IV.

PHYSIOLOGY OF THE NORMAL

Vaginal Bleeding 
MENSTRUAL CYCLE
Monthly repetitive cycle involving changes in ovary and uterus
Date: May 18, 2021
Tutor: Dr. Giselle Alfeche  Made up of ovarian and uterine cycle
 14th day is ovulation – mature egg is released
I. CLARIFICATION OF TERMS  Day before ovulation (1-13): Preovulatory phase
 Vaginal bleeding – flow of blood from the femal reproductive system o Follicular phase
(vagina) o Menstrual and proliferative
 Can be physio or patho process; some maybe from serious causes or
 Postovulatory phase
less serious ones
o Luteal phase
 Physiologyic
o Secretory phase
o Menstrual vaginal bleeding – 1st trimester (implantation
 Due to GnRH from hypothalamus that triggers anterior pit to produce
bleeding); light or spotting
FSH and LH
 Pathologic
 Physiologic cause of vaginal bleeding
o Heavy bleeding in 1st triem and later – pathologic, indicative
 Cycles are regulated by HPG axis
of many causes
o Early – threated abortion; ectopic pregnancy
OVARIAN
o Heavy – Preterm labor, problem with the placenta  Follicular phase
o Post menopausal – 12 months after last LMP o Hyp secretes GnRH stimulating anterior pit to release FSH
o Cancers in cervix or vagina and LH
o Medications and hormone therapy o FSH and LH stimulate ovaries
 Vagina – musculomembranous tube that extends to uterus, interposed o Granulosa cells and thecal cells
between bladder and rectum; proximal to cervix, distal to hymen o LH  thecal cells  progesterone and androstenedione
o Abundant vascular supply o FSH  granulosa cells  recruit maturing follicles in ovary
→ Proximal portion – uterine artery and vaginal artery o Follicles will mature inducing production of estradiol; would
→ Posterior – middle rect
induce negative feedback on pituitary inhibiting release of
→ Distal – internal pudendal art
→ All of which traverse to midline and anastomose FSH
→ If there is occlusion, there are still collaterals for supply o One follicle becomes dominant and would outgrow others and
o Any bleeding in uterus or cervix may also occur here become atretic
 Spotting vs Bleeding o This will induce estradiol to peak and would lead to a positive
o Spotting – light pink, almost brownish, very scanty, usu. only feedback, increasing level of LH
on pantyliner o LH surge will cause ovulation; dominant follicle will release
o Bleeding – heavy, bright red, soaked with blood an oocyte
o Corpus luteum will produce prog inhibiting LH
 Luteal phase
II. STATEMENT OF THE PROBLEM o Degeneration of corpus luteum
 What are the possible conditions/dse that cause vaginal bleeding in o Luteum is first responsible to prepare uterine linings for
pregnant women? implantation; without success  degeneration  decrease
 What are the possible conditions/dse that cause vaginal bleeding of hormones  no maintenance of lining  menstruation
the patient?
MENSTRUAL
 Menstrual phase – no successful implantation, no fertilization
III.HYPOTHESIS
o Lasts few days due to sig production of prog and estrogen and
 Vaginal bleeding originates from the uterus, vaginal wall, or cervix
and can be a part of physiologic (normal menstrual cycle) or may be inhibin becomes ceased  decreased stimulation of
associated with pathologic conditions (infectious [STDs], endocrine, endometrium  involution  menstruation
anatomical [placenta], malignancy [cancers]) o Nonclotting blood – d/t fibrinolysin
 ; It is a part of normal menstrual cycle or may be associated with o Clotting  pathologic
pathologic conditions or pregnancy o Day 4 – basal layer organization
 Bleeding in pregnancy may be due to pregnancy complications  Proliferative phase
(previa, abruptio, ectopic pregnancy, etc.) o Estrogen
o Stromal cell proliferation
o Re-epthelialization
o Production of thin mucus aligned with vaginal lumen to allow
sperm to have means to be directed
 Early proliferative IMPLANTATION
 Day 6 to 8  6-7d after fert; blastocyst  hatches
 Glands straight o Apposition
 Arteries are straight → Initial contact of blastocyst with uterine wall
o Adhesion
Late proliferative  Successful implantation
 Gland coiling o Reqs responsive endometrium
 Vessel coiling o Limited to days 20 – 24 (ard 7-9 days postov)
 Endometrial thickening – glandular hyperplasia → Trophoblast  interact with endometrium  release adhesion
molecules  adherence of blast to decidua
SECRETORY PHASE o Invasion:  secretion of proteases  invasion of uterine
Early secretory stroma
 Marked coiling of glands and artery → Syncytiotrophoblast (outer) and cytotrophoblast (inner)
 Subnuclear vacuolization o Syncitio – 8th day of devt; essential  troph can produce hCG
 Importance of coiling – helps determine kung diin na nga phase ang  detected in preg test
cycle
POST IMPLANT
Late secretory  Cyto  villous troph, extravillous troph
 20 – 25  Day 9: lacunae form in syncitiotrophoblast
 Serrated glands; toothlike projections  Syncitio erode tissue, maternal blood flood lacunae, marking start of
hemochorial placentation
Premenstrual endometrium
 Ischemia Villous trophoblast
 Signs of hemorrhage  Primary chorionic  2nd  3rd
 Arteries coil – rate of lengthening is greater than development of  Primary:
endometrium; there is an increase resistance to blood flow, decreasing o 11-13d
supply to superficial areas  hypoxia  ischemia  necrosis  o Fingerlike projections penetrate and expand to syncitio layer
menstruation o 3rd wk: extraembryonic mesodermal cells grow into these villi
forming loose CT and becomes secondary chorionic villi
 Not everyone has 28 days of interval of cycle
 Embryonic vessels  2nd chorionic villi
o Would usu last 7 days
o Embryonic blood vessels  tertiary villi
o Average blood loss of 35-50mL
 Tertiary villi
o Heavy bleeding – pathological
o Capillary endothelium
o Luteal phase – usu 14 days
o Mesoblast
o Varies in follicular phase
o Cytotroph
o Syncitiotroph
 Menstrual cycle should be regular within 2-4 years of menarche; 10-
o PLACENTAL BARRIER NI SIYA (fetal side!)
16
 Ends with menopause (cessation in 12 months); 48
Extravillous
 Differentiates into endovascular and interstitial trophoblast
 Cervical mucus
 Endovascular
o Changes depending on what hormone is dominant
o Penetrate and replace maternal endothelium
o Fluid becomes watery – egg-white like! When most fertile
 Interstitial
o Luteal phase – becomes rubbery, gummy, sticky
o Surround arteries  differentiation  become low resistance
o Fertility – creamy, smooth, lotion
and increase in diameter
o Invasion of spiral arteries completed  completed maternal
V. NORMAL PLACENTAL DEVELOPMENT side
 Placenta – connecting organ bet. Maternal uterus and fetus
o Supplies nutrients GROWTH AND MATURATION
o Elimination of waste  1st trimester: more rapid than fetus (?)
o Enables gas exchange  17 weeks AOG: growth equal
 Term: weight is 1/6 of fetal weight
PRE IMPLANTATION  Villi vontinue to branch: volume of cyto decrease
 Cellular division  morula (16 cells)  Syncitio thins  vessels of fetus more prominent
 4th day: morula  uterus  blastocyst  Villous stroma  changes 
o Trophoblast (outer) o Branching CT separated by abundant loose matrix
→ Becomes placenta o Stroma becomes denser and become loosely packed
o Syncytiotrophoblast (inner) o Infiltration of holfbauer cells (macorphages)
 → Phagocytic
→ Immunosuppressive phenotype
→ Cytokine formation
→ Paracrine regulation of trophoblastic function
→ Zika virus can infect these cells

