Showing posts with label Obstetrics and Gynecology. Show all posts
Showing posts with label Obstetrics and Gynecology. Show all posts

16 December 2011

Endometrial hyperplasia ppts and recent publications



Endometrial  Biopsy
by Oguchi Andrew  Nwosu, MD, FAAFP, Emory Family  Medicine
http://www.fpm.emory.edu/Family/didactics/powerpint/Endometrial%20Biopsy%20and%20IUD%20Insertion.ppt

Endometrial  Cancer 
by Faina  Linkov, PhD, University  of Pittsburgh Cancer  Institute
http://www.pitt.edu/~super4/34011-35001/34071.ppt

Abnormal  Uterine Bleeding
by Todd  May, M.D.
http://sfghdean.ucsf.edu/barnett/FCM/PGY1/MayUterineBleeding.ppt

Abnormal  Uterine Bleeding
by Peter J.  Chen, M.D., Hospital  of the University of Pennsylvania
http://www.uphs.upenn.edu/obgyn/education/documents/AbnormalUterineBleeding--Studentlecture.ppt

Female  Reproductive System
External  Female Genitals
External  Reproductive Organs
http://www.ed.uab.edu/cpetri/docs/Chapter_2_Female_Reproductive_System.ppt

Sexual  Function in the Geriatric Population
by Vinita  J. Speir, MD
http://www.meded.uci.edu/reynolds/docs/Sexual%20Function%20in%20Geriatric%20Population.ppt

Abnormal  Uterine Bleeding
by Karen  Carlson, M.D., University  of Nebraska Medical  Center
http://www.unmc.edu/obgyn/docs/AbnormalBleeding2010.ppt

Diseases of  Vulva
http://www.nova.edu/noteservice/M2/repro/Path%20MT%20Review-incomplete.ppt

Recent published articles


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Obstetrics and gynaecology ppts from University of Kansas School of Medicine



Dysfunctional Uterine Bleeding
by-Darren Farley, M.D., UKSM-Wichita
http://wichita.kumc.edu/obgyn/slides/farley_DUB.ppt

Surgical  Complications of Pregnancy
by - Matthew  Voth M.D.
http://wichita.kumc.edu/obgyn/slides/voth_scp.ppt

Mullerian  Anomalies
By Elizabeth Diaz
http://wichita.kumc.edu/obgyn/slides/diaz05.ppt

Asthma  in Pregnancy
by Timothy Hoskins,  M.D.
http://wichita.kumc.edu/obgyn/slides/hoskins05.ppt

Pituitary  Disorders
by Jo  Choudhry, M.D.
http://wichita.kumc.edu/obgyn/slides/choudhry05.ppt

Recent published articles on Dysfunctional Uterine Bleeding

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17 October 2011

Occiput Posterior - Abnormal Labor Presentation



What is Occiput Posterior?

The most common position for a baby during labor is head down with the back of the head (occiput) facing the front of the mother (anterior). When the back of the head is facing the back of the mother (posterior) the baby's position is called Occiput Posterior.

Mechanisms of Birth - Complications of Labor
http://w3.palmer.edu/oneill/OBPEDS/PPT%20FW%2007/Complications%20of%20Labor%20(c%20fw06).ppt

Abnormal Labor
by Barbara M. O’Brien, M.D.Women and Infants Hospital, Brown University
https://wiki.brown.edu/confluence/download/attachments/25952305/Abnormal+Labor.ppt?version=1

Pregnancy, Labor and Delivery
by Calla Holmgren, MD, University of Washington
http://faculty.washington.edu/tracyj/Rehab%20400%202008%20Unit%201/pregnancylaboranddeliveryDelivery.ppt

Assessment of Complications During The Labor Process
by Prof. Unn Hidle
http://faculty.lagcc.cuny.edu/uhidle/SCR270/MATERNAL/sixlaboranddeliveryproblems.ppt

Pregnancy Childbirth and Postpartum at Risk
http://www.mccc.edu/~martinl/documents/MODULE4garysp11.ppt

Electronic Fetal Monitors
http://elearning.najah.edu/OldData/pdfs/1156Electronic%20Fetal%20Monitors.ppt


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22 March 2011

Amenorrhea, Asthma in Pregnancy, Dysfunctional Uterine Bleeding, Delayed Puberty and other Gynaecology Presentations



Asthma in Pregnancy
http://wichita.kumc.edu/obgyn/slides/hoskins05.ppt

Mullerian Anomalies By Elizabeth Diaz
http://wichita.kumc.edu/obgyn/slides/diaz05.ppt

Dysfunctional Uterine Bleeding
http://wichita.kumc.edu/obgyn/slides/farley_DUB.ppt

Peripartum Cardiomyopathy
http://wichita.kumc.edu/obgyn/slides/Voth05.ppt

Complementary and Alternative Medicine in Women’s Health
http://wichita.kumc.edu/obgyn/slides/henry05.ppt

Amenorrhea
http://wichita.kumc.edu/obgyn/slides/amenorrhea.ppt

Osteoporosis
http://wichita.kumc.edu/obgyn/slides/webb05.ppt

Thyroid Disease
http://wichita.kumc.edu/obgyn/slides/Kuhlmann05.ppt

Surgical Complications of Pregnancy
http://wichita.kumc.edu/obgyn/slides/voth_scp.ppt

Pituitary Disorders
http://wichita.kumc.edu/obgyn/slides/choudhry05.ppt

Female Sexual Dysfunction
http://wichita.kumc.edu/obgyn/slides/Smette05.ppt

Alloimmunization in Pregnancy
http://wichita.kumc.edu/obgyn/slides/grizzell.ppt

Delayed Puberty Topics in Adolescent Gynecology
http://wichita.kumc.edu/obgyn/slides/wolfe05.ppt

Source: University of Kansas - School of Medicine-Wichita

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03 April 2010

Renal Failure and Dialysis in Pregnancy



Renal Failure and Dialysis in Pregnancy
By:David Shure

Differential Diagnosis
* FSGS -
Pro: HTN, non-remitting, albumin close to NL
Con: expected creatinine to be higher after several years

* Membranous Nephropathy -
Pro: wax/waning course
Con: often with lower albumin, edema

* Diabetic Nephropathy -
Pro: proteinuria, time course
Con:poor evidence for DM
4. FMD - Pro: unequal sized kidneys, young female, HTN hx, renal arteries not commented on in US

Nephrology Consult
* Is there any indication and/ or benefit to the fetus if we begin HD at this time?
* Can we preserve any residual maternal renal function?
* OB team trying to prolong in-utero growth/ length of pregnancy, not sure if pt is masking severe preeclampsia

Why did Ob Deliver the Baby?
* 7/21 pt c/o HA, and 7/23 severe RUQ tenderness and epigastric pain, decision made to deliver fetus based on:
* Severe superimposed Preeclampsia in setting of chronic HTN
* Also, mild thrombocytopenic further led to diagnosis of severe preeclampsia

Normal Physiologic Alterations of Pregnancy
Normal Renal Alterations in Pregnancy

Changes in GFR
* GFR and RBF rise markedly
* Glomerular hyperfiltration results in normal reduction in the plasma creatinine concentration to about 0.4 to 0.5 mg/dL
* Blood urea nitrogen (BUN) and uric acid levels fall for the same reason

Effects of Pregnancy on Renal Disease
* ― cases proteinuria worsen
* ž cases HTN develops
* Worsening edema if nephrotic
* 0-10% women with NL or mild reduction in GFR have permanent decline in renal function

Views on Pregnancy and Dialysis
* ‘Children of women with renal disease used to be born dangerously or not at all - not at all if their doctors had their way’, Lancet, 1975
* ‘Show me a method of birth control more effective than end stage renal disease’, Roger Rodby MD, 1991
* ‘Even if a woman on CAPD ovulates, doesn’t the egg just float away?’, Rodby, 1992

Why don’t uremic women get pregnant?
* Most beyond child bearing age
* Libido/ frequency of intercourse reduced
* Don’t ovulate
* Absence of increase in basal body temperature during the luteal phase of cycle
* Elevated circulating prolactin concentrations
* Elevated PRL impairs hypothalamic-pit function

Actually, they do get pregnant!
* 1st successful term pregnancy in 35 y/o dialysed pt in 1971, Confortini, et al.
* Yr 2000: >15,000 women of childbearing age getting dialysis
* For every person w/CKD 5, 20 have CKD 3 or 4 w/GFR <60, suggesting ~300,000 women w/CKD potentially able to bear children Course of Renal Disease in Pregnancy * Baseline azotemia = more rapid deterioration * As renal dz progresses, ability to maintain nl pregnancy deteriorates, and presence of HTN incr likelihood of renal deterioration * Renal dysfunction - greater risk for complications incl preeclapsia, premature delivery, IUGR Pregancy during dialysis: case report and management guidelines; Giatras, et al. 1998 * 32 y/o AA woman, G4, P2, A1 * FSGS and chronic interstitial nephritis * Renal/obstetric protocol implemented * Increased HD to 4 hrs/ 4 sessions/ week maintain prediaysis BUN <50 * At each HD session, blood flow gradually increased over 1st 30 minutes of HD, from 180 to 300 ml/min * Kt/V 1.02 - 1.66 Giatras Protocol * Dialysis performed in left lateral decubitus position * Est maternal dry wt incrased by 500 g every 10d * EPO administered at each HD session, to maintain HCT 32-34% * Vit D, folic acid and MVI admin * Evid of malnutrition prior to pregnancy, so 3000kcal/day diet w>100g protein/ day

Obstetric Surveillance
* From 25 wks gestation
* Serial BP
* Uterine and umbilical artery perfusion evaluation
* Cont fetal heart rate tracing before, during and after HD
* There were no signif changes in uterine or umbilical artery S/D ratios at any time of HD, and no sig alteration in maternal MAP during HD
* Pt delivered at 32 wks gestation, due to PROM

