OB Exam 4

Diabetes

Most common endocrine disorder associated with pregnancy

General pregnancy findings related to blood glucose

-Glucose levels in the fetus are directly proportional to maternal levels

-Glucose crosses placenta

-Insulin doesn't cross placenta

-Fetus produces its own insulin at 10 weeks gestation

First trimester findings with blood glucose

Rising estrogen and progesterone

-Stimulate insulin production in the pancreas (Promotes increased peripheral use of glucose->Decreased blood glucose, Those with IDDM are prone to hypoglycemia during the first trimester)

Second and third trimester findings with blood glucose

Diabetogenic effect

-Decreased tolerance to glucose

-Increased insulin resistance

-Decreased hepatic glycogen stores

-Increased hepatic production of glucose

Insulin resistance is increased

-Glucose-sparing mechanism that ensures an abundant supply of glucose for the fetus

-Maternal insulin requirements may double or quadruple by the end of the pregnancy

-Maternal insulin requirements gradually increase from 18-24 weeks to 36 weeks

Changes at birth with blood glucose

-Risk of hemorrhage (uterine distension)

-Delivery of the placenta prompts an abrupt decrease in levels of circulating hormones, cortisol and insulinase

-Maternal tissues go back to prepregnancy sensitivities to insulin

-Lactation uses maternal glucose (Mom's insulin requirements remain low)

-ACOG recommends assessing for CHO intolerance with 75-g 2 hour OGTT or fasting at 6-12 weeks postpartum

-Lifelong repeat screening at least every 3 years

Preexisting diabetes in pregnancy

-10% of pregnancies have preexisting DM

-Almost all of these are insulin dependent during pregnancy

-Perinatal mortality is 3 times higher for women with diabetes

Maternal risks/complications with preexisting diabetes

Poor glycemic control in early pregnancy

-Increased miscarriage

Poor glycemic control later in pregnancy

-Increased fetal macrosomia (20-50% of diabetic pregnancies have macrosomic infants, Increased c-section)

Higher rates of preeclampsia and eclampsia

PTL, IUGR, fetal distress, stillbirth, neonatal death

Hydramnios (Polyhydramnios)

-Over 2000 mL of fluid, 10 times more often in diabetic, Associated with PROM, Preterm labor, Postpartum hemorrhage

Increase risk of infection

Hypoglycemia can occur esp. in early pregnancy

-No ill effects on baby

Ketoacidosis

-Diabetic Ketoacidosis occurs at lower blood sugar levels

-DKA can cause fetal death, PTL

Tocolysis increases hyperglycemia

Metabolic acidosis can occur

Fetal/neonatal risks and complications with preexisting diabetes

Congenital malformations

-Most important cause of perinatal loss in pregestational diabetic pregnancy (30-50% of perinatal loss)

Insulin acts as a growth hormone

Macrosomia

-Weight greater than 4500 g, Fractured clavicle Liver or spleen laceration Brachial plexus injury Facial palsy Subdural hemorrhage

Increased risk for RDS

-Hyperglycemia and hyperinsulinemia (Delays pulmonary maturation in fetus)

Neonatal hypoglycemia often occurs within 30-60 minutes after birth

-Interruption of maternal glucose supply

gestational diabetes general

-Any degree of glucose intolerance with the onset or first recognition occurring during pregnancy

-4-7% of all pregnancies in the U.S.

Risk factors for gestational diabetes

Certain ethnic groups

History of GDM

Over age 25

Obesity

Family history of type 2 diabetes

Hx of macrosomic infant

Hydramnios

Unexplained stillbirth

Miscarriage

Hx of infant with congenital anomalies

screening for gestational diabetes

Initial visit if high risk

24-28 weeks is routine

GTT

-1 hour 50-g oral glucose (Lab draw if blood sugar is 130-140 it's a positive screen)

3 hour GTT

-100-g oral glucose

-Lab draw at 1,2, and 3 hours (Diagnosis if two or more values met or exceeded)

Alternative One step screening

-75-g test

Fetal surveillance with gestational diabetes

Twice weekly NST's starting at 32 weeks

Maternal/fetal risk factors with gestational diabetes

Increased risk of developing hypertensive disorders

9.8% if well controlled

18% not well controlled

Cesarean delivery (17-25%)

