Cervical/Vulvar/Vaginal Cancer

Cervical/Vulvar/Vaginal Cancer
By:Steve Remmenga, M.D.
The McClure L Smith Professor of Gynecologic Oncology
Division of Gynecologic Oncology, Department of OB/GYN
University of Nebraska Medical Center

Cervical Cancer

Cervical CA
* International estimates
Pap Smear
* With the advent of the Pap smear, the incidence of cervical cancer has dramatically declined

Cervical CA Etiology
* Cervical cancer is a sexually transmitted disease.
* HPV DNA is present in virtually all cases of cervical cancer and precursors.
* Some strains of HPV have a predilection to the genital tract and transmission is usually through sexual contact (16, 18 High Risk).
* Little understanding of why small subset of women are affected by HPV.
* HPV may be latent for many years before inducing cervical neoplasia.

Cervical CA Risk Factors
* Early age of intercourse
* Number of sexual partners
* Smoking
* Lower socioeconomic status
* High-risk male partner
* Other sexually transmitted diseases
* Up to 70% of the U.S. population is infected with HPV

Prevention
* Educate all providers, men and women regarding HPV and the link to cervical cancer.
* Adolescents are an especially high-risk group due to behavior and cervical biology.
* Delay onset of sexual intercourse.
* Condoms may help prevent sexually transmitted disease.

Screening Guidelines for the Early Detection of Cervical Cancer, American Cancer Society 2003
* Screening should begin approximately three years after a women begins having vaginal intercourse, but no later than 21 years of age.
* Screening should be done every year with regular Pap tests or every two years using liquid-based tests.
* At or after age 30, women who have had three normal test results in a row may get screened every 2-3 years. However, doctors may suggest a woman get screened more if she has certain risk factors, such as HIV infection or a weakened immune system.
* Women 70 and older who have had three or more consecutive Pap tests in the last ten years may choose to stop cervical cancer screening.
* Screening after a total hysterectomy (with removal of the cervix) is not necessary unless the surgery was done as a treatment for cervical cancer.

Pap Smear
* Single Pap false negative rate is 20%.
* The latency period from dysplasia to cancer of the cervix is variable.
* 50% of women with cervical cancer have never had a Pap smear.
* 25% of cases and 41% of deaths occur in women 65 years of age or older.

Symptoms of Invasion
* May be silent until advanced disease develops
* Post-coital bleeding
* Foul vaginal discharge
* Abnormal bleeding
* Pelvic pain
* Unilateral leg swelling or pain
* Pelvic mass
* Gross cervical lesion

Cell Type
* Squamous Cell Carcinoma 80-85%
* AdenoCarcinoma 15%
* Adenosquamous
* Others

Staging
* Clinical Staged Disease
o Physical Exam
o Blood Work
o Cystoscopy
o Proctoscopy
o IVP

Staging Cervical Cancer
* Stage I Confined to Cervix
Microscopic Disease
* Squamous carcinoma of the cervix that has <3mm invasion from the basement membrane
* The diagnosis must be based on a cone or hysterectomy specimen.
* No lymph-vascular invasion
* May be successfully treated with fertility preservation in selected patients
* These patients should all be referred for consultation.





Staging

* Stage III Lower 1/3 Vagina, Sidewall or ureteral involvement
* IIIA Lower 1/3 of Vagina
* IIIB Sidewall or Ureteral Involvement
* Stage IV Bladder, Rectal or Distal Spread
* IVA Bladder or Rectal Involvement
* IVB Distal Spread

Treatment of Early Disease
* Conization or simple hysterectomy (removal of the uterus) - microinvasive cancer
* Radical hysterectomy - removal of the uterus with its associated connective tissues, the upper vagina, and pelvic lymph nodes. Ovarian preservation is possible.
* Chemoradiation therapy

Advanced Disease
* Chemoradiation is the mainstay of treatment

What is Standard Therapy for
Stage IB2 - IVA Cervical Carcinoma?
* External beam pelvic radiation (4,000 to 6,000 cGy)
* Brachytherapy (8,000 to 8,500 cGy to Point A)
* I.V. Cisplatin chemotherapy

Symptoms of Recurrence
* Weight loss, fatigue and anorexia
* Abnormal vaginal bleeding
* Pelvic pain
* Unilateral leg swelling or pain
* Foul discharge
* Signs of distant metastases
* NOTE: must distinguish radiation side effects from recurrent cancer

Management of Recurrence
* Chemoradiation may be curative or palliative, especially in women who have not received prior radiation therapy.
* Isolated soft tissue recurrence may occasionally be treated by resection with long-term survival.
Topotecan in Recurrent Cervical Cancer – Overview of Phase II Studies
Reference Regimen Evaluable Prior CT ORR Median OS
Survival
By Treatment Group
Proportion Surviving
Vulvar Cancer
Vulvar Cancer Etiology
* Chronic inflammatory conditions and vulvar dystrophies are implicated in older patients
* Syphilis and lymphogranuloma venereum and granuloma inguinal
* HPV in younger patients
* Tobacco
* Paget’s Disease of Vulva
Symptoms
* Most patients are treated for “other” conditions
* 12 month or greater time from symptoms to diagnosis
* Pruritus
* Mass
* Pain
* Bleeding
* Ulceration
* Dysuria
* Discharge
* Groin Mass
* May look like:
o Raised
o Erythematous
o Ulcerated
o Condylomatous
o Nodular
* IF IT LOOKS ABNORMAL ON THE VULVA
* BIOPSY!
Tumor Spread
* Very Specific nodal spread pattern
* Direct Spread
* Hematogenous

Treatment
* Primarily Surgical
o Wide Local Excision
o Radical Excision
o Radical Vulvectomy with Inguinal Node Dissection
+ Unilateral
+ Bilateral
+ Possible Node Mapping, still investigational

* Local advanced may be treated with Radiation plus Chemosensitizer
* Positive Nodal Status
* Special Tumor
o Verrucous Carcinoma

Vulva 5 year survival
* Stage I 90
* Stage II 77
* Stage III 51
* Stage IV 18

Recurrence
* Local Recurrence in Vulva
o Reexcision or radiation and good prognosis if not in original site of tumor
o Poor prognosis if in original site
Melanoma
Melanoma Treatment
Clear Cell Carcinoma
Treatment

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Vulvar Lesions

Vulvar Lesions
Presentation by:Anna Mae Smith, MPAS, PA-C
Lock Haven University

Anatomy
* Mons pubis
* labia majora and minora
* clitoris
* vestibule
* urethral meatus
* It covers and protects the entrance to the vagina, vestibule, and urethra.

Vulvar Hygiene
* use mild, nondrying soap
* washing underwear with mild soap and rinsing well
* 100% cotton underwear
* avoid extra layers and tight slacks (unneeded medicines, tinted toilet tissue, all "feminine hygiene" products), excessive sweating without aeration, and public pools and hot tubs
* It is important to be keenly conscious of what "aggravates" the skin.
* A dermatologic cliche is to "dry wet lesions" (soaks and compresses) and "moisturize dry lesions" (creams and ointments).

Vulvar Cancer
* 4th most common site of gynecologic neoplasia
* Squamous neoplasia most common type of neplasia
* HPV (16,18) infections are most commonly associated with squamous cell changes of the vulva, vagina & cervix. However the vulva tends to be more resistant to oncogenesis

Histopathology of Vulvar Neoplasia
* Squamous
* Malignant melanoma
* Sarcoma
* Basal Cell
* Adenocarcinoma
* Paget’s Disease
* Undifferentiated


Classification of VIN
* VIN I - mild dysplasia with hyperplastic vulvar dystrophy with mild atypia
* VIN II - Moderate dysplasia, hyperplastic vulvar dystrophy with moderate atypia
* VIN III - Severe dysplasia, carcinoma in situ, Bowen’s Dz; hyperplastic vulvar dystrophy with severe stypia


Spread of vulvar Ca
* Local growth with extension to the perineum, anus, urethra, vagina & pelvic bone
* Lymphatics - inguinal & femoral nodes to the external iliac, common iliac, & para-aortic chains

Paget’s Disease
* presents with extreme pruritus and soreness, usually of long duration
* red or bright pink, desquamated, exzematoid areas among scattered, raised, white patches of hyperkeratosis
* borders are well demarcated and raised

Basal Cell Carcinoma
* very rare
* associated with a long history of pruritus
* occurs over the anterior two-thirds of the labia majora, with slightly elevated margins
* appears as condyloma
* does not respond to treatment for HPV

Invasive Squamous Cell Carcinoma
* occurs when a woman is in her 60s and 70s
* presents with ulceration, friability, or induration of surrounding tissues

Sarcoma
* occurs in women of all ages
* rapidly expanding, painful mass

Diethylstilbestrol (DES) Exposure
* used extensively in US during the 1940s and early 1950s to prevent miscarriage and premature births
* studies during the late 1950s proved its ineffectiveness
* DES use continued through 1971
* estimated 2 million women were exposed in utero

DES Exposure Sequelae
* structural changes
* vaginal adenosis shows columnar epithelium on or beneath the vaginal mucosa; it is self-limiting and gradually disappears
* clear-cell adenocarcinoma of the cervix or vagina may develop (incidence rises at age 15, and median age at diagnosis is 19 years
* increased incidences of:

Lesions
* Often present with prurutis
* Elevated above the skin
* Gray, white , red or pigmented
* May also look verrucous
* INVASIVE- all the above plus ulcerated & bleeding

Treatments
* Local - laser
* Invasive - total vulvectomy & nodes

Vulvar Lesions
* RED - neoplasm, inflammation, or atrophy
* Inflammation-
o Fungi - most common cause of red, nonulcerative, infectious lesion of the vulva
o Folliculitis - secondary to Staph. Aureus may cause painful, itchy vulva
Vulvar Lesions/ RED
* Noninfectious
* Vestibular adenitis
* Psoriasis
* Seborrheic Dermatitis

White Lesions/ Leukoplakia
* Hyperkeratosis
* Depigmentation
* Absolute or relative avascularity

Vulvar Dystrophy
* Benign epithelial disorders
* Lichen Sclerosis 70%, vulvar hyperplasia accounts for the rest
* Biopsy is mandatory of any white lesion!!!
* VIN - neoplastic, premalignant lesion

Depigmented disorders
* Vitiligo - inherited, autosomal dominant
* Often progressive & often associated with increased incidence of
o Addison’s disease
o Thyroiditis
o DM
o Lymphoma
o Pernicious anemia

Intertrigo
* Nonspecific hyperkeratotic epithelial reaction to inflammation in the skin folds

DARK Lesions
* Usually secondary to increase in melanocytes or melanin production
* Must biopsy any dark lesion of the vulva!
* Lentigo - most common - freckle - no malignant potential
* Nevi - moles. Localized collections of neural crest cells which are usually present from birth
* Asymptomatic and rarely become malignant
* 30% of all malignant melanomas develop from nevi
* Neoplasms
* Reactive Hyperpigmentation
* Seborrheic keratosis