Common Themes in Dialysing Pregnant Patients

1. Keeping BUN < 50 2. Increasing dialysis time and frequency 3. BP control 4. Managing anemia with increasing doses of ESA 5. Fetal monitoring once viability reached BUN <50 Hypothesis? * 1963 150 women varying degrees of CKD, none on dialysis, found the single most important factor influencing fetal outcome was BUN * Fetal mortality directly proportional to BUN * Hypothesis: intensive dialysis in pregnant women w/renal dz might improve fetal outcomes Increasing frequency and time on dialysis? * May be beneficial in reducing incidence of polyhydramnios by reducing urea and water load * Less dialysis-induced hypotension * More liberal diet * American Jrnl Kid Diseases * Spurred by the report of 5 pregnancies in 5 pts on chronic HD in 2 dialysis units bet 1989-1996 * 1st national survey of its kind which revealed a total of 15 pregnancies in HD - all dialysis centers in Belgium questioned for pts bet 1975-1996 Study Population Figures Case Characteristics/ Outcomes Dialysis Dosing * 15 pregnancies went beyond 1st trimester * Frequency of HD was increased immediately or progressively to 16 to 24 hrs * No difference bet successful pregnancies and failed ones for # mths on HD prior to conception or age at conception. * For successful pregnancies + correlation bet birth wt and excess dialysis hrs delivered over entire pregnancy. Success Rate * 80% (4/5) when HD initiated after onset of pregnancy (pregnancy first) * 50% (5/10) when HD was the first event * ‘‘Pregnancy first’ cases have a significant residual renal function and even may benefit from ‘preventive dialysis’, to be taken on dialysis at a stage of renal failure that would not justify dialysis in the eyes of many were it not for the very special setting of a pregnant state’’ Obstetrical Problems * Main Problem: premature births * In this study 3 died due to severe prematurity * Polyhydramnios present in almost all cases, may be cause of preterm labor * Growth retarded babies at highest risk for intrauterine death * Maternal prognosis is good Should we Initiate Dialysis in Pts w/Low Cr Clearance? * Hou, S., Pregnancy in Women on Hemodialysis, 1994, revealed better outcomes of pregnancy in women w/ significant residual renal function or who initiate pregnancy before they need dialysis. * May reduce incidence of polyhydramnios, lower urea and lowers water load, also reducing risk of dialysis-induced hypotension Registry of Pregnancy in Dialysis Patients USRDS Frequency of Prematurity and Low Birth Rate is less in those conceived before beginning dialysis Women who Start Dialysis During Pregnancy * Likelihood of infant surviving is good * Termination of a pregnancy after renal function has begun to deteriorate rarely rescues the kidneys * NEJM, Jones and Hayslett, 1996, looked at 82 pregnancies in 67 women w/CRI, only 15% of those w/deteriorating renal function had a return of renal function to baseline in 6 mths post partum Survival Statistics Renal Failure and Dialysis in Pregnancy.ppt

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Hemolytic Disease of the Newborn and Fetus



Hemolytic Disease of the Newborn and Fetus
By:Renee Newman Wilkins, MS, MT(ASCP), CLS(NCA)
CLS 325/435 Clinical Immunohematology
School of Health Related Professions
University of Mississippi Medical Center

What is HDN?
* Destruction of the RBCs of the fetus and newborn by antibodies produced by the mother
* Only IgG antibodies are involved because it can cross the placenta (not IgA or IgM)
Mother’s antibodies
Pathophysiology
* Although transfer of maternal antibodies is good, transfer of antibodies involved in HDN are directed against antigens on fetal RBCs inherited by the father
* Most often involves antigens of the Rh and ABO blood group system, but can result from any blood group system
* Remember: The fetus is POSITIVE for an antigen and the mother is NEGATIVE for the same antigen

Pathophysiology
* HDN develops in utero
* The mother is sensitized to the foreign antigen present on her child’s RBCs usually through some seepage of fetal RBCs (fetomaternal hemorrhage) or a previous transfusion
* HDN occurs when these antibodies cross the placenta and react with the fetal RBCs

ABO HDN
* ABO incompatibilities are the most common cause of HDN but are less severe
* Usually, the mother is type O and the child has the A or B antigen…Why?
* ABO HDN can occur during the FIRST pregnancy b/c prior sensitization is not necessary
* ABO HDN is less severe than Rh HDN because there is less RBC destruction
o Fetal RBCs are less developed at birth, so there is less destruction by maternal antibodies
Diagnosis of ABO HDN
* Infant presents with jaundice 12-48 hrs after birth
* Testing done after birth on cord blood samples:
Treatment of ABO HDN
* Only about 10% require therapy
* Phototherapy is sufficient
* Rarely is exchange transfusion needed
* Phototherapy is exposure to artificial or sunlight to reduce jaundice
* Exchange transfusion involves removing newborn’s RBCs and replacing them with normal fresh donor cells

Phototherapy
Fluorescent blue light in the 420-475 nm range
Exchange transfusion
* CMV negative
* Irradiated
* Fresh Whole Blood (to avoid Ca++)
* Maternal blood if possible
* Leukoreduced

What type of blood to give fetus:

Rh HDN
* Mother is D negative (d/d) and child is D positive (D/d)
* Most severe form of HDN
* 33% of HDN is caused by Rh incompatibility
* Sensitization usually occurs very late in pregnancy, so the first Rh-positive child is not affected
o Bleeds most often occur at delivery
o Mother is sensitized
o Subsequent offspring that are D-positive will be affected

About 1 in 10 pregnancies involve an Rh-negative mother and an Rh-positive father
FetoMaternal Hemorrhage
* Sensitization occurs as a result of seepage of fetal cells into maternal circulation as a result of a fetomaternal hemorrhage

Risk
* Rh-negative women can be exposed to Rh-Positive cells through transfusion or pregnancy
* Each individual varies in their immune response (depends on amount exposed to)
Pathogenesis
* Maternal IgG attaches to antigens on fetal cells
o Sensitized cells are removed by macrophages in spleen
o Destruction depends on antibody titer and number of antigen sites
o IgG has half-life of 25 days, so the condition can range from days to weeks
* RBC destruction and anemia cause bone marrow to release erythroblasts, hence the name “erythroblastosis fetalis”)

Increased immature RBCs
Pathogenesis
* When erythroblasts are used up in the bone marrow, erythropoiesis in the spleen and liver are increased
Bilirubin
* Hemoglobin is metabolized to bilirubin
Diagnosis & Management
* Serologic Testing (mother & newborn)
* Amniocentesis and Cordocentesis
* Intrauterine Transfusion
* Early Delivery
* Phototherapy & Newborn Transfusions

Serologic testing on mother
* ABO and Rh testing
* Antibody Screen
* Antibody ID
* Paternal phenotype
* Amniocyte testing
* Antibody titration
Marsh score
Example:
Amniocentesis & Cordocentesis
* About 18-20 weeks’ gestation
* Cordocentesis takes a sample of umbilical vessel to obtain blood sample
* Amniocentesis assesses the status of the fetus using amniotic fluid
Analysis of amniotic fluid (example)
Liley graph
What to do?
* Intrauterine transfusion is done if:
* Removes bilirubin
* Removes sensitized RBCs
* Removes antibody

Other treatments
* Early Delivery
* Phototherapy (after birth)
* Newborn transfusion

Postpartum testing
* ABO – forward only
* Rh grouping – including weak D
* DAT
* Elution
Prevention
* RhIg (RhoGAM®) is given to the mother to prevent immunization to the D antigen

Postpartum administration of RhIg
Dose
Rosette Test
* A qualitative measure of fetomaternal hemorrhage

Fetomaternal Hemorrhage:
Kleihauer-Betke acid elution
Calculating KB test
Step 1) stain and count the amount of fetal cells out of 1000 total cells counted
Step 2) calculate the amount of fetal blood in cirulation by multiplying %fetal cells by 50 mL
Step 3) divide mL of fetal blood by 30 (each vial protects against a 30 mL bleed
Step 4) Round the calculated dose up and add one more vial for safety

Considerations
* RhIg is of no benefit once a person has formed anti-D
* It is VERY important to distinguish the presence of anti-D as:
o Residual RhIg from a previous dose OR
o True immunization from exposure to D+ RBCs
* RhIg is not given to the mother if the infant is D negative (and not given to the infant)

* Make sure presence of anti-D is not due to antenatal administration of Rh immune globulin
Hemolytic Disease of the Newborn and Fetus.ppt

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25 March 2010

Chronic Pelvic Pain



Chronic Pelvic Pain
By:Jennifer Griffin, MD
M3 Student Clerkship Lecture
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.

Chronic Pelvic Pain
* Gynecologic
* Gastrointestinal
* Urologic
* Musculoskeletal/ Pelvic Floor
* Psychological
* United Kingdom data:
o Urinary dx 30.8%
o GI dx 37.7%
o Gynecologic 20.2%
o 25-50% have >1 dx
o MC Dx = endometriosis, adhesions, IBS, IC
Getting the History
* Nature of the Pain:
o Sharp, stabbing, colicky, burning?
o Where specifically is it located?
* Timing of the Pain:
o Does it come and go or is it constant?
o Does it occur with certain activities?
o Is it related to menses?
o Is it consistent and predictable?
* Modifying factors:
o Can you do anything to make it better/ worse?

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?
Chronic Pelvic Pain
* 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.

Chronic Pelvic Pain: Cyclic
* Endometriosis
Chronic Pelvic Pain: Cyclic
* Endometriosis: Etiology
* Endometriosis: Classic Triad
* But may present with:
o Chronic pelvic pain
o Adnexal mass
* Endometriosis: Diagnosis
* Endometriosis:
* Endometriosis: Treatment
* Dysmenorrhea
* Leiomyomas
* Adenomyosis
* Dyspareunia
* Vaginismus

Chronic Pelvic Pain: Dyspareunia
* Pelvic Floor Muscle Spasm and Strain
Chronic Pelvic Pain: Non-cyclic
* Pelvic congestion syndrome
* Pelvic organ immobility
* PID
* Infectious causes
* Gynecologic malignancies
* Other Gynecologic origin:
* Treatment of Gynecologic Problems
* Urologic Origin, Level A:
o Bladder malignancy
o Interstitial Cystitis
o Radiation Cystitis
o Urethral Syndrome
* Bladder origin, Level B:
* Urologic origin, Level C:
* Urologic origin
* Urologic origin: Interstitial Cystitis
* Gastrointestinal Origin, Level A:
* IBS
* Irritable Bowel Syndrome
* 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
* Medical treatment of most likely diagnosis.
* Psychiatric evaluation and treatment.
* Pelvic physical therapy.