Type II later in life (up to 70%)

Increased occurrence in future pregnancies

hyperemesis gravidarum general

Excessive prolonged vomiting (10% of women have symptoms that persist throughout pregnancy)

-Concerned if: causing wt loss of 5%, Dehydration, Electrolyte imbalance, Ketosis, Acetonuria

hyperemesis gravidarum risk factors

Nulliparous

BMI(Less than 18.5 or Greater than 25)

Twins

Molar pregnancy

Psychological component

Younger maternal age

Low socioeconomic status

Asthma

Migraines

Preexisting diabetes

Psychiatric illness

Hyperthyroid disorders

Gastrointestinal disorders

Previous pregnancy complicated by hyperemesis

DECREASED RISK of spontaneous abortion

etiology of hyperemesis gravidarum

High estrogen or hCG (having a baby girl)

Transient hyperthyroidism

1.5 increase in female infants

Esophageal reflux

Reduced gastric motility

Decreased secretion of free HCL

Psychosocial

Hyperemesis Gravidarum Treatment

Determine severity

Assessment

-Physical and psychological

IV fluids

Antiemetics

Parenteral nutrition

Supplements

I & O

Hyperthyroidism in pregnancy

Rare in pregnancy (2-17 per 1000 births)

Caused by Graves disease (90-95% of the time)

SxS: Tachycardia, Fatigue, Heat intolerance, Emotional lability, Weight loss, Severe nausea and vomiting, Exophthalmos, Goiter, Altered lab levels

Treatment is meds

Hypothyroidism in pregnancy

Less common in pregnancy than hyperthyroidism (2-12 per 1000)

Associated with menstrual and fertility problems

Increased risk of miscarriage

SxS: Weight gain, Fatigue, Cold intolerance, Constipation, Cool/dry skin, Coarsened hair, Muscle weakness, Altered lab levels

pregnancy induced hypertension

Multi-organ, vasospastic process of reduced organ perfusion(hypoperfusion), activation of the coagulation cascade

Patho:

-Etiology->Origin unknown

-Is related to->Hypoperfusion, Vasospasm, Endothelial cell damage, Platelet aggregation

hypertensive disorders of pregnancy general

5-10% of pregnancies

Major cause of morbidity and mortality

Infant: uteroplacental insufficiency, preterm birth

Mother: renal failure, coagulopathy, cardiac or liver, abruption, seizure, stroke

50,000 maternal deaths annual in the world

-One woman every 7 minutes

>140/90

-HTN if either is elevated

-6 hours apart

-Positioning

-Appropriate sized cuff

Gestational HTN

HTN after 20 weeks if previously normotensive

No proteinuria, No other systemic findings

Systolic over 140, Diastolic over 90

Resolution

-Usually in first postpartum week

-Must resolve by 12 weeks to meet this classification

Preeclampsia

HTN and proteinuria after week 20 or in the early postpartum period in someone previously normotensive. If no proteinuria new onset HTN with new onset of any of these:

-Thrombocytopenia

-Renal insufficiency

-Impaired liver function

-Pulmonary edema

-Cerebral or visual symptoms

Eclampsia

Convulsions or coma not from other causes in a preeclamptic woman

No history of preexisting seizure-related pathology

1 in 2,000 -1 in 3,448 births

50% develop during the pregnancy

Can occur immediately postpartum

Chronic HTN in pregnancy

HTN in pregnant woman which was present prior to the pregnancy or persists longer than 12 weeks postpartum

superimposed preeclampsia

Women with chronic hypertension may acquire preeclampsia or eclampsia

Can be difficult to diagnose

risk factors for preeclampsia

Primigravida

First pregnancy at age extremes (<19 and >35)

Chronic hypertension

Pre-gestational diabetes

Nephropathy

Family History

Vascular and connective tissue disorders

Preexisting diabetes and/or thrombophilia

Maternal infection/inflammation (UTI, periodontal disease)

Obesity

Race

Multiple gestation

Fetal hydrops (baby has fluid where fluid should not be)

Hydatidiform

Preeclampsia in a previous pregnancy

Recurrence of preeclampsia

preeclampsia causes.....