Ulcerative Lesions
* VIRAL - HSV - 48 hrs to 7 days after initial contact
* Bacterial - Syphillis, Granuloma inguinal, pyoderma, cutaneous TB
* Inflammatory/noninfectious

Tumors < 1cm
* Inflammation - condyloma acuminata(HPV) Molluscum contagiosum
* Cysts- epidermal inclusion, vestibular gland, mesonephric duct
* Neoplasia - VIN, hemangioma, hidradenoma, neurofibroma, syringoma
* Other - Accessory breast tissue, acrocordon, endometriosis, Fox-Fordyce Dz., Pilonidal sinus
Tumors > 1 cm

* Inflammatory - Bartholin’s cyst/abscess, lymphogranuloma venereum
* Neoplasm - fibroma, lipoma, verrucous carcinoma, sq. cell carcinoma
* Hernia, Edema
* Hematoma
* Other - skin tag, epidermal cysts, neurofibromatosis, accessory breast tissue

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VULVODYNIA

VULVODYNIA
Clinical Aspects and Research Initiative
Presentation by:Gloria A. Bachmann, M.D. and Nidhi Gupta, M.D.
Women’s Health Institute, UMDNJ-Robert Wood Johnson Medical School


Defining Vulvodynia
The International Society for Study of Vulvovaginal Diseases (ISSVD) defines vulvodynia as ‘chronic vulvar discomfort, characterized by the woman’s complaint of burning, stinging, irritation or rawness’

Types of Vulvar Pain
* PAIN from an IDENTIFIABLE ETIOLOGY
* VULVODYNIA

Pain from an Identifiable Etiology
* Infections such as chronic vulvovaginitis caused by Candida or other pathogens
* Dermatoses and Dermatitis that involve the vulva such as Lichen Sclerosus, Lichen Planus, irritants and allergic dermatitis
* Vaginismus

Vulvodynia: Vulvar Vestibulitis Subtype
* Friedrich’s criteria diagnostic:
* 1. Severe pain on vestibular touch or attempted vaginal entry.
* 2. Tenderness to pressure localized within the vulvar vestibule
* 3. Physical findings confined to vestibular erythema of various degrees
* Pain is provoked and localized
* Commonly seen in women aged 50 years or less

Dysesthetic Vulvodynia Subtype
* Pain is constant and may be felt beyond the confines of vulvar vestibule
* Usually pain is unprovoked
* Diagnosed mainly in women who are peri- or postmenopausal

Vulvodynia: Prevalence Statistics
* Harvard-based study (n=16,000) estimates a 16% life time prevalence*
* UMDNJ-based study estimates:

Vulvodynia: Demographics
* Older data suggest the highest prevalence in white women
* Accounts for 10 million doctor visits/year
* Upwards of 14 million women are affected in their lifetime
* Recent data suggest Hispanic women 80% more likely to have vulvar pain than other racial groups

Etiology: Vulvar Vestibulitis Subtype
* Prior vulvovaginal Candidiasis
* Hypersensitivity to chemicals
* Human Papilloma virus infection
* High levels of urinary oxalates
* Neurological dysfunction

Candida Etiology: Vulvar Vestibulitis Subtype
* In 1989 Ashman and Ott proposed cross reaction between Candida albicans antigens and self-antigen in vulvovaginal tissue
* Affected tissue has locally elevated concentrations of inflammatory cells and pro-inflammatory cytokines
* These suggest a hyper-immune response, possibly from persistent antigen from the Candida

Proposed Etiologies: Vulvar Vestibulitis Subtype
* Calcium oxalate crystals in urine may act as irritant to the vulva
* Reduced estrogen receptor expression causing alteration in vulvar sensation*
* CNS etiology, similar to other regional pain syndromes

Proposed Inflammatory Etiology: Vulvar Vestibulitis Subtype
* An inflammatory event releases cytokines that sensitize nociceptors in the nerve fibers of the vulva*
* Increased intraepithelial nerve endings in vestibulitis patients have been reported. Prolonged neuronal firing sensitizes neurons in dorsal horn of spinal cord, with subsequent abnormal interpretation as pain from touch**

Etiology: Dysesthetic Vulvodynia Subtype
* Etiology not definitively known
* Childhood trauma and OCP’s possible contributors
* Sympathetic pain loops caused by repeated irritation/trauma leads to continuous vulvar symptoms*

Vulvodynia: Assessment of the Patient
* OB/GYN history
* Detailed pelvic exam to exclude pathology
* Vaginal culture (in selected cases)
* Pap smear

Vulvodynia: Assessment of the Patient

* Vaginal pH
* Urinanalysis for oxalate content (select cases)
* Biopsy of abnormal vulvar areas
* Psychosocial assessment

Vulvodynia: Assessment of Pain Intensity
Clinician Assessment:
* Q–tip test
* Vulvalagesiometer- A device developed at McGill University for nominal scale vulvar pain measurement*
* Vulvar Algesiometer- Developed by Curnow to quantify pain by nominal scale**

Vulvodynia: Assessment of Pain Intensity
Patient Assessment:
* McGill-Melzack Pain Questionnaire- 78 pain words grouped in 20 subclasses of 3-5 descriptive words*
* Subclasses are grouped in four sections, sensory, affective, evaluative and miscellaneous.
* Provides information on timeline, location and a quantitative measure of clinical pain.

Vulvodynia: Differential Diagnosis
Exclude other pain causes:

o Vaginitis, Candida, urethritis, interstitial cystitis, Herpes, Bartholin adenitis
o Vulvar Dermatoses and Dermatitis such as eczema
o Vaginismus, entry and deep dyspareunia
o Atrophic Vulvo-Vaginitis

Vulvodynia: Diagnosis
“Diagnosis made after thorough evaluation fails to identify pain etiology”

Vulvodynia: Management
Vulvar Vestibulitis Subtype:
* Non-Pharmacologic
* Pharmacologic
* Surgical

Dysesthetic Vulvodynia Subtype:
* Non-Pharmacologic- Not recommended
* Pharmacologic
* Surgical- Not recommended

NonPharmacologic Management: Vulvar Vestibulitis Subtype
* Patient education and counseling
* Physical therapy and biofeedback
* Life-style modification
* Application of ice and local anesthetics to the vulvar region as needed

NonPharmacologic Management: Vulvar Vestibulitis Subtype
Low Oxalate Diet
* Oxalate is a metabolic breakdown product from certain food types
* Oxalates excreted in urine as crystals
* Vulvar surface contact with oxalate crystals causes irritation and burning
* Low oxalate diet (with calcium citrate supplementation) may be beneficial

NonPharmacologic Management: Vulvar Vestibulitis Subtype
Calcium Citrate and the Low Oxalate Diet
* Surface electromyographic biofeedback data suggest persistent vulvar injury leads to chronic reflex pain, resulting in increased muscle tension*
* Pelvic floor muscle instability may be present
* If pelvic floor abnormalities present, physical therapy often beneficial

Biofeedback: Vulvar Vestibulitis Subtype
Physical Therapy: Vulvar Vestibulitis Subtype
* Physical therapy reduces muscle tension and spasm, decreasing pain levels by 40-60% *
* Physical therapist can retrain dysfunctional pelvic floor muscles

Physical Therapy: Vulvar Vestibulitis Subtype
Physical therapy components:
* Pelvic floor exercise
* Myofascial release
* Trigger point pressure
* Massage
Medical Management: Vulvar Vestibulitis Subtype
* Topical estrogens:
* Topical estrogen creams useful for women with thin vaginal epithelium and/or lose of vulvar adipose tissue
* Can be used with other pharmacologic agents
* Tricyclic antidepressants (Amitriptyline-10mg hs: dose up to 150mg daily)
* Fluconazole
* Gabapentin (anticonvulsant), Venlafaxine-efficacy not proven
* Selective serotonin receptor inhibitors (SSRIs)-efficacy not proven
* Corticosteroids: (topical and injections)
* Topical anesthetics (nitroglycerin & lidocaine)
* Alpha Interferon injections
* Capsaicin cream (immune response modifier)
* Excision of affected vulvar area to remove neural hyperplasia
* Surgery reserved for non- responders to conservative treatments
* Data suggest a success rate varying from 40-100%
* Long term data lacking
* Types: focal excision, vestibuloplasty, vestibulectomy and perineoplasty
* Vestibulectomy excises a U shaped area of the vestibule from 5mm lateral to the urethra and the posterior fourchette
* Perineoplasty excises the vestibule from below and lateral the urethral meatus to the anal canal with the vaginal mucosa undermined 1-2cm.

Pharmacologic Management: Dysesthetic Vulvodynia Subtype
* Amitriptyline: first line therapy
* Other tricyclic antidepressants- desipramine and imipramine-may be effective *
* Selective serotonin reuptake inhibitors efficacy not proven

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Pathology and Neoplasia

Pathology and Neoplasia

1. Describe the pathogenesis and epidemiology of the common nonmalignant neoplasms that affect the external and internal genitalia.
2. Describe the role of oncogenes in the pathogenesis of premalignant lesions of the external and internal genitalia.


Lesions of the Vulva
* Dermatological conditions
* VIN
* Condyloma acuminatum

Condyloma
* Nevus
* Psoriasis
* Seborrheic Dermatosis
* Hidradenitis Suppurativa
* Lichen planus
* Lichen Sclerosis
* Lichen Simplex Chronicus
* Urethral Diverticulum or Caruncle
* Cysts
* Trauma
* Vaginal intraepithelial neoplasia (VAIN)
* Condyloma
* Urethral Diverticulum
* Urethral Caruncle
* Dysontogenetic cysts
* VAIN

Lesions of the Cervix
* Polyps
* Nabothian Cysts-mucous retention cysts, translucent/opaque, caused by normal healing process or cervix
* Fibroids
* Cervical intraepithelial neoplasia (CIN)
* Condyloma
* CIN
* Polyps
* Fibroids

Lesions of the Uterus
* Intravenous leiomyomatosis
* Leiomyomatosis peritonealis disseminata
* Fibroids
* Adenomatoid Tumors
* Paratubal Cysts
* Functional cysts
* Theca lutein cysts
* Tumors
* Fibroma
* Dermoid (Mature Teratoma)
* Brenner’s Tumor (transitional cell tumor)

References
* Comprehensive Gynecology/ Morton A. Stenchever…et al. 4th edition. 2001.
* Precis: an update in obstetrics and gynecology. Gynecology 2nd edition. Oncology 2nd edition.
* Obstetrics and gynecology: principles for practice. Ling, Duff. 2000.
* Urogynecology and reconstructive pelvic surgery. Walters, Karram. 2nd edition. 1999.

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Amenorrhea

Amenorrhea
Presentation lecture by:Jean Amoura, MD, MSc

Amenorrhea
* Primary
o Absence of menses by age 16 with normal secondary sexual characteristics
o Absence of menses by age 14 without secondary sexual development
* Secondary
o Absence of menses for 6 months in a previously menstruating female

Events of Puberty
* Thelarche (breast development)
o Requires estrogen
* Pubarche/adrenarche (pubic hair development)
o Requires androgens
* Menarche
o Requires:
o GnRH from the hypothalamus
o FSH and LH from the pituitary
o Estrogen and progesterone from the ovaries
o Normal outflow tract

Are there secondary sexual characteristics?

