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149 Cards in this Set
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threatened abortion
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slight bleeding (bright red)
mild pain no fetal tissue closed cervical os few days of bedrest should fix |
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inevitable abortion
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moderate bleeding
moderate pain no fetal tissue open cervical os will lose baby no matter the TX |
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incomplete abortion
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heavy bleeding
severe pain some fetal tissue passing open cervical os D&C or suction to remove tissue |
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complete abortion
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slight bleeding
mild pain all fetal tissue passed open cervical os only takes a few days to pass all the tissue monitor VS and bleeding |
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missed abortion
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slight dark brown bleeding
no pain no fetal tissue closed cervical os *baby has died but is not being expelled; can cause severe clotting issues. *TX: D&C |
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habitual abortion
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3 or more spontaneous Abs
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Early hemorrhagic disorders
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Abortions
ectopic PG hydatiform mole |
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Abortion complications
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sepsis
infection hemorrhage |
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Abortion Tx
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*Rhogam shot for all women
*D&C *delay D&C until Anti-Bs in mom if infection is suspected |
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Abortion
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term used to identify the termination of PG prior to the age of viability (20 wks of <500g)
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Ectopic PG
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*fetus implanted outside the uterus
*often mistaken in ER for appendicitis *mostly occurs in tubes & mostly on R side |
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Ectopic PG risk factors
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Hx of STDs
PID tubes tied & didn't work multiple induced Abs > 35 yrs smokers douching |
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S/S of ectopic PG
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**Triad of Symptoms
1. amenorrhea 2. abd/pelvic pain 3. feel adrenal mass on side of PG *will c/o lightheadedness (synchophy), dizzy, neck/shoulder pain, spotting (ask when LMP was) |
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S/S of ruptured ectopic PG
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*bleeding in abd cavity irritates peritoneum.
*have sharp pain *shows s/s of shock if severe *if slow bleed, abd is rigid upon palpation |
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DX of ectopic PG
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US
pelvic exam |
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Tx of ectopic PG
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*methotrexate (chemo) will kill the tissue off, saves integrity of the tube so future PGs possible
*If severe, laparotomy will be done to remove tube *laparascopy to remove the ectopic PG |
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Hydatiform Mole (molar pg)
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noninvasive abnormal placenta with large edlematous vesicular chorionic villi accompanied by various amts of trophoblasts (look like grapes)
*will have + pg test & s/s of Pg b/c of increased Hcg |
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S/S of molar pg
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*severe vag bleeding
*fundus measures larger than usual *hyperemesis gravidum possible *no fetal heart tone *can be benign or malignant |
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RN Considerations for Molar PG
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*2 IV accesses (in case blood needs to be given)
*Monitor for shock *watch output *monitor for infection *grief counseling |
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If hcg level plateau while dropping then:
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choriocarcinoma
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molar PG tx
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*evacuate the mole
*F/U after evacuation is extensive *Hcg levels will be drawn every 2-4 wks until back to normal; then Hcg levels & chest xrays @ 1 yr. *Cannot get PG until 1 year after normal (prob if already delaying PG) *if malignant, would met to lungs |
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low lying placenta previa
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*placenta right at edge of cervix. cord can slide out when water breaks.
*baby putting pressure on placenta (fetal distress) |
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partial placenta previa
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*placenta covers 1/2 of cervix.
*usually delivered by c-section |
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complete placenta previa
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*covers all of cervix.
*c-section is a must *post-partum hemorrhage is common b/c uterus is not contracting in the lower portion where placenta is bleeding; bleeding will not stop |
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causes of placenta previa
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multigravidas
over 35 yrs multigestations previous c-section prior previa smoking cocaine use any previous uterine surgery |
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placenta previa DX
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US
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S/S of placenta previa
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bright red painless bleeding
soft nontender uterus fetal heart tone is stable |
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placenta previa TX
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*options depend on gestational age.
