ANTEPARTAL COMPLICATIONS
 The baby is delivered normally.
BLEEDING CONDITIONS DURING PREGNANCY
 Any type and amount of vaginal bleeding is
considered ABNORMAL.
 Why BLEEDING is a DANGER SIGN?
1) Uterus is a NON-ESSENTIAL ORGAN
 People can survive even
without a uterus.
 Without blood supply to the
uterus and to the placenta,
therefore, no blood supply also
to the fetus.
2) There is a CONNECTION PROBLEM
between the BABY and the MOTHER.
3) BLEEDING might be CONCEALED
 The blood came out in the
vagina MIGHT BE ONLY A
FRACTION OF BLOOD that is
lost.
 Bleeding occurs on the 1st Trimester:
1) Abortion
2) Ectopic Pregnancy
 Bleeding occurs on the 2nd Trimester:
1) Incompetent Cervix
2) Hydatidiform Mole
 Bleeding occurs on the 3rd Trimester:
1) Placenta Previa
2) Abruptio Placenta
3) Preterm Labor
1st TRIMESTER COMPLICATIONS:
1) ABORTION
 Termination of pregnancy before the fetus
reaches the age of viability
 Less than 20-24 AOG
 Weight: <500 gms
 May Occur:
a. EARLY (<6 weeks)
 MILD bleeding
 Area of involvement of uterus
and placenta is small.
b. MIDDLE (6-12 weeks)
 Bleeding is MORE SEVERE
 Area of involvement of uterus
and placenta is moderate.
 Placental attachment is shallow.
 Before the baby is delivered, the
placenta is already detached,
causing massive bleeding.
c. LATE (>12 weeks)
 Area of involvement of uterus and
placenta is large.
 The placental attachment is deep
 Causes of ABORTION:
a. Teratogens
1. Accutane (anti-acne)
 E.g. Eskinol, Maxi-peel
 Topical products having
tretinoin or isotretinoin are
NOT ADVISABLE for pregnant
mothers.
 These chemicals can be
absorbed to the skin and to
the bloodstream.
 When the chemicals are
compounded in the blood, it
is now TERATOGENIC.
2. Toxoplasmosis
3. Syphilis
b. Chromosomal Aberration (LEADING
CAUSE)
 Most of the abortus infants
have physical or congenital
defects
c. Poor Implantation
 Problem in the thickening of
the endometrium during the
menstrual cycle
 (Proliferative Phase)
KINDS OF ABORTION
a) THREATENED
 MILD bleeding & uterine Cramping
 (-) Cervical Dilation
 Avoid strenuous activities for 24-48 hrs
 CBR is not necessary
b) IMMINENT/INEVITABLE
 (+) Cervical dilation
 Premature Rupture of Membranes
 The child is delivered via D&E (Dilation
& Evacuation)
 NURSING CONSIDERATION:
 SAVE ALL PASSED TISSUES
 To determine if there is H mole
or other malignancies
 c) MISSED  (+) Cullen’s sign = bluish discoloration of the
 Also called EARLY PREGNANCY FAILURE periumbiical area
 No increase in fundal height  Shoulder pain = irritation of the phrenic nerve
 Absence of previously heard FHT  Leukocytosis (Increase WBC) = because of
 Confirmed by UTZ TISSUE TRAUMA
 Managed by D&E or inducing labor  Monitor signs of SHOCK
 Complication of RETAINED DEAD FETUS:
 Disseminated Intravascular MANAGEMENT:
Coagulation (DIC)  Not ruptured:
 The mother’s platelet 1. Methotrexate PO until HCG is (-)
count is decreased  Chemotherapeutic drug
because of the  Absorbed in cells having rapid cell
excessive bleeding growth
CELLS having rapid cell
inside the body.  Kill the baby growth:
d) COMPLETE  1. Gastric parietal cells
 Entire products of Conception (Fetus, 2. Bone marrow
Membranes and Placenta) are expelled 3. Hair follicles
4. Fetus
spontaneously without any assistance  If ruptured:
5. Trophoblastic cells
 Bleeding usually slows within 2 hours 1. Salpingectomy
 After the products of Conception are 2. Suturing using a microsurgical technique
expelled, the uterus can contract 3. POST-OP:
normally to STOP the bleeding.  50% fertile (Theoretically)
e) INCOMPLETE  Monitor ABDOMINAL PREGNANCY
 Retention of some products Placental implantation in the
 Managed with D&C (Dilation & internal organs OTHER THAN
Curettage) THE UTERUS
 To STOP the bleeding Most common in the
INTESTINES
2) ECTOPIC PREGNANCY Chances the infant be
 Implantation outside the uterus delivered is SGA and
 Common site is the ampulla MALNOURISHED
 Site of fertilization Mode of Delivery: Laparotomy
 Common site in ectopic
pregnancies FERTILIZATION PROCESS (SEQUENCE)