Placenta at term
 Continues to thickine
 16th to term week: grow circumferentially
 Circular; 15-20cm diameter; 2.5cm thick; 500g; 6:1 fetal:placental

Fetal surface and maternal surface

 Fetal – smooth
o Umbilical cord near center
o Branches of umbilical vessels beneath amnion from the cord
 Maternal – rough spongy with velvety bumps (cotyledons)
o Each cotyledon  with own spiral arteries
o Visible on maternal surface, reps Ca deposition in degenerated
areas

END OF PREGNANCY
 Placenta does not have to function na kay wala na fetus
 May changes
o Inc fibrinous tissue in core villous
o Thickening of capillary basement membrane (fetal)
o Obliterative changes in small caps of villi
o Deposition of fibrinoid on surface of villi

DELIVERY
 Schultz – SHINY emz
o Center
o Fetal side
 Duncan – DIRTY yarn
o More bloody
o Maternal side

 0-13: has low oxygen environment and only becomes high when
spiral artery remodeling starts

TORCH
 Toxo
 Others
 Rubella
 CMV
 Herpes

VI. MANAGEMENT OF A PREGNANT

WOMAN PRESENTING WITH VAGINAL
BLEEDING
 ABCDE
 Unstable  resuscitate
 Based on trimester
 → Adnexal mass
→ Check b-hCG
→ <1500 hCG  early pregnancy; cannot see yet features of
IUP  send mom home and ask comeback after 3 days 
recheck  doubles after  confirm if viable or not and if
implantation bleed
→ No doubling  ectopic  emergency! OR sis! Laparotomy
and laparoscopy

 Bleeding  do PE  check peritoneal or hemodynamic instability 

resuscitate  surgical
 Nonobstetric  diagnose and treat as indicated
o Inflame
o Poly
o Infx
o Others
 With products of conception  incomplete abortion  treated as
indicated
o Inform patient with what to do
o Psych assessment
 Stable, no positives  transvaginal utz and b-hCG