*<37 wks, try to get bleeding to stop (bedrest); if baby is in distress then deliver |
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RN considerations for placenta previa
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*IV access & blood available
*try to get baby to 37 wks *>37 wks, deliver |
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Abruptio placenta
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*premature separation of the placenta after 20 weeks
*Dx: US |
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threatened abortion
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slight bleeding (bright red)
mild pain no fetal tissue closed cervical os few days of bedrest should fix |
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inevitable abortion
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moderate bleeding
moderate pain no fetal tissue open cervical os will lose baby no matter the TX |
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incomplete abortion
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heavy bleeding
severe pain some fetal tissue passing open cervical os D&C or suction to remove tissue |
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complete abortion
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slight bleeding
mild pain all fetal tissue passed open cervical os only takes a few days to pass all the tissue monitor VS and bleeding |
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missed abortion
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slight dark brown bleeding
no pain no fetal tissue closed cervical os *baby has died but is not being expelled; can cause severe clotting issues. *TX: D&C |
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s/s of abruptio placenta
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*may/may not have vag bleeding
*abd pain *uterine irritability *high uterine resting tone (uterus never completely relaxes) *rigid abd *may/may not have fetal heart tones |
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Tx of abruptio placenta
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depends on severity of abruption & amount of bleeding
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causes of abruptio placenta
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uterine anomalies (dble uterus)
multigravidas PIH previous c-section renal/vascular disease trauma abnormally large placenta short cord change in intrauterine pressure smoking cocaine |
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marginal abruption
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placenta pulls loose at edge = bleeding
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concealed abruption
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placenta pulled loose in center, blood pooling b/t abd wall and placenta = no bleeding but more painful
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abruption complications
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shock which causes renal failure, vascular spasms, DIC
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RN considerations for abruptions
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*constant monitoring of mom/baby
*watch VS, bleeding (ensure not developing shock) *accurate I & Os *monitor for DIC ***VS dont match what you see; tachycardia with BP decreasing & no bleeding seen (concealed abruption) ***Bedrest (L lateral), check fibrinogen levels, typed/crossed blood |
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Klein Haur-Betke test
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determnines if any fetal blood in maternal circulation
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Disseminated Intravascular Coagulation (DIC)
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defect in coagulation that consumes large amount of clotting factors
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S/S of DIC
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unusual bleeding
tachycardia bleeding from every orifice decreased fibrinogen & platelets *prolonged PT, PTT (not clotting) *increased FSP |
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Tx of DIC
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*deliver baby immediately
*fix underlying cause, then give PRBCs & clotting factors **in ICU |
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Early signs of shock
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*fetal tachycardia (1st sign, > 160bpm)
*maternal tachycardia *decreased peripheral pulses *increased resp rate *cool clammy skin *BP WNL or slightly decreased |
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late signs of shock
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*decreased BP
*decreased urine output (kidneys shutting down, <30ml/hr) *restlessness *agitation *cold clammy |
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RN considerations for bleeding disorders
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*amt & nature of bleeding
*any pain? *VS? *baby's heart rate pattern *contractions? *OB Hx? *labs? |
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Hypovolemic shock
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*The body will attempt to compensate for decreased blood volume. Hypovolemia is a loss of volume.