 Sharp, stabbing, unilateral pain over the 1) Fertilized egg
lower abdomen 2) Implantation to the upper portion of the uterus
 Causes: CATS (8-10 days)
a. Congenital malformations 3) Forms into a Cleavage (2-celled structure)
b. Adhesions 4) Cell divides into a Murulla (16-celled structure)
c. Tumors 5) Blastocysts
d. Scars from previous surgeries  Made up of 2 Layers
 Estrogen a. Inner layer
 Responsible for uterine growth ONLY Embryoblasts (Fetus)
(no influence on other organs) b. Outer layer
 Responsible for enlargement of breasts Trophoblasts
 Responsible for increase hip diameter (Placenta/Chorionic villi)
 Responsible for vaginal moisture
 Responsible for palmar erythema 2ND TRIMESTER BLEEDING COMPLICATIONS
ASSESSMENT: 1) HYDATIDIFORM MOLE
 Sharp stabbing pain in the lower quadrant  Abnormal proliferation and then
followed by scanty (LIGHT) vaginal bleeding degeneration of the trophoblastic;
 Rigid abdomen from peritoneal irritation
  As the cells degenerate, they become filled
with fluid and appear as clear fluid-filled,
grape-sized vesicles
 Bleeding with a passage of grape-like
vesicles
 Misdiagnosed of multiple pregnancies
 Trophoblastic Cells:
a) Produces HCG (Human Chorionic
Gonadotropin)
 Responsible for the (+) Pregnancy
Test
 Makes the corpus luteum to
continue to survive; initially 10 days;
extended for 2 months
 It takes 2 months the placenta to
mature
b) Fast growing cells
Corpus Luteum
 Secretes Estrogen and Progesterone
 It dies after 2 months
 Placenta will be now the substitute in
secreting Estrogen and Progesterone
 Risk groups:
a) Asians
b) Low protein diet
c) Type A + Type O men
 Symptoms:
a) Hyperemesis gravidarum
 Due to abnormally high levels of
HCG after 2 months causing
REVERSE PERISTALSIS (Vomiting)
b) Large uterus
 Due to abnormal amounts of
trophoblastic cells
 Complications: choriocarcinoma
Types of H mole:
a) Complete mole:
 Trophoblasts swell and become
cystic; comprised of 46XX/46XY
exclusively from the father
 Sperm cell is duplicated to be 46
chromosomes
 Empty ovum
b) Partial mole
 Some villi are formed; 69
chromosomes
 69 chromosomes
 2 sperms in one egg cell
ASSESSMENT:
 Vaginal bleeding with passage of fluid filled
vesicles
 Rapid uterine enlargement
 High levels of HCG (1-2M instead of 400M)
 Marked emesis
 Snowstorm pattern on UTZ
MANAGEMENT:
a) Suction Curettage
 POST OP:
a) Monitor HCG levels every 2 weeks
HCG levels MUST DECLINE
NOTE: if levels either PLATEAU
3x or slight increase, it
indicates CHORIOCARCINOMA
b) Take oral contraceptives for 1 year
 Avoid pregnancy at all costs
 Strictly Monitor HCG levels within this
year
c) Chest radiograph at the 6th month
 To determine if the choriocarcinoma
metastasized to the lungs (Lung cancer)
d) Methothrexate
 As prophylaxis
 Management of choriocarcinoma
e) Methotrexate + Dactinomycin
 Choriocarcinoma has been metastasized
2) PREMATURE CERVICAL
DILATION/INCOMPETENT CERVIX
 Cervix that dilates prematurely
 When does the cervix must dilate?
o Cervical Dilation & Effacement
Phase (1st Stage of Labor)
o 2nd Trimester Bleeding
 Cannot hold a fetus until term
 ASSESSMENT:
a) Painless cervical dilation
b) Pink-stained vaginal discharge
c) Increased pelvic pressure followed by
ROM
 MANAGEMENT:
a) Cervical Cerclage
 Approx. 12-14 weeks
 Purse-string sutures are placed in
the cervix by vaginal route under
regional anesthesia
 Removal of sutures: 37-38 weeks
(for NSVD)
 TWO types:
1. Shirodkar Cerclage
 For Cesarean deliveries
2. McDonald Cerclage
 For NSVD deliveries
3RD TRIMESTER BLEEDING COMPLICATIONS
1) PLACENTA PREVIA
 LOW IMPLANTATION of the placenta
 Clinical Symptom:
 Painless, bright-red vaginal
bleeding
 Occurrence: 30th week AOG (moment of uterine
differentiation)
 The uterus now subdivides itself to
UPPER SEGMENT and LOWER SEGMENT
LOW LOW BLOOD FETAL
IMPLANTATION SUPPLY MALFORMATIONS
 ASSOCIATED FACTORS:
a) Increased parity
b) Advanced maternal age
c) Past cesarean births
d) Past uterine curettage
e) Multiple gestation
 ALL THESE FACTORS WILL RESULT WITH THE
PLACENTA SEARCHING FOR AN EXCHANGE
SURFACE!
