THIRD TRIMESTER CAUSES OF BLEEDING ✔ AMNIOTOMY: artificial rupture of bag of water

1. PLACENTAL PREVIA abnormal low implantation of the placenta ○ Causing fetal head to descent
- low implantation of the placenta so that it overlays affecting mech., pressure @
some/all of the internal cervical OS placental site ctrl of bleeding
Incidence: “ most common cause of bleeding @ 3rdtrimester” ✔ DOUBLE SETUP: I/E in suspected placental previa
Predisposing factors: (DIMM)  2 setups
○ Multiparity-single most impt factor ✔ DELIVERY: vaginal or CS if placental placement
○ Decreased vascularity of upper uterine segment d/t prevents vaginal delivery and if the conditions for
tumor or narrowing watchful waiting are absent
○ Increased age above 35 y/o ✔ HOME MNGT:
○ Multiple Pz *Monitor fetal well-being
TYPE 1 & 2= home mngt
TYPES/ DEGRESS OF P.PREVIA:
Type 3 & 4= hosp for continuous
TYPE 1: LOW LYING
monitoring
placenta @ lower 3rd of uterus not encroach of margins of OS
NURSING CARE:
TYPE 2 : MARGINAL
Placenta lies over the margins of os • Bed & Px’ position: left side lying
TYPE 3 : PARTIAL R: to prevent pressure in the vena cava
Placenta partially covers the os • Assessment(FOBV)
TYPE 4 : COMPLETE/TOTAL Fetal well being
Placenta totally covers the os w/c completely Onset & progress of labor
obstructs the birth canal Blood Loss
S/SX: V/S
*fetal well being: FHT, mov’t., passage of meconium(thru
• painless vaginal bleeding in 3rd trimester(7mos)
vaginal d/c)
• intermittent pain 2nd to uterine contractions • Don’t perform I/E or V/E R: it will increase bleeding
DX:
• Prepare for UTZ to detect placental site
UTZ –95% accuracy
• Institute shock measures prn
Detects site of placenta
○ Bleeding is rarely severe life-threatening but
TX:
may become profuse with I/E
✔ watchful waiting/ expectant mngt/conservative if:
*mother is not in labor • Psychologic and phys. Comfort
*fetus is STABLE; no distress, premature • Conservative mngt = double setup/ CS
*bleeding is not severe Classical CS performed bcoz of LUS is
occupied by placenta
• Observe for bleeding after delivery
2. ABRUPTIO PLACENTA – premature partial/complete separation of the LUS, the site of placental detachment = not
contractile as U.fundal portion
Placenta from its implantation TYPE 2 MARGINAL/OVERT/EXTERNAL BLEEDING
– occurs after 20th wk AOG Placenta separates at the margin
– also called “accidental hemorrhage” and “ablation
c. External placenta”
bleeding, proportional to the amount of internal bleeding
incidence: 2ND leading cause of 3rd trimester bleeding
S/Sx: (SPER)
predisposing factors: MAMST Painful vaginal bleeding @ 3rd trimester
maternal HPN : PIH & renal dse (+) shock
Rigid, boardlike, painful abdomen
sudden uterine decompression as inEnlarged
PZ and polyhydramnios
uterus d/t concealed bleeding
@ labor: titanic contractions c. the absence of alternating contraction & relaxation of uterus.
Advanced age due to insufficiency
Dx: of hormone
Multiparity CLINICAL Dx: s/sx
Short umbilical cord – may pull the
UTZplacenta
says the retroplacental bleeding
Trauma & fibrin defects Clotting studies: reveal “Disseminated Intravascular Coagulation”(DIS)
e.g. massive bleeding causing depletion of blood
Thromboplastin from supply
retroplacental clot enters maternal circulation and
depletion of fibrin Consumes maternal fibrinogen r/t:
*villi separates containing cotyledons that are
*DICattached
– small fibrin clots in the circulation
*villi detachment causing bleeding & rupture of blood vessels of mother
*HYPOFIBRINOGENEMIA & fetus
- normal fibrinogen r/t absence of