Case Studies
Chronic Pelvic Pain
* Conclusions:
o Thorough history and physical
o Imaging and lab studies
o Many treatment options available

Chronic Pelvic Pain.ppt

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Pelvic Pain – Dysmenorrhea and Endometriosis



Pelvic Pain – Dysmenorrhea and Endometriosis

* A 20 y.o. woman presents to her gynecologist with a 4 year history of increasing lower abdominal pain with her menses. The pain begins on the first day of her menses and lasts 2-3 days. She also complains of lower back pain and nausea. Menarche occurred at the age of 13 and her menses occur every 28 days and last 5 days. Physical and pelvic exam are normal.

* How is dysmenorrhea diagnosed? How is it distinguished from other types of pelvic pain?
* What is the pathophysiology of dysmenorrhea?
* What are reasonable approaches to treatment?

Dysmenorrhea
* Dysmenorrhea – severe, painful cramping sensation in the lower abdomen often accompanied by other symptoms – sweating, tachycardia, headaches, n/v, diarrhea, tremulousness, all occurring just before or during menses
- Primary: no obvious pathologic condition, onset < 20 years old - Secondary: associated with pelvic conditions or pathology Primary Dysmenorrhea * Pathogenesis: elevated PG F2α in secretory endometrium (increased uterine contractility) * Treatment: NSAIDs – PG synthetase inhibitors – 1st line treatment of choice * Other treatment options: OCPs, other analgesics Secondary Dysmenorrhea * Etiologies - Cervical Stenosis - Endometriosis and Adenomyosis - Pelvic Infection - Adhesions - Pelvic Congestion - Stress and Tension * Cervical Stenosis - Severe narrowing of cervical canal may impede menstrual outflow – congenital or iatrogenic - can cause an increase in intrauterine pressure during menses - can lead to endometriosis * Cervical Stenosis - Hx – scant menstrual flow, severe cramping throughout menses - Dx – inability to pass a thin probe through the internal os OR HSG demonstrates thin cx canal - Tx – cervical dilation via D&C or laminaria placement * Pelvic Congestion - Due to engorgement of pelvic vasculature - Hx – burning or throbbing pain, worse at night and after standing - Dx – Laparoscopic visualization of engorgement/varicosities of broad ligament and pelvic sidewall veins Evaluation of Pelvic Pain * Detailed history, targeted physical exam, labs (UA, UCx, CBC, HCG, tumor markers), diagnostic imaging studies (US, MRI, CT) as appropriate * Consider age of patient * “OLDCAAR”: onset, location, duration, context, associated sx, aggravating/relieving factors * Temporal characteristics: cyclic (e.g. dysmenorrhea), intermittent (e.g. dyspareunia), non-cyclic * Risk factors * GYN and Non-GYN causes DDx Pelvic Pain - GYN * GYN - Uterus - fibroids, adenomyosis, endometritis - Fallopian tubes - PID/salpingitis, hydrosalpinx, ectopic - Ovaries - cysts – functional, pathological, TOA, torsion; mittleschmerz - Other - endometriosis, adhesions, IUD/infection, severe prolapse DDx Pelvic Pain – Non-GYN * Urologic - UTI/urethritis, interstitial cystitis (IC), OAB, urethral diverticulum, nephrolithiasis, malignancy * GI - constipation, IBS, IBD (Crohn’s, UC), bowel obstruction, diverticulitis, malignancy, appendicitis * Musculoskeletal - trigger points, fibromyalgia, hernias, neuralgia, low back pain * Other - psychiatric – depression, somatization; abdominal cutaneous nerve entrapment in surgical scar; celiac disease Case 1 * At the age of 30, the patient presents with a 2 year history of infertility. Her menses are still regular but she has 2-3 days of spotting before her menses are due. She also complains of pain with intercourse and pelvic pain. In reviewing the patient’s history, the gynecologist notes that over the past year the patient was repeatedly treated by her internist with antibiotics for recurrent microscopic hematuria. * What is the most likely diagnosis? * What are the main theories regarding the pathogenesis in this case? * How would you evaluate and treat this patient? Endometriosis - Symptoms * Variable and unpredictable - asymptomatic - dysmenorrhea - CPP - deep dyspareunia - sacral backache w/ menses - dysuria +/- hematuria (bladder involvement) - dyschezia/hematochezia (bowel involvement) Endometriosis – Physical Exam * Uterosacral nodularity * Adnexal mass (endometrioma) * Normal exam Endometriosis - Incidence * 7-10% of general population * 20-50% of infertile women * 70-85% in women w/ CPP * No racial predisposition * +Familial association with almost 10x increased risk of endometriosis if affected 1st degree relative Endometriosis - Pathogenesis * Retrograde menstruation (Sampson) * Hematogenous or lymphatic spread (Halban) * Coelomic metaplasia (Meyer/Novack) * Iatrogenic dissemination * Immunologic defects (Dmowski) * Genetic predisposition Endometriosis - Pathogenesis * Retrograde menstruation (Sampson’s theory) - Monkey experiments – sutured cervix closed to create outflow obstruction caused development of endometriosis - Clinical observation of retrograde menstrual flow during laparoscopy in humans - Increased risk of endometriosis in women with cervical/vaginal atresia, other outflow obstruction - Increased risk with early menarche, longer and heavier flow - Decreased risk with decreased estrogen levels e.g. exercise-induced menstrual disorders, decreased body fat, + tobacco use Endometriosis - Pathogenesis * Hematogenous or lymphatic spread - Endometriosis found in remote sites – lung, nose, spinal cord, pelvic lymph nodes. Endometriosis - Pathogenesis * Coelomic metaplasia - Mullerian ducts are derived from coelomic epithelium during fetal development - Hypothesize that coelomic epithelium retains ability for multipotential development - Endometriosis seen in prepubertal girls, women w/ congenital absence of the uterus, and RARELY in men Endometriosis - Pathogenesis * Iatrogenic dissemination - Endometriosis has been found in cesarean section scar * Immunologic defects * Genetic predisposition - polygenic, multi-factorial Endometriosis - Diagnosis * Laparoscopy with biopsy proven histologic diagnosis – standard for dx of endometriosis * Empiric medical treatment with improvement in symptoms * CA 125 – NOT considered to be of clinical utility * Imaging – US, MRI, CT – only useful in the presence of pelvic or adnexal masses (endometriomas) * Laparoscopy with biopsy proven histologic diagnosis – standard for dx of endometriosis - Extent of visible lesions do not correlate with severity of sx, but depth of infiltration of lesions seems to correlate best with pain severity - classic powder-burn lesions, endometriomas - lesions can be red, clear or white – more commonly seen in adolescents * Endometrial epithelium * Endometrial glands * Endometrial stroma * Hemosiderin-laden macrophages 2 or more of the following histologic features are criteria for Dx: * Imaging – US, MRI, CT – only useful in the presence of pelvic or adnexal masses (endometriomas) - on US, endometriomas appear as cysts that contain low-level homogeneous internal echoes consistent with old blood (ddx includes hemorrhagic cysts) Endometriosis - Treatment * Medications - Progestins - OCPs – continuous vs. cyclic – if no relief in 3 months, consider tx with Depo Provera or GnRH agonist - NSAIDs - GnRH agonists – most expensive - Danazol – appears to be as effective as GnRH agonist for pain relief but with increased side-effects * GnRH agonists – create a state of relative estrogen deficiency – vasomotor side effects and potential decrease in bone density - 12-month course of GnRH agonist therapy associated with 6% decrease in bone density - No data regarding extended treatment with GnRH agonists beyond 1 year * Add-back therapy is advocated for women undergoing long-term therapy (i.e. > 6 months)
* Some evidence to suggest that immediate add-back therapy may result in even less bone loss
- Add-back regimens: progestins alone, progestins + bisphosphonates, low-dose progestins + estrogens, pulsatile PTH

Endometriosis – Treatment Considerations in Adolescents
* GnRH treatment is NOT recommended for patients < 18 years because the effects of these medications on bone formation and long-term bone density have not been adequately studied * Depo provera used for longer than 2 years has been shown to decrease bone density in adolescents – FDA warning against long-term use * If no improvement in symptoms after 3 months of empiric treatment with NSAIDs and OCPs, diagnostic laparoscopy should be offered Endometriosis - Treatment * Surgery - Laparoscopic laser vaporization vs. cauterization vs. excision - Ovarian cystectomy for endometrioma - Hysterectomy +/- BSO * Medications vs. Surgery - Lack of data to support surgery vs. medical treatment for tx of pain symptoms due to endometriosis - Starting with empiric medical therapy is appropriate - Offer GnRH agonist therapy if initial medical treatment with OCPs and NSAIDs not helping - Cost of comparing empiric medical management with definitive surgical diagnosis is difficult to assess, but 3 months of empiric treatment is less than a laparoscopic procedure .... Pelvic Pain – Dysmenorrhea and Endometriosis.ppt

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14 March 2010

Hematologic Complications of Pregnancy



Hematologic Complications of Pregnancy
By:Joseph Breuner, MD

outline
* Anemia
* Thrombophilias
* Thrombocytopenia

Case #1
* Anemia, pro’s and cons of treating
Which patients will benefit from iron treatment?
What hematocrit at 28 wks should generate attention?
* Dilutional or physiologic
* Iron Deficiency Anemia
* Thalassemias

Physiologic Anemia of Pregnancy
* Pregnancy-induced hypervolemia has several important functions:
1. To meet the demands of the enlarged uterus with its greatly hypertrophied vascular system.
2. To protect the mother, and in turn the fetus, against the deleterious effects of impaired venous return in the supine and erect positions.
3. To safeguard the mother against the adverse effects of blood loss associated with parturition.

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Psychiatric Complications of Pregnancy and the Postpartum



Psychiatric Complications of Pregnancy and the Postpartum
By:Joseph Breuner, MD
Swedish Family Medicine Residency

Objectives
    * Appreciate the postpartum period as a time of increased vulnerability to psychiatric illness
    * Recognize and diagnose psychiatric illness during pregnancy and the postpartum
    * Understand risks to the fetus of psychiatric medications
    * Prevent and treat psychiatric illness in pregnancy and the postpartum

Outline 1
    * Review DSM-IV diagnoses
    * Psychiatric illness during pregnancy
    * Psychiatric illness in the postpartum

But first, a review
DSM-IV Definition of...

