Pregnancy Part 3 – SOGC / TN2014

7 In a pregnant patient presenting with features of an antenatal complication (e.g., premature rupture of membranes, hypertension, bleeding):
a) Establish the diagnosis.
b) Manage the complication appropriately.

Nausea and Vomiting
  • 50-90% of pregnant women, often limited to T1, but may persist
  • Hx/PEx: r/o other causes of N/V & weigh frequently + assess level of hydration
  • Ix: U/A for ketones
Tx:
  • Non-pharmacological:
    • Avoid mixing fluids and solids, frequent small meals
    • Stop prenatal vitamins (folic acid must continue until >12wk)
    • Increase sleep / rest
    • Ginger (max 1000mg/d)
    • Acupuncture, acupressure
  • Pharmacological:
    • Diclectin (10mg doxylamine + B6) 4 tabs po daily to max of 8 tabs
    • Gravol (dimenhydrinate) 50-100mg q4-6h po, hydroxyzine, metoclopramide
    • Vit B6 lollipops
    • If dehydrated, assess fluid replacement needs & resuscitate accordingly
  • Severe / refractory
    • IV fluids + parenteral anti-emetics
Hyperemesis Gravidarum
  • Intractable N/V, usually in T1, 1% of pregnancies
Ix:
  • r/o systemic causes: GI inflammation, pyelonephritis, thyrotoxicosis
  • r/o obstetrical causes: multiple gestation, GTN, HELLP syndrome
  • CBC, lytes, BUN, Creatinine, LFTs, U/A, U/S
Tx
  • Non-pharmacological: same as above
  • Pharmacological: same as above
    • Thiamine supplement
    • Consider ondansetron / methylprednisolone
  • If severe, admit, NPO then small frequent meals, correct hypovolemia, lytes, ketosis, TPN if severe
C/I:
  • maternal: dehydration, lytes, acid/base disturbances; mallory-weiss tear, Wernicke’s encephalopathy, death
  • Fetal: IUGR 15x more common in women losing >5% of pre-pregnancy weight

 Jaundice in Pregnancy

1/1500

Etiology:
  • Viral hepatitis (most common)
  • Hyperemesis gravidarum
  • Hepatobiliary conditions
Unique to pregnancy
1) HELLP syndrome
  • Hemolysis, Elevated Liver enzymes, Low Platelet (unknown pathogenesis)
  • Affects 20% of women with severe preeclampsia
  • Presents >27w GA (11%) & up to 30% after delivery & with no previous signs of HTN
Clinical features:
  • Epigastric / RUQ/Chest pain ± jaundice
  • N/V
  • Preeclampsia symptoms: h/a, blurred vision, thirst
  • Atypical presentations: asymptomatic reduction in platelet count, “flu-like” symptoms
Ix:
  • AST, Total Bilirubin, low platelet count, elevated LDH
  • ± elevated D-dimer / TPA (tissue polypeptide antigen) / fibronectin, fragmented RBCs on smear
Tx:
  • Supportive Care & prompt delivery
  • C/I: sepsis, multi-orgain failure, DIC, death
2) Cholestatic Jaundice of Pregnancy
  • Intense pruritis that precedes jaundice by 7-14 days
  • ? due to increased sensitivity to high estrogen / abn progestational steroids
  • 17-29 wk GA, Chile / Scandinavia (rare in Asian / African)
Clinical Features:
  • Intense pruritus (worse on palms and soles) ± icterus (1-2 wk later)
  • Steatorrhea unusual
Ix:
  • ALT <500, ALP, GGT markedly elevated (levels consistent with moderate to severe cholestasis)
Tx:
  • Ursodiol 20-25mg/kg/d
  • Pruritis: Cholestyramine
  • Prophylactic Vit K before delivery – consider induction of labour
  • Selenium may be protective, strong familial predisposition, correlates with OCP sensitivity
Hepatic Infarct, Hematoma, and rupture
  • Rare consequences of preeclampsia, occur in T3
  • Vasospasm-induced hepatic infarction can lead to hematoma / rupture
  • Hepatic rupture: RUQ abdominal pain, abdominal distention, n/v, HTN (followed by shock)
  • Hemoperitoneum (paracentesis, U/S, CT, MRI showing ruptured liver)
  • Aggressive: rapid delivery & trauma sx to repair liver
  • C/I: death (mother and fetus) if untreated
Acute Fatty Liver of Pregnancy (AFLP)
  • Form of hepatic failure with coagulopathy & encephalopathy
  • Microvascular fatty infiltrate in liver parenchyma
  • 1/7000, T3, high mortality (75%)
  • Resolution of hepatic dysfunction with delivery or termination of pregnancy
Clinical Features (mild to fulminant)
  • Acute N/V; severe upper abd/p preceding jaundice
  • Confusion, preeclampsia, pruritis
Ix:
  • Elevated PTT, low serum fibrinogen, AST>ALT, hypoglycemia, preeclampsia & HELLP features
  • Liver Bx to establish Dx – CT most useful if liver biopsy not possible
Tx:
  • Early Dx with prompt delivery followed by maximal supportive care
  • ABCs, mechanical ventilation, transfusion of blood products, Tx hypoglycemia
  • hepatic encephalopathy Tx: lactulose, catharsis