Normal blood coagulation
ACTIVEBLEEDING – Blood coagulation
Complications:
Hemorrhagic shock
BLOODInfection
CLOTS
DIC
Fibrin becomesCVABIGGER
from DIC
Couvelaire Uterus – bleeding behind the placenta which may cause some
EMBOLUS Of blood to enter the uterine musculature causing uterine
Mngt: Muscles not to contract well once the placenta is delivered.
O2 inhalation L E A D S TO
CS delivery UTERINE ATONY (+) bleeding
Fluid replacement and plasma
Renal expanders
failure
Hypofibrinogenemia
TYPES Fetal distress/demise
TYPE 1 CONCEALED/COVERT/CENTRAL/INTERNAL BLEEDING
Placenta detaches/separates
Nursing @ center causing blood to
Mngt.:
accumulate behind the placentaMaintain bedrest @ LLR
External bleeding is not evident
Careful monitoring of:
Signs of shock not proportional to the amountv/s
Maternal of external bleeding
Uterine pain
FHT Bleeding not proportional to shock
NRSG. MNGT: Labor once/progress
I&O = oliguria/anuria
 [
CRYOCRECIPITATE- blood products that are rich in blood clotting factors
type 4- “Secondary”
Packs of thrombocyte replacement
Administer fluid, –plasma,
Occurs due
blood asto pancreatic tumor/infections or other endocrine disorders due to very slow metabolism
ordered
– Hypothyroidism secretions leads to HYPERGLYCEMIA
Prepare for Dx exams – explain results
Provide psychological
HPL- Humansupport – explain
Placental what is
Lactation = happening,
blocks actionprepare for all exams
of insulin
And inform/explain results.
PhysicallyNORMAL
and emotionally prepare
METABOLIC for emergency
CHANGES birthDM:
affecting either per vagina/CS
Observe for associated problems after delivery
✔ Hormonal production by placenta
*Couvelaire= poorly contracting uterus
*DIC
*neonatal sepsis
✔ Metabolic rate in Pzcausing # of Islets of Langerhans  insulin production but rendered ineffective by
PRE & CO-EXISTING DSES “insulin
OF PZ antagonists” (HPL/HCS)
✔ Activity of the APG  tolerance for sugar
DIABETES MELLITUS
✔ BMR and Co2 combining power raise the tendency of acidosis
, metabolic disorder characterized by a deficiency of insulin production by
✔ Vomiting during pz= CHON intake = ACIDOSIS
Pancreas’ islets of langerhans resulting to improper metabolic interaction of
carbohydrates, Muscular
✔ Fats, activity
proteins, in labor depletes maternal glucose including glycogen stores = requires
and insulin. CHON intake
✔ Hypoglycemia is common
 hyperglycemia due to lack or inadequate insulin In puerperium as involution and lactation occur.
 caused by ✔ If pancreas
heredity, cannot
envi and respond by producing more insulin, glucose crosses the placenta to the fetus where fetal
lifestyle
insulin metabolizes it and by resembling the growth hormone, causing MACROSOMIA
EFFECTS
INCIDENCE: concurrent dseOFin PzPREGNANCY IN DM@ pz
or have its onset
PREDISPOSING FACTORS:
• DM is more difficult to control = difficult to maintain blood sugar
○ Family HX
• Insulin shock and ketaacidosis
○ Rapid hormonal change in Pz
• N-V are predispose to keta-acidosis
○ Tumor/infection of the pancreas –produces insufficient insulin
• Insulin requirements:
○ Obesity
○ Stress ○ 1st 3mos: stable
CLASSIFICATIONS OF D.M.  Insulin may not be
Type 1 – “juvenile-onset”or Dose
“insulin may drop in 1st trimester
dependent”
nd
– Occurs below 2 3mos:
40 y/o rapid
starts @ youth
Type 2 – “maturity-onset”
rd
3 3mos: or “non-insulin
rapid dependent”
– after 40 y/o Postpartum :rapid to prepregnant level
Type 3 - “GESTATIONAL D.M.” Need insulin in the first 24h AC delivery
- onset during pz and ends after termination of pz
-however she becomes DIABETIC after Pregnancy