Primary Amenorrhea
Think hypogonadism or hypogonadotropism
Amenorrhea with Immature Secondary Characteristics
FSH Serum level Low / normal / High
Hypogonadotropic
hypogonadism
Gonadal
dysgenesis

* Hypogonadism
* Enzyme deficiencies
* Kallmann’s syndrome, CNS tumors
* Irradiation
* Chemotherapy
* Galactosemia
* Hypogonadism (gonadal failure)
* Note: gonadotropins (FSH/LH) will be high, similar to menopause

Gonadal Dysgenesis
* Chromosomally abnormal
- Classic turner’s syndrome (45XO)
- Turner variants (45XO/46XX),(46X-abnormal X)
- Mixed gonadal dygenesis (45XO/46XY)
* Chromosomally normal
- 46XX (Pure gonadal dysgeneis)
- 46XY (Swyer’s syndrome)

Primary Amenorrhea with Immature Sexual Characteristics

* Hypogonadotropism
o Hypothalamic dysfunction
+ Kallmann syndrome
+ Anorexia nervosa
+ Space-occupying lesion of CNS
+ Marijuana use
o Pituitary damage (surgery/radiation)
o Constitutional delay

Are there secondary sexual characteristics?
* Is there normal development of secondary sexual characteristics?
* Think
o Pregnancy
o Mullerian anomaly
o Androgen insensitivity
* Mullerian Anomalies
o Mullerian agenesis (Mayer-Rokitansky-Kuster-Hauser syndrome)
o Imperforate hymen
o Transverse vaginal septum

Mayer-Rokitansky-Kuster-Hauser Syndrome (utero-vaginal agenesis)
* 15% of primary amenorrhea
* Normal secondary development & external female genitalia
* Normal female range testosterone level
* Absent uterus and upper vagina & normal ovaries
* Karyotype 46-XX
* 15-30% renal, skeletal and middle ear anomalies

Imperforate Hymen
Androgen Insensitivity
* Normal breasts but no sexual hair
* Normal looking female external genitalia
* Absent uterus and upper vagina
* Karyotype 46, XY
* Male range testosterone level
* Treatment : gonadectomy after puberty + HRT
* Evaluation
o Pregnancy test
o Physical exam to determine presence of uterus
o FSH
o Karyotype

Primary Amenorrhea
Secondary Amenorrhea
* Pregnancy!
* CNS disorders
* Pituitary gland
* Thyroid
* Ovary
* Uterus
* Systemic disorders
* CNS disorders
* Pituitary disorders
* Thyroid disorders
* Ovulation disorders
* Uterine abnormalities
* Drug-induced amenorrhea

Asherman’s Syndrome
Secondary Amenorrhea
Negative Pregnancy.test
TSH ,PROLACTIN, Progesterone challenge test
withdrawal bleeding
without withdrawal bleeding
hypoestrogenic
compromised outflow tract
* Treatment goals
* Sexually active, using condoms
* No recent change in weight, skin, hair
* Occasional heat intolerance
* No cyclic pain
* No gynecologic surgery
* Regular menses (every 28-30 days) prior to past year

* Exam
o Overweight
o No galactorrhea
o Normal hair distribution
o Normal pelvic exam
* Pregnancy test
* Progestin challenge, TSH, serum prolactin
* Estrogen/progestin cycle, FSH

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Chronic Pelvic Pain

Chronic Pelvic Pain
Presentation lecture by:Jennifer Griffin, MD
University of Nebraska Medical Center

Chronic Pelvic Pain
* Definition = Pain of apparent pelvic origin that has been present most of the time for 6 months
* Difficult to diagnose.
* Difficult to treat.
* Difficult to cure.
* =Physician and patient frustration.
Just because you’re a hammer doesn’t necessarily make every problem a nail.

* Gynecologic
* Gastrointestinal
* Urologic
* Musculoskeletal/ Pelvic Floor
* Psychological

Getting the History
* Nature of the Pain:
* Timing of the Pain:
* Modifying factors:

Review of Systems
* Gynecologic:
o Association with menses?
o Association with sexual activity? (be specific)
o New sexual partners/ practices?
o Symptoms of vaginal dryness / atrophy?
o Other changes in menses?
o Use of contraceptives?
o Childbirth history and any associations?
o History of pelvic infections?
o History of other gyn problems/ surgeries?

* Gastrointestinal:
o Regularity of bowel movements?
o Diarrhea/ constipation/ flatus?
o Relief with defecation?
o History of hemorrhoids/ fissures/ polyps?
o Blood in stools, melena, or mucous?
o Nausea, vomiting, or appetite change?
o Weight loss?

* Urologic:
o Pain with urination?
o History of frequent / recurrent UTIs?
o Blood in urine?
o Symptoms of urgency or incontinence?
o Difficulty voiding?

* Musculoskeletal:
o History of trauma?
o Association with back pain?
o Other chronic pain problems?
o Association with position or activity?

* Psychological:
o History of abuse (verbal/ physical/ sexual)?
o Diagnosis of psychiatric disease?
o Association with life stressors?
o Exacerbated by life stressors?
o Family/ spousal support?

* Diagnosis
o History and Physical
o Targeted imaging studies (U/S best for gyn evaluation)
o EMB/D&C
o Laparoscopy
o Cystoscopy/ Colonoscopy
o Physical therapy evaluation

* Gynecologic Origin
o Endometriosis
o Primary Dysmenorrhea
o Leiomyomas
o Dyspareunia
o Vaginismus
o Adenomyosis
o Infectious causes
o Pelvic congestion syndrome
o Pelvic organ immobility
o Cancer


* ACOG Practice


Gyn Causes

* Cyclic:
o Primary dysmenorrhea
o Endometriosis
o Adenomyosis
o Mittleschmertz
* Non-cyclic:
o Pelvic masses
o Adhesions
o Infections
o Non-gyn causes
* Related to intercourse:
o Endometriosis
o Vaginismus
o Vaginal atrophy
o Musculoskeletal
o Any non-cyclic cause could be exacerbated.

* Endometriosis
o 7-10% of women (up to 50% in premenopausal women)
o 33% of women undergoing laparoscopy for pelvic pain will be diagnosed with endometriosis
o Found in 38% of infertile women
o Family history increases risk 10x
o Significant cause of morbidity

Chronic Pelvic Pain: Cyclic
* Endometriosis: Etiology
o Retrograde menstruation
o Hematogenous/lymphatogenous
o Coelomic metaplasia
o Immunologic dysfunction

* Endometriosis: Classic Triad
o Dysmenorrhea
o Dyspareunia
o Infertility
* But may present with:
o Chronic pelvic pain
o Adnexal mass

* Endometriosis: Diagnosis
o Clinical suspicion
o Presence of endometrial glands in biopsy outside endometrial cavity
o Elevated CA-125 without evidence of other pathology
o Relief of pain with empiric GnRH agonist
o Laparoscopy
+ Multiple appearances: red, brown, scar, white, puckering, powder burn, adhesions, endometriomas
+ Multiple locations: ovary, uterosacral ligaments, cul-de-sac, rectovaginal septum, and others

* Endometriosis:
o Classification
o ASRM 1996

* Endometriosis: Treatment
o Laparoscopic removal/destruction
o NSAID’s
o OCP’s
o Danazol
o GnRH analogs x 6-12 months
o LUNA
o TAH-BSO
o Pain clinic/TENS units
o Presacral neurectomy

* Dysmenorrhea
o NSAID’s
o OCP’s
o Vitamins: B6, B1
o Mg++
o Omega-3-Fatty acids

* Leiomyomas
o Pressure
o Pain
o Degeneration
o Treatment:
+ NSAID’s
+ OCP’s
+ Lupron
+ Myomectomy
+ Hysterectomy

* Adenomyosis =endometrial glands within the myometrium

o Rarely diagnosed via ultrasound
o May be inferred with laparoscopy
o Will have complaints related to bleeding and pain.
o May be anemic.
o Definitive Dx and Tx: hysterectomy/pathology

* Dyspareunia
o Endometriosis
o Adnexal masses
o Vulvovaginitis
o Chronic endometritis
o Vaginal dryness
o Vaginal atrophy
o Obstetrical trauma
o Surgical scars
o Vaginismus

* Vaginismus
o Primary
o Secondary
o Treatment:

* Pelvic Floor Muscle Spasm and Strain
o Piriformis m.
o Coccygeus m.
o Levator ani m.
o Peripartum pelvic pain syndrome
o Treatment:

Chronic Pelvic Pain: Non-cyclic

* Pelvic congestion syndrome
* Pelvic organ immobility
* PID
* Infectious causes
* Gynecologic malignancies
* Other Gynecologic origin:
o IUD
o Intra-uterine, cervical polyps
o Ovulatory pain (Mittelschmerz)
o Ovarian retention/remnant syndrome
o Adhesions
o Adnexal cysts
o Pelvic relaxation

* Treatment of Gynecologic Problems
o Empathic listening
o Analgesics (preferably NSAID’s, avoid opioids)
o OTC products (Astroglide, Replens, KY)
o OCP’s
o Antibiotics
o Removal of IUD, polyps
o GnRH analogs
o Surgery (Destruction/removal lesions, adhesiolysis, LUNA, hysterectomy, presacral neurectomy etc)
o Biofeedback/PT
o Antidepressants and Psychotherapy
o Marital/partner counseling
o Massage
o Acupuncture
o Exercise

* Urologic Origin, Level A:
o Bladder malignancy
o Interstitial Cystitis
o Radiation Cystitis
o Urethral Syndrome

Chronic Pelvic Pain
* Bladder origin, Level B:
o Uninhibited Bladder Contractions (Detrusor dyssynergia)
o Urethral diverticulum

* Urologic origin, Level C:
o Chronic UTI
o Recurrent, acute UTI
o Urolithiasis
o Urethral caruncle
o Urologic evaluation:
+ Urinalysis
+ Urine culture
+ Urine cytology
+ Cystourethroscopy +/- hydrodistension
+ IVP

* Urologic origin: Interstitial Cystitis
o Urinary urgency/frequency
o Glomerulations
o Potassium chloride test
o Emuron
o Antihistamines
o Tricyclic antidepressants (Imipramine 25-50mg @ hs)
o Intravesical treatments: DMSO, BCG
o Avoidance of acidic foods

* Gastrointestinal Origin, Level A:
o Carcinoma of colon
o Constipation
o Inflammatory bowel disease
o Irritable Bowel Syndrome
* IBS

Chronic Pelvic Pain
* IBS Treatment
* Colon carcinoma
* Constipation
* Inflammatory Bowel Disease
* Gastrointestinal origin, Level C (no Level B):
* Musculoskeletal, Level A:
* Musculoskeletal origin, Level B:
* Musculoskeletal origin, Level C:
* Other Non-Gynecologic Origin, Level A:
* Psychological
* Other Non-Gynecologic origins, level B:
* Other Non-Gynecologic origin, Level C:
Clinical Pearl of Wisdom
Pelvic Pain Treatment Triad
6 Case Studies
* Conclusions:

Chronic Pelvic Pain.ppt

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PELVIC ORGAN PROLAPSE

PELVIC ORGAN PROLAPSE
Presentation lecture by:Neena Agarwala,M.D.
Laparoscopic Surgery & Urogynecology

Elements comprising the Pelvis
* Bones
o Ilium, ischium and pubis fusion
* Ligaments
* Muscles
o Obturator internis muscle
o Arcus tendineus levator ani or white line
o Levator ani muscles
o Urethral and anal sphincter muscles
* Endopelvic fascia
o Meshwork of collagen, elastin and smooth muscle
o Extends from the level of uterine artery to the fusion of the vagina and levator ani
o Attached to uterus is parametrium – cardinal-uterosacral ligament complex
o Attached to vagina is paracolpium – pubocervical and rectovaginal fasciae

Normal Vaginal Support Anatomy
* Bladder, upper two-third vagina and rectum lie in a horizontal axis
* Urethra, distal one-third vagina and anal canal are vertical in orientation
* Pelvic floor is horizontal and like a hammock – levator plate
* Levator ani muscles and perineal body support the vertical orientation

The axes of pelvic support
* Three support axes
* Upper vertical axis (cardinal-uterosacral ligament complex)
* Horizontal axis leads to lateral and paravaginal supports
o Two platforms pubocervical fascia and rectovaginal septum
* Lower vertical axis supports the lower third of the vagina, urethra and anal canal

DeLancey’s three levels of vaginal support
* Apical suspension
o Upper paracolpium suspends apex to pelvic walls and sacrum
o Damage results in prolapse of vaginal apex
* Midvaginal lateral attachment
o Vaginal attachment to arcus tendineus fascia and levator ani muscle fascia
o Pubocervical and rectovaginal fasciae support bladder and anterior rectum
o Avulsion results in cystocele or rectocele
* Distal perineal fusion
o Fusion of vagina to perineal membrane, body and levators
o Damage results in deficient perineal body or urethrocele

Fascial and Muscular layers of the Pelvic Floor
Attachments of cardinal/uterosacral ligaments
Perineum
External genital muscles and the Urogenital diaphragm
Pelvic Relaxation
* Cystocele
* Stress urinary incontinence
* Rectocele
* Enterocele
* Uterine and vaginal prolapse

Boat in dock analogy
* Boat- pelvic organs
* Water- levator muscles
* Moorings- Endopelvic fascial ligaments
* Problem is with the water or moorings or both
* Result is sinking of the boat
* Really the boat itself is fine

PROLAPSE

* Mutifactorial involving both neuromuscular and endopelvic fascial damage
* Relaxation of the tissues supporting the pelvic organs may cause downward displacement of one or more of these organs into the vagina, which may result in their protrusion through the vaginal introitus.

Factors promoting prolapse
* Erect posture causes increased stress on muscles, nerves and connective tissue
* Acute and chronic trauma of vaginal delivery
* Aging
* Estrogen deprivation
* Intrinsic collagen abnormalities
* Chronic increase in intraabdominal pressure

Clinical Evaluation
* Hormonal and neurologic evaluation
o Level of estrogenization
o Sensory and sacral reflex activity
* Quantitative site-specific assessment of pelvic floor components
o in lithotomy position, patient sitting
o at rest and with valsalva
o ability to contract levator and anal sphincter muscles

Patient position for evaluating pelvic floor defects
Anterior compartment defects
* Urethral hypermobility
* Cystocele
Evaluation of a cystourethrocele
Posterior compartment defects
Rectocele
Evaluation of a rectocele
Apical defects
Uterine prolapse
Complete Uterovaginal procidentia
Complete genital procidentia
Enterocele
Principles of reconstructive pelvic surgery
Conservative treatments

PELVIC ORGAN PROLAPSE.ppt

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Complications of Early Pregnancy & Pregnancy Loss

Complications of Early Pregnancy & Pregnancy Loss
Presenttaion by: Dotun Ogunyemi, MD

TOPICS
• Spontaneous abortions :
pregnancy
termination prior to 20 weeks' gestation or
less than 500-g birthweight
• Congenital abnormalities
• Chromosomal abnormalities
• Hyperemesis gravidarum
• Ectopic pregnancy: extra-uterine
gestation
• Gestational trophoblastic disease

OBJECTIVES
• To be aware of the different types and
causes of abortions
• To understand the causes and risks
factor of birth defects
• To obtain knowledge on types of
abnormal early pregnancy
• To be aware of the effects of severe
vomiting in early pregnancy

Threatened Abortion
• Bleeding through a closed cervix in first half of
pregnancy
• Bleeding of expected menses, decidual reaction,
Cervical lesions
• No effective therapy
• Half will abort
• Increased risk for preterm delivery, low birthweight,
& perinatal death
• Vaginal sonography, serial serum quantitative
human chorionic gonadotropin (hCG) levels, serum
progesterone values
• Anti-D immunoglobulin because up to 5 % of D-
negative women become isoimmunized

Inevitable Abortion
• Leaking amniotic fluid
• Cervical dilatation
• Heavy bleeding
• Severe pain
• Impending abortion
• Risk of incomplete abortion or sepsis
• Uterine evacuation

Incomplete Abortion
• Partial expulsion with retained products
of conception (POC)
• Open internal cervical os, bleeding,
• Ultrasound or pelvic exam shows POC
• Hemorrhage, Sepsis
• Uterine evacuation
• Complete Abortion
• Closed internal cervical os
• Ultrasound = Normal endometrial stripe

Missed Abortion
• Dead products of concept is
retained inside uterus
• Maybe associated with
coagulation defects
• Expectant, medical or surgical
management

Recurrent Abortion
• 3 or more consecutive spontaneous
abortions
• Risk of 1 loss = 10-15 %,
• Risk of 2 losses = 2.3 %
• Risk of 2 losses = 0.34 %
• Parental cytogenetic analysis
• Antiphospholipid antibodies
• If previous liveborn; risk for subsequent
abortion was 30 %.
• If no liveborn, the risk of subsequent
abortion was 46 %

Frequency of chromosomal anomalies in abortuses & stillbirths.
First- and second-trimester spontaneous abortions
by maternal age.
Findings in Abortuses
Abnormality not specified
Sex chromosome polysomy
Mosaic trisomy
Autosomal monosomy G
Others—XXY, monosomy 21
Triple trisomy
Double trisomy
Structural anomaly
Tetraploidy
Triploidy
Monosomy X (45,X)
Autosomal trisomy
Abnormal (aneuploid)
Normal (euploid), 46,XY& 46,XX

Chromosomal Studies
Incidence in Percent
Chromosomal Findings in Abortuses

Etiology ofAbortions
FETAL
Abnormal Zygotic
Development (40%)
Aneuploid Abortion (50%)
MATERNAL: Systemic
Infections
Chronic Diseases
Tuberculosis
carcinomatosis.
Celiac sprue
MATERNAL: ENDOCRINE
Hypothyroidism
Diabetes Mellitus
Progesterone Deficiency
MATERNAL: Environment
Tobacco Alcohol
Caffeine
Radiation
intrauterine devices failure
anesthetic gases
MATERNAL: Systemic
Antiphospholipid
antibodies
Inherited Thrombophilia
MATERNAL: Local
Uterine leiomyomas
Asherman syndrome
Müllerian duct defects
DES offsprings
Incompetent Cervix
Physical Trauma
PATERNAL
FACTORS

Cervical Incompetence
• Painless cervical dilatation in 2nd
trimester, with prolapse and ballooning of
membranes into the vagina, followed by
expulsion of an immature fetus.
• Transvaginal ultrasound cervical length &
funneling
• Previous trauma to the cervix—dilatation
and curettage, conization, cauterization, or
amputation, delivery
• Abnormal cervical development,
diethylstilbestrol
• McDonald cerclage or Shirodkar cerclage

McDonald cerclage

Abortion Techniques
Medical Techniques
Intravenous oxytocin
Intra-amnionic hyperosmotic
fluid saline or urea
Prostaglandins
Intra-amnionic injection
Extraovular injection
Vaginal insertion
Parenteral injection
Oral ingestion
Antiprogesterones—RU 486
(mifepristone) & epostane
Methotrexate—intramuscular
& oral
Various combinations
Surgical techniques
Cervical dilatation
followed by uterine
evacuation
Curettage
Vacuum aspiration
(suction curettage)
Dilatation and
evacuation(D & E)
Dilatation and
extraction (D & X)
Menstrual aspiration
Laparotomy:
Hysterotomy
Hysterectomy

Septic Abortion
• Criminal abortion Spontaneous abortion
• Legal elective abortion
• Anaerobic bacteria; coliforms, Haemophilus
influenzae, Campylobacter jejuni, group A
streptococcus
• COMPLICATIONS:
• Severe hemorrhage
Bacterial shock
• Acute renal failure
Uterine infection
• Parametritis
Peritonitis
• Endocarditis
Septicemia
• DIC
Infertility
• TREATMENT:
• supportive care; antimicrobials & evacuation

Hyperemesis gravidarum (HEG)
• Nausea and vomiting occurs in 50-90% of
pregnancies (morning sickness)
• HEG =persistent nausea & vomiting
associated with ketosis and weight loss (>5%
of prepregnancy weight)
• ETIOLOGY
• Unknown
psychological,
• sociocultural factors,
HCG levels,
• estradiol levels,
gastric dysrhythmias
• Vestibular and olfaction dysfunction

HEG: Risk Factors
• Hyperthyroid disorders
Psychiatric d
• Previous molar disease
Gastrointestinal d.
• Pre-gestational diabetes
Asthma
• Female fetuses
Multiple fetuses
• Occupational status
Fetal anomalies
• Increased body weight
Infertility
• Nausea & vomiting in a prior pregnancy
• Prior intolerance to oral contraceptives.
• Maternal smoking & older maternal age
decreased risk.
• DIAGNOSIS OF EXCLUSION.

HEG treatment & outcome
• Intravenous fluids
Diet
• Anti-histamines
Vitamin B6
• Anti-emetics
Ginger
• Promotility agents
Parenteral Nutrition
• if low pregnancy weight gain, increased risks
of:
• Low birth weight,
• Small for gestational age,
• Preterm delivery
• 5-minute Apgar <7.