 Normal in less than 20 weeks pregnancy

 Bleeding due to implantation and due to cervix kay damo blood
vessels para maka supply sa developing egg sa embryo

2ND OR 3RD TRIME

Major risks of bleeding
 Abruption
 Vasa previa
 Uterine rupture
 Gestational troph disease

management
 Stabilize, ABCDE
 Ask for OB profile
 Duration of bleeding is noted, as well as amount and color
 Amount  can be concelead by placenta and uterine wall  not
reflective with what is actually occurring
 More than 20 weeks  not rec transvag utz esp if previa not
diagnosed  could cause massive bleeding so do Abdominal first
 Syncope, hemorrhage, risk factors

 Contact OR for surgical management Risk factors of major bleeding

LESS THAN 20 WEEKS AOG  HTN
o Do pelvic exam and determine if it is coming from the internal
 Age
os
 >40 previa
o If not: polyp, neoplasm, laceration, infection
 >30 abruption
o If yes: determine if cervix is dilated
 Smoker
→ Dilated: abortion, ectopic pregnancy with clots
 Cocaine use
→ No clots: cervical insufficiency
→ Manage with evacuation and curettage  Trauma
→ Administer antibacterial agents  Previous CS
 If cervix is closed  perform transvaginal utz
o Note intrauterine pregnancy Later term bleeding  antepartum hemorrhage
→ Yolk sac  Bleeding at 24 weeks or more but before labor
→ Fetal pole  Usu. unexplained and due to marginal placental bleeds
→ Fetal heart rate
 Pathologic causes are minimal, but when detected should be manged
o Implantation bleeding if IUP (+)
appropriately
o If not  determine if ectopic or not
→ Free fluid in pelvis of abdomen
 Maternal causes  cervical erosion, ectoprion, local infection, GT
tumors, varicose, trauma Associated symptoms:
 Fetal cause  vasa previa o Changes in urinary and bowel changes: none
o Breast changes: none
Management in late pregnancy o Back pain: none
 Hemodynamic instability  immediate IV access, fluid, blood o Pressure on pelvic area: none
products o Dizziness during bleeding: none
 Baseline lab tests  CBC, coag, BT, antibody screen, RhD o Leakage other than blood: none
prophylaxis
 Continuous fetal monitoring  check for decreased decelerations and  Prior trauma: none
variability because it may be persistent despite management of
mother  Bleeding: 3hrs prior to consult; **appearance not stated

VII. HISTORY TAKING OB AND MENSTRUAL HISTORY

GENERAL DATA  Menarche: 13 years old; regular monthly interval, lasting 3-5 days
Name: CV  Consumes 2-3 pads per day, moderately soaked, no associated
Age: 22
symptoms
Sex: F
Address: Pavia, Iloilo  LMP: May 15, 2020
Civil Status: S  PMP: April 18, 2020
Occupation: sales clerk for cellphone stall for 1 year  Date of consult: December 28, 2020
Religion: **not stated
 Primigravida
Folks: **not stated
Educational attainment: **not stated  AOG: 32 – 3/7 weeks AOG (3rd trimester)
Date: December 28, 2020  OB Score: G1P0 (0-0-0-0)
 EDD: February 22, 2021
CHIEF COMPLAINT
 Vaginal bleeding PAST MEDICAL HISTORY
 No previous hospitalization
HISTORY OF PRESENT ILLNESS  Not diabetic, not hypertensive, not asthmatic
Last felt well: 2 weeks prior to consult
 Allergies: NSAIDs and crustaceans
o No nausea and vomiting
o No headache Prenatal check-ups: Nearing end of 1st trimester
o No fever  Poor prenatal care
o Weight: no loss nor gain  Prescribed multivitamins and prenatal milk
o Change in appetite: none  Patient did not comply; no monthly prenatal visits; only returned 6
o Dizziness/weakness: none months AOG
o Fatigue: none  Check check check!
o Contractions: none o Fundal height
o Pressure at back of neck: none o Heart beat
o Cyanosis of fingers: none o VS
o Edema: swelling of lower extremities, level of ankles (bipedal → BP: 140/100
edema), noted at the end of the day → Given methyldopa, 3x/d, good compliance
 Did not return! Only sang ER consult na
PRIOR TO CONSULT
 Progression of bipedal edema FAMILY HISTORY
 Parents
 Swelling of fingers
o State of health: not stated**
 Periorbital edema noted upon waking up
 Siblings
 Address edema: no consult done
o Sister: gestational hypertension
o No medications
o 1 sister and brother
o No consult
 Diabetes – both sides of the family
Pain: 1d prior to consult  Cancer – not stated**
 Location: hypogastric pain  Cardiac problems – not stated**
 Character: regular  Identical condition – sister (gestational HTN)
 Occasional shortness of breathing when lying flat – decided to stay at  Bronchial asthma – both sides of the family
home and rest  Twin pregnancy – not stated**
 1d prior – tolerable and irregular  Miscarriages/abortions – not stated**
 3h prior – regular and painful  Anticoagulation disorders – not stated**
 Soaking 1 sanitary pad
 PERSONAL, SOCIAL, AND ENVIRONMENTAL HISTORY
 Nonsmoker VITAL SIGNS
 Nonalcoholic beverage drinker  Blood pressure: 180/100
 No illicit drugs  Temperature: 36.8 deg. C
 Planned or not – not stated**  Oxygen Saturation: 99%
 Sexual partners  Pulse rate: 90bpm
o 1 partner  Respiratory rate: 24breaths/min (tachypneic)
 Contraception – no history of use
ANTHROPOMETRICS
 No history of STDs
 Weight: 132lb
 Anorgasmia – not stated** (and of partner)
 Height: 5ft, 2inches
 Disinterest in sex – not stated**
 BMI: 24.19 (normal)
 Bleeding after sex – not stated**
 Diet – no data**
 Environment – no data** SKIN
 Education – not stated**  No data**
 Work time – not stated**
 History of abuse – not stated** HEAD, EYES, EARS, NOSE, THROAT
 Fam dynamics – not stated** Eyes
o periorbital edema
o anicteric sclerae
o pinkish conjuctiva
o pupillary reflex – not stated**

