Endometriosis
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Endometriosis
Definition
Endometriosis is a common chronic inflammatory condition defined by the presence of endometrial glands and stroma in extrauterine locations. It affects an estimated 5-10% of women of reproductive age and is found in nearly half of women with infertility.
- Bailey and Love's Short Practice of Surgery, 28th Ed.
- Robbins & Kumar Basic Pathology
Types
Three distinct subtypes are recognized:
| Type | Description |
|---|---|
| Superficial peritoneal endometriosis | Small implants on serosal/peritoneal surfaces |
| Ovarian endometriosis (endometriomas) | Cystic lesions filled with old blood ("chocolate cysts"); reported in 17-44% of cases |
| Deep infiltrating endometriosis | Tissue >5 mm beneath the peritoneum; involves uterosacral ligaments, vagina, bowel, bladder, ureters |
Risk of malignant transformation is mainly confined to the deep infiltrating type.
Pathogenesis
The exact mechanism remains elusive. Four leading theories are proposed:
Pathogenesis of endometriosis - Robbins & Kumar Basic Pathology, Fig. 17.9
- Regurgitation theory (most widely accepted): retrograde flow of menstrual endometrium through the fallopian tube implants at ectopic pelvic sites.
- Benign metastasis theory: endometrial tissue spreads to distant sites (bone, lung, brain) via blood vessels and lymphatics.
- Metaplastic theory: coelomic epithelium (mesothelium) undergoes metaplasia into endometrial tissue - explains extraperitoneal sites.
- Extrauterine stem/progenitor cell theory: bone marrow-derived stem cells differentiate into endometrial tissue.
Why implants persist
Endometriotic stromal cells produce high levels of aromatase, leading to increased local estrogen synthesis from androgens - creating a self-sustaining estrogen-rich microenvironment. Implants also express elevated PGE2, VEGF, and MMPs, partly released by recruited macrophages (via COX-2), promoting survival, angiogenesis, and invasion.
Sites of Involvement
Common pelvic sites:
- Ovaries (most common)
- Pouch of Douglas
- Uterosacral ligaments
- Fallopian tubes
- Peritoneum / pelvic sidewall
Extrapelvic sites (less common):
- GI tract: sigmoid colon and small bowel loops in 12-37% of cases; cecum also affected
- Bladder, ureters
- Lungs (causing catamenial hemoptysis or recurrent pneumothoraces at time of menstruation)
- Periumbilical tissues, laparotomy scars
- Rarely: bone, brain
Gross and Microscopic Appearance
Typical ("powder burn") lesions:
- Black, dark brown, or bluish puckered nodules on ovaries, serosal surfaces, and peritoneum
- Represent old hemorrhage surrounded by fibrosis
Atypical / "subtle" lesions:
- Red implants (petechial, vesicular, polypoid, red flame-like)
- Serous or clear vesicles
- White plaques/scarring
- Yellow-brown peritoneal discoloration
Endometriomas ("chocolate cysts"):
Ovarian endometrioma - Robbins & Kumar Basic Pathology, Fig. 17.10
- Cystic masses 3-5 cm in diameter, filled with thick dark brown fluid ("tar-like")
- Densely adherent to peritoneum of the ovarian fossa, fallopian tube, and posterolateral uterus
- Distinguishable from simple hemorrhagic ovarian cysts by their adherence pattern
Microscopically: functioning endometrial glands + stroma undergoing cyclic bleeding, with hemosiderin deposition and fibrous adhesions. Diagnosis requires both glands and stroma at ectopic sites.
Clinical Features
Cardinal symptoms (the "4 Ds"):
- Dysmenorrhea - pain related to menstruation (most common symptom)
- Dyspareunia - deep pain during intercourse
- Dyschezia - pain on defecation (with bowel involvement)
- Dysuria - pain on urination (with bladder involvement)
Other symptoms:
- Chronic pelvic pain (cyclical and non-cyclical)
- Infertility - presenting complaint in 30-40% of patients
- Fatigue
- Rectal bleeding (haematochezia), hematuria
- A significant proportion remain asymptomatic
Important caveat: There is little correlation between the extent/severity of disease on classification systems and the type or severity of symptoms experienced.