 DEGREES OF PLACENTA PREVIA
a) PLACENT PREVIA MARGINALIS
 Placenta is near the edge of
cervix
 MOD: NSVD
b) PLACENTA PREVIA PARTIALIS
 Placenta is partly
obstructed the cervix
 MOD: NSVD
c) PLACENTA PREVIA TOTALIS
 Placenta completely
obstructed the cervix
 MOD: Cesarean Delivery
d) LOW LYING PLACENTA
 Placenta is at the lower
portion of the uterus, not
obstructing the placenta.
 MOD: NSVD
e) VASA PREVIA
 Umbilical cord is on the
entrance of the cervix
 NURSING CONSIDERATIONS
a) NEVER ATTEMPT a pelvic or rectal
examination with painless bleeding
late in pregnancy
 Agitation of the cervix when
there is placenta previa
may initiate massive
HEMORRHAGE!
2) ABRUPTIO PLACENTA
 RISK FACTORS:
a) Trauma
b) Short umbilicus
 As the fetus (with short
umbilicus) tends to move, it
can gradually pull the
placenta from its
attachment site.
c) Degeneration of the DECIDUA
 DECIDUA – mucosal lining
of the uterus from its
attachment
 When the decidua DRIES
UP, the placenta will
gradually move away from
its attachment site.
 FACTORS OF DEGENERATION OF DECIDUA
1. Cocaine & Smoking
 Has VASOCONSTRICTING
effects
 Reduced blood supply to
the decidua
2. Advance maternal age
 The higher number of age,
the lesser blood supply
3. PIH & Chronic Hypertension
 Due to vascular spasms
 Reduced blood supply to
the decidua
 DEGREES OF ABRUPTIO PLACENTA
a) ABRUPTIO PLACENTA PARTIALIS
 PARTIAL separation of the
placenta from its central
portions to the attachment
site
 Bleeding is CONCEALED
 DARK RED BLEEDING
b) ABRUPTIO PLACENTA TOTALIS
 COMPLETE separation of
the placenta from its
attachment site
 Bleeding is CONCEALED
 DARK RED BLEEDING
ASSESSMENT
 May occur LATE in labor
 Tenderness upon palpation
 Brought about by the CONCEALED
bleeding
 Heavy bleeding – DARK RED BLEEDING
 The blood is trapped in the central areas
of the placenta before it eventually
released outside the vagina
  Couvelaire uterus (RIGID)
 Fetal prognosis: Depends on the extent of INCREASE BLOOD PRESSURE
the placental separation (Pathophysiology)
 Maternal prognosis: depends on how PLATELETS
promptly treatment can be instituted INCREASED
CARDIAC OUTPUT
ENDOTHELIAL
WALL INJURIES
RELEASES
CLOTTING
FACTORS

DISSEMINATED INTRAVASCULAR COAGULATION (DIC)

 Acquired disorder of blood clotting
INCREASED
 Fibrinogen levels fall to below effective limits INCREASE BLOOD SYSTEMIC NARROWED
PRESSURE VASCULAR BLOOD VESSELS
 CAUSES: RESISTANCE
a) PIH
b) Retained Dead Fetus
c) Placenta Previa
REDUCED BLOOD
d) Abruptio Placenta SUPPLY
 TEST TUBE TEST
1. After 30 minutes, a clot should not only
form but retract (becomes lesser volume 2. Proteinuria
than the serum)  PROTEINS
2. The volume of serum in the tube SHOULD  Responsible for colloid osmotic
EXCEED THE SIZE of the clot. pressure
 MANAGEMENT:  Orthostatic Proteinuria
1. STOP the CAUSE  Considered NORMAL
a) Abruptio placenta  Elevated protein levels of
b) Retention of the Dead Fetus pregnant mothers in an upright
2. Administer HEPARIN position
3. Give:  Positive indication:
a) Fresh Frozen Plasma (FFP)  (+) Proteins in urine
b) Platelets (PLT)  Urine test was taken in the
c) Blood Transfusion (BT) AFTERNOON
PREGNANCY-INDUCED HYPERTENSION (PIH)  Kidney problem
 Condition in which vasospasm occurs during  Positive indication:
pregnancy in both small and large arteries  (+) Proteins in urine
 Formerly as TOXEMIA  Urine test was taken in the
 RISK FACTORS: EARLY MORNING
a) Pre-existing heart diseases
b) Pre-existing Diabetes
 TRIAD SYMPTOMS:
DECREASE GFR INFLAMMATION
1. Hypertension REDUCED BLOOD
(GLOMERULAR RESPONSE OF
SUPPLY TO KIDNEYS
Considered NORMAL SIGNS for FILTRATION RATE) KIDNEYS
Pregnant Mothers:
a) Increased Blood Volume
b) Increased BP
c) Increased CO EXCRETION OF PROTEINS IN THE
EXPANSION OF