Nose
o Nasal flaring – none
o Nasal congestion – none
o Nose bleeding – none

Oral Cavity
 Oral cavity – moist lips and buccal mucosa
VIII. DIFFERENTIAL DIAGNOSIS  Bad breath – not stated**
Preeclampsia  High blood pressure  Oral thrush – not stated**
 Shortness of breath – pulmonary edema  Ears – grossly normal
 Edema Neck
 Diabetes in family  No lymphadenopathy
 Gestational hypertension in sister  Thyroid enlargement – not stated
Gestational  Family history  JVP – not stated
diabetes
Abruptio placenta  Late trimester painful bleeding
CHEST AND LUNGS
 Hypertension  Paradoxical motion/effort of breathing – none
 Painful bleeding  Deformities – none
Preterm labor  Due to bleeding  Symmetry of expansion – symmetrical
 Regular contractions  fremitus – not done**
Placenta previa  Contractions  Breast – not stated**
 Bleeding  Lesions or scars – not stated**
 Before 37 weeks of pregnancy  Breath sounds – decreased, bibasal
Pulmonary edema  Lung findings  Adventitious sounds – crackles, upper lung fields (occasional)

IX. PHYSICAL EXAMINATION CARDIOVASCULAR

GENERAL SURVEY  PMI – no data**
 Wheelchair  Auscultation – no murmurs
 Alert  Regular cardiac rhythm
 Speak in full sentences – not stated**
 Anxious/scared – not stated** ABDOMEN
 General appearance –  Fundic height: 29cm
 Cardiopulmonary status – in distress; GCS15  Cutaneous signs: not stated**
 Fetal movement:  GTT: not done*
 Surgical scars: none  Random blood sugar: not done*
 Bowel sounds: not stated**  HbA1C: 4.9%
 Leopold’s maneuver:  Lactate dehydrogenase: 100
o L1: breech  Sodium: 135
o L2: fetal back, maternal right  Potassium: 3.6
o L3: cephalic, unengaged  Blood urea nitrogen: 6.08
o L4: N.A.**  Total protein: 60.27
 Fetal heart beat: 105bpm  Albumin: 23.25
 Tetanic uterine contractions  Globulin: 37.02
ABG  None
EXTREMITIES Serologic test  Anti treponema pallidum: neg
 Edema of hands and lower ex  HBsAg: nonreactive
 hCG: not tested*
OB PELVIC EXAM
RT-PCR  not done
 Normal external genitalia
Abdominal  Not done**
 Vaginal bleeding moderate
 IE not done
Transvaginal utz  Not done**
 Speculum and rectovaginal examination – not done