Congenital abnormalities
• Malformation: "programmed" to develop
abnormally; thus intrinsically genetically
abnormal.
• Deformation: a genetically normal structure
develops an abnormal shape because of
mechanical forces imposed by the uterine
environment
• Disruption: severe change in form or
function when genetically normal tissue is
modified due to a specific insult
• Phenocopies

Spina bifida
anencephaly

omphalocele
gastroschisis

Endocardial cushion defect
Hypoplastic Left Heart
4 chambered heart

Teratology
• Dose:
• No effect at low dose,
• Organ effect at immediate dose
• Severe effect/abortion at high dose
• Timing:
• Up to 2 weeks gestation: all or none effect
• 3-8 weeks gestation is period of
organogenesis when can birth defects occur
• After 4
th
month usually decreased growth

Oligohydramnios, growth restriction, limb
shortening, maldevelopment of calvarium
ACE Inhibitors = renal
ischemia,
Microcephaly & severe brain damage
Methyl Mercury:
neuronal
& cell division migration
skull defects, cutis aplasia, porencephaly,
subependymal/periventricular cysts, ileal
atresia, cardiac anomalies; visceral infarcts
Cocaine: vascular
disruption
ileal atresia; hydrocephaly, hand defects,
microcephaly, omphalocele, gastroschisis,
cleft lip/ palate,
Tobacco: vascular
disruption
Phocomelia; Limb-reduction defects
Thalidomide
dysmorphogenesis/disruption
CNS & skeleton defects

Antifungals
vaginal clear-cell adenocarcinoma,adenosis,
cervix/vagina defects, hypospadias
Diethylstilbestrol (DES)
25%
Ear defects, cardiac outflow tract defects ,
hydrocephaly system, & thymus aplasia
Isoretinoin

Clefts, cardiac anomalies, urinary tract
malformations
Phenobarbital 10–20%
Neural-tube defects
Carbamazepine
Valproate 1–2%
Fetal hydantoin syndrome: craniofacial
anomalies, fingernail hypoplasia, growth
deficiency, developmental delay, cardiac
defects, facial clefts
Phenytoin 5–11%
accumulation in fetal tissues of
free oxide radicals, with
toxic,carcinogenic, mutagenic
effects.
Fetal warfarin syndrome: nasal & midface
hypoplasia; stippled vertebral and femoral
epiphyses.
Dorsal CNS dysplasia, mental retardation
Coumarin: 9%
inhibiting
posttranslational carboxylation
of coagulation proteins.
hemorrhage leading
to disharmonic growth and
deformation from scarring
IUGR, craniosynostosis , microcephaly,
limb abnormalities
Anti-neoplastic drugs
Fetal alcohol syndrome: Craniofacial
anomalies; Cardiac defects; Behavior
disturbances, Failure to thrive, ADD
Alcohol

Fetal alcohol syndrome. A. At 2 ½ years. B, C. At 12 years. Note persistence of short palpebral fissures
Fetal alcohol syndrome

Toxoplasmosis
Syphilis
Rubella
CMV
HSV
Varicella
Congenital Infections

Intracranial
Infections
Hydrops: Features
Scalp edema
Ascites
Dilated ventricles with
bilateral perventricular
calcifications (arrows)
Congenital Infections
Hepatomegaly,
Splenomegaly

ANEUPLOIDY
• Trisomy: extra chromosome nondisjunction
of meiosis I increases with maternal age
• Only autosomal trisomies 13, 18, and 21
result in viable term pregnancies
• Monosomy: missing a chromosome
monosomy X,
• Polyploidy: number of haploid chromosomal
complements hydatidiform mole fertilization
of one egg by two sperm
This is 45 slides presentation in pdf format

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Abnormal Uterine Bleeding

Abnormal Uterine Bleeding
Presentation by:Lloyd Holm, D.O., FACOG
Associate Professor
Department of Obstetrics and Gynecology
University of Nebraska Medical Center

Abnormal Uterine Bleeding
* Definitions
* Etiologies
* Evaluation and workup
* Case presentation
* Management and options

Definitions
Normal
abnormal
Average blood loss with menstruation
Definitions
Menorrhagia
Prolonged
Synonymous with hypermenorrhea
Metrorrhagia
Oligomenorrhea:
Amenorrhea
Etiologies
* Organic
o Systemic
o Reproductive tract disease
o Iatrogenic
* Dysfunctional
o Ovulatory
o Anovulatory

Systemic Etiologies
* Coagulation defects
* Leukemia
* ITP
* Thyroid dysfunction

Most Common Causes of Reproductive Tract AUB
Reproductive Tract Causes
* Gestational events
* Malignancies
* Benign
o Atrophy
o Leiomyoma
o Polyps
o Cervical lesions
o Foreign body
o Infections
* Gestational events
o Abortions
o Ectopic pregnancies
o Trophoblastic disease
o IUP
* Malignancies
o Endometrial
o Ovarian
o Cervical
Incidence of Endometrial Cancer in Premenopausal Women
Reproductive Tract Causes of Benign Origin
* Atrophy
* Leiomyoma
* Polyps
* Cervical lesions
* Foreign body
* Infection

Proposed Etiologies of Menorrhagia with Leiomyoma
* Increased vessel number
* Increased endometrial surface area
* Impeded uterine contraction with menstruation
* Clotting less efficient locally

Leiomyoma in any location is associated with increased risks of gushing or high pad/tampon use.
Iatrogenic Causes of AUB
* Intra-uterine device
* Oral and injectable steroids
* Psychotropic drugs
To determine if DUB is ovulatory or anovulatory
Evaluation and Work-up: Early Reproductive Years/Adolescent
Evaluation and Work-up: Women of Reproductive Age
Evaluation and Work-up: Post-menopausal Women
EMB
Incidence of Endometrial Cancer in Premenopausal Women
Endometrial Cancer Risk Factors
Possible Path Reports with EMB
Hysteroscopy
Management
Management Options:
* Progestins
* Estrogen
* OCs
* NSAIDs
* Antifibrinolytics
* Surgical
Progestins: Mechanisms of Action
Management: Progesterone
Progestational Agents
Intrauterine System
Treatment of menorrhagia with IUD vs endometrial resection
Endometrial Hyperplasia
Management: Estrogen
Management: NSAIDs
Cyclooxygenase Pathway
Arachidonic Acid
Prostaglandins
Thromboxane
Prostacyclin*
Antifibrinolytics:
Surgical Options:
* Laser ablation
* Thermal ablation
* Resection
* Hysterectomy
Comparison of Ablative Techniques
Case Presentation
Summary

Abnormal Uterine Bleeding.ppt

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Uterine Artery Embolization

Uterine Artery Embolization
Presentation by:Dennis DeSimone, MIV
Virginia College of Osteopathic Medicine

Background
* Menorrhagia is a very common gynecologic complaint
* The complaint of heavy menstrual bleeding accounts for nearly 30% of all hysterectomies
Uterine Fibroids - a source of significant uterine bleeding
* Surgical management has been the standard of treatment in menorrhagia due to organic causes
o Dilatation and curettage
o Transcervical resection of the endometrium
o Endometrial ablation
o Uterine balloon therapy
o HydroThermAblator
o Hysterectomy
* Modern gynecology dictates the trend toward conservative therapy
o Cost containment
o Patient’s desire to preserve their uterus
o Evidence that nearly 50% of uterine pathology findings from hysterectomies for menorrhagia are free of disease and histopathologic abnormalities.
* Uterine artery embolization
* A relatively new approach to treating fibroid tumors.

significant improvement
* Tumors shrink by 50%
* Uterus shrinks by 40%
* Main risks:
o Pain
o Secondary
amenorrhea

Uterine artery embolization
Before and after
Methods
Results
Conclusions

* UAE has a low MAJOR complication rate
* Hospital stay, time off from work, and time until resumption of normal activities for UAE patients is reduced
* Short term minor complications of the procedure include hematoma, pain, nausea
* UAE may be a reasonable alternative to hysterectomy
References

Uterine Artery Embolization.ppt

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Menstrual Disorders

Menstrual Disorders
Presentation by:Oguchi A. Nwosu M.D.
Assistant Profressor
Emory Family Medicine Dept.

Menstrual Cycle
Definitions
* Menorrhagia Excessive (>80ml) uterine bleeding Prolonged (>7days) regular
* DUB Abnormal Bleeding, no obvious organic cause usually anovulatory
* Oligomenorrhea Uterine bleeding occurring at intervals between 35 days and 6 months
* Amenorrhea No menses x at least 6 months

Metrorragia, Menometrorrhagia, Polymenorrhea
Ovulatory vs Anovulatory cycles
Oligo or Amenorrhea +/- Menorrhagia
DUB
-Defn: Excessively heavy, prolonged or frequent bleeding of uterine origin that is not due to pregnancy, pelvic or systemic disease
-Diagnosis of exclusion
- Anovulatory
-Usually extremes of reproductive life and in pts with PCOS

DUB pathophysiology
* Disturbance in the HPO axis thus changes in length of menstrual cycle
* No progesterone withdrawal from an estrogen-primed endometrium
* Endometrium builds up with erratic bleeding as it breaks down.

DUB management
– sample endometrium
Usually followed by OCP or progestin
Menorrhagia

-Heavy vaginal bleeding that is not DUB
-Usually secondary to distortion of uterine cavity- heavy with or without prolongation (anatomic).
Uterus unable to contract down on open venous sinuses in the zona basalis
-Other causes organic, endocrinologic, hemostatic and iatrogenic
-Usually ovulatory

Menorrhagia, Management
sample endometrium
Other tests as INDICATED by HX and PE
Endometrial evaluation of menorrhagia
Endometrial Biopsy
Procedure of choice (detection and cost)
Menorrhagia, medical management
* NSAID’s, 1st line, 5 days, decrease prostaglandins
* Danazol, Androgen and prog. competitor , amenorrhea in 4-6 weeks, androgenic side effects
* OCP’s, esp. if contraception desired, up to 60% dec. supp. HP axis
* Continous OCP’s
* Oral continous progestins (day 5 to 26), most prescribed, antiestrogen, downregulates endormetrium
* Levonorgestrel IUD (Mirena), High satisfaction rate that approaches surgical techniques
* GnRH agonists, Inhibit FSH and LH release– hypogonadism, bone
* Conjugated estrogens for acute bleeding
* Other treatments as indicated e.g. DDAVP for coagulation defects

Menorrhagia, surgical management
Amenorrhea, physiologic causes
Primary Amenorrhea
-Vaginal agenesis
-Androgen insensitivity syndrome
-Turners syndrome
Amenorrhea, causes
Amenorrhea, management
Evaluation of Secondary Amenorrhea
Causes of Amenorrhea
Hyperprolactinemia
Antipsychotics
Antidepressants
Antihypertensives
Histamine H2 receptor blockers
Opiates, cocaine
Empty sella syndrome
Pituitary adenoma
Hypergonadotropic hypogonadism
Gonadal dysgenesis
Turner's syndrome*
Other*
Postmenopausal ovarian failure
Premature ovarian failure
Autoimmune
Chemotherapy
Galactosemia
Genetic
17-hydroxylase deficiency syndrome
Idiopathic
Mumps
Pelvic radiation
Hypogonadotropic hypogonadism
Anorexia or bulimia nervosa
Central nervous system tumor
Constitutional delay of growth and puberty*
Chronic illness
Chronic liver disease
Chronic renal insufficiency
Diabetes
Immunodeficiency
Inflammatory bowel disease
Thyroid disease
Severe depression or psychosocial stressors
Cranial radiation
Hypogonadotropic hypogonadism
Excessive exercise
Excessive weight loss or malnutrition
Hypothalamic or pituitary destruction
Kallmann syndrome*
Sheehan's syndrome
Normogonadotropic
Congenital
Androgen insensitivity syndrome*
Müllerian agenesis*
Hyperandrogenic anovulation
Acromegaly
Androgen-secreting tumor (ovarian or adrenal)
Cushing's disease
Exogenous androgens
Nonclassic congenital adrenal hyperplasia
Polycystic ovary syndrome
Thyroid disease
Outflow tract obstruction
Asherman's syndrome
Cervical stenosis
Imperforate hymen*
Transverse vaginal septum*
Other
Pregnancy
Thyroid disease
*-Causes of primary amenorrhea only.