FILTRATION SITES
 To supply blood for PROTEIN THROUGH BLOOD PASSES
(GLOMERULAR
URINE THROUGH
themselves as well as her CAPILLARIES)
infant
d) Increased Blood Loss
 Compensatory mechanism
of the body of the pregnant
mother removing the
produced blood
 For the purpose of
pregnancy
 3. Edema 1) To avoid seizures:
 Ankle Edema (Physiologic) a) Darken the room
 Considered NORMAL b) Limit visitors
 Facial Edema (Pathologic) c) Minimize noise
 Considered (+) for PRE- 2) Weigh daily
ECLAMPSIA 3) Monitor BP
 Tightening of the Wedding Ring 4) High Protein Diet
(Pathologic)  Patient is (+) Proteinuria
5) Administer meds as ordered: MgSO4

LACK OF PROTEINS IN
IMBALANCE OF MAGNESIUM SULFATE
ABSENCE OF COLLOID HYDROSTATIC PRSSURE
THE BLOOD
OSMOTIC PRESSURE AND COLLOID OSMOTIC  Cathartic (accelerates defecation)
(DUE TO PROTEINURIA)
PRESSURE
 Pulls the excess fluids from the
extravascular spaces in to the intestines
causing diarrhea
 S/E: DIARRHEA
FLUIDS TRAVELS
FLUIDS WILL
EXTRAVASATE
 CNS depressant
EDEMA
THROUGH TISSUES (GOES OUT from the  In decreasing of brain activity, it stops the
vascular wall)
existing eclamptic seizures from worsening.
DEGREES OF PIH  Therapeutic Range: 5.0-8.0 mg/dL
GESTATIONA MILD PIH SEVERE ECLAMPSIA  <5.0 mg/dL of MgSO4: SEIZURES
L HTN PIH  >8.0 mg/dL of MgSO4: TOXICITY
BP of 140/90 BP of BP of SEVERE  Antidote: Calcium Gluconate
140/90 160/110 SEIZURES  Magnesium can ONLY BE EXCRETED through
NO EDEMA MILD SEVERE or COMA URINE!
EDEMA EDEMA along with  Low/No Urine Output = No excretion of Mg
NO +1 or +2 +3 or +4 signs of PIH
PROTEINURIA ASSESSING MgSO4 TOXICITY
 SEIZURES in ECLAMPSIA Signs of toxicity Nursing considerations
 Due to the SEVERE EDEMA that Reduced Urine Output Must be 30 cc/hr
compresses the brain of excess Low LOC Must be responsive
fluids.
Reduced DTR Must be +2
 TREATMENT: MgSO4
(average DTR)
 If seizures are not treated early or
Shallow Respirations Must be 12 cpm
immediately, 90% of eclampsia
WITHHOLD ANY OF THESE FACTORS
cases, the baby will die.
MEDICATION IF: ARE LOW OR NOT MET!
MANAGEMENT of MILD PIH
1) Administer LOW-dose ASPIRIN  How much blood does a mother loss in NSVD?
 Prevent platelet aggregation  500 mL
2) Promote bed REST
 The body excretes sodium at a faster  How much blood does a mother loss in
rate when the body is in a state of rest Cesarean Delivery?
3) Promote GOOD NUTRTION  1000 mL (1 L)
a) Na restriction is recently no longer
included in the diet  How much blood loss does it need for Blood
 Absence of sodium in the diet Transfusion?
will activate RAAS activation  2 units (1000 mL) for BT
 Causing REBOUND
HYPERTENSION  Blood Pressure = Cardiac Output x Systemic
Vascular Resistance
 BP = CO x SVR
MANAGEMENT of SEVERE PIH RH INCOMPATIBILITY (ISOIMMUNIZATION)
 Rh NEGATIVE mother carries a Rh POSITIVE fetus
 What is the meaning of the (+) and (-) in blood
typing?
 Indication of whether or not the person has
a D antigen
 Protein that is found in the cell walls of
every RBC
 If have D antigen: Blood type is
POSITIVE
 If have absence of D antigen: Blood
type is NEGATIVE
 How does Rh Incompatibility Happens?
 When an Rh NEGATIVE person exposed to
a (+) D antigen blood ONLY!
 The Rh NEGATIVE person will regard the
(+) D antigen blood as an INVADING
ORGANISM.
 DEFENSE MECHANISM of the Rh (-)
person:
 Forms ANTIBODIES to the (+) D
antigen blood
 In the 1st pregnancy of the Rh (-) mother to
a Rh (+) fetus:
 NO COMPLICATIONS; NORMAL
 The beginning problem comes in the 3rd
Stage of LABOR (PLACENTAL STAGE)
 In the separation and expulsion of
the placenta, the placental barrier
dissipates.
 The fetus Rh (+) blood gains access
to the mother’s Rh (-) blood
 This time, the Rh (-) mother will
form ANTIBODIES against the
fetus Rh (+) D antigen blood.
