Benign Breast Di

– Incidence begins during 2nd decade of life, peaks in the 4th/5th

INFLAMMATORY

–ACUTE MASTITIS:

  • Not to be mistaken for Inflammatory Breast CA, skin biopsy if suspicious.
  • Usually within first 3 months postpartum. Cellulitis, not affecting ducts.
  • Can progress to abscess and speticemia.
  • Improper latch vs. stress and sleep deprivation => lower immune status and inhibition of milk flow.

–GRANULOMATOUS MASTITIS

  • Foreign material, autoimmune (sarcoid or Wegener’s), Tuberculosis
  • Possible autoimmune response to retained and extravasated fat/protein-rich secretions in the duct
  • Complete surgical excision.
  • Silicone/paraffin for augmentaiton/reconstruction. => granulomatous rxn.
  • Multinucleated giant cells surround silicone => fibrosis and contractions

–MAMMARY DUCT ECTASIA

  • Periductal mastitis: seen in middle aged to elderly parous women => nipple discharge, palpable subareolar mass, noncyclical mastalgia, nipple inversion or traction.
  • SMoking implicated as risk factor.
  • Microcalcifications seen on mammography => mimim IDC.
  • Difference is in dilation of major ducts in subareolar region.  => calc from inspissation of luminal secretion.
  • Histology shows eosinophils and foamy histiocytes.

-ZUSKA-ATKINS (Recurring Subareolar Abscess)

  • Bacterial infection of breast => Draining cutaneous fistula from subareolar tissue, chronic pasty discharge from nipple, hx of recurrent abscess.
  • Squamous metaplasia of lactiferous ducts from smoking toxicity => keratin plugs => obstruction => rupture.
  • Complete excision upon drainage necessary.

FIBROCYSTIC CHANGE

  • Seen in 50% of women clinically; generally affects premenopausal women between 20 and 50 yrs old.
  • Multifocal, bilateral.
  • Presents with breast pain and tender nodularities in breasts
  • Pathogenesis: hormonal imbalance => estrogen predominance over progesterone.
  • Nonproliferative, proliferative without atypia, proliferative with atypia. 70% nonproliferative. 80% of patients with atypical hyperplasia will not develop invasive cancer in their lifetime.

–CYSTS

  • Cysts seen in 1/3 of women from 35-50 yo. Subclinical microcysts in 25%.
  • US or FNA needed to evaluate difference from solid mass clinically.
  • Derived from terminal duct lobular units.
  • Complex cyst has internal echoes or septations, irregular/thick walls, absent posterior enhancement.

–ADENOSIS

  • Increased density of glandular components, mostly involving lobular units.
  • Disordered acinar, myoepithelial and connective tissue elements.
  • Association with proliferative elements =>invasive breast cancer
  • Can be confused with tubular carcinoma, but differentiated by presence of basal lamina (laminin or type IV collagen stain)

EPTIHELIAL HYPERPLASIA

  • Breast ducts usually lined by two cuboidal layers, any more is regarded as epithelial hyperplasia. Mild is 3-4 cells layers, Moderate >4 layers.
  • No architectural distortion.  Overlapped uneven distribution of nuclei (mixture of cell types)
  • ATYPICAL Ductal Hyperplasia: mimic low grade ductal carcinoma in situ. Small, focal <2mm.  Detected on mammography with calcifications and found on biopsy. Patients have increased risk for invasive breast CA. CA within 10-15 years, but after 15 years risk decreases. Risk related to menopausal status. Consider chemoprevention.

RADIAL SCAR LESION

  • Pseudoinfiltrative lesions of uncertain significance.
  • Fibroelastic core with entrapped ducts, surrounded by radiating ducts with variable hyperplasia.
  • Excision b/c core biopsy may miss occult cancer. Mammographically similar to CA (spiculations) and leads to increased risk.