Abnormal Menstruation
Here’s what you need to remember!!
* Always R/O pregnancy, check pap
* Try to differentiate anovulatory from ovulatory bleeding
* Good history and physical is key( this applies to amenorrhea as well)
* Do a focused work up based on your H & P rather than a random set of studies
* In amenorrhea, where no indication of cause based on H & P, follow the stepwise algorithm for diagnosis
* Know the INDICATIONS for endometrial sampling
References

Menstrual Disorders.ppt

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Fetal distress

Fetal distress
Presentation by:LIN QI DE

Fetal distress is defined as depletion of oxygen and accumulation of carbon dioxide,leading to a state of “hypoxia and acidosis ” during intra-uterine life.

Definition
Maternal factors

* Microvascular ischaemia(PIH)
* Low oxygen carried by RBC(severe anemia)
* Acute bleeding(placenta previa, placental abruption)
* Shock and acute infection
* obstructed of Utero-placental blood flow

Etiology
Placenta umbilical factors
* Obstructed of umbilical blood flow
* Dysfunction of placenta
* Fetal factors
* Malformations of cardiovascular system
* Intrauterine infection

Hypoxiaaccumulation of carbon dioxide
Respiratory Acidosis
Intestinal peristalsis
Relaxation of the anal sphincter
Meconium aspiration
Fetal or neonatal pneumonia
Pathogenesis
Acute fetal distress

Clinical manifestation Acute fetal distress
Acute fetal distress
Chronic fetal distress
Management

Fetal distress.ppt

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Fetal Development

FETAL DEVELOPMENT
Presentation by:Peggy Pannell RN, MSN

Learning Goals
* Normal Fetal Development
o From ovulation to birth
* Teratogen
o Definition and potential effects on development
Vocabulary
* Blastocyst
* Conception
* Ductus arteriosus
* Embryo
* Fertilization
* Fetus
* Foramen Ovale
* HCG
* Implantation
* L/S ration
* Gestational age
* Vernix
* Zygote
* Placenta
* Quickening
* Surfactant
* Teratogens
* Umbilical Cord

FERTILIZATION
* Begins with 46 pair of chromosomes, splits off to 23 then combine for a unique new 46 pair.

Stages and Time Frames
* Ovum
* Zygote
* Morula
* Blastocyst
* Embryo
* Fetus

IMPLANTATION
First weeks of human development:
Blastocyst embedded in endometrium.

PRIMARY GERM LAYERS
* Ectoderm
* Mesoderm
* Endoderm

GESTATIONAL AGE
* Gestational age=Time since last menstrual period (LMP)
* EDC, EDD, EDB
* 266 Days after fertilization
* 280 Days after onset of LMP

Nagele’s Rule
Trimester
1st = week’s 1-13
2nd = week’s 14 - 26
3rd = week’s 27 and on (38-40 WEEKS)

STAGES OF DEVELOPMENT
FETAL MEMBRANES
* Amnion
* Chorion

Decidua capsularis
Decidua basalis
Developing placenta
Yolk sac
Amniotic cavity
Intrauterine cavity
Decidua vera
Mucus plug (operculum)
Chorion (blends with placenta)
Amnion (blends with umbilical cord)

Umbilical cord (funis)
Lacunae in decidua basalis filled with maternal blood
Intrauterine cavity
Decidua capsularis
Decidua vera

1 Month
Month 2
Month 3
Month 4
Month 5
Month 6
Month 7
Month 8
Month 9
Third Trimester
At the end of 9 months:
* Baby is 19 to 20 inches long
* Weight is about 7 to 7 1/2 pounds
* The lungs are mature
* Baby is now fully developed and can survive outside the mother's body
* Skin is pink and smooth
* Baby settles down lower in the abdomen in preparation for birth and may seem less active

AMNIOTIC FLUID
* Clear, yellowish fluid surrounding the developing fetus.
* Average amount 1000 ml.
* Having < 300ml – Oligohydramnios, associated with fetal renal abnormalities.
* Having > 2 L – Hydramnios, associated with GI and other malformations.
* Protects Fetus
* Controls Temperature
* Supports Symmetrical Growth
* Prevents Adherence to amnion
* Allows Movement
* Source of oral fluid
* Acts as a excretion-collection repository

UMBILICAL CORD
Connecting link between fetus and placenta.
* Transports oxygen and nutrients to fetus from the placenta and returns waste products from the fetus to the placenta.
* Contains: 2 arteries and 1 vein supported by mucoid material (wharton’s jelly) to prevent kinking and knotting.
* Contains NO pain receptors.

PLACENTA
MOM
Baby
Produce protein hormones:
* Human chorionic gonadotrophin (HCG)- 8-10 days past conception, is basis for pregnancy test
* Progesterone
* Estrogen
* Human Placental Lactogen
* Sieve/filter – allows smaller particles through and holds back larger molecules. Passage of materials in either direction is effected by:
o Diffusion: gases, water, electrolytes
o Facilitated transfer: glucose, amino acids, minerals.
o Pinocytosis: movement of minute particle
* Mother transmits immunoglobulin G (IgG) to fetus providing limited passive immunity.
* Leakage: caused by membrane defect: may allow maternal and fetal blood mixing.

VIABILITY
RESPIRATORY SYSTEM
CARDIOVASCULAR SYSTEM
FETAL CIRCULATION
* HEPATIC SYSTEM
* MUSCULO-SKELETAL SYSTEM
GASTROINTESTINAL SYSTEM
RENAL SYSTEM
NEUROLOGICAL SYSTEM
ENDOCRINE SYSTEM
INTEGUMENTARY SYSTEM
IMMUNE SYSTEM
MULTIFETAL PREGNANCY
Teratogens
STAGES OF DEVELOPMENT

FETAL DEVELOPMENT.ppt

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Nursing Management During Pregnancy

Nursing Management During Pregnancy
presentation from:Los Angeles Valley College

Preconceptual Counseling
* Why is it important?
* Medical- past or current problems
* Sexual- STI
* Reproductive-AB or losses
* Psychosocial-support system
* Counseling- Folic acid, iron, wgt. SA, violence diseases, genetics

Taking History
* Current pregnancy- any problems
* Past pregnancy-problems, type of delivery,newborn info
* Current/past medical hx
* Family-Religion-Culture
* Age-old vs. young
* Identify high risk problems early

Vocabulary
* Nagle’s rule minus three months + 7days
* Ab- before 20 weeks
* Nullipara- no births before 20 weeks
* Primpara -one birth after 20 weeks
* Gravida- pregnancy regardless of duration
* P- after 20 weeks before 37 wks
* Living- number of living children

Head to Toe
* Head and Neck- Evaluate thyroid, dental
* Chest- HR, murmur, SOB, breast exam
* Abdomen- check fundal hgt
* Extremities- varicosities, edema, calfs
* Pelvic exam-Lesions, discharge, hematomas
* Pelvimetry- gynecoid, assess for adequate pelvis
* Labs- CBC, Rh, Rubella, Hepatitis, HIV, VDRL,RPR

Prenatal Care Visits
Fetal Movement
* Used to determine fetal well being
* Cardiff- lie or sit, count 10 fetal movements
* Call healthcare provider if more than 1 hour
* Sadovsky- lie on left after eating.
* Should feel 4 movements in 1 hr
* Count movements second hr.
* Call HCP if criteria not met


Assessment of Fetal Well Being
* UTZ- Low risk assessment tool
* Doppler Flow-Eval for absent or reversed diastolic flow
* AFP-16-18wks Eval for NTD or Down’s
* Marker Screening test- AFP ,unconjugated estriol, hCG and Inhibin A- more accurate
* Amniocentisis—chromosomes and metabolic defect



Assessment of Fetal Well Being
* Nsg-Consent, risk of AB, empty bladder
* Assess for FHT and UC- Rhogam?
* Give labor precautions
* CVS-Tissue sample- Get results sooner
* Nsg- same as amniocentisis
* PUBS- blood collected from fetus
* High Risk- Monitor fetus
* NSG-FKC- S/S of infection, cramping

Assessment of Fetal Well Being
* NST- Fetal Movement = Fetal Well Being
* Reactivity= 2 accelerations above baseline lasting 15 seconds within 20 minutes
* Nsg- Apply monitors, give marker, displace uterus to left lateral
* Need for NST determined by risk factors
* CST- Ability of fetus to tolerate stress and fetal reserve
* Decrease in oxygenation with uc’s
* Initiate 3 ucs in 10 minutes
* Eval. FHR for variations
* Negative results are GOOD
* Positive - 50% of ucs = late decelerations

Biophysical Profile
Promotion of Self-Care

* Treat holistically-promote well being
* Personal Hygiene/Dental Hygiene
* Breast Care- Sears or J.C. Penny
* Clothing- loose comfortable
* Balance exercise with rest
* Pelvic Tilt and Kagel’s
* Sleep- use pillows- limit fluids
* Sexual activity- encourage intimacy
* Employment- evaluate risk factors
* Travel- move q 2 hrs
* Immunizations- no live vaccines
* OTC meds- should consult HCP

Classifications of Drugs
* A- controlled studies- no fetal risks
* B- use frequently- r/t little harm
* C- likely to cause harm risk vs. benefits
* D- fetal risk benefits outweigh risk
* X risks outweigh benefits

Promotion of Self Care
* Urinary frequency-need 2000 cc/day. Limit 2-3 hrs before bed
* Fatigue- feel best 2nd trimester
* N/V- Avoid foods and smell. Crackers, sit up, rise slowly- S/S of dehydration
* Constipation- increase fiber-Do not strain
* Nasal- epitaxis-use air vaporizer
* Cravings- Weight? Avoid sodium/sugar

Promotion of Self Care Second Trimester
* Backache- Good body mechanics
* Leg cramps-increase calcium/magnesium
* Ankle edema- common- legs above heart
* Hemorrhoids- avoid straining
* Constipation- bulk in diet- prune juice
* Flatulence- avoid carbonation, cheese

Promotion of Self Care Third Trimester
* SOB-pressure on diaphragm, sit up, avoid large meals- Lightening
* Constipation- hydration- fruits and vegetables
* Heartburn- sit up, avoid large meals
* Ankle edema- eval for PIH
* Braxton Hicks- Cervix preparing for labor