    *   For at least one week (or less, if hospitalized) the patient's mood is
    *   abnormally and persistently high, irritable or expansive.
    *   To a material degree during this time, the patient has persistently had 3 or
    *   more of these symptoms (4 if the only abnormality of mood is irritability):
    *   -Grandiosity or exaggerated self-esteem
    *   -Reduced need for sleep

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11 February 2010

Tools of Prenatal Diagnosis



Tools of Prenatal Diagnosis
By:Julie Moldenhauer, MD
Reproductive Genetics
Maternal Fetal Medicine
Obstetrics and Gynecology

Objectives:
* Discuss various prenatal screening and testing tools
* Discuss the timing of the various tools in gestation
* Discuss benefits and risks of various options
* Review the difference between screening and testing
Baseline Risk for Birth Defects in the General Population is 3-5%
What Can We Diagnose in the Prenatal Setting?
* Structural Abnormalities
o Congenital heart disease
o Spina bifida
o Gastroschisis
* Chromosomal Abnormalities
o Trisomy 21
o Triploidy
* Infections
o Parvovirus
o Cytomegalovirus
o Toxoplasmosis
* Growth Abnormalities
* Hematologic Abnormalities
o Anemia
o Thrombocytopenia
* Functional Defects
o Arthrogryposis
o Renal dysfunction
* Syndromes
o Skeletal Dysplasia
o Diabetic embryopathy

Prenatal Diagnosis Tools

* History
o Personal History
o Family History
* Population Screening
* Serum Screening
* Ultrasound
* Fetal MRI
* Invasive Diagnosis
o Chorionic villus sampling
o Amniocentesis

History is a Screening Tool!
o Maternal Age
+ > 35 years at delivery
o Obstetric History
+ Prior baby born with Down syndrome
+ Prior stillbirth
o Medical History
+ Is mom diabetic? How well controlled is her sugar?
+ Does she have PKU?
+ Is she hypertensive?
o Medication Exposures
+ What medications?
+ When was the exposure?
o Environmental Exposures
+ Does she work in a preschool and was exposed to parvovirus?
+ Is she exposed to high doses of radiation?
o Family History
+ Brother with hemophilia
+ Uncle with cystic fibrosis
+ Ethnic background
+ Consanguinity

As maternal age increases, the risk for aneuploidy increases. This is due to maternal meiotic nondisjunction.
Maternal age > 35 at the time of delivery is considered “Advanced Maternal Age” or AMA
The risk for recurrence of chromosome abnormalities is dependent upon the genetic mechanism involved.
Trisomy: 1% or maternal age-related risk
Translocation:
Maternal carrier: 10-15%
Paternal carrier: 2%

Down syndrome phenotype caused by trisomy 21
Down syndrome phenotype caused by 14;21 translocation

Maternal Diabetes: Reproductive Risks
* Fetal and Neonatal
o Congenital anomalies: 6-12%
o Intrauterine fetal demise
o Macrosomia – Shoulder dystocia
o Growth restriction
o Hyperbilirubinemia
o Hypoglycemia
o RDS
o Polycythemia
o Organomegaly
o Long term – obesity and carbohydrate intolerance
* Obstetric
o Spontaneous preterm labor
o Polyhydramnios
o Preeclampsia (15-20%)
o Intrauterine growth restriction
o Shoulder dystocia
o Cesarean delivery

Caudal Regression Syndrome
Teratogen Exposure
Fetal growth
Organogenesis complete
Eyes, heart, lower limbs
Axial skeleton, limb buds, musculature
CNS
None, “ALL or NONE”
* Examples:
* Accutane
* ACE inhibitors
* Lithium
* Antiepileptic drugs (AEDs)
* Anticoagulants: warfarin
* Antidepressants
* Methotrexate
* Thalidomide

Teratogen Exposure
* Fetal effects are timing and dose dependent

* Each medication is assigned a pregnancy category based on available data; A-D, X
* www.Reprotox.org
* www.otispregnancy.org

Ultrasound images of fetal hydrops – abnormal collection of fluid in multiple body compartments.
Mom works at a daycare where there was a Parvovirus B19 or Fifth Disease outbreak 4 weeks ago. Parvovirus causes fetal aplastic anemia that can be life-threatening.

Suspicion of diagnosis by altered maternal serum titers of Parvo IgG and IgM and confirmed by amniotic fluid PCR for Parvo.
Confirmed Parvo infection in a fetus with hydrops can be treated with intrauterine blood transfusions.

Fetal Ultrasound Showing Cardiac Rhabdomyoma
Fetal MRI Showing Tubers
Prenatal Findings Consistent with Tuberous Sclerosis Confirmed as Neonate
Screening for Genetic Disease
Ethnic Group Disease
African American Sickle Cell Disease: 1/12
Mediterranean Beta-Thalassemia: 1/30
Southeast Asian Alpha-Thalassemia: 1/20
Caucasian Cystic Fibrosis: 1/25

ASHKENAZI JEWISH ANCESTRY
GENETIC CARRIER TESTING
Gaucher’s disease
Bloom syndrome
Mucolipidosis IV
Niemann-Pick disease type A
Fanconi Anemia Group C
Familial Dysautonomia
Cystic Fibrosis
Canavan disease
Tay-Sachs disease
Detection rate
Carrier Frequency
Disease Incidence
Testing and screening options should be made available to all pregnant women
Prenatal Screening & Testing
When Screening
(risk estimate)
Definitive
(Invasive)
First Trimester
FIRST screen*
Ultrasound
CVS

Second Trimester
Maternal Serum Screen*
Ultrasound
Amnio
Cordo
*First and Second Trimester Integrated and Sequential Screening

Test Performance
* Detection rate – the percentage of affected that are test “positive”
o (the higher, the better)
* False positive rate – the percentage of unaffected that are test “positive”
o (the lower, the better)

Goals in Prenatal Screening:
* High sensitivity - low false positive rate
* Wide availability
* Reproducibility and accuracy
o Human error, testing conditions

First Trimester Screening
o 11-13 6/7 weeks (CRL 39-79 mm)
o Maternal serum sample for PAPP-A and Free b-HCG
o Ultrasound for Nuchal translucency
o Detection Rates:
+ 80% for Trisomy 21
+ 90% for Trisomy 18
+ Does not screen for NTDs

PAPP-A
b-HCG
T21
T18

Increased NT vs Cystic Hygroma
* Increased NT > 95th%
o With or without septations
* Structural defects
o Heart defects most common
* Syndromic associations
* Chromosomal defects
o Exponential increase with increased NT
o 50% Down syndrome
o 25% Trisomy 13 or 18
o 10% Turner Syndrome
o 5% Triploidy
o 10% other

NT > 3 mm is ABNORMAL
Second Trimester Serum Screening: Chromosome Abnormalities

* Maternal Serum Screening
o 15-20 weeks
o Triple screen: 60% for T21
o Quad screen: 70% for T21
o Gestational Age Dependent**
* Targeted Ultrasound
o 50% aneuploid fetuses will have ultrasound markers
AGE +AFP +hCG +uE3 +InhA
DR at 5% FPR
2nd trimester
single double triple quadruple
Serum Screening Test Performance at a fixed 5% False Positive Rate (Dating by Ultrasound)

Prediction
SURUSS
FASTER
Second Trimester Serum Screening: Neural Tube Defects
* Neural Tube Defects
o Spina Bifida
o Anencephaly
* AFP increased in “open” defects
* Sensitivity
o 90% anencephaly
o 80-85% open spina bifida
* False positive – 3-4%
Interpreting a Quadruple Screen

Bottom Line: AFP is increased with NTDs and decreased with chromosome abnormalities

Elevated MSAFP
* Incorrect Dates – most common reason
* Multiples
* Congenital Nephrosis
* Ventral Wall Defects
* IUFD
* Adverse Pregnancy Outcomes
o Stillbirth
o Placental abruption
o Preterm labor
o Oligohydramnios
o IUGR

Ultrasound detection of aneuploidy
Nuchal Fold
CPC
Duodenal atresia
Pyelectasis
Clinodactyly
Second trimester sonographic markers of Down syndrome
AV Canal
Trisomy 18
Edward Syndrome
* Close to 90% detected by prenatal scan
* US:
o Growth restriction
o Clenched fists
o >90% with cardiac defects
o Multiple malformations
* Grim prognosis
o 50% Stillbirth
o 50% die within the first week
o 5-10% survive the first year

Trisomy 13
Patau Syndrome
Fetal Anatomy by Ultrasound
Ventral Wall Defect
Gastroschisis
NTDs
Lemon Sign
Banana Sign
Meningomyelocele Sac
Meningomyelocele Sac on Newborn
PGD: Preimplantation Genetic Diagosis
Pearls for Invasive Testing
* Risk for Sensitization
o Mom Rh negative – Rhogam
o Other antibodies may increase risk
* Risk for Infection transmission
o Hepatitis B
o Hepatitis C
o HIV
o Need to know familial mutations prior to performing invasive testing

Chorionic Villus Sampling
* Performed 10-14 weeks
* Does not test for ONTD
* Technique – “Placental biopsy”
o Transabdominal
o Transcervical
* Risk for limb reduction defects if performed < 9 weeks
* Loss rate 1/100-1/200
* Risk for mosaicism (~1%)

Transcervical
CVS
Transabdominal
Performed at 10-14 weeks
Amniocentesis
* > 15 weeks
* Loss rate 1/200 (probably closer to 1/300-1/500)
* Tests for ONTD
* Technique
o Fine gauge needle
o Ultrasound guidance
o Aspiration of 20-30 cc of fluid

PERFORMED ROUTINELY 15-20 WEEKS
Ultrasound Guided Procedure
AMNIOCENTESIS
Cordocentesis
* Percutaneous Umbilical Blood Sampling
* Loss rate 1/100-1/200
* Typically done after 18 weeks
* Ability for:
o Rapid karyotype
o Blood/platelet counts
o Direct fetal injections/transfusions

Fetal Blood Sampling
“PUBS”
Conclusions

* Many options for screening and testing.
* Prenatal screening should provide the most effective test to the greatest number of women.
* The best method of screening is yet to be determined.
* Patient preference should be considered.
* Testing and screening should be available to all women.

