Everything about Meig’s - Decoded

Meigs syndrome:

• The presence of triad consisting of solid benign ovarian mass, associated with ascites and pleural effusion that resolve after the resection of the adnexal mass define Meigs' syndrome.
• Histologically, the benign ovarian tumor may be a fibroma, thecoma, cystadenoma, or granulosa cell tumor.of which ovarian fibromas are the most common cause of Meigs syndrome.

The most likely pathogenesis of peritoneal and pleural effusions ascribes filtration of interstitial fluid in the peritoneum through the tumor capsule, and diffusion to the pleural space, usually at the right side, through diaphragmatic lymphatic vessels and apertures, as well as through intercellular gaps and small areas where muscular tissue of the diaphragm is replaced by areolar tissue.

Pseudo-Meigs' syndrome :

• It is a condition characterized by  ascites and pleural effusion caused by pelvic tumors other than solid benign ovarian tumors.

• The pseudo-Meigs syndrome is clinically important because it resembles metastatic pelvic cancer. Especially in patients with malignant ovarian tumors, cytologic examination of the body cavity effusions is essential to differentiate between reactive process and metastatic tumor spread. While detection of malignant cells is a marker of metastatic disease and a sign of bad prognosis, benign effusions of pseudo-Meigs syndrome affect neither disease stage nor the patient's prognosis. Determination of the presence or absence of tumor spread is based primarily on cellular morphology study, but if distinction between reactive mesothial and cancer cells is difficult, immunocytochemistry may be necessary.
• At this point, must be underlined that an ovarian mass combined with pleural and peritoneal effusions not always represents an advanced malignancy, even with elevation of CA 125 value. There are some benign pelvic lesions causing pseudo-Meigs syndrome, which are associated with elevated levels of this tumor marker, such as struma ovarii, ovarian cystadenomas, uterine leiomyomas and broad ligament leiomyomas 
• CA 125 levels decline to the normal range after tumor resection.

Atypical Meigs :

Ii is characterized by a benign pelvic mass with right-sided pleural effusion but without ascites . As in Meigs syndrome, pleural effusion resolves after removal of the pelvic mass.

Pseudo-pseudo Meigs syndrome:

• It is a term that describes patients with ascites, pleural effusion, and enlarged ovaries secondary to systemic lupus erythematosus.
• The ovaries in pseudo-pseudo Meigs syndrome may be enlarged, but without evidence of a tumor.
• Ascites in pseudo-pseudo Meigs syndrome is usually exudative, and may be associated with activated mesothelial cells in systemic lupus erythematosus .

Carpal tunnel syndrome – Important signs.

Phalen sign:Hyper flexion of the wrist for 60 seconds may elicit paresthesia in the median nerve distribution.

Tinel sign :Tapping the volar wrist over the median nerve may produce paresthesia in the median distribution of the hand.

Flick sign :Shaking or flicking one's hands for relief during maximal symptoms.

Various Lines in Ophthalmology

Arlt's Line :

• Horizontal line of conjunctival scarring in sulcus subtarsalis of superior palpebral conjunctiva.
• Seen in Trachoma.

Ehrlich-Turk Line :

Vertical linear deposition of KPs in uveitis.

Ferry's Line :

Corneal epithelial iron line at the edge of filtering blebs of glaucoma surgery.

Hudson-Stahli Line :

Iron deposition line in the corneal epithelium, which commonly seen in the junction between middle and lower third cornea.

Khodadoust Line :

• Corneal graft endothelial rejection line composed of inflammatory cells.
• Khodadoust's line separates immunologically damaged endothelium - usually originating from neovascularization in the same area - from the unaffected endothelium. In the area of damage the endothelium is decompensated resulting in stromal and epithelial edema. Timely immuno-suppression can reverse this process.

Endothelial rejections :Most severe form of corneal rejection as this layer doesn’t have regenerative property & significant cell loss can cause chronic graft edema.

• Classic endothelial rejection presents with an endothelial rejection line (Khodadoust line) that usually begins at a vascularized portion of the peripheral graft-host junction and progresses, if untreated, across the endothelial surface over several days. The rejection line consists of mononuclear white cells that damage endothelial cells as the line sweeps across the endothelium.
• Generally, a mild-to-moderate anterior chamber reaction is present. The damaged endothelium is unable to properly dehydrate the corneal graft; as a result, the donor cornea is clear ahead of the rejection line and is cloudy and edematous behind it.
• A second variant of endothelial rejection is more diffuse in character, with scattered keratic precipitates and an anterior chamber reaction indicative of endothelial rejection and damage. In this type of endothelial rejection, stromal edema typically is not localized, but rather generalized throughout the graft, consistent with the generalized endothelial damage. The combination of keratic precipitates, an anterior chamber reaction, circumcorneal injection, and regions of corneal edema should be diagnosed as corneal graft rejection. In some cases, it may be difficult to distinguish graft edema from rejection and graft edema from endothelial insufficiency. Since rejection may be reversible, it is best in these situations to treat patients as if they have graft rejection.

