm extorting your precious time.

-Sushrut

Sunday, April 28, 2019

Strabismus/Squint

Hello Everyone!

                 Strabismus has been confusing me for long, so I decided to come up with a chart:


You can download the chart at https://drive.google.com/file/d/1leP_Ir3FZU0J-0isZcYHkgd5x_ujQFX8/view?usp=sharing

Thanks!

Chaitanya Inge
Upasana Yadav

Wednesday, April 10, 2019

Unique iris behavior in bleeding

Iridodialysis bleeds profusely as the circulus major arteriosus lies near it's root.
Conversely, sphincterotomies or YAG iridotomies hardly bleed. Why? Because the vessels in the iris away from it's root are intertwined within it's musculature. The muscles contract immediately, halting any hemorrhage.

-Sushrut 

Thursday, February 28, 2019

Cogan's Syndrome

●Cogan's syndrome (CS) is a chronic inflammatory disorder that most commonly affects young adults. Clinical hallmarks are interstitial keratitis (IK) and vestibuloauditory dysfunction, and associations between CS and systemic vasculitis, as well as aortitis, also exist. There are a range of pathologic findings, most of which reflect immune-mediated injury of the affected tissues; however, despite an association with systemic vasculitis, eye and inner ear specimens of those with CS do not reveal any evidence of vasculitis. The underlying mechanisms responsible for the eye and inner ear disease in CS are unknown.

●The predominant ocular feature of CS is IK, which typically causes eye redness, pain, photophobia, and blurred vision. Slit-lamp examination commonly demonstrates a patchy, deep, granular corneal infiltrate. IK is not essential for the diagnosis; ocular inflammation may involve other parts of the eye and may lead to iridocyclitis, conjunctivitis, episcleritis, anterior or posterior scleritis, or retinal vasculitis.

●The inner ear manifestations of CS are Ménière-like attacks consisting of vertigo, ataxia, nausea, vomiting, tinnitus, and hearing loss. Vestibular dysfunction may also cause oscillopsia, and caloric testing often reveals absent vestibular function. Recurrent episodes of inner ear disease frequently result in profound sensorineural hearing loss. Noninflammatory down-fluctuations in hearing may be difficult to distinguish from those of inflammatory origin. If hearing loss is associated with eye inflammation or other features of active CS or does not resolve within three to five days, an inflammatory origin is more likely.

●When present, the systemic vasculitis associated with CS is a large- or medium- to small-sized vessel vasculitis or an aortitis. The pattern of vessel involvement may be overlapping. Other systemic manifestations of CS include fever, fatigue, weight loss, lymphadenopathy, hepatomegaly, hepatitis, splenomegaly, pulmonary nodules, pericarditis, abdominal pain, arthralgia, arthritis, myalgia, and urticaria. An association with inflammatory bowel disease has also been observed.

●Evaluation of the patient with possible CS requires ophthalmologic examination to establish the presence of IK, scleritis, or episcleritis and to exclude other diseases and ocular pathology; neurologic and otologic examination to establish the presence of vestibuloauditory abnormalities; and rheumatologic examination to seek evidence of systemic vasculitis. We diagnose CS based upon the presence of characteristic inflammatory eye disease and vestibuloauditory dysfunction. The eye and inner ear are nearly equally likely to be the cause of presenting symptoms, while less than 5 percent of patients initially present with systemic manifestations

Bhopalwala. H

Tuesday, February 26, 2019

Eye Findings in GCA

●Anterior ischemic optic neuropathy – At least 80 percent of cases of vision loss in patients with GCA are caused by AION . The ischemic insult in arteritic AION is typically the consequence of occlusion of the posterior ciliary artery, a branch of the ophthalmic artery from the internal carotid artery, and the main arterial supply to the optic nerve.

Only about five percent of the total occurrences of AION are due to GCA, the majority being nonarteritic and secondary to atherosclerotic disease . About 40 percent of patients who suffer nonarteritic AION regain some amount of visual acuity, in contrast to visual loss due to GCA, which is more often massive and irreversible .

●Central retinal artery occlusion – CRAO is responsible for approximately 10 percent of the cases of visual loss in GCA . On the other hand, approximately two percent of older patients with CRAO have underlying GCA . Bilateral CRAOs in an older adult should prompt evaluation for GCA.

●Posterior ischemic optic neuropathy – PION occurs in less than five percent of patients with GCA . It results from the interruption of blood flow to the retrobulbar portion of the optic nerve. Histopathologic examination typically reveals inflammatory occlusion of the short nutrient posterior ciliary arteries .