Tools of Prenatal Diagnosis.ppt

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Physiologic Changes in Pregnancy



Physiologic Changes in Pregnancy
By:Thomas S. Ivester, MD, MPH
Maternal-Fetal Medicine

Relevance of OB physiology
* 5-10 % of women in ER are pregnant
o Many don’t know or show
* Any female of reproductive age could be pregnant
o Should be assumed so!
* Virtually every organ system affected
* Can touch almost any specialty

Case history
Case 1

* 36 y.o. female presents to ER
* CC: Fatigue, dyspnea, chest pain
* HPI:
o Progressive SOB and dyspnea over several weeks.
o Poor exercise tolerance and easy fatigability
+ ‘get winded after 1 flight of stairs’
o Substernal chest pain, peaks in morning and night
o Nocturnal cough, semi-productive – clear
o Leg swelling
o polyuria
* PMH
o Mild obesity
* Ob/gyn – menses at age 12; irregular menses; no pregnancies
* Meds
o Oral contraceptives
o multivitamins
* Social
o Married for 2 years. No exposures

Case 1: PE
* Skin
o warm, clammy. Mild facial acne and increased hair – medium coarseness
* HEENT
o NC/AT. Nasal mucosa slightly hyperemic.
o Mild non-nodular thyromegaly
* CV
o Tachycardia (HR 107)
o + JVD
o 2/6 systolic murmurs over pulmonic and aortic v.
* Chest
o Clear bilaterally. Diaphragm elevated with decreased excursion
* Ext
o 1+ pretibial pitting edema
* Abd
o Skin – spider angiomata and striae. Medium course hair, infraumbilical.
o Distended, firm, non-tender.

Studies / labs
* EKG:
o Sinus rhythm; tachy; Left axis deviation
* CXR:
o Lungs clear. Cardiomegaly. Increased vascular markings
* Labs:
o Hct 32% (low); WBC 12 (high)
o Cholesterol 300 mg/dl
o D-dimer elevated
o Potassium and creatinine low

What does she have???
General Principles
* Most changes begin early
o Even before pregnancy recognized
* Most are hormonally driven
o Progesterone, estrogen, renin / aldosterone, cortisol, insulin
o Some ‘mechanically’ driven
* Designed to optimize conditions for fetus & prepare for delivery
o Delivery of oxygen & nutrients
Cardiovascular & Hematologic
* Vascular
o Decreased tone / vaso-relaxation
+ SVR decreased 20%
o Positional effects
o Placenta – low resistance shunt
* Hematologic
o Blood volume increases 50-100%
o RBC increases 25-40%
+ Relative anemia (“physiologic”)

Hematologic
* Hypercoagulable
o Estrogen & Vascular stasis
o Increased risk for thromboembolic disease
+ Increase in fibrinogen, all coag factors except II, V, XII
+ Fall in protein S and sensitivity to APC
* Fall in platelets and factor XI and XIII
* Increase in WBC

Changes in the Pump
* Cardiac axis displaced cephalad and left
o PMI lateral & elevated (not just due to baby!)
+ Altered thoracic dimensions
o Left axis deviation
* Murmurs > 96%
o Virtually all valves
+ Esp. Aortic and Pulmonary
+ Mammary Souffle
* Rate – increased (80’s typical)
* Ventricular distention – 25% increase
* Rhythm
o Non-specific ST & T changes
o Increase in dysrhythmias
+ Physiologic hypokalemia
* Anatomy
o LVH & Pericardial effusion
* Function
o Increased & markedly fluctuating output

Blood Pressure
Pregnancy Adaptations
Anatomical considerations
Uterine Position over Time
Cardiac Output – Positional Effects
* Aorto-caval Compression
Labor Changes
* SVR – Increased 10-25% with CTX
* Volume – autotransfusion 300-500cc
* Cardiac output -
o <3cm Increased 17%
o 4-7cm Increased 23%
o >8cm Increased 34%
The Fetus and Placenta
* Fetus (aka – “the parasite”)
o A sensitive survivor
o A window
* Placenta
o A veritable hormone factory
o Receives 20-25% of cardiac output*
+ 750-1000 ml/min
+ Refractory to vasoactive meds
o Uses as much O2 as fetus

Normal physiology or disease?
Signs & Symptoms of Normal Pregnancy that may Mimic Heart Disease
* Signs
o Peripheral edema
o JVD
* Symptoms
o Reduced exercise tolerance
o Dyspnea
* Auscultation
o S3 gallop
o Systolic ejection murmur
* Chest x-ray
o Change in heart position & size
o Increased vascular markings
* EKG
o Nonspecific ST-T wave changes
o Axis deviation
o LVH
Other systems
Changes in the Filter
* Renin – stimulated by progesterone
o Also made by placenta
o Angiotensinogen Angiotensin I Angiotensin II Aldosterone Distal tubule
+ Net absorption of Na+
+ Excretion of K+
+ Water retention: 6-8 liters
* Increased renal blood flow
o 50-75% increase
o GFR – 50% increase
o Decreased Albumin = lower colloid oncotic pressure

Other urinary tract changes
* Ureteral dilation / hydroureter
o Smooth muscle relaxation
o Later exacerbation by uterine obstruction
o Urinary stasis*
* Dilation of pelves and calyces
* Increased kidney size
Lungs and respiration
Respiratory Adaptations
o No change in rate or IRV
o Thorax
+ Tr. Diameter 2cm; circumference 5-7cm
o Increased minute ventilation
o Reduced FRC – 20%
o Increased Tidal Volume – 30-40%
o Compensated respiratory alkalosis
+ pH 7.4+
+ PaO2; PaCO2 (40 – 30)
+ Drives gradient b/w mom and fetus

Respiratory Changes
Gastrointestinal
* Slowed GI motility
o Constipation, early satiety
* Relaxation of LES
o GERD
* Nausea / vomiting
o Often proportional to HCG level
* Liver / gallbladder
o Biliary stasis, cholesterol saturation
+ More stones
o Coagulation factors
o Increased binding proteins (thyroid, steroid, vitamin D)
Other “Adaptations”

* “I can’t see my feet!!!”
o Altered center of gravity
o Altered gait
o Greater joint laxity
+ Widening of symphysis pubis
+ Affects other joints
+ Thorax; widened costovertebral angle
o Fatigue / somnolence

Integumentary Changes
* Spider angiomata and palmar erythema
* Hair growth (abdomen and face)
* Mucosal hyperemia
* Striae gravidarum
* Hyperpigmentation (esp. linea nigra)
o Rashes and acne relatively common
Other Endocrine
* Pancreas
o Carbohydrate metabolism -Insulin resistance
+ Human placental lactogen, cortisol
* Thyroid Function
o Increased TIBG (via liver)
o Increased total T4 and T3
+ free levels unchanged
+ HCG suppresses TSH
* Adrenal function
o Free plasma cortisol is elevated
+ CRH from placenta stimulates ACTH
Immunology

* Must adapt to accept ‘allograft’
* Immune response altered, but not deficient
* Modulates away from cell-mediated cytotoxic effects
o Progesterone effect
o NK cells decrease by 30%
o Enhanced humoral / innate immunity
+ Immunoglobulins still active
+ IgG crosses placenta
o More susceptible to CMV, HSV, Varicella, Malaria
o Decrease in symptoms of some autoimmune disorders

Pregnancy – not a disease

* Profound changes in physiology and anatomy
* Affects most organ systems
* Can dramatically impact disease states, susceptibility, and treatment
* Almost all will encounter and treat pregnant women
o Even if you don’t know it
* Under-appreciation of changes will lead to suboptimal treatment or outright mistakes

Physiologic Changes in Pregnancy.ppt

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27 September 2009

SGA and IUGR



SGA and IUGR
By Tina Burleson Stewart, MD

What is the difference between SGA and IUGR?
Can these terms be used interchangeably?
SGA - small for gestational age infants
* an infant whose weight is lower than the population norms
* defined as weight below 10th percentile for gestational age or greater than 2 standard deviations below the mean
* cause may be pathologic or nonpathologic

IUGR - intrauterine growth retardation
* defined as failure of normal fetal growth
* caused by multiple adverse effects on fetus
* due to process that inhibits normal growth potential of fetus


So what is the difference between SGA and IUGR?
* These terms are related but not synonomous.
* Not all IUGR infants are small enough to fit the qualifications for SGA.
* Not all SGA infants are small because of a growth-restrictive process, and therefore, do not meet criteria for IUGR.

Incidence
* 3-10% of all pregnancies
* 20% of stillborn infants
* perinatal mortality 4-8 times higher
* half have serious or long-term morbidity

Epidemiology
* more common in low socioeconomic class
* more common in those of African-American race
* leading cause in third world countries is inadequate nutrition of mother
* leading cause in US is uteroplacental insufficieny

Causes of IUGR
* maternal factors
* fetal factors
* placental factors
* environmental factors

Maternal causes of IUGR
* inadequate nutrition of mother
* multiple gestation
* uteroplacental insufficiency
* hypoxia
* drugs

Mother’s Malnutrition
* lack of adequate food supply
* poor weight gain
* chronic illness
* malabsorption

Multiple Gestation
* difficult to provide optimal nutrition for greater than one fetus
* uterine capacity limitations

Uteroplacental Insufficiency
* preeclampsia
* chronic HTN
* renovascular disease
* vasculopathy from diabetes
* drugs

Hypoxia
* maternal hemoglobinopathies - sickle cell
* maternal anemia
* maternal cyanotic heart disease
* mom living at high altitudes

Maternal Drug Use and Toxin Exposure
* cigarettes
* cocaine
* amphetamines
* antimetabolites - MTX
* bromides
* heroin
* hydantoin
* isoretinoin (Accutane)
* methadone
* alcohol
* methyl mercury
* phencyclidine
* phenytoin (Dilantin)
* polychlorinated biphenyls
* propanolol
* steroids - prednisone
* toluene
* trimethadione
* warfarin (Coumadin)

Fetal Causes of IUGR
* genetics
* congenital infection
* inborn errors of metabolism

Chromosome Disorders associated with IUGR

* trisomies 8, 13, 18, 21
* 4p- syndrome
* 5p syndrome
* 13q, 18p, 18q syndromes
* triploidy
* XO - Turner’s syndrome
* XXY, XXXY, XXXXY
* XXXXX

Syndromes associated with low birth weight
* Aarskog-Scott syndrome
* anencephaly
* Bloom syndrome
* Cornelia de Lange syndrome
* Dubowitz syndrome
* Dwarfism (achondrogenesis, achondroplasia)
* Ellis-van Creveld syndrome
* Familial dysautonomia
* Fanconi pancytopenia
* Hallerman-Streiff syndrome
* Meckel-Gruber syndrome
* Microcephaly
* Mobius syndrome
* Multiple congenital anomalads
* Osteogenesis imperfecta
* Potter syndrome
* Prader-Willi syndrome
* Progeria
* Prune-belly syndrome
* Radial aplasia; thrombocytopenia
* Robert syndrome
* Robinow syndrome
* Rubinstein-Taybi syndrome
* Silver syndrome
* Seckel syndrome
* Smith-Lemli-Opitz syndrome
* VATER and VACTERL
* Williams syndrome