Diagnosis
Gold standard: Laparoscopy with histological confirmation
Non-invasive imaging:
- Transvaginal/transrectal ultrasound: reliable only for severe forms (endometriomas, deep pelvic endometriosis)
- MRI: can detect hemosiderin deposits in abdominal organs; demonstrates low-signal fibrotic plaques; increasingly used for deep disease
MRI pelvis - deep rectovaginal endometriosis obliterating the pouch of Douglas - Grainger & Allison's Diagnostic Radiology
- Sigmoidoscopy: useful for assessing level of bowel involvement; distance of rectal lesion from anal verge affects surgical planning (lesions 5-8 cm from the anal verge carry higher risk of anastomotic leak)
- Serum CA-125 is neither sensitive nor specific enough for routine diagnosis
Management
Medical (hormonal suppression - estrogen-dependent disease)
| Drug Class | Examples | Mechanism |
|---|---|---|
| Combined OCP | Ethinylestradiol/levonorgestrel | Suppresses ovulation, induces pseudopregnancy |
| Progestogens | Norethisterone, Medroxyprogesterone, Levonorgestrel IUS | Decidualization and atrophy of implants |
| GnRH agonists | Leuprorelin, Goserelin | Medical castration; hypoestrogenic state |
| GnRH antagonists | Elagolix | Rapid FSH/LH suppression |
| Danazol | Synthetic androgen/antigonadotropin | Androgenic/anabolic state, suppresses LH surge |
| COX-2 inhibitors | Celecoxib | Reduce PGE2, anti-inflammatory |
| Aromatase inhibitors | Letrozole, Anastrozole | Block local estrogen production in implants |
All medical treatments are suppressive, not curative - symptoms typically return after stopping treatment.
Surgical
Indications: failed medical therapy, desire for fertility, severe or deep disease, diagnostic uncertainty
- Conservative surgery (laparoscopy): excision or ablation of endometriotic lesions, lysis of adhesions, cystectomy for endometriomas - preferred approach for fertility preservation
- Bowel surgery: segmental resection, rectal shaving, disc excision for deep bowel endometriosis; low rectal lesions (5-8 cm from anal verge) carry higher risk of anastomotic leak and transient neurogenic bladder dysfunction
- Definitive surgery: hysterectomy ± bilateral salpingo-oophorectomy for women who have completed their families with severe refractory disease
Complications
- Infertility (mechanism: adhesions distorting tubo-ovarian anatomy, impaired folliculogenesis, altered peritoneal environment)
- Extensive fibrous adhesions obliterating the pouch of Douglas
- Bowel obstruction / ureteral obstruction
- Malignant transformation - rare; mainly from deep infiltrating endometriosis (clear cell and endometrioid carcinomas)
- Recurrent pneumothorax / catamenial hemoptysis (thoracic endometriosis)
Recent Evidence (2024-2026)
Three recent systematic reviews are worth noting:
- Fibrosis in endometriosis (PMID 39067455): A 2024 systematic review in Human Reproduction Update identifies fibrosis as a key driver of deep infiltrating endometriosis and pain - a potential therapeutic target beyond hormonal suppression.
- Diagnosis delay (PMID 39373298): A 2025 systematic review in BJOG confirms persistent diagnostic delays of 6-8+ years globally, with significant regional variation - underscoring the importance of clinical suspicion.
- Exercise and physical activity (PMID 39946383): A 2025 meta-analysis finds physical activity reduces pain and improves quality of life in women with endometriosis, supporting its role as an adjunct to medical/surgical care.
Sources: Bailey and Love's Short Practice of Surgery (28th Ed.) | Robbins & Kumar Basic Pathology | Grainger & Allison's Diagnostic Radiology
In detail acute congestive glaucoma for opthalmology Final mbbs?students
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Acute Congestive Glaucoma (Acute Primary Angle-Closure Glaucoma)
Ocular Emergency - requires immediate treatment to prevent permanent blindness
Definition
Acute congestive glaucoma (now formally called Acute Primary Angle Closure - APAC) is a sudden, dramatic rise in intraocular pressure (IOP) caused by occlusion of the trabecular meshwork by the peripheral iris (iridotrabecular contact - ITC), which obstructs aqueous outflow. It was historically called "acute glaucoma" and remains the classic ophthalmic emergency tested in Final MBBS.