Diet

* 30 mg ferrous sulphate/600mcg of folic acid
* Normal weight gain 25-35 pounds
* Alterations in weight- thin vs. obese
* Culture variations
* Special Diets- Lactose Intolerant- Vegans
* Use Dieticians
* Evaluate for Pica

Perinatal Education
* Knowledge = Better Birth Experience
* Lamaze- psychophrophylactic- Breathing controls pain
* Bradley-Enjoy process of childbirth-no pain medications
* Dick Read- Break cycle of Fear-Tension-Pain

Birth Options
* Hospital Based Care-Birthing Suites – Family Centered Care
* Birthing Center- No Rush- Midwife
* Home Birth- Must be low risk
* Choosing a health care provider
* Doula- Continuous support during labor and birth

Breast vs. Bottle
* Breast is best
* Bonding
* Less infection
* Promotes involution
* Less allergies
* Less obesity
* More digestible
* Bottle
* Need more to get same nutrition
* Expensive
* Less digestible
* No microwave
* Do not prop bottle
* Father can feed

Danger Signs of Pregnancy
Class activities
GTPAL
Maslow
Diet

Nursing Management During Pregnancy.ppt

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Antepartum Fetal Testing

Antepartum Fetal Testing: Examining the Evidence
Presentation lecture by:Jay J Bringman, MD
University of Tennessee Health Sciences Center, Memphis

Objectives
* Understand physiology behind antepartum fetal testing
* Review evidence for antepartum fetal testing
* Indications for testing
* Review what test to use
* What to do with an abnormal test
* When to start and the frequency in which to test

Cerebral Palsy
* Case-control study of term infants weighing >2500g in Australia
* Case: neonate with diagnosed moderate or severe neonatal encephalopathy in first week of life
* Control: term neonate without diagnosis of neonatal encephalopathy
* Evaluated role of preconceptional, antepartum and intrapartum factors in neonatal encephalopathy
* Strongest antepartum risk factor for NE is IUGR; OR 38.2 (9.4-154.8)
* Other risk factors:

Physiologic basis for antenatal testing
* Fetal testing designed to assess for fetal hypoxia

Non-stress test physiology
* Afferent signals:
* When stimulated, send afferent impulses to brain to increase FHR
* Efferent signals increase FHR
* If movement and accelerations observed, reasonable to conclude the afferent and efferent limbs intact and cardioregulatory neurons adequately oxygenated

NST: How to do it
* Patient in lateral tilt position
* Tracing observed for 40 minutes
* Accelerations peak (but do not necessarily remain) at least 15 BPM above baseline
* Last for 15 seconds
* Reactive: 2 or more accelerations within 20 m period
* Nonreactive: one that lacks sufficient accelerations over 40 minute period
* No contraindications

The preterm fetus
* Frequently nonreactive
Evidence for use of NST
Randomized trials
Caveats
NST versus VAS
NST and nonrandomized data
Caveat for observational data
Contraction stress test
CST interpretation
Biophysical profile
What score tells you…

* Normal acute variables and AFI
* Normal pH and blood gases secondary to compensation
* Abnormal blood gases and normal AFI
* Abnormal acute and abnormal blood gases
* Goal is to recognize asphyxia and deliver prior to morbidity and mortality

Cesarean delivery
IOL for abnormal testing
Induction of labor
Nonrandomized data
Biophysical profile
Fetal movement assessment
Indications for antepartum monitoring
Maternal and Fetal Indications
Which test to use?
* Most evidence points to use of NST as first line test
* Imperative to remember that it should not be used a sole test
* Other tests should be used in situation of nonreassuring testing such as BPP or CST
* NST can be used in conjunction with Doppler studies in IUGR

What to do if test is abnormal?
* True false-positive test results not known
o Test introduced without rigorous evaluation of utility
* Abnormal result in context of clinical situation
o Did maternal condition change?
o Abnormal test usually followed by other test
+ 90% of NRNSTs followed by negative CST
o If NRNST followed by positive CST, delivery warranted in morphologically normal fetus

Abnormal BPP
When to start?
How frequently?

Antepartum Fetal Testing.ppt

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PREGNANCY 1st and 2nd Trimesters

PREGNANCY 1st and 2nd Trimesters
Presentation lecture from: Orangecoastcollege

* General
o Sonography used after 4-5 weeks
o Events prior to this time:
1. Ovulation
2. Fertilization
3. Implantation
4. Placentation
5. Embryonic Development

OVULATION
A. Definition: a cyclic event controlled by two hormones (FSH and LH) that occurs monthly

1. ~ 20 ova begin maturing
2. Only one completes the maturation process
Phase??
3. After ovulation, ovum moves into uterine tube
4. If fertilized, the zygote begins to divide
5. Implantation begins in ~6 days

FERTILIZATION
A. Definition: penetration of the ovum by one spermatozooan

1. Hyaluronidase (from acrosome):enzyme that allows penetration
2. Lack of acrosome/enzyme: infertility
3. Polyspermy: More than one sperm penetrates ovum

B. Sperm and ovum are haploid (N)
C. Genetic material in nuclei fuses to form zygote (2N)
D. Zygote begins cell division (mitosis!) immediately
E. Differentiation: prior to reaching uterus, zygote has developed into morula
+ Cells continue to divide, form blastula or blastocyst
# trophoblast
# inner cell mass or blastoderm
G. Trophoblast will give rise to placenta
H. Inner cell mass will give rise to the embryo
1. Ectoderm (outer layer or “outer skin”)
2. Endoderm (inner layer or “inner skin”)
3. Mesoderm (middle layer or “middle skin”)


Primary Germ Layers

Implantation
The Uterus
Perimetrium
Myometrium
Endometrium
Placenta & Fetal Membranes
Placental formation
Chorion Frondosum
Formation of Umbilical Vessels
Fetal membranes
Umbilical Cord
Anomalies
Meckel’s Diverticulum
May indicate fetal demise, premature rupture of membranes
Omphalocele
Ectopic Pregnancy
Metastatic Carcinomas
Spread via lymph circulation
Rectouterine Pouch (of Douglas) or cul-de-sac
Hydrocephaly
Hydrocephalus
Anencephaly:
Porencephaly
Doppler U/S of the Circle of Willis in utero
Circle of Willis
Fetal circle of Willis: 3D U/S
Ultrasound-guided Prenatal Diagnosis
Amniocentesis and CVS
Pelvic masses
Uterine Anomalies
Uterus bicornis
Uterus didelphys
Uterus unicornis

PREGNANCY 1st and 2nd Trimesters.ppt

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High Risk Pregnancy

High Risk Pregnancy
Presentation By:Susan Sienkiewicz

Adolescent Pregnancy: Contributing Factors
Implications of Adolescent Pregnancy
Socioeconomic:
* reliance on welfare
* cycle repeats itself

Maternal health:
* CPD
* PIH
* anemia
* nut deficits
* mortality

Fetal Health:
* LBW
* prematurity
* resp complications
* cp
* cognitive deficits
* death

Adolescent Pregnancy: Assessment
* Risks
* fundal height
* # of sexual partners
* knowledge of infant care/needs
* family unit/support system
* baseline VS/weight

IMPLICATIONS OF DELAYED PREGNANCY
* Pre-existing conditions
* Preterm labor SGA/LBW
* IUGR
* PIH Abruption
* C-section
* Uterine fibroids PP hemorrhage
* Chromosomal abnormalities


DELAYED PREGNANCY: ASSESSMENT
* Pre-existing conditions
* Fundal height
* Anxiety
* Psychosocial issues

TYPES OF SPONTANEOUS ABORTIONS
Spontaneous Abortion Management
Threatened
Inevitable
Incomplete
Missed
Post Abortion Education
SITES OF ECTOPIC PREGNANCY
S & S Ectopic Pregnancy
Surgical Management of Ectopic Pregnancy
Med Mgmt of Ectopic PG
MTX
S & S Hydatiform Mole
Therap. Mgmt: vacuum aspiration & curettage
Spontaneous Abortion Matching – Choose all that apply.
Medical Mgmt of Placenta Previa
Mom stable,fetus immature
Fetus > 36 wks
S&S Abruptio Placentae
Med Mgmt of Placental Abruption
Placental Bleeding
Thromboplastin release
Clot formation (systemic response)
clotting factors (fibrinogen, plts, PTT, FDP)
inability to form clots
profuse bleeding
Hemorrhagic Conditions: Abruption & DIC
ASSESSMENT
The Pathological Processes of Pre-eclampsia
S&S Pre-eclampsia
Treatment of Pre-eclampsia
Mild: diastolic
Severe: diastolic
S&S Eclampsia/HELLP Syndrome
* Eclampsia
* HELLP Syndrome
Treatment of Eclampsia/HELLP Syndrome
* Bedrest
* Meds
* Delivery
Assessment: Hypertensive Disorders of Pregnancy
Risk Control Strategies for Hypertensive Disorders of Pregnancy
Incompetent Cervix
Treatment
Premature Labor/Rupture of Membranes
Nursing Care for PTL/PROM
Postterm Pregnancy
Disorders of Amniotic Fluid
Risks of Multifetal Gestation
(Fetal) S&S Rh Incompatibility
Sequence of Assessments for Rh Sensitization
Blood Test for Type & Rh Factor
Management of Rh Incompatibility
Prenatal
Hyperemesis Gravidarum
Glucose Tolerance Test
Gestational Diabetes is diagnosed with FBS > 105 or with 2 of the following BS results:
Effects of Pre-Existing DM
* Maternal
* Fetal
Treatment of Pre-existing DM
Effects of Gestational Diabetes
Diabetes: Patient Education
PPCM: Manifestations
PPCM: Energy Management
PPCM: Cardiac Care
PPCM: Patient Education
Sickle Cell Disease
Systemic Lupus Erythematosis
AIDS
Treatment:
CASE STUDY

High Risk Pregnancy.ppt

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Pelvic Masses

Pelvic Masses
Preentation by:Anna Mae Smith, MPAS, PA-C
Lock Haven University

Central Pelvic Masses
* Pregnancy
* Leiomyomata - uterine fibroids
* Endometrial malignancy or uterine sarcoma
* Ovarian or other laterally located masses may present centrally
* Bladder

Leiomyomas
* benign smooth muscle tumors of the uterus
* commonly called “fibroids”
* estrogen dependent
* rarely occur before menarche or after menopause
* grow larger during pregnancy
* rarely malignant
* most common indication for pelvic surgery in women

Leiomyomas in Pregnancy
* interfere with fetal growth and nutrition
* increase the risk of
o spontaneous abortion during the first and second trimesters
o preterm labor

Epidemiology of Leiomyomas
* develop from smooth muscle cells by means of metaplasia
* cause for growth is unknown
* occurs in 20% of women of reproductive age
o most often occurs among African American women
o nulliparous women
o women older than 35
o nonsmokers
o oral contraceptive or IUD users


Classification of Leiomyomas
* submucous - protrude into the uterine cavity
* intramural - within the myometrial wall
* subserous - growing toward the serous surface of the uterus
* intraligamentous - located in the cervix or in between the folds of the broad ligament