Congenital Infections associated with IUGR
* rubella
* cytomegalovirus
* toxoplasmosis
* herpes
* syphilis
* varicella
* hepatitis B
* coxsackie
* Epstein-Barr
* parvovirus
* Chagas disease
* malaria

Metabolic disorders associated with low birth weight
* agenesis of pancreas
* congenital absence of islets of Langerhans
* congenital lipodystrophy
* galactosemia
* generalized gangliosidosis type I
* hypophosphatasia
* I cell disease
* leprechaunism
* maternal and fetal phenylketonuria
* maternal renal insufficiency
* maternal Gaucher disease
* Menke syndrome
* transient neonatal diabetes mellitus

Placental Causes of IUGR
* placental insufficency
o very important in the 3rd trimester
* anatomic problems
o infarcts
o aberrant cord insertions
o umbilical vascular thrombosis
o hemangiomas
o premature placental separation
o double vessel cord
* microscopic changes
o villous necrosis
o fibrinosis

Environmental Causes of IUGR
* high altitude - lower environmental oxygen saturation
* toxins

IUGR classification
* SYMMETRIC
* height, weight, head circ proportional
* early pregnancy insult: commonly due to congenital infection, genetic disorder, or extrinsic factors
* normal ponderal index
* low risk of perinatal asphyxia
* low risk of hypoglycemia
* ASYMMETRIC
* head=height, both > weight
* brain growth spared
* later in pregnancy: commonly due to uteroplacental insufficiency, maternal malnutrition, hypoxia, or extrinsic factors
* low ponderal index
* increased risk of asphyxia
* increased risk of hypoglycemia

Ponderal Index
* The ponderal index is used determine those infants whose soft tissue mass is below normal for their stage of skeletal development. Those who have a ponderal index below the 10th % can be classified as SGA.
* Ponderal Index = birth weight x 100 crown-heel length

Diagnosis
Prior to delivery, it is necessary to determine the correct gestational age.
* last menstrual period - most precise
* size of uterus
* time of quickening (detection of fetal movements)
* early ultrasound - the earlier the better accuracy
o biparietal diameter
o abdominal circumference - best sensitivity
o ratio of head to abdominal circumference
o femur length
o placental morphology and amniotic fluid

Diagnosis after delivery (OUR JOB!)
* low birth weight - this parameter alone misses big IUGR infants and overdiagnoses constitutionally small infants
* appearance - thin with loose, peeling skin; scaphoid abdomen; disproportionately large head; may be dysmorphic
* ponderal index
* Ballard/Dubowitz - accurate within 2 weeks of gestation if birth weight >999g, most accurate within 30-42 hrs of age
* birth/weight curves

Complications
* hypoxia
o perinatal asphyxia
o PPHN
* hematologic - polycythemia
* meconium aspiration
* metabolic
o hypoglycemia
o hypocalcemia
o acidosis
* hypothermia
* neurological
o more tremulous
o more easily startled
o less visual fixation
o less activity
o less oriented to visual and auditory stimuli

Management in utero
* serologic testing if desired by parents
* decrease mother’s activity
* stop or decrease risk factors if possible
* closely monitor with biophysical profile or nonstress testing or amniotic fluid measurements
* ultrasound every 10-21 days
* teach mom fetal kick counting
* deliver if reaches 36 weeks

Management after birth
* obtain history of risk factors
* appropriate resuscitation
* prevent heat loss
* watch for hypoglycemia
o check glucoses
o early feeding
o parenteral dextrose
* check hematocrit
* screen for congenital infections
* screen for genetic abnormalities
* check calcium

Outcome

* depends on cause of IUGR/SGA and neonatal course
* symmetric IUGR - poor outcome because early insult
* asymmetric IUGR - better outcome because brain spared
* very bad if brain growth failure starts at < 26 weeks
* school performance influenced by social class
* 25-50% likelihood of neurodevelopmental problems


SGA and IUGR.ppt

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16 July 2009

Nervous system in the abdomen and pelvis



Nervous system in the abdomen and pelvis

Targets of NS in abdomen and pelvis
Abdominal muscles (motor)
Body wall & parietal peritoneum (sensory)
Perineal muscles (motor)
(eg. external anal sphincter)
Perineal skin (sensory)
Sweat glands, erector pilae & sm mm of BVs in abdominal and perineal skin
Foregut smooth muscle & glands
Midgut smooth muscle & glands
Kidneys and suprarenal glands
Hindgut smooth muscle & glands
Blood vessels of GIT
Pelvic viscera and blood vessels
Smooth muscle & glands of reproductive tract
Blood vessels in erectile tissue

SYMPATHETIC
Gray rami of chain
ganglia
Thoracic
splanchnic nerves:
Lumbar splanchnic nerves
Sacral splanchnic Nerves
Prevertebral ganglia


PARA-SYMPATHETIC
Vagus
Pelvic splanchnic nerves
Intramural ganglia/enteric nervous system
SOMATIC
Abdomino-inercostal nerves
L1 spinal nerve
Pudendal nerve
ANS in the abdomen and pelvis:
important principles
Autonomic nerves are found in plexuses along the blood vessels or other major structures
In thorax:
In abdomen:
In pelvis:
Prevertebral plexus for abdominal viscera
Several parts: named for adjacent vessel or region

Lecture Plan
* Parasympathetic innervation of GIT and other structures
* Sympathetic innervation of GIT and other structures
* Referred pain
* Somatic nerves of the abdomen, pelvis and perineum
* Sympathetic
* Parasympathetic
ANS Divisions
Parasympathetic division
Intramural neurons are part of the enteric nervous system:
Parasympathetic Vagal trunk dissection
Left and right vagus nerves
Anterior (left) and posterior (right)
vagal trunks
Esophageal plexus
Parasympathetic
Pelvic splanchnic nerves
Targets of NS in abdomen and pelvis
Foregut smooth muscle & glands
Midgut smooth muscle & glands
Hindgut smooth muscle & glands
Pelvic viscera
Blood vessels in erectile tissue
Supply motor fibers to intramural ganglia
Greater thoracic splanchnic nerve
Targets of NS in abdomen and pelvis
Foregut smooth muscle & glands
Midgut smooth muscle & glands
Kidney, adrenal gland
Blood vessels of GIT
Hindgut smooth muscle & glands
Pelvic viscera (involuntary sphincters)
Smooth muscle and glands of reproductive tract
Lumbar splanchnic nerves
Sacral splanchnic nerves
Gray rami of chain ganglia
Lecture plan
* Parasympathetic innervation of GIT and other structures
* Sympathetic innervation of GIT and other structures
* Referred pain
* Somatic nerves of the abdomen, pelvis and perineum
Pain in the abdomen
Somatic pain
Example of visceral pain afferents
conveyed with sympathetic system
e.g. from stomach
* Pain originating from one structure but perceived as coming from another. Thus, pain from an organ can be perceived as originating from a somatic structure.
* Due to cross-talk in the CNS sensory pathways? brain misperceives origin of pain
* You can predict the site of referral, if you know the entry segment of visceral afferents, and the body’s dermatome map.
Involvement of parietal serous membranes
and much more are covered in this presentation.

Nervous system in the abdomen and pelvis.ppt

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Fetal outcomes: Comparison of gestational diabetes



Fetal outcomes: Comparison of oral agents with diet controlled and insulin controlled gestational diabetes
By:Amanda Hatton, MD
Investigators
* Amanda Hatton, MD
* Selman Welt, MD
* Samuel Prien, PhD

Background
* Gestational diabetes affects from 1-14% of pregnant mothers1
* Levels of diabetogenic placental steroids and peptide hormones (estrogen, progesterone, chorionic sommatomammotrophin) rise linearly throughout the second and third trimester resulting in progressively increasing tissue resistance to insulin2
* Maternal insulin resistance requires a significant increase in pancreatic insulin production to more than twice non-pregnant levels
* Failure to adequately compensate for increased demand of insulin production leads to maternal hyperglycemia followed by fetal hyperglycemia

Fetal health implications
* Fetal hyperglycemia leads to fetal hyperinsulinemia which has detrimental consequences to fetal growth and well-being2
* Promotes storage of excess nutrients leading to macrosomia
* Drives catabolism of oversupply of fuel, using energy and depleting fetal oxygen stores
* Episodic fetal hypoxia leads to increased adrenal catecholamines causing hypertension, cardiac remodeling, and hypertrophy
* Hypoxia also causes stimulation of erythropoietin which in turn increases hematocrit level and causes poor circulation and postnatal hyperbilirubinemia
* At birth fetal hyperinsulinemia in absence of maternal glucose supply leads to hypoglycemia

Treatment of GDM
* Glycemic monitoring, dietary regulation and medical therapy are used to control diabetes and prevent postnatal sequelae
* Insulin discovered in 1922, successful management of diabetic pregnancies became possible and the frequency of antepartum fetal death decreased by one half2
* Glycemic control must be instituted early and aggressively if excellent newborn outcome is to be achieved
* Oral agents such as acarbose and glyburide are aimed at augmenting insulin supply, decreasing insulin resistance, and limiting postprandial hypoglycemia
* These agents have been shown to be an effective and safe alternative, since they do not significantly cross the placenta in vitro3

Objectives
* To compare fetal outcomes in mothers with gestational diabetes treated with:
* Diet - ADA diet, weight dependent, 3 meals and 3 snacks
* Oral agents
* Acarbose - alpha-glucosidase inhibitor, reversibly inhibits enzymes in the small intestine, delaying cleavage of oligosaccharides and disaccharides to monosaccharides
* Glyburide - sulfonylurea compound, stimulates insulin release from the pancreatic beta cells, reduces glucose output from the liver and also increases insulin sensitivity at peripheral target sites
* Insulin – weight based split mix dose of NPH and Novolog, insulin pump therapy, or long acting insulin with supplementation
* This study was submitted to the IRB and was found to be exempt from formal IRB review

Experimental Design
* Retrospective chart review
* Identify mothers seen at Texas Tech Health Science Center (Lubbock) with gestational diabetes who were treated and delivered between January, 2005 and January, 2008
* Includes pregestational diabetics and those diagnosed by random blood sugar >200mg/dL or at least two abnormal values on a 3 hour 100g glucose challenge
* All patients were provided with diabetic education, including nutrition guidance at the onset of their prenatal care in the case of preexisting diabetes or soon after diagnosis