Placental ischemia

-Endothelial cell dysfunction

Generalized vasospasm

-Poor tissue perfusion in organs (Increased peripheral resistance and BP, Increased endothelial cell permeability)

-Reduced kidney perfusion

-Plasma colloid osmotic pressure decreases

-Decreased liver perfusion

Neurologic complications

-Cerebral edema

-Cerebral hemorrhage

-Central nervous system irritability

Preeclampsia management/assessments

Low dose ASA (81 mg) may help

Accurate BP measurement

Assessment of edema (no longer included in definition of preeclampsia)

Assess for hyperactive reflexes

-DTR's

-Clonus

Proteinuria

-24 hour urine

-Little relationship between degree and outcome

Assess for

-Headache

-Epigastric pain

-RUQ pain

-Visual disturbances

Goals for Gestational HTN and Preeclampsia without severe features

Goals:

-Ensure maternal safety

-Manage outpatient if possible

-Monitor Labs

-Deliver healthy newborn as close to term as possible

-Monitor Fetus

-No bedrest

Goals/Intrapartum care or Gestational HTN and preeclampsia with severe features

Goals:

Ensure maternal safety

Formulate a plan for delivery

Expectant management

-For women less than 37 weeks

-Hospitalization (Antihypertensive meds, Corticosteroids)

Intrapartum Care:

-Continuous FHR and uterine contraction monitoring

-Bed rest with side rails up

-Darkened environment

-Assess for signs of abruption

preeclampsia interventions

Magnesium Sulfate

-Prevents and treats seizure

-IV piggyback on a pump

-Initial loading dose then maintenance

-Little effect on maternal BP

-Unclear mechanism of action

-High alert medications

Control BP

-Antihypertensive medications

preeclampsia postpartum care

Vital signs

DTR's

LOC

Magnesium sulfate x 24 hours

Severe features of preeclampsia

Progressive renal insufficiency

-Serum creatinine concentration >1.1mg/dL or a doubling of serum creatinine concentration in the absence of other renal disease

Pulmonary Edema

Visual disturbances

-flashing lights, auras, light sensitivity, blurry vision, spots in vision

Markedly elevated blood pressure

- > or equal to 160 over > or equal to 110 x 2 (Taken 4 hours apart on bedrest)

Platelet count <100,000

Elevated liver enzymes to twice normal

Severe persistent epigastric or RUQ pain unresponsive to meds

eclampsia causes

Cause of seizure is unknown, could be:

-Cerebral vasospasm

-Hemorrhage

-Ischemia

-Edema

-Platelet and fibrin clots that occlude cerebral vasculature

Eclampsia SxS

Premonitory signs

-Persistent headache and blurred vision

-Epigastric or RUQ pain

-Altered mental status

Seizures can appear without warning

Eclampsia Tx

Ensure patent airway and safety

Note time of onset and duration of seizure

Call for help (remain calm)

Remain at bedside

eclampsia complications

Periods of hypoxia in mother and fetus

Risk of aspiration

CVA

Cerebral edema

Anoxia

Coma

Maternal death

HELLP Syndrome

Hemolysis

Elevated

Liver enzymes

Lowered

Platelets

HELLP syndrome labs

CBC

CMP

Uric Acid - increases

BUN -increases

24 hour urine for protein and creatinine clearance

Serum creatinine - increase

pathophysiology of HELLP

RBC are destroyed as they travel through constricted vessels

-Hemolytic anemia

-RBC morph

-Reduced oxygen carrying capacity

-Elevated bilirubin and jaundice d/t hemolysis of RBC's

Elevated liver enzymes

-Vasospasm decreases blood flow to the liver

-Serum Liver enzymes become elevated

-Hepatic pain->RUQ, Epigastric, N & V, Tenderness to liver palpation

Platelets gather at site of damaged vascular endothelium causing platelet consumption and thrombocytopenia (possible DIC)

Platelet transfusions may be needed

implications/complications of HELLP

Eclampsia

Abruptio placenta

Disseminated intravascular coagulation

Acute renal failure

Hepatic failure

Pulmonary edema

Acute adult respiratory distress syndrome

Cerebral hemorrhage

Stroke

cerebral hemorrhage

Common cause of maternal death

Watch for

-Progressive decrease in patient's level of consciousness or stupor

-Complaints of flashes of light

Focal neurologic deficits (Nuchal rigidity, seizures, slurring of speech, local or unilateral motor weakness)