FIBROADENOMA

  • Most common lesion of breast. Peak incidence between 15 and 35.
  • Hormone dependent neoplasm that lcatates during pregnancy and involutes in perimenopause.
  • Association with oral contraceptives before age 20
  • Epstein-Barr virus association in immunosuppressed patients
  • Mobile, firm, nontender, palpable breast mass; unilateral.
  • Fibroadenomas in older women associated with CA; CA can be included in fibroadenoomatous tissue (complex)
  • Can manage conservatively, ?US guided cryo-ablation.

LIPOMA

  • Well circumscribed smooth or lobulated mass that is soft and usually  nontender.
  • FNA with fat cells.
  • F/U palpation in 6 months.
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GYN SURG: Urinary Tract Injury

INCIDENCE: 1% of women undergoing pelvic surgery. If not fixed intraoperatively => genitourinary fistula.

RISK FACTORS: distortion of anatomy, loss of planes

  • prior pelvic surgery, endometriosis, UT abnormalities (duplicated ureter, pelvic kidney – 1/500-3000 individuals), irradiation, obesity, large pelvic mass.
  • Prior C/S doubles to quadruples riks of UT injury.

ANATOMY

  • Ureters enter pelvis at the brim (Lateral to Medial), anterior to bifurcation of common iliacs. Descend into pelvis within peritoneal sheath (ureteric fold) attached to medial leaf of uterine broad ligament.
  • Inferior to internal cervical os, ureter passes under uterine arteries in the cardinal ligament. => pass along anterior fornix and enter posterior aspect of the bladder.
  • Bladder divided into dome and base. Base has urethra and trigone, including the ureters.

Primary Prevention

  • LIGATION OF OVARIAN VESSELS: open retroperitoneum to visualize ureter directly and palpate.  Ligate and divide round ligament to create an opening in the broad ligament => dissect laterally to external iliac. Dissect out ureter which should be anterior to common iliac (can be traced from external iliac). Palpate.
  • LIGATION OF UTERINE ARTERIES: Mobilize bladder form anterior cervix and displace inferiorly to shift ureters inferior to uterine arteries prior to clamping.

INTRAOPERATIVE EVALUATION

  • Cystoscopy > Visual inspection for urinary tract injury.
  • Require repair: transection, crush injury, ligation, kinking, cystotomy.
  • No clinical consequence: transmural bladder suture => absorption, abrasion
  • Routine intraoperative cystoscopy: reduced rate of injury postop. [systematic review]. Visual => underreporting. Observe for efflux of indigo carmine from both ureteral orifices.
  • COMPLICATIONS: cost, time, training, having to treat incidental findings or overtreating conditions that don’t require tx.
  • ACOG Rec: Perform intraop cysto for bladder and ureteral dmage after all prolapse or incontinence procedures where urinary tract at risk of injury. Consider for hysterectomy or oophorectomy patients with risk factors, i.e. endometriosis, pelvic irradiation hxs

SIGNS of INJURY

  • Bladder catheter seen, ureter proximity to clamp/suture/staple, urine in field, ongoing hematuria vs hematuria that clears (transient from insertion of catheter or retractor compression), gas in bladder catheter in LSC surgery.

INSPECTION

  • Ureter peristalsis is good for identification but not for test of integrity.
  • Intravenous/Intravesical dye:” good for pinpointing defects but false negative in case of bleed/leak into retroperitoneum.
  • INTRAVESICAL 200-500mL of methylene blue through the bladder catheter [No methylene blue IV b/c >7mg/kg leads to methemoglobinemia] => Consider TRIPLE LUMEN CATHETER: 1 for balloon, 2 for output, 3 for input.
  • INTRAVENOUS 2.5mL of 0.8% solution: put pt in reverse Trendelenberg to speed flow of dye. Can add 20mg Furosemide to pts w/out renal compromise. If blue urine, can be assured that at least 1 ureter is functioning.
  • Can consider prophylactic ureteral catheters for accurate palpation of ureters and prevention of kinking/scarring effect. Place with cystoscope.