X. INITIAL IMPRESSION
G1P0
Pregnancy, uterine
32 3/7 weeks AOG
Preeclampsia
Abruptio placenta
Gestational Diabetes
Placenta previa
Pulmonary Edema
XI. DIAGNOSTIC TESTS
CBC  Hemoglobin – 114mg/dL
 Hematocrit - 33%
 Red blood cell – 3.96
 White blood cell – 14.53
o Segmenters – 64%
o Lymphocyte – 28%
o Monocyte – 8%
 Platelet – 245
 Mean corpuscular hemoglobin – 28.7
 Mean cell volume – 82.6
 Mean corpuscular
concentration – 34.8
Urinalysis  Color: Straw
 Sugar: (-)
 Protein: 2+
 Pus: 0-1
 RBC: 0-1
 Amorphous urates: few
 Squamous cells: few
Blood typing Not stated**
Coagulation studies  Prothrombin time: 100%
Chem  Serum glutamic
transmainase: 35
 Serum glutamic pyruvate transaminase:
90.34
 Creatinine: 86.22
 Troponin: none*
XII. FINAL DIAGNOSIS
Preeclampsia  High blood pressure
 Shortness of breath – pulmonary edema
 Edema
 Diabetes in family
 Gestational hypertension in sister
Gestational  Family history
diabetes
Abruptio placenta  Late trimester painful bleeding
 Hypertension
 Painful bleeding
Preterm labor  Due to bleeding
 Regular contractions
hemoglobin Placenta previa  Contractions
 Bleeding
 Before 37 weeks of pregnancy
Pulmonary edema  Lung findings
G1P0, Pregnancy uterine, 32 3/7 weeks AOG, in preterm labor,
abruptio placenta secondary to preeclampsia, pulmonary edema
XIII. ILOS
 Read on preeclampsia
 Interpret laboratory exams
oxaloacetic  Management
 Pathophysiology
 Risk factors
 Indications sa dif delivery; CS etc.
 o Acute rise in blood pressure even in normotensive patients,
bisan <140/90 but nag add 30 sa systolic or 15mmHg sa
diastolic  indicative
→ Note sudden rises in BP and MAP
→ BP be taken twice after 4 hours from the first measurement
 If there is multiorgan involvement regardless of proteinuria 
diagnosis
o Seizures
o Renal dysfunction

EPIDEMIOLOGY
 5-8% incidence worldwide
 500000 featl deaths per year
 2015, top leading cause  eclampsia (19%), preeclampsia (17%)
 Trend for maternal deaths is decreasing, but stil the same na
eclampsia and preeclampsia ang leading cause
 Improvement, work to be done
 Preeclampsia + varying degrees of preterm birth
o Highest in PH, NG, JM
o 24-36 wks AOG (7.2/1000 In Filipino women)

RISK FACTORS
XIV. INTERPRETATION OF LAB RESULTS  Young and nulliparous  more vulnerable**
 Acute anemia d/t decrease in hemoglobin and hct – bleeding o 3-10% incidence
o Bleeding experienced o Most prevalent
 Urinalysis o If first na pregnancy or nulliparous, the mother has not yet
o 2+ protein – protein in urine developed, less exposed pa sa paternal antigens 
o Urine protein 2+ is one of criteria sued by ACOG in diagnosis sensitization  antibodies
of preeclampsia and is an indication to deliver pregnancy prior o Primiparity not only at high risk, but also first child with new
to 37 weeks and risk for developing maternal HTN and fother
perinatal mortality o Interpregnancy intervals too short or too long
 Decreased albumin and increase in globulin  hepatocellular damage o For pregnancies of diff paternities  higher risk!!!!! Ghrl
o A/G ratio  decreased  kidney disease  loss of alb in  Older women  chronic HTN with superimposed preeclampsia
circulation  SLE
o Renal insufficiency  Age<35; may greater than 35; (?)
 Decreased CBC numbers  increased blood volume  hemodilution  Prior stillbirth
 High ALT  hepatic involvement  extreme elevation signifies  CKD
HELLP syndrome  ART
 Creatinine  significant increase  renal insufficiency  BMI>30
o Decreased GFR  Multifetal gestation
 Platelet  decreased <100k  HELLP syndrome  Prior abortion
 Diabetes
XV. PREECLAMPSIA  Prior preeclampsia – HIGHEST RISK!
DEFINITION  Chronic HTN -2nd highest risk
 One of HTN disorders that complicates pregnancy  Antiphospholipid antibody
 Pregnancy-specific, can affect any organ  Family history – 20% of daughters whose mother had preeclampsia,
 POGS: new-onset HTN after 20 weeks AOG + new onset proteinuria develop man, 11-30% sisters nga may preec nag develop man 
 Preg complication  endothelial dysfunction  HTN + signs of genetic!  many genes assocd but mainly from the mother
organ damage (liver and kidneys)  Molar pregnancy – trophoblast has abnormal growth
 Syndrome  Vitamin D deficiency  preeclampsia + FGR
o HTN  Calcium deficiency
o Edema  Women nonsmokers, higher risk of preeclampsia
o Proteinuria
 Proteinuria  not objective marker since there are instances where ETIOPATHOGENESIS
there are late manifestations of proteinuria ……
o Not a prerequisite to diagnose as 10% of seizures may develop Haha
even before proteinuria is detected  2-stage disorder
 o Stage 1 : faulty trophoblastic invasion; normally there is a
change of spiral arteries from 12 weeks  goal is to increase
the diameter of arteries and make it less resistant for good
perfusion
→ First time pregnancy: increased sLT 1  antiangiogenic
protein regulating vessel formation
→ Because of increase, endovascular troph will have a hard time
changing the landscape of spiral arteries, so instead nga
matapos na siya earlier, with increased levels, placental
growth factors and VEGF, small lumen is retained, increasing
lumen resistnace and decreasing perfusion  preeclampsia
→ Endothelial cell activation  oxidative stress  toxic
radicals  injury  cytokines and interleukins  oxidative
stress  preeclampsia
→ Production of lipid-laden macrophage, activation of
microvascular coagulation  thrombocytopenia
→ Increase capillary permeability  edema
→ Proteinuria
PATHOPHYSIOLOGY
 Multiorgan involvement
Early onset
 <34 weeks AOG
 More severe conditions
 Poorer outcomes
Late onset
 >34 weeks
 Sudden elevation in systemic BP exceed normal autoregulatory
capacity
o Mismatch in vasodilation and vasoconstriction of blood
vessels  sirupt capi pressur e extravasation to tight
junctions of RBCs
o Combination of theories/
CLINICAL MANIFESTATIONS
 Severe headache
 Visual disturbance (scomata)  blindspot emz
 Confusion
 Epigastric pain, RUQ
CLASSIFICATIONS
Preeclampsia without severe features
 BP >=140 systolic; >=90mmHg diastolic
 But not lesser than 160/110mmHg
With severe features
 >160/110mmHg
 Oliguria, cerebral or visual disturbances, pulmonary edema, epigastric
pain, impaired liver function (severe persistent RUQ pain, elevated
liver enzymes)n, thrombocytopenia (<100000), renal insufficiency
(serum crea >1.1mg/dL + pulmonary edema)
 Proteinuria may not occur – removed as absolute req in diagnosis of
preeclampsia