 Bleeding in Pregnancy

T1/T2 bleeding

Hx:

  • Risk factors for ectopic:
    • Previous ectopic, Hx of STI/PID, IUD use, previous pelvic Sx, smoking
  • Previous SA
  • Recent trauma
  • Characteristics of the bleeding (any tissue passed)
  • Characteristics of the pain (cramping ? SA)
  • Hx of coagulopathy
  • Gyne/OB hx
  • Dizziness (sig blood loss – ?rupture ectopic)
  • fever (may be associated with septic abortion

PEx:

  • Vitals (including orthostatic changes), Abdomen (SFH, tenderness, CTX?), perineum (signs of trauma, genital lesions)
  • Speculum (cervical os open / closed, presence of active bleeding / clots / tissue)
  • Pelvic exam: uterine size, adnexal mass, uterine / adnexal tenderness

ddx:

  • Physiologic bleeding: spotting due to implantation of placenta – normal serial b-HCGs
  • Abortion (threatened, inevitable, incomplete, complete)
  • Abnormal pregnancy – hydatidiform mole
  • Trauma – post-coital / after pelvic exam or Genital lesion (cervical polp, neoplasms)

Ix:

  1. CBC, group and screen, b-HCG
  2. U/S (confirm intrauterine pregnancy & fetal viability) – r/o ectopic

Tx:

  • IV NS for hemorrhagic shock, Tx underlying cause

 Antepartum hemorrhage: vaginal bleed 20wk to term

Ddx:

  • Bloody show (shedding of cervical mucous plug) – most common in T3
  • Placenta previa
  • Placenta abruption – most common pathological etiology in T3
  • Cervical lesion (cervicitis, polyp, ectropion, cervical cancer)
  • Uterine rupture
  • Other: bleeding from bowel / bladder, placenta accreta, abnormal coagulation

Hx:

  • How much bleeding?
  • Are there contraction / cramping / pain?
  • Description? color, clotting etc
Placenta Previa
  • Placenta edge mm away or overlap from the internal os
  • >20 mm of overlap over the internal os in T3 / overlap after GA35wk – predictive of c/s
Clinical Features
  • Painless bright red vaginal bleeding (recurrent), mean onset is 30wk GA

PEx:

  • no VE until u/s r/o placenta previa
  • Uterus soft & nt, presenting part high or displaced
  • FHR usually normal
  • Shock / anemia correspond to degree of apparent blood loss

C/I:

  • Fetal: mortality (low), prematurity (bleeding dictates c/s), intrauterine hypoxia (acute or IUGR), fetal malpresentation, PPPROM, risk of fetal blood loss from placenta
  • Maternal: <1% mortality, Sheehan syndrome – pituitary necrosis, hemorrhagic / hypovolemic shock, anemia, AKI, placenta accreta, hysterectomy

Ix:

  • Transvaginal U/S > transabdominal U/S – repeated at regular intervals if 20mm overlp – 20mm away from internal os
  • CBC, INR/PTT, plt, fibrinogen, FDP, type and cross match
  • U/S: determine fetal viability, GA, placenta status/position
  • Kleihauer-Betke – determine extent of fetomaternal transfusion – dose of Rhogam

Tx:

  • Stabilize and monitor: IV, O2, Vitals, U/O, EFT
  • Keep intrauterine pregnancy until the risk of delivery < risk of continuing pregnancy
    • GA<37wk + min bleeding: expectant Tx – admit, limited physical acitivity, no douches, enemas, intercourse
      • consider corticosteroids for fetal lung maturity, delivery when fetus is mature / hemorrhage
    • Term / profuse bleeding / L/S ration is >2:1 – deliver by C/S
Placenta abruption
Classification: most are mixed
  • total (fetal death inevitable) vs Partial
  • External / revealed / apparent: blood dissects downward toward cervix
  • Internal / concealed (20%): blood dissects upward toward fetus
Risk Factors:
  • previous abruption
  • DM, HTN, preeclamsia, renal disease
  • trauma, shock from other cause
  • cocain use
Presentation
  • Painful (80%) vaginal bleeding, uterine tenderness, uterine contactions – sudden onset, constant, localized to lower back and uterus
  • shock / anemia out of proportion to apparent blood loss
  • ± fetal distress, fetal demise, bloody amniotic fluid, coagulopathy
C/I:
  • Most common cause of DIC in pregnancy, AKI, anemia, hemorrhagic shock, Sheehan syndrome, amniotic fluid embolus
  • Fetal mortality 25-60%, prematurity, intrauterine hypoxia
Ix: – clinical dx
  • U/S not sensitive for diagnosing abruption