-New onset vomiting

-Sudden increase in BP (Sign of intracranial bleeding)

How the cardiac system is affected by HTN during pregnancy

HTN first sign

-d/t elevated systemic vascular resistance

-Left ventricle also working harder

-BP may vary d/t intermittent vasospasm

Edema least valid

Proteinuria may be late in onset

Fluid shifts from intravascular to extravascular

-d/t/ endothelial dysfunction and increased capillary permeability (Hypovolemia, Edema->Inclusive of pulmonary)

-hemoconcentration (Rise in hematocrit)

Leaking of albumin and other plasma proteins

-d/t endothelial dysfunction

-Causes decrease in colloid osmotic pressure (Higher risk for pulmonary edema)

How the renal system is affected by HTN during pregnancy

Endothelial cells in renal system are injured

Vasospasm

-Decreases in renal blood flow and GFR

Glomerular membrane is damaged from vasoconstriction

-Increases permeability to proteins

Severest forms of preeclampsia may have no edema

-Oliguria

-Intravascular fluid volume depletion

-Renal vasospasm

-Decreased cardiac output (d/t vasospasm and increased vascular resistance)

how postpartum is affected by HTN during pregnancy

Auto transfusion and extra vascular to intravascular fluid shifts

-Cause drop in COP (d/t dilution, 6-24 hours postpartum, Greatest risk for pulmonary edema, Lowest cardiac contractility)

How the CNS is affected by HTN during pregnancy

HA in pregnancy

-Question cerebral vasoconstriction (Leads to cerebral ischemia, Seizures, Hemorrhage)

Visual changes

-Retinal arteriolar spasms

-Petechial hemorrhages

-Retinal edema

-Retinal detachment (Can result in permanent blindness)

How the Hematologic system is affected by HTN during pregnancy

Hemoconcentration

Thrombocytopenia

-Platelet consumption

-Platelets adhere to damaged vessel walls

-Hepatic dysfunction contributes

Platelet count usually returns to normal within 72 hours postpartum

-More severe = longer recovery

-Count is o.k. but function may not be normal d/t meds (MgSO4, Aspirin, Steroid therapy)

Higher risk of DVT's ◦ Fibrinogen and blood coagulation

MgSO4 (magnesium sulfate)

Preferred drug for preventing and treating eclamptic seizure

Improves cerebral circulation and perfusion

Interferes with platelet aggregation

-Predisposes to bleeding

Changes serum osmolality

-May increase risk for pulmonary and cerebral edema

BP may decrease

-Relaxant effect on smooth muscle

-Use other medications for direct TX

Contraindicated in those with Myasthenia gravis (respiratory failure)

Contraindicated with heart block, myocardial insufficiency and possibly renal disease

Excreted via kidneys

-Oliguria or elevated serum creatinine levels may lead to high levels

Cardiac monitoring needed if given with IV labetalol

-Dysrhythmias and bradycardia

MgSO4 dosing

IV bolus 4-6 grams over 20-30 minutes

Maintenance infusion of 2-4 grams

-Usually is 2 grams per one hour

-Watch dose r/t renal ability

-Use cautiously with other meds that are CNS depressants (Additive effects/ potentiate->Barbiturates, Narcotics)

MgSO4 therapeutic levels

Normal 1.5-2

Therapeutic 4-7

ECG Changes 5-10

Loss of reflexes 8-12

Respiratory distress 15

Cardiac arrest 25

OVERLAP with therapeutic and ECG changes

MgSO4 side effects

Flushing

Lethargy

Nausea

Diaphoresis

Blurred vision

Hypocalcemia

Depressed reflexes

Depressed platelet aggregation

Cardiac dysrhythmias

Respiratory paralysis

Circulatory collapse

nursing interventions with MgSO4

I & O

Vitals

-Q 5-15" with loading dose

-Q 30-60 depending upon status

Hourly reflexes

Monitor for toxicity

Provide seizure precautions

Assess lung sounds

Antepartal use vs. postpartum use

Monitor for signs of toxicity

Monitor for worsening condition

-Shock

-Respiratory distress

-Arrhythmias

-S/S DIC

safety/antidote with MgSO4

Pre mixed solution, Standard strength, Label lines, Use smart pump, Remove medication completely if finished with it, Double check