Leiomyomas: Symptoms
* usually asymptomatic
* symptoms increase as tumors grow
* common symptoms
o pelvic pressure
o bloating
o pelvic congestion
o feeling of “heaviness”
o urinary frequency
o dysmenorrhea
o dyspareunia
o menorrhagia
o pain - less common
* may report infertility
* pregnant women complain more of pain

Leiomyomas: Physical Exam
* absence of ascites
* normal bowel sounds
* enlarged uterus that is firm and irregular but not tender
* may be mistaken for adnexal mass if situated laterally
* if mass moves with the uterus, likely to be a leiomyoma

Leiomyomas: Diagnostic Tests
* CBC to determine if anemic
* UA to r/o urinary tract infection
* Pregnancy test
* Hemoccult
* Ultrasound
* Barium enema
* IVP
* Endometrial biopsy

Leiomyomas: Differential Diagnoses
* ovarian neoplasm
* tubo-ovarian inflammatory mass
* diverticular inflammatory mass
* pregnancy
* ectopic pregnancy
* adenomyosis
* pelvic kidney
* malignancy

Leiomyomas: Treatment
Leiomyomas: Conservative Surgery
* myomectomy
* Leiomyomas: Hysterectomy
* GI Tract

Lateral Pelvic Masses
* Ovary
* Normal premenopausal ovary - 3x2x1.5cms
* Early Menopausal ovary - 2x1.5x0.5cms
* Postmenopausal ovary - 1.5x0.75x0.5cms
* GI causes
* Pelvic kidney
* PID with tubo-ovarian abscess
* Ectopic pregnancy

Ectopic Pregnancy
* Potentially life-threatening condition in which the embryo implants outside the uterine endometrial cavity.
* Leading cause of pregnancy-related death during the first trimester
* Must be considered in all sexually active women of reproductive age who have abdominal pain or abnormal vaginal bleeding

Risk Factors for Ectopic
* current IUD use
* previous tubal surgery
* history of pelvic inflammatory disease
* history of infertility
* In-utero DES exposure
* H/o STD’s
* Smoking
* Progesterone only contraception
* Use of fertility drugs

Classic Triad of Symptoms
* Amenorrhea
* Irregular vaginal bleeding
* Pelvic pain

Physical Findings of Ectopic Pregnancy
* Prior to rupture may feel nothing…usually some form of abnormal bleeding present
* Ruptured:
o Hypovolemic/orthostatic hypotension
o Peritoneal signs
o Positive CMT & adnexal tenderness
o Bulging cul-de-sac of Douglas

Ectopic Testing
Fallopian Tube
Dermoid Cyst/Teratoma
Ovary
Laparoscopy

Pelvic Masses.ppt

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Acute Abdomen in Pregnancy

Acute Abdomen in Pregnancy
Presentation by:Kate Pettit, MS III

DDx of Abdominal Pain in Pregnancy
* Divided into three categories:
1) Conditions incidental to pregnancy
2) Conditions associated with pregnancy
3) Conditions due to pregnancy

Conditions Incidental to Pregnancy

* Acute appendicitis
* Acute pancreatitis
* Peptic ulcer
* Gastroenteritis
* Hepatitis
* Bowel obstruction
* Bowel Perforation
* Herniation
* Meckel’s Diverticulitis
* Toxic megacolon
* Pancreatic pseudocyst
* Ovarian cyst rupture
* Adnexal torsion
* Ureteral calculus
* Rupture of renal pelvis
* Ureteral obstruction
* SMA syndrome
* Thrombosis/infarction
* Ruptured visceral artery aneurysm
* Pneumonia
* Pulmonary embolus
* Intraperitoneal hemorrhage
* Splenic rupture
* Abdominal trauma
* Acute intermittent porphyria
* Diabetic ketoacidosis
* Sickle Cell Disease

Conditions Associated with Pregnancy
* Acute pyelonephritis
* Acute cystitis
* Acute cholecystitis
* Acute fatty liver of pregnancy
* Rupture of rectus abdominus muscle
* Torsion of pregnant uterus

Conditions Due to Pregnancy
* Ectopic pregnancy
* Septic abortion with peritonitis
* Acute urinary retention due to retroverted uterus
* Round ligament pain
* Torsion of pedunculated myoma
* Placental abruption
* Placenta percreta
* HELLP Syndrome
* Acute Fatty Liver of Pregnancy
* Uterine rupture
* Chorioamionitis

Ectopic Pregnancy
* Classic Symptoms
o Abdominal pain
o Amennorrhea
o Vaginal Bleeding
* Diagnosis
o Transvaginal U/S (TVS)
o Serum quantitative HCG
* Management
o Option of medical vs surgical management if pt is hemodynamically stable and no rupture has occurred.
o Emergent surgical management if rupture has occurred and/or patient is hemodynamically unstable
* Prognosis
o Ruptured ectopic pregnancies account for 4- 10 percent of all pregnancy related deaths.

HELLP Syndrome
Hemolysis – Elevated Liver Enzymes – Low Platelets
Acute Fatty Liver of Pregnancy
Definition of Acute Abdomen
* Stedman's Medical Dictionary, 27th Edition defines acute abdomen as "any serious acute intra-abdominal condition attended by pain, tenderness, and muscular rigidity, and for which emergency surgery must be considered.”
Epidemiology
# 1 Acute Appendicitis
# 2 Acute Cholecystitis

Challenges of Diagnosis
* Symptoms
* Physical Exam
* Labs

Which conditions require urgent surgical management in pregnancy?
* Trauma
* Acute appendicitis
* Intestinal obstruction
* Perforated duodenal ulcer
* Spontaneous visceral rupture
* Ectopic pregnancy
* Ovarian or uterine torsion

Timing of Surgery
* 1st trimester (wks 1-12)
o 12% SAb rate
* 2nd trimester (wks 13-26)
o 0 - 5.6% SAb rate
o 5% rate of preterm labor
* 3rd trimester (wks 27-40)
o 30-40% rate of preterm labor

Imaging Options

* U/S: No known adverse effects.
* X-ray: Presence of adverse effects depends on total radiation dose.
* CT: Presence of adverse effects depends on total radiation dose.
* MRI: No known adverse effects.
* ERCP: Only recommended for therapeutic use, not for routine imaging.

Radiation during pregnancy
Use of ERCP in Pregnancy
American Society for Gastrointestinal Endoscopy Guidelines

* ERCP should only be used when therapeutic intervention is intended (usually for biliary pancreatitis, choledocholithiasis, or cholangitis).
* Several studies have confirmed the safety of ERCP in pregnancy.
* With precautions, fetal exposure is well below the 5- to 10-rad level.
o Kahaleh et al. reported an estimated fetal radiation exposure of 40 mrads (range 1-180 mrad).
* Precautions for reducing radiation exposure:
o Lead shields placed under the pelvis an

Reducing Radiation in Pregnancy
* X-ray: PA exposures lowers the radiation dose by 2 to 4 mrad compared with the traditional AP exposures because the uterus is located in an anterior pelvic position.
* CT: Narrow collimation and wide pitch (the patient moves through the scanner at a faster rate) results in a slightly reduced image quality, but provides a large reduction in radiation exposure.

Sequelae of Radiation in Pregnancy
* May cause failure of implantation, malformation, growth retardation, CNS abnormalities, or fetal loss.
* Exposure <10 rads (100 mGy) does not  the risk of fetal death, malformation, or developmental delay.*
* Highest risk of radiation damage during embryonic period of organogenesis (weeks 3-9).

*International Commission on Radiological Protection.
Childhood Leukemia and Radiation
Use of contrast in pregnancy
MRI as an imaging modality
American College of Radiology Paper on MRI Safety
MRI should only be used in pregnancy when:
o The information requested from the study cannot be obtained from nonionizing means.
o The information is needed to care for the pt and fetus during pregnancy.
o The ordering MD does not feel it is prudent to delay diagnosis until after pregnancy.

MRI in Pregnancy
* No studies have shown adverse effects on the fetus or the outcome of the pregnancy.
* However, arbitrarily MRI is NOT usually performed in the 1st trimester 2/2 to this being the period of organogenesis.
* When MRI is used, informed consent must include the possibility that a previously undiagnosed fetal abnormality may be found.

Appendicitis
Signs and Symptoms
* RLQ pain: Most reliable sx
* Anorexia and vomiting: Not sensitive nor specific.
* Direct RLQ tenderness: ~100%
* Rebound tenderness: 55-75% of pts
* Abdominal muscle rigidity: 50-65% of pts
* Psoas sign: Observed less frequently.
* All findings are less common in 3rd trimester due to laxity of abdominal wall muscles.

Adler Sign
Appendiceal Location
Laboratory Evaluation
1st Line Imaging for Appendicitis
2nd Line Imaging for Appendicitis
MRI
Risks for Mother and Fetus
Recommendations for Diffuse Peritonitis
Acute Cholecystitis
Pathophysiology:
Hormones and biliary disease
Epidemiology
Presentation and Diagnosis
Initial Management of Cholecystitis
* IV hydration
* Bowel rest
* Pain control
* Antibiotics
* Fetal monitoring
* Nasogastric decompression if necessary

Surgical Management of Cholecystitis
* Cholecystectomy is now recommended as the primary treatment for cholecystitis because of:
o Recurrence rate during pregnancy of 44-92%, depending on date of 1st presentation
o Reduced use of medications
o Shorter hospital stay and fewer hospitalizations
o Elimination of risk of subsequent gallstone pancreatitis
o Minimizing development of potentially life-threatening complications such as perforation, sepsis, and peritonitis

Other Indications for Cholecystectomy During pregnancy
* Choledocolithiasis (after ERCP)
* Gallstone Pancreatitis
* Recurrent symptomatic cholelithiasis

Laparotomy vs Laparoscopy?
Choosing Surgical Technique
Laparotomy
* Currently considered 1st line approach.
* Always preferred approach when diffuse peritonitis is present, as it is associated with a lower complication rate than laparoscopy in this setting.
Laparoscopy
* First offered in 1991 for pregnant patients for appendectomy and cholecystectomy.
* Many new studies show this technique to be safe in pregnancy for routine appendicitis, especially during the 2nd trimester.
Recommendations to improve safety of laparoscopy during pregnancy
* Obstetrical consultation should be obtained preoperatively.
* When possible, operative intervention should be deferred until 2nd trimester.
* Procedure should be performed with pt in supine, left lateral decubitus position and degree of reverse Trendelenburg should be minimized.
* Open Hasson technique should be used to prevent puncture of uterus.
* Pneumoperitoneum pressures should be minimized to 8-12 mm Hg with maximum 15 mm Hg.
* Administration of tocolytic agents and perioperative monitoring of fetal heart tones should be considered.
* Pneumatic compression devices should always be used as both pneumoperitoneum and the condition of pregnancy are a risk for venous stasis.

Optimizing Delivery
Use of Tocolytics for Preterm Labor
Types of Tocolytics I
Types of Tocolytics II
Use of corticosteroids to improve fetal outcomes in premature delivery
Steroids and peritonitis?
References

Acute Abdomen in Pregnancy.ppt

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