CYSTOSCOPY

  • Intraabdominal operations: can consider repositioning patient from dorsal supine to lithotomy, but can also place scope through dome of bladder and tie the opening with a purse-string suture.
  • If in lithotomy position intraop, use self-retaining retractor that does not interfere with thighs (Bookwalter)
  • BOOKWALTER
  • URETEROGRAPHY also an option.

POSTOPERATIVE RECOGNITION of INJURY

  • Presentation within 2 weeks. Mean time to dx = 5.6 days.
  • Leak urine from vagina or abdmoinal incision, unilateral /bilat flank pain, hematuria, oliguria, anuria, abd pain/distension, N/V, Ileus, Fever.
  • Stasis or urine => pyelonephritis. Can be masked by post-op analgesics.
  • LAB EVAL: b/l obstruction leads to acute renal failure, unjilateral complete ureteral obstruction => Cr increase. Mean 0.8mg/dL increase above baseline Cr.

TREATMENT

  • Relieve pressure with ureteral stent.
  • Nephrostomy if operation must be delayed before complete repair
  • Reanastomosis in cases of crush, transection, or thermal injury [thermal injury from harmonic scalpel/electrosurgery => thermal spread from 2mm to 22mm]
  • Bladder dome management = expectant if small (i.e. <2mm injury from pneumoperitoneum needle)
  • If bladder injury <1cm, can repair or leave bladder catheter in for one week and allow to heal on its own.
  • Repair cystostomy with one or two layered runnning closure with absorbable suture.  One layer if <2cm.

NEUROGENIC BLADDER DYSFNXN

  • 9% of women have postoperative urinary retention
  • Treat with bladder catheterization => normal function returns within several days.
  • Results from perivesical dissection seen in radical hysterectomy with interruption of parasympathetic innervation due to resection of uterosacral and cardinal ligaments.
  • Operative trauma => edema and hematoma => problem with urine collection/micturition.
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Cysts of the Breast

19% incidence of macroscopic cysts on Autopsy.

27% incidental cysts among women with breast excision for cancer.

Cysts are lined by a single layer of epithelium: tall columan vs. flattened cells

  • Determines secretory status.
  • Aspiration does not eliminate cysts: they’re impalpable afterwards because they are less tense; decreased intracystic pressure =>laxity and merging into breast tissue of similar consistency.
  • Blood in cysts is pathognomonic for neoplasms

 

PATHOGENESIS

  • Apocrine epthelium in terminal ductal lobular unit: excess secretion and osmotic pull of secretion products => progressive dilation of terminal duct unit => microcyst.
  • Type1: active secretion to create intracellular fluid-like content. Low Na+, High K+. Higher pH (K+in, H+out). Tight junctions & secretory function.
  • Type2: extracellular fluid-like content. High Na+, Low K+. Loose junctions, Passive diffusion of contents.
  • Type 1: Cyst from secretion in excess of reabsorptive capacity => increased propensity towards cysts, increase in subsequent cancer risk.
  • Type 2: Obstruction of ductule draining lobule via periductal fibrosis seen in involution => kinking => back pressure and dilation.
  • Premenopausal etiology: hyperestrogenism.
  • Postmenopausal: ? Hormone replacement therapy => hyperestrogenism.

CLINICAL FEATURES

  • Frequently asymptomatic but can be painful when large, distending breast, or with leakage of fluid => chemical irritation.
  • 55% of cysts in L breast and 45% in right. Same as in Fibroadenoma.
  • 2/3rds of cysts in the upper outter quadrant. Cysts uncommon in lower half of breast => embryologic migration of breast tissue

AGE

  • Increased frequency from 35 years to 45 years. Rarely seen before age 30.
  • Rapid disappearance after menopause.
  • Rare cysts in elderly => think papillary tumor!

NATURAL HISTORY

  • Greater number of cysts, shorter interval to recurrence.
  • 1/8 new cysts detetd between mammographic screening incrase in size; 60% resolve in one year; 80% resolve in 4 years.