 WHY is it SUCCESSFUL for the Rh (-) mother
to have a NORMAL delivery of an Rh (+)
fetus?
 REMEMBER: The baby is out in the
2nd Stage of LABOR (Delivery of the
Baby)
 Meaning, the baby is out before the
placenta had dissipated in the
uterus.
 The ACTUAL PROBLEM comes in the 2nd
pregnancy of the Rh (-) mother with Rh (+)
fetus.
 The maternal blood of the Rh (-)
mother was pre-exposed before
during her 1st pregnancy;
ANTIBODIES HAVE ALREADY
FORMED!
 The ANTIBODIES can now CROSS
THE PLACENTAL BARRIER!
 The ANTIBOIES can now DESTROY
the fetus’ RBCs, resulting to a
EXCESSIVE LOSS OF RBCs (Hemolytic
Anemia), leading to a condition
ERYTHROBLASTOSIS
called
FETALIS!
 Why do people have Rh NEGATIVE blood?
 85% of people have Rh POSITIVE
Blood
 15% of people will have Rh
NEGATIVE blood.
 This happens when the MOTHER is
HOMOZYGOUS(Rh NEGATIVE gene)
and the FATHER is HETEROZYGOUS
o one copy is Rh NEGATIVE
gene
o one copy is Rh POSITIVE
gene
 50% chance to have a Rh NEGATIVE
baby
MANAGEMENT:
1) Administer RHOGAM within 72 hours
 Prevents formation of antibodies (anti-
D antigen)
 RHOGAM must be administered every
after delivery of the Rh (-) mother
 RHOGAM lasts only for 2 months
 ALL Rh (-) WOMEN with UNTYPABLE
PREGNANCIES must take RHOGAM!
2) Anti-D Titer Screening (COOMBS TEST)
 Determines if the mother has
ANTIBODIES (Anti-D antigen)
 Types of Coombs Test:
a) DIRECT COOMBS TEST
o Fetal blood sample is tested
b) INDIRECT COOMBS TEST
o Maternal blood sample is
tested
ASSESSMENT:
1) ALL Rh (-) WOMEN should undergo COOMBS
TEST
a) If test is NEGATIVE/LOW:
1. Receives RHOGAM at 28 weeks (7
months)
 For PROPHYLACTIC measure
 To prevent seepage of the
placenta filled with Rh (+) blood
 Prevent sensitization of the
mother
2. within 72 hours postpartum
b) If test is POSITIVE/HIGH:
 1. The mother is sensitized; TOXIC to
the baby
2. Do not give RHOGAM
3. Fetus is monitored via DOPPLER
VELOCITY
c) DOPPLER VELOCITY is ABNORMAL:
 Indicates child has ANEMIA
 RBCs has been destroyed
d) DOPPLER VELOCITY is NORMAL:
 CHILD is likely to be Rh (-)
GESTATIONAL DIABETES MELLITUS
 A condition where the mother either has:
a) ABSENCE of insulin
b) Has insulin yet harbors RESISTANCE to
insulin
 Why is INSULIN IMPORTANT?
 Insulin is the KEY
 Without INSULIN, Glucose cannot
enter any of the cells in the body.
 Insulin must attach itself in the
receptor sites of every cell for the
glucose to enter into the cell.
 GLUCOSE
 is absorbed totally in the
Duodenum (Small
Intestine)
 Is USELESS if not INSIDE the
cell.
 TYPES of DM:
1. TYPE 1 DM
 Considered as Juvenile Onset DM
 Occurs in childhood
 Represents failure of the pancreas
to produce adequate insulin
 Glucose cannot enter into the cells
of the body because of there is
absence of insulin
 Regarded as an AUTOIMMUNE
condition
2. TYPE 2 DM
 Considered as Adult Onset DM
 Common in older adults
 Cause by gradual failure of insulin
production that occurs in aging
 Glucose cannot enter into the cells
of the body because of the cells
does not recognize glucose,
meaning resistance.
3. Gestational DM
 Insulin resistance as pregnancy
progresses
 Insulin does not seem as effective
during pregnancy
 CAUSE: Human Placental Lactogen
hormone (HPL)
o Ensures the baby receives
glucose through its anti-
insulin effect
o 80% of the mother’s
nutritional intake (glucose)
goes to herself
o 20% of the mother’s
nutritional intake (glucose)
goes to the infant
o The fetus will release its own
insulin, resulting of glucose
entering the fetus’
circulation.
 Not all pregnant mothers can
tolerate the effects of HPL.
o The effects of HPL can
AGGRAVATE when the
pregnant mother has pre-
existing DM.
o DOUBLES the chance of
getting Gestational DM
WHAT HAPPENS IF THE PREGNANT MOTHER HAS NO
INSULIN?