Antidote is calcium gluconate or calcium chloride

-Have on unit!

protective changes in pregnancy against blood loss

Hypervolemia

Increased vascular resistance

Plasma volume increases

RBC mass increases

-Meets metabolic demands of mother and baby

-Protects against the potentially deleterious impairment in venous return caused by pressure of enlarging uterus

-Safeguards against blood loss at birth

Antepartal Hemorrhage

Leading cause of maternal death

-Highest incidence of maternal mortality (Ruptured ectopic, Abruption)

Miscarriage general

Pregnancy that ends as a result of natural causes before 20 weeks gestation

Fetal weight less than 500 g may be used as definition

10-20% of all confirmed pregnancies end in miscarriage

Early miscarriage

-Before 12 weeks gestation

-90% before 8 weeks

50% of early miscarriages

-Chromosomal abnormalities

causes of early miscarriage

Endocrine imbalance

-uncontrolled diabetes, hypothyroidism, etc.

Immunologic factors

-E.g. antiphospholipid antibody syndrome: maternal immune system attacks the placenta, leading to clot formation and pregnancy loss, etc.

Infections

-TORCHES, listeria, etc.

Systemic disorders

-Uncontrolled hypertension, renal disease, etc.

Genetic factors

-Chromosomal abnormality e.g. trisomy 16, etc.

late miscarriage

12-20 weeks

Usually maternal causes:

-Advanced maternal age and parity

-Chronic infection (PID, bacterial vaginosis, syphilis)

-Premature dilation of cervix

-Anomalies of reproductive tract

-Chronic debilitating disease (Diabetes, HTN, etc.)

-Inadequate nutrition

-Recreation drug use

prevention of miscarriage

Immunization

Early prenatal care

Treatment of pregnancy complications

Types of miscarriage

-Threatened: Spotting, os closed, mild uterine cramping present

-Inevitable: Moderate to heavy bleeding with open os, tissue may be present, mild to severe cramping

-Incomplete: Same symptoms as inevitable. Fetus is expelled and placenta is retained

-Complete: All fetal tissue is passed, cervix is closed, slight bleeding, mild uterine cramping

-Missed: Fetus has died but products are retained in utero. No bleeding or cramping. Os is closed

Habitual miscarriage

Recurrent spontaneous abortion

-3 or more consecutive pregnancy losses before 20 weeks gestation

Unclear etiology

-multifactorial

Increased risk for:

-preterm birth, previa, fetal anomalies

Septic miscarriage

Fever

Abdominal tenderness

Vaginal bleeding is malodorous

Requires surgical intervention

monitoring/management/home care for miscarriage

Monitoring

-Lab results :hCG

-Ultrasound

-HgB: Blood loss

-WBC: Infection

Management

-Depends upon the type of miscarriage

-Bed rest and supportive care

-D & C

-D & E (After 16 weeks)

-Outpatient vs. inpatient

-Misoprostol, pitocin, laminaria -

-Rhogam

-Control bleeding

-Psychologic care

Home care

-Discharge teaching

-Follow up

incompetent cervix general

Recurrent premature dilation of the cervix

Passive and painless dilation during the second trimester

Acquired or Congenital

Cervical Length

-Less than 25mm

Etiology of incompetent cervix

History of:

-Cervical lacerations

-Excessive dilation for curettage or biopsy

-DES from pt's mother: diethylstilbestrol->Synthetic estrogen to prevent miscarriage and preterm labor, Discontinued 1971->Reproductive tract anomalies

-Short cervix: Cervical funneling, Effacement of internal os

Management of incompetent cervix

Bed Rest

Hydration

Tocolysis

Cerclage

-Inserted at 10-14 weeks

-Removed at 37 weeks for vaginal delivery or c-section

Cerclage

Treatment of choice for cervical insufficiency

80-90% of pregnancies treated with cerclage result in live viable birth

Suture around the cervix to constrict the os

Abdominal cerclage->Suture (Mersilene tape) is placed at the junction of the lower uterine segment and the cervix