Paton's Line :

• Circumferential retinal folds in peripapillary region due to papilledema.
• Papilledema is defined as optic nerve head edema secondary to increased intracranial pressure. The main cause of optic nerve head swelling is blockage of the axoplasma transport and the blockage occurs at the lamina cribrosa.
• The optic nerve head can swell to the extent where it is extended forward into the vitreous as well as laterally. This lateral swelling causes the retina to buckle inward at the temporal aspect of the optic nerve head. The buckling is know as Paton's lines or folds.

Sampaolesi line :

• Wavy line of Increased pigmentation anterior to Schwalbe's line.
• Occurs in

1. pseudoexfoliation syndrome
2. pigment dispersion syndrome
3. trauma
4. iris melanoma

Scheie's Line or Zentmayer's line :

• Pigment on lens equator and posterior capsule in pigment dispersion syndrome.
• Peripheral pigmentation of the posterior lens capsule anterior to the junction between the anterior hyaloid face and the posterior lens capsule (ligamentum hyaloideo-capsulare of Wieger)
• "Scheie's line" is considered to be pathognomonic for pigment dispersion syndrome.

Schwalbe's Line :

• Termination of Descemet's membrane .
• Line where corneal scleral meshwork terminates anteriorly .Delineates the outer limit of the corneal endothelium layer.

Stockers Line :

Corneal epithelial iron line at the edge of pterygium.

White lines of Vogt :

• Sheathed or sclerosed vessels seen in Lattice degeneration.
• Lattice degeneration of the retina is a fairly common degenerative disease of the peripheral retina characterized by the presence of lattice lines created by fibrosed blood vessels.
• Crisscrossing fine white lines that account for the name lattice degeneration are present in roughly only 10% of lesions and most likely represent hyalinized blood vessels.

Corneal Pigmentation – Decoded

 

Corneal Pigmentation

Type of Pigment	Name of Deposit	Disorder	Location in Cornea
Iron	Stocker’s line	Pterygium	Epithelium
	Hudson-Stahli line	In old age	Epithelium
	Ferry’s line	Filtering bleb	Epithelium
	Fleischer’s ring	Keratoconus	Epithelium
	Coat’s white ring	Previous Metallic foreign body injury	Bowman’s layer
		Siderosis	Stroma
		Blood staining of cornea	Stroma
Copper	Kayser-Fleischer ring	Wilsons’s Disease	Descement’s membrane
Melanin	Krukenberg’s spindle	Pigment dispersion syndrome	Endothelium
Silver		Argyrosis	Stroma
Gold		Chrysiasis	Stroma

Stockers line:

• Iron deposition line in the corneal epithelium, located at the corneal leading edge of a pterygium.
• present at the leading edge of non-growing pterygium
• yellow to golden brown.

Hudson-stahli line:

• Iron deposition line in the corneal epithelium, which commonly seen in the junction between middle and lower third cornea (corresponding to the line of lid closure).
• Often seen in elderly.
• bilateral & symmetric
• Causes no symptoms or clinical significance.

Ferry’s line:

• Seen in front of filtering bleb in glaucoma.
• Filtering bleb is a blister of conjunctiva resulting from glaucoma surgery by which a flap of sclera is created in the eye wall, allowing aqueous humor to percolate out of the eye and underneath the conjunctiva, thus lowering intraocular pressure. To know more about it, check this MedRounds link.

Coat's White Ring:

• A form of iron deposit at the level of Bowman's layer.
• Clinical features:
  • Asymptomatic
  • Small, granular, oval white ring
  • Commonly associated with previous corneal foreign body injury
• Requires no treatment.

Fleischer Ring :

• Partial or complete iron deposition ring in deep epithelium encircling the base of the cone.
• Formed when hemosiderin (iron) pigment is deposited deep in the epithelium
• Characteristic in eyes with keratoconus.

Kayser-Fleischer ring:

• Deposits of copper producing golden-brown discoloration in the peripheral cornea. Their earliest appearance consists of colored crescents at the superior and inferior quadrants of the cornea that eventually become circumferential.
• The Kayser-Fleischer ring is the single most important diagnostic sign in Wilson's disease
• It is found in 95% of patients.
• Virtually all patients with Kayser-Fleischer rings have neurological manifestations.
• Diseases associated with Kayser-Fleischer rings

1. Wilson's disease
2. primary biliary cirrhosis
3. chronic cholestasis
4. cryptogenic cirrhosis

Krukenberg’s spindle:

• a vertically oriented deposition of pigment on the posterior endothelial surface of cornea.
• Seen in Pigment dispersion syndrome.
• In Pigment dispersion syndrome, the iris is bowed posteriorly causing it to rub against the lens zonules. this results in the loss of pigment epithelium& hence the transillumination and the endothelium deposition of pigment. The vertical orientation of pigment is due to conventional current.
• Pigment granule accumulation in the trabecular meshwork then leads to progressive trabecular dysfunction and ocular hypertension with or without associated glaucomatous optic neuropathy.About 1/3 of them develop pigmentary glaucoma.
• The classic triad of clinical signs of PDS consists of a

1. Krukenberg spindle,
2. slit-like, radial, mid-peripheral iris transillumination defects, and
3. pigment deposition on the trabecular meshwork (Sampaolesi’s line)