 The mother’s nutritional intake (glucose) to
herself is 0%
 100% of the mother’s nutritional intake
(glucose) goes to the infant
 This results to the infant having
MACROSOMIA (LGA)
PLACENTA FUNCTIONS: IRENE
a) IMMUNOLOGIC (has Immunoglobulin M A G D E)
 When can the infant start receiving
antibodies?
o 24 weeks AOG
1. Pupils starts to react to light
2. Start of the first hearing
3. Receives IgG
 IgG
o Only immunoglobulin that can CROSS
THE PLACENTAL BARRIER.
b) RESPIRATION
 Allows GAS EXCHANGE of the infant via:
 UMBILICAL CORD (AVA) (21 inches)
 c) EXECRETORY
 Excretes nitrites and ammonia from fetus to ASSOCIATED CONDITION
the mother a) Infants of women with poorly controlled
d) NUTRITION diabetes tend to be LARGE
 Glucose enters in to the placenta for the  Due to increase insulin by the fetus
infant’s nutrtion  To compensate, the fetus must produce
e) ENDOCRINE ORGAN increase insulin to counteract
 Secretes: overloading of glucose that it receives.
1. Estrogen
2. Progesterone ASSESSMENT:
3. HCG 1. Screening for FBS
4. HPL  >126 mg/dL:
o The pregnant mother has
FASTING BLOOD SUGAR LEVEL (FBS) to undergo a next level
 NORMAL: 80-120 mg/dL test using 50-g oral
 If levels are 150 mg/dL: excessive glucose is glucose challenge
excreted to urine (Glucosuria)  >160 mg/dL in 1 hour on the 50-g:
o Proceed to another test
4 CLASSICAL SIGNS OF DM (3 P’s) (100-g oral glucose
a) POLYPHAGIA challenge for
 Feeling of extreme hunger. confirmatory)
 When glucose remains in the blood for
long periods of time, the cells signals MANAGEMENT:
the brain to as “a state of hunger”. 1. INSULIN
 The liver then converts fats into  Mixed with short acting and intermediate
glucose (gluconeogenesis) acting insulin
b) POLYDIPSIA  SHORT ACTING INSULIN: given In the
 Feeling of extreme thirst. MORNING
 To compensate by the body’s excessive  INTERMEDIATE ACTING INSULIN: given In
excretion of water through urine the EVENING
(Polyuria), the body signals THIRST a) AVOID ORAL HYPOGLYCEMIC AGENTS
RESPONSE.  IT HAS A TERATOGENIC EFFECT
c) POLYURIA b) Early pregnancy of woman with DM
 The body urinates more than usual.  May need less insulin than before
 Glucose is an OSMOTIC DIURETIC pregnancy
o PULLS or CARRIES water  REASON: Fetus is using so much
together with glucose to glucose for rapid cell growth
be excreted in urine. c) Later pregnancy of woman with DM
 The body compensates to excrete  Increased amount of insulin
excess glucose in the blood causing  REASON: To increase metabolic
GLUCOSURIA (150 mg/dL) rate
o (+) Glucose in the urine is 2. CESAREAN SECTION DELIVERY (For Macrosomic
indication of EXCESSIVE babies)
GLUCOSE IN THE BLOOD  To prevent SHOULDER DYSTOCIA of the
d) WEIGHT LOSS macrosomic infant.
 Due to glucose cannot enter inside the  To prevent dysfunctional labor.
cell; there is no cell metabolism that 3. LOW-GLUCOSE DIET
will occur. 4. REGULAR EXERCISE
 There is NO CELL GROWTH, developing
weight loss.
IRON DEFICIENCY ANEMIA (IDA) MANAGEMENT:
 A condition which the mother lacks iron in the 1. IRON THERAPY
blood. a) Supplementation: 60 mg
Amount of NUTRIENTS required DURING PREGNANCY b) IDA therapy: 120-200 mg
FOLIC ACID 400 mcg c) SEVERE CASES: IRON DEXTRAN IM in Z-
(FO-FO-FOUR HUNDRED) track
d) If given liquid form:
PHOSPHORUS 800 mg o Use straw to avoid teeth staining
(multiplied by 2 of FOLIC ACID) e) Best absorbed together with Vitamin C
(acidic environment)
CALCIUM 1200 mg f) S/E:
(TOTAL between FOLIC o Constipation
ACID and PHOSPHORUS) o Dark stools
g) HEALTH TEACHING:
VITAMIN A 800 mcg o Iron-rich food intake:
(AY-AY-AYT HUNDRED)  Organ meats
 Green vegetables
VITAMIN C 7 mg  Beans
(C-C-C-ven)  Dried fruits

VITAMIN E 8 mg URINARY TRACT INFECTION

(E-E-Eight)  Pregnancy is a RISK FACTOR for the
development of UTI:
VITAMIN D 10 mcg a) Dilated ureters
(D-D-Dyes or 10)  Influence of PROGESTERONE
ZINC 15 mg b) Shorter urethra in females
(ZINC backwards “KEN-ZE”)  Due to close proximity to the anal
region
IRON 60-100 mg c) Minimal glucosuria in pregnancy
(SUPPLEMENTAL)  Invites pathogens (E.coli)
 WHY does PREGNANT WOMEN
120-200 mg have slightly increase of glucosuria?