Risks: ROM, Preterm, Chorioamniotis

ectopic pregnancy general/risk factors

Gestational sac is implanted outside the uterine cavity

-fallopian tube (95% of cases), abdominal cavity, ovary, cervix

Responsible for 3% of maternal mortality, Leading pregnancy related cause of first trimester maternal mortality, Leading cause of infertility, Higher risk of future ectopic pregnancies

risk factors: Sexually Transmitted Infection(PID), Reversal of tubal ligation

Sxs of ectopic pregnancy

Missed period

Adnexal fullness and tenderness

Pain

-Unilateral, bilateral or diffuse: Blood irritates peritoneal cavity, Pain increases with rupture, Referred shoulder pain (Diaphragmatic irritation by blood in peritoneal cavity)

Bleeding (50-80% of the time)

Dx of ectopic pregnancy

Screen for if

-Abdominal pain

-Vaginal spotting or bleeding

-Positive pregnancy test

hCG

Ultrasound (transvaginal)

ectopic pregnancy tx

Surgical

Treatment of hypovolemia if applicable

Methotrexate

-Folic acid analog

-Destroys rapidly dividing cells

-Similar results to surgery

-High success, Low complications

-Good reproductive potential

molar pregnancy

Benign proliferative growth of the placental trophoblast in which the chorionic villi develop into edematous cystic transparent vesicles that hang in a grapelike cluster

1 in 1000 pregnancies in U.S.

Unknown etiology

-Ovular defect

-Nutritional deficiency

Risk factors

-Ovulation stimulation

-Early teens or over 40

-History of miscarriage

complete molar pregnancy

Fertilization of an egg with lost or inactivated nucleus

Resembles bunch of grapes

Fluid filled vesicles grow rapidly

-Uterus is bigger than expected

Usually has no fetus, placenta, amniotic membranes or fluid

Hemorrhage into uterine cavity and vaginal may occur

-No placenta to receive blood

20% progression towards choriocarcinoma

partial molar pregnancy

Two sperm fertilizes a normal ovum

Have embryonic or fetal parts and an amniotic sac

Congenital anomalies are usually present

6% malignant transformation

Sxs of molar pregnancy

Normal pregnancy symptoms

Vaginal bleeding later 95%

-Prune juice discharge or bright red

-Larger than expected uterus (25% have smaller)

management of molar pregnancy

Most abort spontaneously

Suction curettage

No induction

-Increased risk of embolization

Rhogam if needed

Ultrasound

hCG

Chemotherapy

placenta previa types

Four types

1)Total

2)Partial: Incomplete coverage

3)Marginal: An edge of placenta extends to the margin of internal os

4)Low lying: Lower uterine segment, but doesn't touch the os

placenta previa risk factors

History of previa

Hx of c-section

Endometrial scarring

Multiple gestation

Closely spaced pregnancies

Maternal age older than 35

African or Asian ethnicity

Smoking

Cocaine use

Multiparity

History of suction curettage

Living at higher altitude

placental previa SxS/Dx

70% painless vaginal bleeding

Suspect if bleeding after 24 weeks

Bright red bleeding

Pregnant women can lose 40% of their blood volume without signs of shock

Usually diagnosed with ultrasound before bleeding

vasa previa

Unprotected fetal vessels pass across the cervical os in front of the presenting part of the fetus

Vessels surrounded only by the amnion and are not covered with Wharton's jelly

Risk of laceration->Esp during ROM

Associated with higher fetal morbidity and mortality

Examiner may feel a pulsing vessel

Velamentous insertion of the cord

Rare

Associated with previa and multiple gestation

-Cord vessels branch at membranes and then into placenta

Rupture of membranes or traction

-Can tear the vessels->Fetus bleeds to death

Battledore (marginal) insertion of the cord

cord inserts at edge of placenta

succenturiate placenta

Lobed placenta

Retained fragments likely

Placental abruption and risk factors

Premature separation of placenta

Risk Factors

-Maternal hypertension

-Cocaine use (Causing hypertension)

-Abdominal trauma (Motor Vehicle Accident, Abuse)

-History of abruption (25% recurrence rate)

-Smoking

-Preterm Pre-labor Rupture Of Membranes

SxS of placental abruption

Vaginal bleeding

Uterine tenderness

Contractions

s/s hypovolemia

Board like abdomen

(couvelaire uterus)