CVS Patient:
 Increased cardiac afterload d/t hypertension  SBP >160mg/dL
 Reduced cardiac preload d/t abnormal intravascular volume  Impaired liver function d/t elevated SGPT
expansion
 Pulmonary edema – indicator of severity
 No intravascular expansion  reduced afterload
 Renal insufficiency
 Endothelial activation  extravasation of fluid  pulmonary edema
 Elevated crea dec GFR

Renal
POGS – changed non severe/severe
 Release of soluble VEGFr  release of endothelin 1 
 Misleading ang mga mild and severe
vasoconstriction  inc resistance to blood flow  hypertension
 Indi ma feel ang danger sang preeclampsia so nalimtan nga bisan
(kidney is susceptible)
mild lang pero pwede japon mapatay kag magkasakit so gin change
 Vasoconstriction  dec BV  dec perfusion
sang POGS
 Cell damage  decrease filtration capacity  oliguria, proteinuria
 Preeclampsia with severe features as Dx
Fluid
o New onset of HTN and proteinuria after 20weeks AOG,
 Volume of ECF fluid  edema greater than in nonpregnant
recent data suggest that it may develop before 20 weeks and
 Increased oncotic pressure  extravasation  generalized edema after 48hrs postpartum or in the absence of typical symptoms
o Can still be diagnosed even if it is still <20wks AOG
Liver
 Periportal hemorrhage  hepatic necrosis + hemorrhage
o RUQ pain, stretch of glisons capsule
 Elevated serum ALT and AST
 Shock liver d/t subcapsular hematoma
 Abnormalities in coagulation

Brain
 Headaches and visual disturbances
 Risk of developing convulsions  eclampsia
 Response to acute and severe HTN, crebrovacular regulation 
vasospasm DIAGNOSIS AND WORKUP
 Low cerebral blood flow, ischemia  Starts when patient visits at first prenatal, noting history
 POGS: best way to id:
 o Combi biomarker + uterine vessel doppler utz
o Biomarkers for 1st trim
→ Dec PP13, inc GF, dec PIGFa, dec inhibin a,
o Uterine vessel doppler utz
→ Notching, persistence after 24wk indicative of inadequate
trophoblast invasion  strong association
→ Normally, 18-24 not seen! Kay ang lumen kag resistance
reduced na
 Other tests
Maternal assessment
 CBC
 Liver enzymes
 Serum crea
 Performed every other day If px is stable
 Contractions
 Rupture and bleeding
 Abdominal pain
 Severe preec symtpoms: dyspnea, nausea vomiting
Fetal
 BPP
 NST
 Twice weekly
 Fetal growth

COMPLICATIONS
 Eclampsia 2/200 women
 HELLP syndrome
 IUGR
 Preterm birth 28-31 weeks; 32-36 weeks
 Placental abruption
o Extent of separation
o Location of separation
o Clinical presentation RISK FACTORS
→ Revealed: vaginal bleeding  Preeclampsia
→ Concelead: remains in uterus, not visible but can cause shock  Prior abruption
o Clinical severity  Increased age of parity
 Chorioamnionitis
 PPROM
 multifetal gestation
 Cirgarette smoking
 leiomyoma