●Branch retinal artery occlusion – BRAO is distinctly uncommon in GCA, though it has been described.

●Cerebral ischemia — Homonymous hemianopia is a visual field defect involving either the two right or the two left halves of the visual fields of both eyes. The most common cause in GCA is an occipital lobe infarction resulting from a lesion in the vertebrobasilar circulation. In rare cases, bilateral occipital lobe involvement leads to bilateral homonymous field defects and to the development of cortical blindness.

Bhopalwala. H

Monday, February 25, 2019

Vision Loss in Giant Cell Arteritis

Causes of vision loss —

Permanent loss of vision in GCA results from arteritic anterior ischemic optic neuropathy (AION), central or branch retinal arterial occlusion (CRAO/BRAO), posterior ischemic optic neuropathy (PION), or, rarely, cerebral ischemia

●Anterior ischemic optic neuropathy – At least 80 percent of cases of vision loss in patients with GCA are caused by AION . The ischemic insult in arteritic AION is typically the consequence of occlusion of the posterior ciliary artery, a branch of the ophthalmic artery from the internal carotid artery, and the main arterial supply to the optic nerve.

Only about five percent of the total occurrences of AION are due to GCA, the majority being nonarteritic and secondary to atherosclerotic disease . About 40 percent of patients who suffer nonarteritic AION regain some amount of visual acuity, in contrast to visual loss due to GCA, which is more often massive and irreversible .

●Central retinal artery occlusion – CRAO is responsible for approximately 10 percent of the cases of visual loss in GCA . On the other hand, approximately two percent of older patients with CRAO have underlying GCA . Bilateral CRAOs in an older adult should prompt evaluation for GCA.

●Posterior ischemic optic neuropathy – PION occurs in less than five percent of patients with GCA . It results from the interruption of blood flow to the retrobulbar portion of the optic nerve. Histopathologic examination typically reveals inflammatory occlusion of the short nutrient posterior ciliary arteries .

●Branch retinal artery occlusion – BRAO is distinctly uncommon in GCA, though it has been described.

●Cerebral ischemia — Homonymous hemianopia is a visual field defect involving either the two right or the two left halves of the visual fields of both eyes. The most common cause in GCA is an occipital lobe infarction resulting from a lesion in the vertebrobasilar circulation. In rare cases, bilateral occipital lobe involvement leads to bilateral homonymous field defects and to the development of cortical blindness.

Bhopalwala. H

Thursday, December 27, 2018

Vestibulo ocular reflex

The vestibulo-ocular reflex is a reflex, where activation of the vestibular system causes eye movement. This reflex functions to stabilize images on the retinas during head movement by producing eye movements in the direction opposite to head movement, thus preserving the image on the center of the visual field. For example, when the head moves to the right, the eyes move to the left, and vice versa. Since slight head movement is present all the time, VOR is necessary for stabilizing vision.

Circuit:

1)It starts in the vestibular system, where semicircular canals get activated by head rotation and send their impulses via the vestibular nerve and end in the vestibular nuclei in the brainstem.In addition the hair cells of opposite ear are inhibited because endolymph in that ear flows away from hair cells.

2)From these nuclei, fibers cross to the contralateral cranial nerve VI nucleus.

3a)There they synapse with 2 additional pathways. One pathway projects directly to the lateral rectus of the eye via the abducens nerve.
  b) Another nerve tract projects from the abducens nucleus by the medial longitudinal fasciculus to the contralateral oculomotor nucleus, which contains motorneurons specifically activating the medial rectus muscle of the eye through the oculomotor nerve. 

4)For instance, if the head is turned clockwise, then excitatory impulses are sent from the semicircular canal on the right side via the vestibular nerve to the right vestibular nuclei in the brainstem. From this nuclei excitatory fibres cross to the left abducens nucleus.There they project and stimulate the lateral rectus of the left eye via the abducens nerve. In addition, by the right medial longitudinal fasciculus, fibers cross and go to right oculomotor nuclei, they activate the medial rectus muscles on the right eye. As a result, both eyes will turn counter-clockwise.

-Srikar Sama

Friday, December 14, 2018

Horner Syndrome

Horner syndrome is a classic neurologic syndrome whose signs include miosis, ptosis, and anhidrosis.