*natural response is to compensate by shunting blood to brain/heart; uterus is not considered essential by the body, baby will not get blood. |
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RN considerations for shock
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*IV access needed
*blood needed *need volume expander (LR) *correct problem (underlying issue) |
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Triad of symptoms for PIH
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progressive HTN
proteinuria generalized edema |
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PIH
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aka: toxemia/preeclampsia
*common in teens & moms over 40 *cyclic aterial vasospasms lead to increased peripheral resistance & decreased perfusion |
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Dx of PIH
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systolic > or = 160 OR
diastolic > or = 90 **if BP normally high/low then use 30 pts over baseline systolic and 15 pts over baseline diastolic **must have 2 elevated BPs taken 6 hrs apart to DX |
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symptoms of mild PIH
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systolic > 140 but < 160
diastolic > 90 but < 110 1 to 2+ proteinuria 2+ edema 5 lb wt gain in 1 week |
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symptoms of severe PIH
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systolic > 160
diastolic > 110 (on bedrest) 3-4+ protein 3-4+ edema visual disturbances decreased output increased creatinine |
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management of mild PIH
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monitor BP
daily wt urine check daily kick counts bedrest |
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management of severe PIH
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hospitalized
complete bedrest with foley hourly VS, I&Os, reflexes quiet room (no tv/lights) limited visitation anti-HTN used sparingly **seizures possible which compromises mom/baby's O2 **Mom's safety is key |
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RN responsibilities with PIH
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<34 wks; mag sulfate til 34 wks
>34 wks will deliver if uncontrollable **4-6g bolus of mag in 30 mins; 1-3g/hr after **amp of calcium gluconate at bedside (antidote for mag) |
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RN considerations for Mag Sulfate
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hourly VS
DTR's outputs monitor for deterioration |
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Eclampsia
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*development of seizures, or coma in a patient with preeclampsia
**tonic-clonic seizures that start with facial twitching>rigidity>apnea |
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eclampsia complications
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pulmonary edema
aspiration abruption cardiac failure intracranial bleeding transient blindness |
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eclampsia management
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*control seizures (mag sulfate)
*correct hypoxia (O2) *control HTN (apresoline - diuretic - last stop drug, used sparingly, works fast then gone) *delivery (after mom is stable) |
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HELLP Syndrome
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*hemolytic anemia elevated liver enzymes low platelets
*higher risk with white multigravida over 25 yrs *vasospasms in arteries destroy RBCs which causes anemia |
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S/S of HELLP
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epigastric pain
N&V flu like symptoms malaise HTN possible edema possible severe increase in BP |
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Tx of HELLP
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delivery
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Outcomes of HELLP
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poor maternal and fetal outcomes
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complications of HELLP
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high chance of complete renal failure, hepatic rupture, DIC, death
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Chronic HTN
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*defined & graded by specific diastolic pressures
Mild = 90-104 moderate = 105-114 severe = >115 **elevations occur PRIOR to 20 wks (after 20 wks is PIH) |
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Chronic HTN management
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*diet (increased protein & low sodium)
*meds (anti-HTN is DBP>100; aldomet; apresoline only used in crisis) |
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blood incompatibilities
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Rh+ Rh- mothers
ABO - type O mothers |
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Rh incompatibility
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***Mother MUST be Rh- & fetus Rh+
*Occurs when fetal & maternal blood mix usually in the 3rd stage of labor when placenta delivers (only takes 1 drop of baby's blood) *1st child not affected |
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subsequent fetus issue in Rh compatibility
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**Subsequent fetus: antibodies cross the placenta & attack & kill off RBCs of fetus; baby develops jaundice which causes encephalopathy; baby is forced to produce immature RBCs which can't carry enough O2 (erythroblastosis fetalis)
*Anemia is so severe it leads to hydrops fetalis and then death |
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Tx for Rh compatibility
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Rhogam shot
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ABO incompatibility
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**Mother type O; fetus type A, B, AB
*develop anti-A or anti-B antibody titers that become either IgG or IgM (IgG crosses placenta) |
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Coombs Test
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done on cord blood after delivery; if positive then ABO incompatibility
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TX for ABO incompatibility
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phototherapy
warmer *wear eye patches |
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ABO incompatibility causes
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jaundice occuring w/i 1st 24 hrs of life. Extremely high bilirubin levels. Will form bilirubin deposits in brain (kernicterus) that cause CNS damage.
***If bilirubin levels continue to rise an exchange transfusion of type O blood will be given to baby (replace most of baby's blood with Type O) |
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Concurrent Disorders
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*mother already has a disease process (DM, HTN)
*Conditions: anything that affects fluid/electrolyte balance, affects cardio/resp system, certain infections *risk factors: homeless, no PNC, no support system, poor coping skills, infection, genetic predisposition, age |
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Diabetes (type 1)
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*body either doesn't produce enough insulin or doesn't utilize insulin properly.