- Kanski's Clinical Ophthalmology, 10th Ed.
Aqueous Humor Physiology (Essential Background)
Aqueous humor is produced by the ciliary processes, passes from the posterior chamber → anterior chamber through the pupillary aperture, then drains through the trabecular meshwork → Canal of Schlemm → episcleral veins.
Normal IOP = 10-20 mmHg. Any obstruction to outflow raises IOP dramatically.
Anatomy of the Angle - Shaffer Grading System
Shaffer angle grading - Kanski's Clinical Ophthalmology, Fig. 11.31
| Grade | Angle (degrees) | Visible Structures | Clinical Significance |
|---|---|---|---|
| 4 | 35-45° | Ciliary body visible | Widest; typical in myopia |
| 3 | 25-35° | Scleral spur visible | Open - incapable of closure |
| 2 | 20° | Trabeculum only, no scleral spur | Should undergo gonioscopy |
| 1 | 10° | Schwalbe line ± top of trabeculum | Very narrow - dangerously occludable |
| 0 | 0° | Iridocorneal contact | Closed |
Van Herick method (slit lamp): compares peripheral AC depth to corneal thickness - a space <1/4 corneal thickness = gonioscopy urgently needed.
Pathophysiology - Mechanism of Angle Closure
The relative pupillary block is the primary mechanism in most cases:
Anatomically predisposed eye (hypermetropic, short axial length, shallow AC)
↓
Posterior iris surface contacts anterior lens surface
↓
Aqueous CANNOT flow freely from posterior → anterior chamber
↓
Pressure builds in posterior chamber
↓
Peripheral iris bows FORWARD (iris bombé)
↓
Peripheral iris occludes trabecular meshwork
↓
Aqueous CANNOT drain → IOP rises rapidly to 50-80 mmHg
↓
Ischemia of cornea, iris, lens, optic nerve
Why pupillary mid-dilation is the danger zone:
- Miosis → iris taut → pulls away from lens → flow unblocked
- Mydriasis → iris folds peripherally → angle may open
- Mid-dilation (4-6 mm) → maximum lens-iris contact area → maximum block
Predisposing Factors (Risk Factors)
| Factor | Detail |
|---|---|
| Refractive error | Hypermetropia (short axial length, shallow AC) - most common |
| Age | Elderly - lens increases in volume with age, displacing iris anteriorly |
| Sex | Females more commonly affected |
| Race | Particularly prevalent in Far Eastern and Indian Asians |
| Family history | Genetic factors important but poorly defined |
| Axial length | Short eyes (nanophthalmos <20 mm) - very high risk |
| Cataracts | Large lens → phacomorphic element |
Precipitating Factors
An attack is triggered by anything that produces pupillary mid-dilation or forward iris displacement:
- Dim lighting (cinema, watching TV in the dark) - physiological mydriasis
- Pharmacological mydriasis - atropine drops, cyclopentolate (e.g. during fundus examination - a key MBBS exam point)
- Systemic drugs: anticholinergics (antihistamines, antispasmodics), sympathomimetics, cold/flu remedies, motion sickness patches, inhalers
- Topiramate and other sulfonamide derivatives - cause ciliary body effusion pushing the lens-iris diaphragm forward
- Semi-prone reading position
- Acute emotional stress
- Rarely: pilocarpine (miosis-induced forward iris shift in certain eyes)
Clinical Features
Symptoms
| Symptom | Mechanism |
|---|---|
| Severe unilateral eye pain | Very high IOP → stretching of ocular coats |
| Periocular/brow pain | Referred pain via trigeminal nerve |
| Headache | IOP-mediated |
| Blurred vision | Corneal epithelial edema |
| Coloured halos around lights | Corneal epithelial edema diffracting light ("rainbow around lights") |
| Nausea and vomiting | Vagal reflex; may simulate acute abdomen |
| Redness | Circumcorneal injection |
Classic exam point: Nausea and vomiting can be so severe that the patient may present to a general physician with apparent abdominal pain, and the eye problem is missed. Always check the pupil.