(if have IDA)  There is decrease of renal
 HOW FE is STORED? threshold during pregnancy
 IRON is made available by: ASSESSMENT:
a) Absorption from duodenum into 1. FREQUENCY
bloodstream after it is ingested. 2. URGENCY
 In the bloodstream ,the IRON is: 3. DYSURIA (BURNING upon urination)
a) Bounded by TRANSFERRIN 4. MALAISE, FEVER & CHILLS
b) Transported to LIVER, SPLEEN, 5. LOW BACK PAIN
and BONE MARROW. 6. (+) URINE TEST for WBC, PUS & RBC
 Incorporated into MANAGEMENT:
HEMOGLOBIN 1. TREATMENT IS NECESSARY because UTI is
 Stored as FERRITIN common factor that leads to PRE-TERM LABOR
 PERSONS AT RISK: (PTL)
a) Poor intake of foods rich in iron 2. C&S prior to antibiotic therapy
b) Heavy menses 3. Encourage oral fluids
c) Closely-spaced pregnancy (less than 2 4. Acidify the urine
years gap between pregnancies) 5. 3 W’s
a) WASH every after urination
b) WEAR cotton panties
c) WIPE from front to back
 6. Give Amoxicillin, Ampicillins or Cephalosporins  PHYSIOLOGIC RETRACTION RING:
as ordered  NORMAL
 SULFONAMIDES ARE CONTRAINDICATED!  In 30th week AOG (moment of
 Causes hyperbilirubinemia in newborns uterine differentiation), the uterus
will subdivide into UPPER and
CAUSES OF PRE-TERM LABOR: LOWER SEGEMENTS in preparation
1. CHORIOAMNIONITIS of labor
 Infection of the chorionic villi/amniotic  Causing a slight indention of the
membrane abdomen
2. UTI  Assessed by PALPATION:
3. DEHYDRATION (MOST COMMON) a) SEVERE Horizontal indention across the
 Whenever the body is dehydrated, the abdomen
body responses to hypothalamus to  EFFECT:
produce ADH and secretes it by the a) Fetus is GRIPPED
posterior pituitary gland. b) Placenta is GRIPPED in the PP
 Also it accidentally the posterior pituitary  MANAGEMENT:
gland secretes oxytocin, together with a) Inhalation of AMYL NITRITE
ADH.  To relax the constriction ring
 Due to oxytocin is also secreted to the  Prevents continual gripping of
body; it now leads to preterm uterine the fetus and placenta
contractions (Braxton Hicks contractions).  Prevents neurological damage
 MANAGEMENT: of the fetus
a) HYDRATION b) Cesarean Delivery
b) IV fluids  COMPLICATIONS:
a) Neurologic damage to fetus
INTRAPARTAL COMPLICATIONS b) Uterine rupture
 CAUSES:
1) INEFFECTIVE UTERINE CONTRACTIONS a) Excessive Oxytocin administration
A. HYPOTONIC CONTRACTIONS b) Uncoordinated contractions
 DURING Inactive Phase c) Obstetric manipulation (Fundal Push)
 MANAGEMENT:
a) OXYTOCIN 3) PRECIPITUOUS LABOR
B. HYPERTONIC CONTRACTIONS  Labor that is completed in fewer than 3 hours
 DURING Latent Phase  Associated with:
 MANAGEMENT: a) Grand Multiparity
a) TOCOLYTICS:  “Suki nang Prenatal”
1. Ritodrine b) Oxytocin administration
2. Yutopar c) Post Amniotomy
3. Terbutaline  Artificial puncturing of the amniotic
4. Bricanyl sac (This will cause a gushing of fluid).
 Determining Amniotic Fluid:
2) PATHOLOGIC RETRACTION RING (BANDL’S RING) USING NITRAZINE PAPER (yellow):
 A hard band that forms across the uterus at the a) Remains YELLOW: Urine
junction of the upper and lower uterine (acidic)
segments. b) Turns to BLUE: Amniotic Fluid
 INDICATION: impending uterine rupture. (alkaline)
 Due to the low lying position of the  MANAGEMENT:
placenta (attachment is in midway to the a) TOCOLYTICS:
segments of the uterus) 1. Ritodrine
 This uterine differentiation will stretched 2. Yutopar
the placenta which results to bleeding. 3. Terbutaline
4. Bricanyl (relaxes smooth muscle)
  COMPLICATIONS:
a) Abruptio Placenta
b) Subdural hemorrhage in Fetal Head
c) Perineal lacerations (MOST COMMON)
4) UTERINE RUPTURE
 Occurs when a uterus undergoes more strain
that is capable of sustaining
 Preceded by a Bandl’s Ring
 SIGNS & SYMPTOMS:
a) Tearing sensation on a strong labor
contraction
 CAUSES:
a) Unwise us of Oxytocin
b) Traumatic maneuvers on labor (Fundal
Push)
c) Prolonged Labor
TYPES OF UTERINE RUPTURE:
1. COMPLETE (Endometrium-Myometrium-
Perimetrium INVOLVEMENT)
 ALL LAYERS of uterus are involved
 2 swells are visible, the extra-uterine
fetus and the retracted uterus
 SEVERE BLEEDING follows oozing from
torn vessels
2. PARTIAL (Endometrium-Myometrium
INVOLVEMENT)
 No Perimetrium Involvement
 Localized tenderness
 Persistent aching pain over the area of
the lower uterine segment
5) UTERINE INVERSION
 Uterus turn inside out with either:
a) In the Birth of the fetus
 Pressure is applied in the fundus of an
uncontracted uterus (Fundal Push)
 Fundal Push maneuver must be
performed together with the mother
pushing.