NEUROANATOMY - Horner syndrome can result from a lesion anywhere along a three-neuron sympathetic pathway that originates in the hypothalamus:
●The first-order neuron descends caudally from the hypothalamus to the first synapse, which is located in the cervical spinal cord (levels C8-T2, also called ciliospinal center of Budge).

●The second-order neuron travels from the sympathetic trunk over the lung apex. It then ascends to the superior cervical ganglion, located near the bifurcation of the common carotid artery.

●The third-order neuron from superior cervical ganglia then ascends within the adventitia of the internal carotid artery, through the cavernous sinus. In the orbit and the eye, the oculosympathetic fibers innervate the iris dilator muscle as well as Müller's muscle, a small smooth muscle in the eyelids responsible for a minor portion of the upper lid elevation and lower lid retraction.
First-order syndrome - Lesions of the sympathetic tracts in the brainstem or cervicothoracic spinal cord can produce a first-order Horner syndrome.
The most common causes are:
(a)occlusion of PICA, which produces Horner syndrome as part of the Wallenberg syndrome.
(b)Brown-Séquard syndrome above T1, patient may present with ipsilateral Horner syndrome due to damage of oculosympathetic pathway.

Second-order syndrome — Second-order or preganglionic Horner syndromes can occur with trauma or surgery involving the spinal cord, thoracic outlet, or lung apex.Other causes include pancoast tumor involving the lung apex.

Third-order syndrome — Third-order Horner syndromes often indicate lesions of the internal carotid artery such as an arterial dissection, thrombosis, or cavernous sinus aneurysm

CLINICAL FEATURES -The classic signs of a Horner syndrome are ptosis, miosis, and anhidrosis.
1)The ptosis occurs as a result of paralysis of the Müller's muscle.
2)The degree of anisocoria is more marked in the dark than in light.
3)Anhidrosis is present in central or preganglionic (first- or second-order) lesions because the sympathetic fibers responsible for facial sweating branch off at the superior cervical ganglion along the external carotid artery and its branches.
4)Horner syndrome is also a common feature of cluster headache.

SOURCE-UpToDate, Kaplan.

-Srikar Sama.

Sunday, October 7, 2018

Question: Caloric test

#Medicowesome
#Ent

Q) Caloric test was done on right side with cold water and eyes were moved to opposite side. Which of the following correspond to interpretation of nystagmus in this test?
1) Eyes moves slowly to right
2) Eyes moves slowly to left
3) ‎Eyes moves rapidly to left
4) ‎Eyes moves rapidly to right
Answer in 24 hours with explanation of Caloric test.

Wednesday, September 26, 2018

Inverse glaucoma

In normal eye aqueous humour flow from ciliary body to anterior chamber. In Malignant glaucoma or Aqueous misdirection syndrome, aqueous humour escapes into posterior chamber. Now posterior chamber has two fluids - aqueous and vitreous. This mixture now push our lens forward. This leads to formation of shallow AC.

Now in this case if I give Pilocarpine then ciliary zonules will be slacked which will ultimately causes lens to move more anteriorly, leading to shallow AC.

Remember: Pilocarpine is DOC for acute congestive glaucoma and it is C/I in inverse glaucoma.

So I will need to give drugs which will cause tightening of ciliary zonules. This can happen when I will relax ciliary muscle. Now relaxation of ciliary muscles is done by cycloplegic drugs. Example - Atropine/ Homatropine.

Did you see the contrast?
Atropine is C/I in Acute ACG but it is DOC for inverse glaucoma!

Hope it helps!

That's all
-Demotional bloke

Tuesday, September 11, 2018

Question: Squint manifestations

#Medicowesome
#Ophthalmology
Question)

A patient presented with his head tilted towards right. On examination, he was having Left hypertropia which is increased on looking towards right or medially. The muscle which is mostly likely paralyzed is?
1) Left superior oblique
2) ‎Left inferior oblique
3) ‎Right superior oblique
4) ‎Right inferior oblique
Answer in 24 hours

Answer is 1) Left superior oblique

So, you can see above question is based on Park 3 steps method. I will try to simplify it as much as possible. Let us try to find out what essential information we get from above from above question. So I find three things.

-Left hypertropia.
-Increases on looking towards right.
-Head tilted towards right  (For compensating diplopia)

To proceed further, I want you to take care of two things .
1) Draw clinical eye movement diagram for squint not anatomical diagram
2) In this technique we go with parameters which increases diplopia for patients.

So, hold your horses and let us get started.