*Pts should go to precounseling to ensure levels are good before getting PG *Severe hypoglycemia possible if lots of N&V b/c still taking insulin but not eating (give IV dextrose) |
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Gestational diabetes
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*screening done at 26 wks
*usually shows up in 2nd trimester b/c insulin resistance usually shows up here |
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Risk factors for gestational DM
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*Obesity before PG
*>30 yrs *LGA of prev baby (>4000g or 8.5lbs) *family history of DM *unexplained loss of baby in past *congenital anomalies in prev baby |
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Maternal symptoms of gestational diabetes
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*excessive thirst
*usually lose wt (10-15lbs) *blurred vision *increased UTIs *increased yeast infections *excessive amniotic fluid (polyhydramnios) |
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Fetal symptoms of gestational diabetes
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usually large (macrosomic babies) which causes complications at delivery
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maternal effects of gestational diabetes
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Risk For:
PIH ketoacidosis UTI hydramnios c-section hemorrhage |
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fetal effects of gestational diabetes
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Risk for congenital anomalies
macrosomia or IUGR |
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newborn effects of gestational diabetes
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cardiac dysfunction
hypoglycemia hypocalcemia hyperbilirubinia RDS (resp distress syndrome) |
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management of gestational diabetes
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*usually regular (short-acting) insulin is given.
*check sugar before meals & at bedtime. *at 26 wks, moms come in often for NST to monitor baby (DM's more prone to PIH) *delivery timing is important b/c of large baby. |
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Postpartum gestational diabetes needs
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usually problem disappears; insulin might be needed for 1st few days post delivery & then back to usual dosage
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Cardiac disease
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*major complications r/t congenital defects, rheumatic fever & advanced maternal age.
*s/s are hard to identify |
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warning signs of cardiac disease
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severe chest pain
SOB (w/w-out activity) extreme fatigue dyspnea syncope |
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Type 1 Cardiac Disease
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*uncompromised
*mitral valve prolapse *before they have any kind of procedure done, they need prophylactic anti-Bs d/t susceptibility to endocarditis. *few activity limitations on these pts *usually asymptomatic |
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Type 2 cardiac disease
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*few limitations on activity
*most likely on bedrest *ordinary activity can result in dyspnea & fatigue *chest pain on exertion |
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Type 3 cardiac disease
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*marked limitations on physical activity
*Pts usually comfortable at rest *ordinary activities pretty difficult for pts, can lead to excessive fatigue, palpitations & chest pain **ex: rheumatic fever, mitral stenosis |
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Type 4 cardiac disease
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unable to perform any kind of physical activity without pain
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Left sided heart failure
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*normal tachycardia of PG shortens diastole & decreases time available for blood to cross valve > back pressure on pulmonary trunk > distention, decreased BP, pulmonary HTN > fluid leaks interstitial spaces > pulmonary edema.
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causes of left sided heart failure
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coarctation
stenosis rheumatic fever |
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symptoms of left sided heart failure
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fatigue
drop in BP tachycardia |
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risks/complications of left sided heart failure
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*high risk of spont abs, fetal demise, PTL b/c body is unable to compensate for increased blood levels.
*Pt unable to nourish the PG d/t inefficient O2/CO2 exchange |
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Right sided heart failure
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output of RV is less than what RA receives causing back pressure > congestion of systemic venous circulation & decreased cardiac output to lungs.