Hypoglycemics are c/I in Pz due to:

 • secretion of pancreas @ GDM
Dx:
• Normal 1. production but not
OGTT (oral used in
glucose Pz
tolerance test) 100 g GTT is sensitive
Abnormal results:
EFFECTS OF DM  POLYPHAGIA – excessive appetite
Mother BABY
 POLYDIPSIA- excessive thirst
○ Infertility d//t  POLYURIA- excessive
○ Congenital anomalies urine
2. 2hr postprandial
chronic or persistent (3x) dueblood sugar – greater than 120mg/dl
to persistent
○ PIH 3. Urine glucose monitoring
BS depletion BSinaccurate
@ as the urine of a pregnant woman is normally with sugar (+1 – normal
○ Spontaneous value) baby
abortion Nursing Mngt.: ○ Polyhydramnios
○ Infections 1. – Participate in Macrosomia(LGA)
○ early detection
○ Fetal
Moniliasis 2. Encourage early, hypoxia(IUFD)
frequent medical and prenatal mngt and supervision
○ UTI Intrauterine
Every 2wks prenatal visit fetal
until 30th wk, then weekly
○ Uteroplacental death
3. Provide health teachings:
insufficiency ○ Stillbirths
a. NATURE OF DM: effects on pregnancy, and effects of DM
○ Premature Labor ○ Perinatal mortality
b. S/sx of hypo/hyperglycemia
○ Hypoglycemia/Hype ○ Neonatal
c. Need for exercise not only to regulate glucose level but also to enhance feelings of well-being and to control
r hypoglycemia @
weight birth/postpartal
○ Dystocia- too large
shoulders
d. Insulin
○ regulations/self
Prematurity administration of insulin
○ CS if indicated e. Prompt ○ reporting
RDS of danger signs and signs of infection
○ Postpartal4. Promote control of DM
○ Hypocalcemia
hemorrhage a. DIET cornerstone of mngt
○ From uterine atony Calories: 35 cal/kg DBW 1800-2000 daily
CHON : 30-45% milk/bread @ 200mg/day
ASSESSMENT FINDINGS: PROTEIN: ½- 2KG BW of 70g daily
a. Hx FATS: saturated
*Familial Taken regularly
*previous large infant
b. weighing
Exercise400g/more
: exercise the need for insulin
* “ c/ congenital defects- polyhydramnios
c. Insulin: oral diabetogenic agents are C/I
*fetal wastage, abortion, stillbirths
i. Need for insulin @ 2nd and 3rd 3mos
*obesity c/ very rapid weight gain
@ 3rd3mos needs may be tripled tendency to ketoacidosis
* incidence of vaginal moniliasisand UTI
ii.Regular insulin and NPH insulin are used
b. Abdominal enlargement, marked from polyhydramnios and LGA
c. S/Sx of Hypoglycemia iii.Rapid-acting regular insulin used in labor
1. Onset of action: 30 mins to 1hr
2. Peak of action : 2-4 h
d.weight loss bcoz it is not properly metabolized
3. Duration of action: 4-6 hrs
4.
e. blood and urine sugar

 Indications of Early termination of PZ:

4. prevention of infection and stress
5.promote adherence to dietary regimen 1.UTZ: fetal growth detection
6.encourage hospitalization m< AOG by m< BPD
Purposes: *CTRL OF INFECTION 2.Urine/blood estriol levels : determine feto placental sufficiency
*REGULATION OF INSULIN 3.AMNIOCENTESIS: determines lung maturity
*ASSESSMENT OF FETAL JEOPARDY OR INDICATIONS FOR 2:1)
(L/S ratio EARLY means mature lungs, above 36wks.
TERMINATION OF PREGNANCY:
L/S ration may be elevated in DM
7. prepare for early hospitalization for possible early labor induction for CS
4.PHOSPHATIDYGLYCEROL(PG) using amniotic fluid
*The baby of a diabetic is large and when allowed to reach term a CPD may
Complicate a labor
-more accurate way of estimating fetal lung maturity by
*the final time of terminating Pz depends on fetal and maternalDetermining lung surfactant
well-being
5. STRESS and
8. Continued monitoring, mother and fetus, during the intrapartal periodNONSTRESS TESTS
○ Electronic fetal monitoring
○ Left lateral recumbernt R: to preventCARDIAC PROBLEMS
supine hypotensve syndrome
○ Ensure fluid and electrolyte balance
 of all cases-RHEUMATIC
 D5IMB needed to maintain glucose
PREDISPOSI Variety of heart conditions both congenital and acquired, 90% NG FACTORS:
 Insulin added to IV of 5-10% D5IMB, tiltrated to maintain glucose
✔ Rheumatic fever
Between 100-150 mg/dl
9. provide postpartum care
✔ Arteriosclerosis
○ There is a in insulin needed to ½ to 2/3 Pulmonary
✔ pregnant dses
dose on
st
1 postpartum day if on full diet ✔ Renal dses
✔ Heart surgery
○ Be alert for complications in the postpartum/prevention of:
 HEMORRHAGE ✔ Congenital defects of the heart
CLASSIFICATION
 INFECTIONS = candidiasis, OF HEART DSE:
UTI “avoid cathetherization”
 INSULIN SHOCK Class 1 NO limitation of activity
 PIH Regular activities do not produce SX
Encourage breastfeeding --- it has
ClassANTIDIABETOGENIC
2 affect
SLIGHT limitation of activity
 Hypoglycemia raises adrenaline level resulting to milk supply and
Asymptomatic @ rest, but regular activities produces
○ Let down-reflex
Palpitations, fatigue, dyspnea and angina pains
ACETONURIA : stop breastfeeding while insulin/diet are being adjusted
Class 3 MARKED limitations of activities
May pump breast to maintain milk production
Less than ordinary activities causing Sx
Encourage contraception : reinforce Dr’s recommendations
○ Oral contraceptive pills C/I CHOClass 4 MARKED limitation of activities
tolerance
Less
○ Barrier using diaphragm/condom recommended than regular activities cause Sx
TX: DIGITALIS
○ IUD c/I due to poor response  meds that regulate heart rhythm and heart rate
to infection
COMPLICATIONS OF HEART DSES(SHIMP)
In labor, analgesia anesthesia as there should be NO PAIN in labor = FORCEPS DELIVERY
➢ Spontaneous Abortion
➢ HEART FAILURE c/I: scopolamine, oral contraceptives, Oxytocin
➢ Intrauterine growth retardation
✔ as they further circulating volume
➢ Maternal Dysrythmias
✔ promotes retention of fluid
➢ Premature labor
✔ enhance dev’t of thromboembolism