Signs (APAC - the full examination findings)
Acute congestive glaucoma - mid-dilated vertically oval, non-reactive pupil with corneal haze - Kanski's Clinical Ophthalmology, Fig. 11.36
| Sign | Detail |
|---|---|
| Visual acuity | 6/60 to hand movements (HM) |
| IOP | Very high: 50-80 mmHg (can approach diastolic BP) |
| Conjunctiva | Violaceous circumcorneal (ciliary/pericorneal) injection |
| Cornea | Hazy, cloudy due to epithelial edema |
| Anterior chamber | Shallow + aqueous flare (protein-rich exudate) |
| Pupil | Mid-dilated, vertically oval, fixed/non-reactive - CLASSIC SIGN |
| Fellow eye | Typically shows an occludable angle (same anatomical predisposition) |
| Penlight test | Shadow on nasal side of iris when light shone from temporal side = shallow AC |
Acute angle-closure glaucoma - cloudy cornea, injected conjunctiva - Rosen's Emergency Medicine, Fig. 57.22
Sequelae After an Acute Attack (Post-Congestive Changes)
| Finding | Significance |
|---|---|
| Glaukomflecken | Small anterior subcapsular lens opacities - pathognomonic of previous acute attack; caused by ischemic necrosis of lens epithelium |
| Spiral-shaped iris atrophy | Sector iris atrophy from ischemia |
| Posterior synechiae | Adhesions between iris and lens |
| Corneal folds (Descemet membrane) | Residual corneal edema |
| Optic atrophy | Combined pallor and cupping from optic nerve ischemia |
| Peripheral anterior synechiae (PAS) | Permanent angle closure requiring surgery |
Investigations
- IOP measurement (tonometry - applanation/Tonopen): typically >30-80 mmHg
- Gonioscopy (gold standard for angle assessment): shows Grade 0-1 angle; confirms ITC; indentation gonioscopy distinguishes appositional from synechial closure
- Slit lamp examination: corneal edema, shallow AC, flare, pupil changes, glaukomflecken
- Penlight test: Oblique illumination - shallow AC casts a shadow on nasal iris
- Visual field testing: after acute phase
- Optic disc assessment: cupping, pallor
Differential Diagnosis
| Condition | Distinguishing Features |
|---|---|
| Acute iritis/uveitis | Miosed pupil (vs. mid-dilated), keratic precipitates, IOP normal/low, photophobia |
| Acute conjunctivitis | Discharge, normal vision, normal IOP, no corneal edema |
| Corneal ulcer | Staining with fluorescein, history of trauma/contact lens |
| Migraine | No red eye, no corneal edema, normal IOP, visual aura |
| Paroxysmal hemicrania | Autonomic symptoms, normal IOP |
| Cataracts | Painless, no acute red eye, gradual onset |
| Acute abdomen | Missed if vomiting dominating - ALWAYS examine the eyes |
Management
Immediate (Emergency) Treatment - Lower IOP Fast
Step 1: Reduce aqueous production
| Drug | Dose | Route | Mechanism |
|---|---|---|---|
| Acetazolamide (carbonic anhydrase inhibitor) | 500 mg IV (if IOP >50 mmHg) OR 500 mg oral (if IOP <50 mmHg) | IV / PO | Reduces aqueous secretion by ciliary epithelium |
| Timolol 0.5% (beta-blocker) | 1-2 drops | Topical | Reduces aqueous production |
| Apraclonidine 0.5%-1% (alpha-2 agonist) | 1 drop | Topical | Reduces aqueous production, mild increased outflow |
Step 2: Increase aqueous outflow / miose the pupil
| Drug | Dose | Route | Mechanism |
|---|---|---|---|
| Pilocarpine 2% | 1 drop to affected eye; repeat after 30 min. 1% to fellow eye | Topical | Miosis → pulls peripheral iris away from angle → opens drainage |
| Prednisolone 1% | 1 drop | Topical | Reduces intraocular inflammation |
Critical exam point: Pilocarpine should NOT be repeated if IOP remains >40 mmHg - ischemia of the iris sphincter impairs its action, it may exert a forward iris vector and excessive dosing carries systemic toxicity risk.