Placental abruption morbidity/mortality

Mortality rate

-1%

-Leading cause of maternal death

Prognosis depends upon

-degree of placental detachment

-Blood loss

-DIC

-Time between placental detachment and birth

Perinatal mortality rates (15-30%)

Mortality

-fetal hypoxia

-preterm birth

-status as SGA

Morbidity

-neurologic defects

Non reassuring FHT's

-60% of the time (Decreased variability, Late decels)

Hyper stim and increased resting tone may be noted

Abnormal clotting factors

placental abruption Tx

Expectant Management

Delivery: Vaginal or Cesarean

DIC def/risk factors

Consumptive coagulapathy

-Diffused clotting

-Consumes clotting factors

Blood cells are destroyed as they pass through fibrin-choked vessels

Always a secondary diagnosis

Risk factors:

-Abruption

-Retained dead fetus

-Amniotic fluid embolus

-Severe preeclampsia

-HELLP syndrome

-Gram-negative sepsis

perinatal loss/grief

Ectopic pregnancy or fetal death, miscarriage and induced abortion

-Hidden or silent

Stillbirth

-Usually later term

-Parents are planning on welcoming a healthy newborn (End of life decisions)

Difficult with perinatal loss

-Society belief that there are no barriers to getting pregnant

-Expectation that pregnancy will result in a healthy live baby

-Society minimizes perinatal loss

-Lacks understanding of associated pain (May not get the support that they need)

Lack of identifiable cause

-Complicates grief

-Women feel responsible (Repeated loss)

Parental Grief Box

Acute distress

-Shock, numbness, intense crying, and depression

Intense Grief

-Loneliness, emptiness, and yearning, guilt, anger, resentment, bitterness, irritability, fear and anxiety (esp. about getting pregnant again)

-Disorganization, difficulties with cognitive processing, sadness and depression, and physical symptoms

Reorganization

-Search for meaning, reduction of distress, reentering normal life activities with more enthusiasm, can make future plans, including another pregnancy

family grief of baby

Grandparents

-Sadness for their own child as well

-Survivor guilt (Infant deal is out of order)

Siblings

-Depends upon age and stage (Understanding, response and grief)

actualizing the loss of a baby

Tell honestly

Use the term miscarriage, dead and died

-Avoid (Lost or gone)

Let them recount, and listen

See, hold, name

-Acquaint and separate

-Offers closure

important decision making with infant loss

Autopsy

Organ donation

Baptism

Burial

Cremation

what/what not to say with infant loss

What to say:

-I'm sad for you

-How are you doing with all of this

-This must be hard for you

-What can I do for you

-I'm sorry

-I'm here and I want to listen

What not to say:

-God had a purpose for her

-Be thankful you have another child

-The living must go on

-I know how you feel

-It's God Will

-You have to keep on going for her sake

-You're young. You can have another

-We'll see you back here next year and you'll be happier

-Now you have an angel in heaven

-This happened for the best

-Better for this to happen now, before you knew the baby

-There was something wrong with the baby anyway

perinatal mood disorders

Set of disorders that can occur anytime during pregnancy as well as in the first year postpartum and can include:

-Depression (postpartum depression)

-Bipolar disorder

-Postpartum psychosis

1 in 7 women affected by perinatal mood disorders

Postpartum depression

-Negative effects on child development

Maternal suicide

-20% of postpartum deaths in depressed women

Dx of perinatal mood disorders

Rule out:

-Thyroid

-Anemia

Signs and Symptoms of major depression

Edinburgh Postnatal Depression Scale

perinatal mood disorders care management/nursing interventions

Care management

-Antidepressants

-Cognitive-behavioral Therapy or interpersonal psychotherapy

nursing interventions

-Educate (Depression as an illness, Plan of care, Medications)

-Discuss alternative treatments respect refusal of meds

Dx of depression

5 of the following nearly every day:

-Depressed mood

-Spontaneous crying

-Diminished interest in all activities

-Insomnia or hypersomnia

-Weight changes

-Psychomotor retardation or agitation

-Fatigue or loss of energy

-Feelings of worthlessness or inappropriate guilt

-Diminished ability to concentrate

-Suicidal ideation

risk factors for depression during pregnancy

Prior history

-Self

-Family

Lack of social support

Stressful life events

Partner discord

History of PMS