Dx of heart dse in Pz is not easy asNURSING

there areMNGT:
signs of mimic dse:
1. Encourage early & regular prenatal care-supervision
2. Encourage compliance w/ medical therapeutic regimen
a. Workload of the heart
i. Rest and sleep = 10h
Criteria for establishing Dx of Cardiac Dses
ii.Tx of early anemia & infections
✔ Persistent Diastolic/presystolic murmurs
iii.Prevent exhaustion, fatigue and stress
✔ Loud systolic murmur
iv.Avoid acts that O2
✔ Permanent/unequivocal cardiomegaly
v.Avoid constipation
✔ Severe dysrythmias
b. Proper nutrition
✔ Severe dyspnea prior to stage of pressure in the diaphragm
i. Sodium, adequate protein, h2O, fruits and veggies
Signs of cardiac decompensation:
ii. Fats & CHON
Moist cough
iii.Well balanced diet
Pedal edema – signs of pulmo edema
c. Frequent prenatal visit
Dyspnea w/ minimal act
d. Early hospitalization – pz puts more stress on the cardio system, mother needs more
Tachycardia
rest b4 labor
Tachypnea – rapid, weak pulse
3. Provide care in labor
Chest pains on exertion
a. Position @ semi-recumbent c/ hands & legs supported
Cyanosis
b. O2 prn
Heart murmurs
c. NPO
d. Continuous cardiac monitoring, be alert for Sx of cardiac failure and pulmo edema
Meds:
i. PR = most sensitive and reliable indicator of CHF
DIURETICS
ii.Report stat PR above 200 bpm
ANTIBIOTICS  prophylaxis against rheumatic fever
iii.RR more than 24 cpm
Tx of bacterial infection in Pz
IRON SUPPLEMENTS prevents anemia & treats it
O2 prn
e. strict/asepsits to prevent infection
f. provide emotional support ✔ poor absorption as in stomach and intestinal dses
r: to reduce stress and encourage cooperation-participation
g. episiotomy and foreceps PROGNOSIS
nd
r. to shorten the 2 stage Associated with fetal problems – IUGR, perinatal mortality
h. encourage Lamaze technique or other DBE patterns Increased incidence :
INSTRUCT not to BEAR DOWN / PUSH ABORTION PREMATURE LABOR
i. Prepare for regional anesthesia PIH POST PARTAL HEMORRHAGE
ii. Administer drugs as ordered,: HEART FAILURE
a. Digitalis, INFECTION
b. Diuretics S/SX :
c. Antibiotics OBJ: pale skin and mucus lining
d. Oxytocin production Pearly-white sclera
PROVIDE POSTPARTAL CARE Brittle, flattened nails
Cardiac failure/ decompensation is likely to occur the postpartal periodAltered V/S rise in Systolic pressure c/ widened pulse pressure
Because of the ff factors: Tachycardia
1. Loss of placental circulation 30-50% blood volume is reabsorbedTachypnea
2. Normal dieresis circulating blood volume SUBJ:
Fatigue
3. Rapid in intraabdominal pressure ff delivery resulting to vasocongestion
andrapid @ C.O. Shortness of breath on exercise, headache, anorexia,
POSTPARTAL CARE Menorrhagia, heartburn, flatulence
1. Rest physically and emotionally Dx:
2. Frequent monitoring of V/S – RR & PR Physical signs
3. Pain-relief R: to prevent neurogenic shock Lab. Findings:
4. Monitor blood loss, i&O fluid rate flow HgB (less than 10g/100ml)
5. Freq. assessment of S/Sx of bleeding,sepsis & CHF HcT (less than 37% in first tri)
6. Provide care typical of a normal postpartum mother (less than 35% @ 2ND TRI)
LESS THAN 33% @ 3RD 3MOS
Serum Iron less than 65 mmg/100ml blood
ANEMIA NURSING MNGT:
Decrease in 02-carrying capacity of blood d/t hemoglobin
➢ Use @ z-Tract
blood injection method
PREDISPOSING FACTORS: ➢ Inject 0.5ml of air before withdrawing needle to prevent tissue
✔ Nutritional intake/malnutrition necrosis
✔ Heredity, cultural practices, fads ➢ Do not rub site
✔ Demands Pz and adolescence ➢ Instruct not to wear constricting garments after injection
➢ Keep warm free from injection
○ No water bottles/heating pads because of decreased