CLINICAL MANIFESTATIONS
 Vaginal bleeding
 Abdominal pain
 Uterine tenderness/rigidity
 Uterine contractions
 Back pain

 Gas exchange and nutrient exchange inadequate

XVI. PLACENTAL ABRUPTION  Fetus increased heart rate

DEFINITION  Fetal tachycardia
 Separation of placenta even before delivery  If placenta cannot compensate  fatigue of fetus  no compensation
 hypoxia  bradycardia  absent accelerations and late
decelerations

 INDICATORS OF SEVERITY immediate CS
 Magnesium sulfate – fetal
neuroprotection, prevention of
convulsions of mother
 Inform doctors, Peds, OB, Anes
 Assess if pwede CS or NSVD
Determine need for  Hypertensive crisis (emergency) 
hospitalization admission
 Transfer to ICU before or after delivery
Determine need for  Prompt delivery is safest option for
delivery mother and fetus if there is PE and
suspected AP
 If there is severe bleeding  emergency
 Moderate CS
 Thrombocytopenia  higher maternal
DIAGNOSIS AND WORKUP and fetal morbidity and mortality
 No specific and definitive diagnostic test Diagnosis of labor  If present is in labor
 Mostly thru PE Course for delivery  Nonreassuring fetal status but ok mother
 Some use ultrasound but low sensitivity esp with bleeding  DELIVER via CS
 Kleihauer-Betke test Prophylaxis  Corticosteroid for FLM
o 1st dose admnx even if 2nd dose
XVII. MANAGEMENT unlikely
IMMEDIATE MANAGEMENT o Kahit deliver 24hrs, must always
give to improve prognosis
Stabilization  ABCDE  34 wks  betamethasone, dexa
 IV access with wide-bore cannula  Beta 12mgIM every 6h 2 doses
o G18 for possible blood  Dexa 6mgIM every 12h 4 doses
transfusion
 Magnesium sulfate
 Blood extraction for lab tests CBC, BT, o 4-6g dilute in 100mL IV fluid 
coag profile
15-20mins
 Monitoring of hemodynamic status such o Maintain at 5.5-7.5mg/dL
as BP, PR, volume status, urine output
Preparation for CS  Check for DR availability
 Continuous fetal monitoring delivery  Informed consent
 Take note of HTN  emergent therapy
 Preoperative care
for acute onset, give hydralazine
o Prophylactic antibiotics  single
o 5mg IV/IM, 5-10mg every 40mins
IV B-lactam cephalosporin or
until BP controlled, then every 3
extended spec penicillin
hours
 Surgical safety
o If no success, use other drugs
o Documentation
o Note possible adverse effects such

as fetal distress and maternal
hypotension Contact folks  Medicolegal purposes
Unstable  Immediate delivery via CS
Stable  Assessment of fetal wellbeing SHORT-TERM MANAGEMENT
o Confirm gestational age
o Continue external fetal monitoring Preparation for  Check for DR availability
o NST, kick, BPP CS delivery  Informed consent
Establishment of  Hx, PE, diagnostic tests e.g. CBC +plt,  Preoperative care
diagnosis CTBT, BUN, urinalysis, LFT< crea, o Prophylactic antibiotics  single IV
electrolytes, serum alb, HbA1C, CXR, B-lactam cephalosporin or extended
sero, RTPCR spec penicillin
If stabilized with  Expectant management  Surgical safety
hydralazine (POGS) o Delivery o Documentation
o However, based on clinical  Mother  put on NPO at least 12h prior
picture, there is PE and o Reduce vomiting and complications
progressive renal insufx, and (lung)
nonreassuring fetal test d/t o Reduce mess
bradycardia,  might not do  IV access to maintain tissue and fluid
 homeostasis
o Lactated ringers (preferred)
o 0.9NSS
 Foley catheter insertion
o Drain bladder
o Monitor urine output
 Monitoring devices
 Clear labs and imaging of the patient for
surgery and by anes
 Regional anesthesia
o For women with severe features
Anesthesia  Regional anes preferred
 General – aspiration, failed intubation, stroke
d/t increased intracranial pressure
Cutting  Incisions
o Low segment transverse
→ Transverse incision of lower anterior
abdomen and uterine fundus
→ Pfenienstel(?) – common 2-3cm above
symphysis and slightly curved
→ Joel and Cohen – ASIS, 3cm below;
straight
 Ligate/meds to stop bleeding if it still
continues
Monitoring of  72hrs post-partum, 7-10 days after delivery
BP  Prevent seizure  magnesium sulate, cont
24hrs after delivery
 Transfer to NICU
 Monitor mother for complains of pain kay basi
dula na effect sang anes
Address PE
 Wait for mother to pass flatus before siya
maka eat again
 But promote gid early intake kay ga bulig siya
early restoration of status kag angulation
decreases length of stay
Bleeding  Ligation, uterotonic agents
 But if no response  hysterectomy
 Since G1 ang px, last resort
Pain  NSAIDs -> inc. BP don’t give
 Give opioid instead
Wound care and  Risk for thromboembolism, thus suggested na
ambulation mag walk pa bathroom, assisted, brief walking
 Removal of surgical dressing after 24 hrs then
inspect incision daily
 Taking a bat after 3 days is ok
Discharge  As long as okay ang baby, may good suck na,
criteria etc, can discharge