General Treatment Guidelines
Materials and Methods
* Review mother’s and infant’s charts to compare outcomes of different treatment modalities
* Class of gestational diabetes
* Treatment and changes in treatment
* Level of control
* Complications of pregnancy
* Mode of delivery
* Fetal weight
* Delivery complications
* Fetal complications (hypoglycemia, hyperbilirubinemia, respiratory distress)
* Patients diagnosed 36 weeks gestation will be excluded

Statistical Analysis
* Continuous data will be evaluated with an analysis of variance (ANOVA)
* Discrete data will be evaluated with a Chi-Square or Mann-Whitney U test
Results
* We expect to find similar fetal outcomes in diabetic mothers with blood glucose levels that are well controlled by diet, oral agents or insulin
* Thus far we have noted that there are no noticeable differences in outcomes pending a greater number of chart reviews and statistical analysis

References

Fetal outcomes: Comparison of gestational diabetes.ppt

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Ultrasonographic features of endometrium



Ultrasonographic features of endometrium in pre- and postmenopausal women
By:C. Tracy Suit, MD
Cornelia de Riese, MD
Samuel Prien, PhD
Kelsey Kelso, BS

Background

* The endometrium is a dynamic tissue
o Menstrual cycle
o Postmenopausal
o Exogenous hormones

Transvaginal US
* Non-invasive
* Relatively inexpensive
* Good safety profile
* Readily available

Normal endometrium
* Menstrual phase
* Proliferative phase
* Secretory phase
* In the follicular phase, the endometrium becomes relatively hypodense
* As the cycle progresses the endometrium becomes more hyperechoic
* Ovulatory period = trilaminar endometrium
* Usually disappears 48 hours after ovulation
* Postmenopausal women
* A small amount of fluid may be considered normal

Premenopausal—Differential Diagnosis
* Often due to normal proliferation under hormonal influences
* Can include:
o Polyps
o Polypoid growths
o Hyperplasia or cancer
o Submucosal fibroids
Postmenopausal
* Important distinction: symptoms
* Exogenous hormones
Postmenopausal—differential diagnosis
* Polyps
* Hyperplasia or cancer
* Fibroids
Associated sonographic findings
* Polyps: cystic spaces
* Hyperplasia: regular/homogeneous echotexture
* Cancer: irregular margins, indistinct borders between the endometrium and myometrium, heterogeneous echotexture, complex fluid

Study objective
* To evaluate the predictive value of endometrial thickness and descriptive sonographic appearance on pathology in pre- and postmenopausal women
Methods
* 1903 gynecologic ultrasounds of the endometrium were performed between January, 2004 and January 2009
* Stratification: Of these, 367 had pathology performed within 3 months of the ultrasound
* The patients were then divided into either pre- or post menopausal after review of the chart
* Each US was critically evaluated for:
o Endometrial thickness
o Descriptors of the endometrium
Exclusion criteria
* No corresponding pathology (EMB, curettage, or hysterectomy) within 3 months of the US
* No measurement of the endometrial thickness or distortion by fibroids so that the endometrium could not be meaningfully evaluated
* Patient less than 18 years old
Methods
* Pathology was classified into groups:
o Benign: proliferative or secretory, atrophic, or chronic endometritis
o Precancerous or cancerous: simple hyperplasia with or without atypia, complex hyperplasia with or without atypia, endometrial cancer
Statistics
* Endometrial descriptors were compared with pathology using a Chi-Square analysis
* Endometrial thickness and age were compared using a Student’s t-test
Results
Result: Postmenopausal group
Results: Premenopausal group
Conclusions
* Confirmed that endometrial thickness is increased in pathological conditions such as hyperplasia and cancer
* But hyperplasia was diagnosed often within the “normal” ranges, especially in the premenopausal women
* In the postmenopausal group, complex hyperplasia and cancer were diagnosed with an endometrial thickness of 3 and 5 mm, respectively
* In premenopausal women, the average endometrial thickness in women with pathology was still in the normal range for secretory endometrium
* In addition, no simple hyperplasia was diagnosed in the postmenopausal group—when pathology was found, it was much more likely to have become frank cancer
* Heterogeneity and irregularity in echo pattern were significantly more likely to be associated with hyperplasia or cancer in the premenopausal group. It may have not reached significance in the postmenopausal women due to the smaller sample size.
* One weakness of the study is the low rate of pathology
* DO THE EMB in symptomatic women
OUTLOOK

* What can the sonohysterogram add?
* We need to correlate findings to ethnicity, metabolic and exogenous as well as endogenous hormonal influences to further define high risk scenarios.

Ultrasonographic features of endometrium in pre- and postmenopausal women.ppt

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18 June 2009

Conditions of the Vulva and Vagina



Conditions of the Vulva and Vagina
By:Marjorie Greenfield MD
Department of Reproductive Biology
a.k.a
Obstetrics and Gynecology

Learning Objectives
* Know surface anatomy of vulva and vagina
* Name and describe common vulvar conditions—skin, subcut, glandular
* Understand the concept of the vagina as an ecosystem influenced by hormones
* Use the ecosystem model to describe four types of vaginitis

Vaginal structure
The vaginal wall
Vaginal function: sexual
Vaginal function: reproductive
Benign conditions of the vagina
The vagina as ecosystem
Where are the bacteria?
Lactobacilli are the good guys because they make acids
The vaginal ecosystem: estrogen present
The vaginal ecosystem
Vaginitis: Why do you need to know?
Common causes of vaginal symptoms
Bacterial vaginosis: a synergistic bacterial infection
Amsel’s criteria for BV:
Repercussions of BV
Bacterial vaginosis:
Is BV a sexually transmitted infection?
Candida vulvovaginitis
Candida likes an estrogenized environment
Asymptomatic yeast carriage
What determines symptomatic candida vulvovaginitis?
Microscopic diagnosis
Wet prep
KOH prep
Role of culture in the diagnosis
Trichomonas vaginitis
Comparative exudates
Atrophic vaginitis
Approach to the Evaluation of Vaginitis
Evaluation of Vaginitis Symptoms
The Vulva
Vulvar function
Vulvar Tissue Types
Vulvar conditions
Skin processes Vulvar dermatoses
Vulvar dystrophies:
Non-neoplastic epithelial disorders
Lichen sclerosis
child
Squamous cell hyperplasia
Other skin processes
* Infections—mostly STDs
* Neoplasms
Subcutaneous processes
* Inclusion cysts
* Fibroma, lipoma, hernia, female hydrocele
* Breast tissue
endometriosis
lipoma
Gland processes
* Skenitis
* Bartholin gland cyst or abscess
Summary
Pathology correlation
Lichen sclerosus
Normal skin
Squamous cell hyperplasia
Normal skin

Conditions of the Vulva and Vagina.ppt

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24 May 2009

Childbearing & the Pelvic Floor



Childbearing & the Pelvic Floor: A Review of the Literature
By:Nancy H. Sullivan, CNM, MS, FACNM

Types of pelvic floor disorders
* Pelvic pain
* Nerve damage
* Pelvic organ prolapse: cystocele, rectocele, enterocele, uterine prolapse
* Urinary incontinence: stress, urge, mixed
* Fecal incontinence

Prevalence of pelvic floor disorders
* Pelvic organ prolapse is common and is seen in 50% of parous women.
* Around 10% of women in the community undergo surgery at some time of their lives for the management of prolapse (Olsen et al.).
* Urinary and fecal incontinence are common and prevalence estimates vary from 9% of women over 15 (UK study) to 38% of women over 60 (US study).
* Studied 2070 women who sought care for UI or PFD at Kaiser Permanente, San Diego.
* Forty-six percent had undergone previous hysterectomy; ten percent had undergone previous anti-incontinence surgery; six percent had undergone previous anterior or posterior repair (or both).
* Median age of women seeking care was 61; half of women were from 30-60 years of age.
* Genuine stress incontinence was more common in younger patients than in older patients (78% vs 57%);
* Detrusor instability/urge incontinence was more common in older women than in younger ones (67% vs 56%);
* Mixed incontinence was common; 38% of all patients had this diagnosis.
* Pelvic organ prolapse was similar in both groups (27% vs 30%).
* Population survey in South Australia; 3010 interviews in respondent’s homes
* Prevalence of all types of incontinence in women was 35.3%.
* Pregnancy >20 weeks, regardless of mode of delivery, greatly increased the prevalence of major pelvic floor dysfunction.
* Significant increase in PFD for women with history of instrumental delivery over women with CS, but not for women with SVD over women with CS
* Other risk factors for PFD were age, obesity or increased BMI, coughing, osteoporosis, arthritis, and reduced quality of life scores.

Additional associated factors identified in the literature:
* Menopause and estrogen depletion
* However – HRT increases the risk of developing urinary incontinence in post-menopausal women, according to new data from the Nurses’ Health Study (Grodstein et al, 2004) and from the Australian Longitudinal Study of Women’s Health (Miller et al, 2003).
* This increased risk does not vary by route of administration, type of hormone, or dose taken, but is diminished upon cessation of use.
* Depression; individuals with UI more likely to be depressed- which comes first?
* Impaired mobility; relationship among UI, urinary urgency, and falling – which comes first?
* Medications, bladder irritants
* Smoking – possibly because of smoker’s cough?
* Work environment, including limited access to bathroom, heavy lifting, bending, walking, or standing.
* Chronic disease causing cognitive impairment, peripheral neuropathy or decreased mobility. Examples are Alzheimer’s Disease, stroke Parkinson’s Disease, diabetes, multiple sclerosis.
* Physical and occupational activity, especially high-impact exercise, are risk factors.
* But…there is evidence that women who have better ability to absorb impact forces (more flexibility) have less stress incontinence.
* Nygaard et al (1996) studied the relationship between urinary incontinence in elite nulliparous athletes and force absorption as assessed by foot arch flexibility, and found a significant correlation between decreased foot flexibility and stress urinary incontinence.