BP aorta decreases > increased pressure in vena cava > vein distention > liver & spleen congestion > increased abdominal fluid > acsites > peripheral edema |
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assessment of maternal cardiac disease
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*need complete health Hx
*exercise level *presence of dyspnea or cough *VS *EKG *echocardiogram & chest xray *check CRT & JVD *encourage rest *need good nutrition *avoid infection risks *evaluate current heart meds to decide if any increases are necessary |
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assessment of fetal cardiac disease
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*inadequate circulation can effect fetal growth & result in LBW, PTL, & fetal distress
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Delivery considerations for mom's with cardiac disease
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*should not push (baby can descend on own & can use vacuum/forceps to deliver)
*monitor closely (keep heart rate < 100, position on left side, HOB elevated 30 degrees, no fluid bolus & be careful w/fluid intake, keep environment quiet & admin O2 *4th stage (recovery period of 1 hr after delivery; about 500ml of blood returns to circulation; need close monitoring d/t possibility of cardiac overload. Keep pt legs down, DON'T MASSAGE UTERUS) *Postpartum considerations (d/t rapid blood return, pt is placed on complete bedrest until their cardio system stabilizes. can take 24-48 hrs. Pt w/bedrest run risk of DVTs, put on anti-coagulants) |
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Hematology disorders
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*Pseudoanemia
*Iron deficiency *Sickle Cell *Folic Acid |
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Pseudoanemia
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normal d/t dilution of the blood
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Iron deficiency
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*Hct < 30, Hgb < 10
*seen in younger pts d/t poor nutrition *predisposes client to infection & hemorrhage |
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characteristics of iron deficiency
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microlytic anemia
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symptoms of iron deficiency
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severe fatigue
exercise intolerance HA tachycardia |
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Tx for iron deficiency
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*prenatal vitamins with iron & an add'l iron supplement.
*s/b taken with OJ, vitamin C aids in the absorption of iron *if PO cannot be tolerated, iron injections are available |
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Sickle Cell
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*recessive inherited hemolytic anemia caused by an abnormal amino acid in the beta chain
*RBCs are abnormal in shape *PG increases risk |
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Assessment of PG sickle cell pt
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*pt requires sickle cell screening as initial prenatal panel.
*usually pts have Hgb of 6-8, in crisis Hgb can drop to less than 5; elevated bilirubin level |
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Management of PG sickle cell pt
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*need to be on folic acid
*8-8oz glasses/day (MUST stay hydrated) *exchange transfusion if necessary *in crisis, give O2 & analgesic |
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Folic Acid
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*essential component for fetal cell growth & formation of RBCs
*maternal needs double with PG *increases risk for SAB, abruption, anomalies, NTD *dietary: liver, kidney/lima beans, green leafy vegs |
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Renal disorders
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*in PG, renal plasma volume increases by 60-80% & GFR by 30-50%; decrease in BUN & creatinine
*reabsorption of glucose, amino acids, & protein decrease >glycosuria > bacterial growth *structures change |
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UTI
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*common in all women
*asymptomatic > pyelonephritis > PTL, PROM, FD *frequency associated to PG *pain/burning is only symptom pt would notice |
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Organism to blame for UTI's
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E Coli
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symptoms of pyelonephritis
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severe flank pain
N&V high fever |
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Dx of UTI
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clean catch UA (CCUA)
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Tx of UTI
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ampicillin
genomycin (if early in PG, sulfa drug) (no sulfa later in PG) NO tetracycline |
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Asthma
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*wheezing & dyspnea gets progressively worse
*uterine pushing on diaphragm *TX: aggressive, epinephrine administered; usually on theophylline or anticholinergic *if asthma cannot be maintained: can effect fetal growth & cause possible IUGR |
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Pneumonia
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*usually confines to one lobe
*affected area has fluid buildup & impairs O2/CO2 exchange *bacterial or viral (viral=mycoplasma) |
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Pneumonia symptoms
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Strep or mycoplasma:
*Strep = tachypnea, high fever, coughing *mycoplasma = possible cough, patchy infiltrates in lungs |
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Pneumonia mangement
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Tx: IV penicillin (bacterial)
*severe case can affect outcome of PG, often experience PTL; some moms need ventilator support |
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Appendicitis
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*Hard to DX during PG
*Hx important for differentiation *pain is usually higher in PG pts, important to determine difference b/t appendicitis & either round ligament issue, ectopic PG & GB |
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Sickle Cell
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*recessive inherited hemolytic anemia caused by an abnormal amino acid in the beta chain
*RBCs are abnormal in shape *PG increases risk |
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Assessment of PG sickle cell pt
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*pt requires sickle cell screening as initial prenatal panel.