Step 1: Left hypertropia= Right hypotropia

So, basically you have to solve now question for two eyes instead of one. This is the same reason option 3 and option 4 could be right as well. So, when you draw clinical diagram for same you have to highlight muscles which are paralyzed leading to above criteria.

So, left hypertropia is caused by paralysis of the inferior muscles - Superior oblique and Inferior rectus.
In right hypotropia, superior muscles are paralyzed -Inferior oblique and Superior rectus. 
So our diagram will be as follow. We need to concentrate on four muscles only

Step 2: Now let us go to second clue. Diplopia increases on looking towards right. So, out of our four selected muscles let us see which muscles moves eyeball towards right.
 In right eye, it is Superior rectus.
In left eye, it is Superior oblique.

Our diagram will be as follow and your muscles will be narrowed down to two. Each from one eye.


Step 3: So this is final step. The End game. (Reminds me Taylor swift!)

  We have one last finding and that is patient's head is tilted towards right. Remember that this is compensatory method of patient for avoiding diplopia which actually suggests that patient is experiencing diplopia maximum when head is tilted towards left.

So in our last step we will be using clue as head tilted towards left! (Remember we go to maximum diplopia.)

So, this time hold your pencil in the centre of our clinical diagram and tilt it towards left. Obviously do this for both eyes individually. Simply like this
Now, this will narrow down your two muscles into one. Let us do it for right eye first. We will get muscle IO which is not among of our selected two muscles so discard it. Now go to left eye, do same over here. You will get answer as SO

Hope that makes your job easy as far as squint is considered.
-Demotional bloke








Monday, September 10, 2018

Question: Dengue and eye

#Medicowesome
#Ophthalmology

Q) In Dengue, all are seen w.r.t eye except:-

1) Cataract
2) Optic neuritis
3) Vitreous hemorrhage
4) Maculopathy

So, you basically cannot solve above problem if you don't know which portion dengue affects in eye.

Dengue affects posterior portion of the eye. So accordingly answer is
Cataract-Option 1

Some basics to cover over here.

Eyeball is divided into two segments or portion.

Anterior segment: Cornea to lens.
Volume - 0.31mL of Aqueous humor.

Posterior segment: Lens to retina.
Volume - 4mL of Vitreous humor.

Anterior segment is divided into two parts:-

Anterior chamber: Cornea to iris.
Volume- 0.25mL of Aqueous humor

Posterior chamber: Iris to lens.
Volume- 0.06mL of Aqueous humor

-Demotional bloke.

Friday, September 7, 2018

Question: Diabetic 3rd nerve palsy

Question:
In Diabetic 3rd nerve palsy all are seen except
A) Pupil dilation
B) Outward and downward gaze
C) Ptosis
D) Impaired pupillary reflex

Let us start with the basic.

Mnemonic for extraocular muscles nerve supply
LR6 SO4 Rest3

Lateral rectus is supplied by 6th nerve or abducence nerve and superior oblique by 4th nerve or trochlear nerve and rest all  muscles including LPS are supplied by 3rd muscle or  occulomotor nerve.

In pupillary reflex,
Afferent nerve: Optic nerve
Efferent nerve: Occulomotor nerve.

So in case of 3rd nerve palsy, we will have less or no actions of all EOM except lateral rectus and superior oblique.
So we will have downward gaze (due to superior oblique) and outward gaze (due to lateral rectus) and Ptosis (because LPS is supplied by 3rd nerve! ).
Pupillary reflex is also disturbed so option 4 is also ruled out.

Here is a trick in this question. In DM and HTN, microangiopathy is seen due to which central fibers are affected.
Central part do not contribute to pupillary reflex.
This leads to no pupil dilation. In case of surgical conditions and trauma, peripheral fibers are affected which causes impaired pupillary reflex or pupil dilation.

-Demotional bloke.

Wednesday, August 29, 2018

Hering's law of equal innervation

Now to study this law, we need to know clinical function diagram of eye muscles.


So according to this diagram,
Right SR is responsible for elevating right eye to right side.
Similarly, Left IO is responsible for elevating left eye to right side.

Since both the muscles are performing same action on two different eyes using two different muscles they are called yoke muscles of each other.
This is Hering's law of equal innervation.

Now, here is a trick to solve problem without looking into the diagram:

Right gets converted to Left.
S (Superior) gets converted to I (Inferior)
O (Oblique) gets converted to R (Rectus)
So the mnemonic for remembering muscle change is
ROSI (You can remember it as ROSS from friends!)
R gets converted to O.
S gets converted to I.
-Demotional bloke