Childbearing is a leading cause of pelvic floor disorders.
* Research studies are heterogeneous in definition and design, controversial, and inconclusive.
* Pregnancy itself, regardless of mode of delivery, is a risk factor. However, much of the professional as well as the lay literature ignores or minimizes this and focuses the blame on the birth process.
* Significant confounding factors are age and hysterectomy; by around 60 years of age, nulliparous women have the same rate of incontinence as parous women.
* However, most studies show an increased risk with vaginal delivery or cesarean after trial of labor over elective cesarean.
* Survey by the authors reported that 61% of women in a Dublin population (n=7771) reported the onset of symptoms of urinary incontinence before or during pregnancy.
* In another study, the authors compared two groups of healthy physio-therapists, 20-28 years, one nulliparous (n=10)and one primiparous (VD only) (n=10).
* Each group was assessed with a manual digital exam, electromyography (EMG) and perineometry on one occasion only.
* Statistical analysis of digital assessment data showed significant differences between groups for all four types of assessment, with the nulliparous group scoring higher.
* Despite measured loss of pelvic floor integrity in primiparous group, none of the subjects had symptoms of urinary incontinence.
* Authors suggest program of pelvic floor exercises for all women postpartum.

Urinary incontinence after vaginal delivery or Cesarean section
* Did not investigate the effect of instrument-assisted deliveries, shown to be a major factor in other studies
* Did not look at length of second stage or pushing phase
* Found no significant difference between rate in elective CS and CS after labor, shown to be a factor in other studies
* Found no association of incontinence with mode of delivery for women over 50, consistent with other studies
* Mean age of nulliparae lowest, women who had a vaginal birth highest
* Gestational age and birthweight significantly higher in vaginally-delivered group than in cesarean group
* Concluded that an individual woman’s risk of moderate or severe incontinence would be decreased from about 10% to about 5% if she delivered all her children by CS. This decrease would apply only until 50 years of age.
* For women having had two CS, odds still lower than for women with a VD; however, by third CS, odds were the same.
* Women who performed daily antenatal pelvic floor exercises had lower rate than those who did not; women with higher BMI and parity of 5 or greater had higher rates.

The case against elective cesarean section.
* Medial episiotomy increases anal tears (up to 22-fold in one study).
* Even without extending, episiotomy is associated with 2.4 times more fecal incontinence than spontaneous second-degree lacerations.
* Three months after childbirth, primiparae with intact perineums had the strongest pelvic floors, followed by women with spontaneous tears, women with episiotomies, and, weakest of all, women whose episiotomy extended.
* Compared with nulliparity, pelvic floor dysfunction is significantly associated with cesarean section (OR 2.5), with spontaneous vaginal delivery (OR 3.4) and with at least one instrumental delivery (OR 4.3). The difference between cesarean and instrumental delivery was significant, but not the difference between CS and VD.
* Looked at elective CS vs SVD vs CS performed for obstructed labor
* Study population 363 primiparae delivering in maternity ward in Tel Aviv; interviewed them one year postpartum regarding symptoms of SUI; excluded those with SUI prior to childbirth
* Subgroups comparable with respect to age, weight/height, gestational age at delivery, Apgar scores, and use of epidural anesthesia
* Women with postpartum SUI significantly heavier, older, and had increased prevalence of SUI during pregnancy; duration of first and second stage of labor significantly longer in these women.
* Aim of study was to quantify the changes that occur in the levator ani muscles after vaginal delivery using MRI.
* Scanned 6 women one day, one, two and six weeks, and six months postpartum
* Changes noted at one day postpartum had completely returned to normal by 6 weeks postpartum in 5 out of six women, and on one side in the sixth.
* Timing of sampling is very important.
* Vaginal delivery leads to increased anterior vaginal wall mobility.
* These alterations are more marked in women with limited pelvic organ mobility prior to childbirth.
* Postpartum sampling varied from 2-5 months, a variation of 3 months during which substantial changes may be happening.
* Current advanced imaging studies can delineate clearly the musculo-fascial defects associated with vaginal birth and could enhance our understanding of post-cesarean incontinence.
* Incidence of anal incontinence similar in primiparae with elective CS and non-instrumental VD; higher in primiparae with forceps delivery; SUI more frequent after all VD than after CS.
* Prevalence of both increases with parity, but the association with UI is lost in the elderly (hence, study showing elderly nuns with SUI).
* Postpartum urinary incontinence can persist, resolve spontaneously, or symptoms can arise de novo within a 7-year period. Primagravidae who develop incontinence in the immediate postpartum period usually regain continence within three months.

Pelvic floor exercises – Can they prevent PFD? Review of the evidence.
prevents urinary incontinence during pregnancy and after childbirth.”

* 268 primigravidae with bladder neck mobility of >5mm randomized to (1)supervised PFE with PT from 20 weeks until delivery or (2) usual advice from midwives.
* Fewer women in study group reported postpartum SUI. No difference in bladder neck mobility or in pelvic floor strength.
* Difference attributed to “the knack” of contracting pelvic floor muscles prior to exertion, cough, sneeze, etc.
What else can we learn from the literature?
Counseling Women About Elective Cesarean Section

Childbearing & the Pelvic Floor.ppt

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Pelvic Floor Disorders: Evaluation and Treatment



Pelvic Floor Disorders: Evaluation and Treatment
By:Elisa Rodriguez Trowbridge, MD
Departments OB/GYN and Urology
Division of Female Pelvic Medicine and Reconstructive Surgery



3 General Categories of Disorders

* Urinary Incontinence
* Pelvic Organ Prolapse
* Anal Incontinence

Urinary Incontinence
Types of Urinary Incontinence
* Stress Incontinence
* Urge Incontinence
* Mixed Incontinence
* Overflow Incontinence

Stress Urinary Incontinence (SUI)
* Generally occurs with sudden movements or increases in intra-abdominal pressure- coughing, laughing, sneezing, or running.
Urge Incontinence
* Typically preceded by an urge to void, and can involve a trigger such as running water, opening a door, removing undergarments.
* Mixed urinary incontinence: Involuntary leakage associated with urgency and also with exertion, sneezing, or coughing (SUI).

Overactive Bladder
* Urgency- DRY
* Frequency- DRY
* Urge Urinary Incontinence (UUI)- WET

Urinary Incontinence- Evaluation
* History
* Exam
Incontinence Physical Exam
* Standing or Supine Stress Test
Post Void Residual & Urine Dipstick
Voiding Diary
* Normal Voiding
Overflow incontinence
* Obstruction of urethra
* Poor contractile bladder muscle
* Must find out PVR !!
** Must stop anticholinergics!!
Simple Cystometry (Urodynamics)
Multichannel Urodynamics
Indications:
* Uncertain diagnosis
* Fail respond to treatment
* Prior failed surgery
* Complex

Risk factors of UI
* Sex: Women are more likely than men to have stress incontinence –pregnancy, childbirth, and menopause.
* Age: As you get older, the muscles in your bladder and urethra lose some of their strength. Changes with age reduce how much your bladder can hold and increase the chances of involuntary urine release. However, getting older doesn't necessarily mean that you'll have incontinence. Incontinence isn't normal at any age — except during infancy.
* Obesity: Being overweight increases the pressure on your bladder.
* Smoking: A chronic cough can cause episodes of incontinence or aggravate incontinence that has other causes. Smokers are also at risk of developing overactive bladder.
* Other diseases: Having kidney disease or diabetes may increase risk of urinary incontinence.

Treatment Urinary Incontinence
* Lifestyle modification
* Pads
* Physical Therapy- Kegels, biofeedback
* Pessary
* Medications- eg anticholinergics (Detrol)
* Botox (OAB)
* Surgery (many!!)

Pelvic Prolapse
3 Compartments of Prolapse

* Anterior
* Middle or Apical
* Posterior
3 Compartments: Normal Support
3 Compartments of Prolapse
Cystocele (Anterior)
Symptoms: bulging, pressure, “mass”, difficulty voiding, incomplete emptying, splinting vaginal wall, difficulty inserting tampon, pain with intercourse.
Vaginal vault prolapse/ Enterocele (Middle/Apical)
Symptoms: bulging, pressure, “mass”, difficulty voiding, incomplete emptying, splinting vaginal wall, difficulty inserting tampon, pain with intercourse.
Rectocele (Posterior)
Symptoms: bulging, pressure, “mass”, difficulty defecation, incomplete defecation, splinting vaginal wall or perineum, difficulty inserting tampon.
Complete eversion (All compartments)
* Uterine Procidentia
* Complete uterine prolapse

Pelvic Organ Prolapse Quantification System (POP-Q)
* Patient straining, 6 specific sites are evaluated, at rest 3 sites measured.
* Measure each site (cm) in relation to the hymenal ring, which is a “fixed”. The hymenal ring is the zero point of reference.
* If a site is above the hymen, assigned a negative number.
* If site prolapses below the hymen, the measurement is positive.

POP-Q: Normal
* What type of prolapse
* What compartment?
Prolapse treatment options
* Expectant Management
* Physiotherapy???
* Pessary
* Surgery (Many!!)
o Abdominal
o Vaginal
o Laparoscopic
o Robotic assisted Laparoscopy
o Mesh kits
Abdominal Sacralcolpopexy
Vaginal Hysterectomy
Mesh repairs
Anal Incontinence
Anal incontinence (AI)
* Anal Incontinence is the inability to control passage of gas, liquid or solid stool from the rectum.
* Affects two to 15 percent of adults in the United States.
* This condition affects men and women of all ages, but because people are embarrassed to talk about their symptoms, many people go untreated because they are unwilling to ask for help.

Types of Anal Incontinece
* Flatal incontinence:
* Double incontinence:
* Rectovaginal fistula:

Evaluation- AI
* History
* Pelvic exam
* Transanal ultrasound: Assess integrity of external and internal anal sphincter. A probe is about the size of a finger is place in the anorectum.
* MRI: Muscles of the pelvic floor, CNS or spinal cord lesions.
* Defecography: Barium paste is placed into your rectum and vagina and patient sits in the toilet simulationg defecation.
* Anal manometry: Assessment of muscles, capacity and sensation of the anorectum. A small air-filled balloon is inserted into your rectum.

Treatment of AI
* Lifestyles modifications
* Medications
* Physical Therapy
o Electrical Stimulation
o Biofeedback
Surgery for Separated Anal Sphincter
Anal sphincteroplasty
* Performed if involuntary loss of stool is caused by an injured/separated sphincter muscle.
* Opening made between the vagina and anus. Separated muscles are identified and approximated with sutures.
Treatment AI
* There are effective treatments that can help, or even cure, the problem. However, fecal incontinence has long been a neglected subject, and for some fecal incontinence problems, we do not yet have completely effective treatments.

Pelvic Floor Disorders: Evaluation and Treatment .ppt

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