*usually pts have Hgb of 6-8, in crisis Hgb can drop to less than 5; elevated bilirubin level |
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Management of PG sickle cell pt
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*need to be on folic acid
*8-8oz glasses/day (MUST stay hydrated) *exchange transfusion if necessary *in crisis, give O2 & analgesic |
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Folic Acid
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*essential component for fetal cell growth & formation of RBCs
*maternal needs double with PG *increases risk for SAB, abruption, anomalies, NTD *dietary: liver, kidney/lima beans, green leafy vegs |
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Renal disorders
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*in PG, renal plasma volume increases by 60-80% & GFR by 30-50%; decrease in BUN & creatinine
*reabsorption of glucose, amino acids, & protein decrease >glycosuria > bacterial growth *structures change |
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Appendicitis management
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*c-section, if close to term, to remove baby & appendix
*if early, can do laparascopic appendectomy *ruptures can cause sepsis for mom/baby |
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Cholecystitis
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*gallbladder inflammation
*associated w/>40 yrs, obesity, multiparas, high fat diet *c/o pain/pressure in epigastric area *TX: low fat diet if acute: IVFs, pain meds & laparascopic surgery |
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Lupus
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*immune disorder
*S/S: severe joint pain, photosensitivity *high rate of SAB *often born with congenital heart block |
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Antiphospholipid Syndrome
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*characterized by the production of antibodies that cause thrombus formation.
*Not uncommon for these pts to experience stroke/PE/DVTs *PG related complications: SAB, preterm delivery, severe preeclampsia |
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HIV
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*progressive, severe weakening of the immune system by a rotovirus that attacks the T-lymphocytes disabling the body's ability to fight infection
*no routine screening; should be ordered if mother possesses any risk factors but maternal consent is needed. *Can use ELISA test |
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HIV symptoms
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based on progression
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HIV transmission
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body fluids (minus perspiration)
*does cross placenta & blood-brain barrier *can occur d/t blood transfusions |
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HIV risk factors
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multiple sex partners
bisexual IV drug users transfusions |
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HIV progression
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1. Initial invasion
2. Sero-conversion 3. Asymptomatic 4. Symptomatic |
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Initial invasion (HIV)
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flu-like symptoms
little lymphadenopathy |
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Sero-conversion (HIV)
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*virus is actually active in their system, asymptomatic.
*could take anywhere from 6 wks to a year after initial invasion. |
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Asymptomatic (HIV)
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"wasting syndrome"
anywhere from 2-6 yrs |
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Symptomatic (HIV)
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*begin to observe opportunistic infections in these pts.
*Odd infections d/t low T-cells |
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HIV delivery
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*attempt to prevent transmission to baby
*limit fetal contact w/maternal blood as much as possible *not eligible to have amnio *no fetal scalp electrode *no forceps or vacuum extraction *shots given AFTER bathing |
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HIV consequences
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*LBW infants
*PTL *Pneumocystic pneumonia (tx for this is tetragenic) *kaposi sarcoma (chemo needed) *thrombocytopenia *untreated |
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HIV TX
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*treat newborns with AZT starting at approx 6 wks in attempt to sero-convert these babies back to negative status
*PCR 2-4 wks, after that ELISA test is done. 2 negative tests w/i 4 months = negative infant |
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Trauma
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*injury by force
*rare in PG *6-7% mostly last trimeseter (abusive relationships can worsen during last trimester) |
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Changes in PG that affect trauma
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*blood volume - lose a significant amt of blood before signs of shock occur. Hypovolemic shock will shunt blood away from uterus & baby
*WBCs increase |
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Trauma assessment
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*quick
*brief Hx *document circumstances (is degree of injury appropriate for story told) **may need emotional reassurance |
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Trauma management
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2 phases:
1. plan the care to get her stabilized 2. continuation of care *if greater than 24 wks, severe trauma is reason to c-section & deliver baby |