INVESTIGATION

  • US multiple, bilateral. Excess to those seen clinically/mammographically.
  • Rounded, ovoid; very similar characteristics clinically to a fibroadenoma. => Need for US.
  • Complex cyst => septations and inflammation.
  • Blood from a cyst can come from a traumatic tap vs. papillary tumor: differentiate by gross appearance of blood (old and profound vs bright stained)

DIFFERENTIAL

  • cystic form of fat necrosis
  • galactocele
  • cystic papillary tumors, adenoma, carcinoma.
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Analgesics in Pregnancy

ASPIRIN: potent prostaglandin inhibitor => possible premature closure ductus arteriosus, but NEVER seen with fetal echo studies
ACETAMINOPHEN: no association with anomalies (Pastore 1999, Thulstrup 1999)
NSAIDS: Ibuprofen, naproxen, ketoprofen
  • Indomethacin used as a tocolytic, but CAN result in constrction of fetal ductus arteriosus => pulmonay hypertension.  Also decreases urine output and amniotic fluid volume after prolonged use. Can be used to treat hydramnios.
  • Non-teratogenic; largely reversible fetal effects if used short term in 3rd trimester.
NARCOTICS: No association with fetal anomalies. Chronic ingestion associated with neonatal withdrawal.
MIGRAINE HA MEDICATION: Most rx for HA are vasoconstrictors
  • 1st Trimester Ergotamine: possible NTD;s
  • 3rd Trimester Ergotamine: fetal bradycardia from uterine contractions and decreased uterine blood flow
  • Sumatriptan: Vasoconstriction, but no effect on uterine vessels. Sumatriptan exposure Pregnancy Registry 2002 shows 3.8% incidence of diverse defects => similar to background rate.
From Williams Obstetrics (22nd Edition)
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Fallopian Tube Cancer

Incidence

  • Rare, more likely to be secondary to local mets.
  • Underestimated: primary for PAPILLARY SEROUS OV CA. Widespread dissemination (fimbriae => ovary => peritoneum).
  • Left and right involved with equal frequency
  • Mostly adenocarcinomas, specifically papillary serous => 50% poor differentiation at diag

Risk Factors

  • BRCA1/2 (up to 29x higher than gen pop)
  • Primary infertility is common (40-70% nulliparity)
  • PID, HPV, GC/CT, sterilization, hysterectomy are not RFs

Clinical Manifestation

  • Presentation btwn 50s-60s, vague complaints
  • LATZKO’S TRIAD (15%):
  • 1 Serosanguinous Vag Discharge (hydrops tubae profluens) => shrinkage of adnexal mass
  • 2 Pelvic Pain => peristalsis/distention of tube
  • 3 Pelvic Mass
  • Fallopian Tube CA pain > Ov CA pain => earlier presentation and stage
  • Abnl Pap smear, but negative w/u for endometrial/cervical CA

Diagnosis and Evaluation

  • Same as Ov CA, usually made post-operatively

Laboratory & Imaging

  • CA125 elevation
  • Pelvic US: neovascularization or ascites => malignancy
  • CT/PET only useful for potential mets if pt already has palpable/visualized mass.

Treatment

  • Same as Ov CA: Surg => Chemo
  • TAH/BSO, tumor debulking, full staging
  • Chemo: Paclitaxel and Carboplatin
  • Radiation not recommended 2/2 spread of disease to upper abdomen (excess morbidity)
  • Follow CA125

Prognosis

  • Survival correlated with Stage
  • Invasion of tubal wall
  • Recurrence outside pelvis within 2-3 years of dx

Posttx surveillance

  • First 2 YEARS: q2-4mo
  • s/p 2 YEARS: 3-6mo
  • s/p 5 YEARS: annually
  • CA125 at each visit , tx of elevation alone not valuable. Correlate with PET/CT/XR findings
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