Hysterotomy  Incision
LONG-TERM MANAGEMENT
 Delivery of fetus
 Delivery of placenta Monitor BP  At least 1 week after discharge
 Uterine repair  Establish baseline BP if may preeclampsia
 Abdominal closure gidman or if nag progress
Why CS?  Provide drugs safe for breastfeeding
 preferable in pregnancies less than 30-32 o Nifedipine, captopril
weeks of gestation especially if there are signs
 Use aspirin kung mag pregnant liwat
of fetal compromise like abruptio placenta.

 Prompt delivery is the safest option for the
Educate  Possible recurrence in next pregnancy
woman and her fetus when there is evidence of
 Prenatal check up
pulmonary edema, renal failure, and abruptio
placenta, DIC, eclampsia, nonreassuring fetal  Adhere to sched every 4 weeks next 24 weeks
tesitng or fetal demise.  Every __
 Every week 37 weeks and beyond
Upon delivery  EINC cannot completely be done due to CS  Breastfeeding
but continue eval of neonate  Family planning
 <85%O2  intubate  Wait at least 6 weeks (postpartum intercourse)
 Resuscitate if unstable  Avoid special positions
 Start IV  Vaccination
 Incubator to prevent hypothermia  Continuous check ups of neonate
Postpartum  1st 4 days  anti HTN  Explain diagnosis d/t increased risk
persistence of o Oral methyldopa or nefidipine o Lifestyle modifications like regular
HTN exercise
o Slow release preparation
Surfactant  Supplement deficit of surfactant o Fatty acids from fish oil
therapy  Monitor signs of complications of prematurity Supplements  Vitamin D
 Calcium
After delivery  Close monitoring of mom and baby Maternity leave
Psychosocial  Recommend to go to organizations where they
 support can go and ask for help  50% develop ASD  important to check for developmental
 milestones of baby
Privileges  HB 10% discounts to VAT for necessity of  Baseline data for Filipino women
children(?)

XVIII. PROGNOSIS
PREECLAMPSIA
 Preeclampsia – 14% maternal deaths annually
 Mortality and morbidity is d/t complications present
 Recurrence – 10%
XXI. COURSE IN THE CLINIC
 Severe preeclampsia – 20% recurrence
 Admitted
PLACENTAL ABRUPTION
 Start IV
Fetal – depends on timing of abruption and severity
 Hydralazine 5mg IV, every 20mins.
 Extremely preterm gestation + 50% separation of placenta  high
 MgSO4 – 4mg load, continued drip 1g/hr
risk death
 Foley catheter inserted, urine output monitored
 Abruption recognize early + promt delivery  good
 O2, nasal prongs
Maternal prognosis  Labs taken
 Amount of blood loss, severity, coagulopathy  Scheduled for STAT CS
 Absence  better prognosis  Regional anesthesia, subarachnoid block
 AF clear and adequate, no oligohydramnios
XIX. PHILHEALTH COVERAGE  Live preterm baby girl, cephalic
 CS -19000  30 weeks AOG
o 11000 – PF  Placenta with infarct, 100mL retroplacental clot
o 7400 – IF  Bilateral ovaries and tubes were normal
 Severe preeclampsia – 6800  Estimated blood loss 500cc
o 3040 - PF  Post op, BP acceptable range
o 3716 – IF  RR 12-20cpm
o Can get as much as 71000!  O2 – 2L nasal prong
 Abruptio placenta – 7700  CXR @ PACU – Pulmonary edema
o 2310  Responded to meds to augment pulmonary status
o 5390  Discharged on 27th post op day with home medications
 NBB (Social service)
o 0 FEE!!!! XXII. FINAL DIAGNOSIS
o Discharge WITHOUT ANY spending  G1P1 (0-1-0-1), Pregnancy uterine, delivered to a live preterm baby
girl in cephalic presentation, with birth weight of 1165 grams,
APGAR score 6,7 , clinical aging 30 weeks via primary cesarean
XX. AREAS OF RESEARCH section under regional anesthesia (RA-SAB) for abruptio placenta
secondary to preeclampsia with severe features, pulmonary edema
resolved