 REQUIREMENTS FOR FUNDAL PUSH:
1. Synchronization together as the
mother pushes.
2. Firm abdomen
b) Delivery of the placenta
 Traction of the umbilical cord to
remove the placenta (Pulling of the
cord)
 INITIAL SIGN: Sudden gush of blood
 Bleeding continues as the uterus does
not contract in an inverted state
 MANAGEMENT:
1. Give uterine relaxants (Tocolytics)
FIRST
 To relax the inverted uterus
2. REPLACE the inverted uterus
3. Give Oxytocin
 DO NOT GIVE OXYTOCIN FIRST!
o The uterus is cannot contract
to its inverted state
o To prevent rigidity of the
inverted uterus on replacing
the inverted uterus.
4. Give prophylactic antibiotics
 Uterus is exposed to an external
environment
 OTHER MANAGEMENT:
1. CAUTION: NEVER ATTEMPT to replace
an inversion
 Handling of the uterus may
increase BLEEDING
2. Administer O2 via mask
6) CORD PROLAPSE
 Loop of the umbilical cord slips down in front
of the presenting fetal part where:
a) Umbilical cord is in the entrance of the
cervix
b) Umbilical cord is in the entrance of the
vagina
 Most commonly follows:
a) After Rupture of Membranes (ROM)
 Every CORD PROLAPSE, there is Cord
Compression
a) Note for variable decelerations
VEAL CHOP
VARIABLE DECELARATIONS CORD COMPRESSION
EARLY DECELERATIONS HEAD COMPRESSION
ACCELERATIONS OKAY!
LATE DECELERATIONS PLACENTAL
INSUFFICIENCY
b) EARLY DECELERATIONS in EARLY
LABOR: Cephalopelvic disproportion
(CPD)
 pelvis of the mother is not a
gynecoid type
c) EARLY DECELERATIONS in LATE
LABOR: Head compression
 NORMAL
 Fetal head is compressed in the
pelvic brim
PHASES OF A UTERINE CONTRACTION BIRTH TECHNIQUE:
 As the uterine contracts, the FHR must 1. If infant will be born vaginally:
INCREASE! a) Mother is allowed to push after full
 The fetus (FHR) must compensate of the dilatation is achieved
temporary stoppage of blood supply.  STARTED WITH THE:
1. INCREMENT a. BREECH
2. ACME (Peak of contraction) b. TRUNK
3. DECREMENT c. SHOULDERS
d. Lastly, the HEAD
MANAGEMENT: 2. Piper Forceps may be used
 GOAL: RELIEVE CORD PRESSURE  To aid the delivery of the head
1. Place the mother on a KNEE-CHEST position or 3. The hazardous part:
on a TRENDELENBURG a) Delivery of the head
 This relieves cord pressure 4. C/S is highly recommended.
2. Place a gloved hand into the vagina and lift the
presenting part
3. Administer O2 @ 10 LPM via face mask
4. Administer Tocolytics
5. If the cord is exposed, cover it with saline
gauze.
 Prevent from drying.
6. DO NOT ATTEMPT TO PUSH IT BACK
 This may add more compression
7. Amniofusion
 Sterile catheter into the cervix attached
to IV tubing with a warm NSS.

7) BREECH POSITION
 The fetal buttocks + legs take up more space
than the fetal head.
 ALL INFANTS are assumed at BREECH POSITION
 But at 36th week AOG, the fetus will assume
VERTEX position
 Which part of the passenger least likely to pass
through the passageway?
 Fetal Head
 COMPLICATIONS:
a) Anoxia from a prolapsed cord
b) Traumatic injury to the after coming
head
c) Fracture of the spine or arm
d) Dysfunctional labor
ANTHROPOMETRIC MEASUREMENTS
HEAD 34-35 cm
CHEST 32-33 cm
ABDOMEN 30-31 cm
LENGTH 43-53 cm
WEIGHT 2500 – 3500
gms