Step 3: Systemic osmotic agents (resistant cases)
| Drug | Dose | Route |
|---|---|---|
| Mannitol 20% | 1-2 g/kg IV over 1 hour | IV |
| Glycerol 50% | 1 g/kg | Oral |
| Isosorbide | 1-1.5 g/kg | Oral |
Also:
- Analgesia and antiemetic
- Patient lying supine helps aqueous lens-iris separation
Drug Summary Box (from Rosen's Emergency Medicine):
Drugs for acute glaucoma - Rosen's Emergency Medicine, Box 57.1
Definitive Treatment - Breaking the Anatomical Block
Laser Peripheral Iridotomy (LPI) - Treatment of Choice
- Creates a small full-thickness hole in the peripheral iris
- Equalizes pressure between posterior and anterior chambers
- Breaks the pupillary block mechanism
- Performed within 24-48 hours once the cornea has cleared (glycerol 50% drops can be used to clear corneal edema first)
- Bilateral - prophylactic LPI should be performed on the fellow eye as it has the same anatomical predisposition
Surgical Options (if laser fails or not available):
- Peripheral iridectomy (surgical - the historic gold standard before laser)
- Lens extraction (phacoemulsification + IOL) - deepens the AC, corrects hypermetropia, opens the angle; highly effective - EAGLE trial shows this may be preferred over LPI in eyes with early PACG
- Goniosynechialysis - to break peripheral anterior synechiae
- Trabeculectomy - if IOP remains elevated despite open angle
- Cyclodiode laser - cyclodestruction in refractory cases
- Paracentesis - effective emergency option but risk of lens damage; reserved for extreme cases
Subsequent / Follow-up Treatment
After IOP is controlled and cornea clears:
- Pilocarpine 2% four times daily to affected eye
- Pilocarpine 1% four times daily to fellow eye
- Topical steroids (prednisolone 1%) four times daily if acutely inflamed
- Continue timolol/apraclonidine as needed by IOP response
- Gonioscopy repeated to confirm angle is open
- Bilateral LPI performed electively once attack resolved
Contraindications to Remember
- Acetazolamide - contraindicated in sulfonamide allergy AND angle closure secondary to topiramate (sulfonamide derivative - giving acetazolamide worsens ciliary body effusion)
- Mannitol - contraindicated in cardiac failure, renal failure, pulmonary edema
- Pilocarpine not to be repeated when IOP >40 mmHg
MBBS Exam High-Yield Summary
| Feature | Key Fact |
|---|---|
| Most common cause | Hypermetropic middle-aged/elderly female |
| Mechanism | Relative pupillary block → iris bombé → angle closure |
| Classic precipitant | Pharmacological mydriasis (atropine, cyclopentolate, dark cinema) |
| IOP in attack | 50-80 mmHg |
| Pathognomonic sign | Mid-dilated vertically oval fixed pupil |
| Pathognomonic sequela | Glaukomflecken (anterior subcapsular lens opacities) |
| Gold standard investigation | Gonioscopy |
| First drug given | Acetazolamide 500 mg IV/oral |
| Miotic used | Pilocarpine 2% |
| Definitive treatment | Laser peripheral iridotomy |
| Fellow eye treatment | Prophylactic LPI (same anatomy, high risk) |
| Must not miss trap | Nausea/vomiting masking as acute abdomen - examine the eye |
| Race with highest prevalence | Far Eastern and Indian Asians |
Sources: Kanski's Clinical Ophthalmology - A Systematic Approach, 10th Ed. | Rosen's Emergency Medicine, 10th Ed. | Goldman-Cecil Medicine, International Ed.
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