Tx:

  • Stabilize and monitor: IV NS, O2, VS, B/W (CBC, PTT/PT, Plt, fibrinogen, FDP, type and cross match), EFM
  • Blood products on hand: red cells, platelets, cryoprecipitate (DIC risk)
  • Rhogam prn – Kleihauer-Betke may confirm abruption
  • Mild abruption
    • <37 – serial Hct to assess concealed bleeding, deliver if fetus mature or hemorrhage
    • term – stabilize and deliver
  • Moderate / severe
    • Hydrate, restore blood loss, correct coagulopathy
    • Vaginal delivery if no c/i and no evidence of fetal or maternal distress OR fetal demise
    • C/S if live fetus & fetal / maternal distress, FTP or vaginal delivery c/i
Vasa Previa – 1/5000, higher in twin pregnancies
  • Unprotected fetal vessels pass over the cervical os – associated with velamentous insertion of cord into membranes of placenta or succenturiate lobe
  • Painless vaginal bleeding & fetal distress – 50% perinatal mortality, 75% if membrane rupture (most infants die of exsanguination)
Ix:
  • Apt test – NaOH mixed with the blood – fetal (supernatant turns pink), maternal (turns yellow)
  • Wright stain on blood smear – nucleated red blood cells (cord)
Tx:
  • emergency c/s

 PROM (premature rupture of membranes) / amniorrhexis

  • Rupture of membrane prior to labour
  • prolonged ROM: >24 hr elapsed between ROM and onset of labour
  • Preterm ROM: ROM before GA37 (associated with PTL)
  • PPROM: ROM <37 & prior to onset of labour
Risk Factors:
  • Maternal:
    • family Hx of PROM,
    • multiparity, cervical incompetence,
    • infection – cervicitis, vaginitis, STI, UTI
    • low socioeconomic class / poor nutrition
  • Fetal:
    • congenital anomaly
    • multiple gestation
  • PTL risk factors
Hx:
  • Hx of fluid gush or continued leakage
O/E:
  • Avoid introducing infection with exam (don’t do a bimanual exam)
  • Sterile speculum exam
  • pooling of fluid in the posterior fornix
  • may observe fluid leaking out of cervix on cough / valsalva (“cascade”)
  • Nitrazine turns blue (low specificity) ddx: blood, urine, semen
  • Ferning – more specific

Ix:

  1. u/s:
    • decreased AFV
    • r/o fetal anomalies, assess GA, BPP
  2. L/S ratio (Lecithin:Sphingomyelin ratio) – Assess fetal lung maturity
    • Lecithin levels increase rapidly after GA35, sphingomyelin remain constant.
    • less than 2:1 indicates pulmonary immaturity
    • affected by blood / meconium in the amniotic fluid
  3. Cx (cervix for GC, lower vagina for GBS)
Tx:
  • Deliver urgently if evidence of fetal distress / chorioamnionitis
  • <24 wk – consider termination
  • 24-25 wk – individual consideration – RE risks to preterm infants
  • 26-34 wk – expectant as prematurity complications are significant
    • consider betamethasone to accelerate maturity if <32 wk & no evidence of infection
    • Consider tocolysis x 48 hr to permit administration of steroids if PPROM induces labour
  • 34-36wk – risk of death from RDS vs neonatal sepsis
    • Admit for expectant management and monitor VS Q4h, daily BPP, WBC count
    • If not in labour or labour not indicated, consider abx (controversial)
      • broad spectrum coverage increase the time to onset of labour from PROM by 5-7 d
  • Term – IOL – risk of death from sepsis > RDS
C/I:
  • Corde prolapse,
  • chorioamnionitis,
  • premature delivery,
  • limb contracture

Decreased Fetal Movements
  • Healthy pregnant women without risk factors for adverse perinatal outcomes should be made aware of the significance of FM in the third trimester and count FM if they perceive decreased movements.
  • Daily monitoring of fetal movements starting at 26 to 32 weeks should be done in all pregnancies with risk factors for adverse perinatal outcome
  • <6 FM/2hr require further antenatal testing and should contact their caregivers  asap
    • a complete evaluation of maternal and fetal status, including NST ± biophysical profile.
    • An anatomical scan to rule out a fetal malformation should be done, if none been done.
    • Management should be based upon the following:
      • normal NST and no risk factors: the woman should continue with daily FM counting.
      • Normal NST and risk factors or clinical suspicion of IUGR/oligohydramnios: an U/S for either BPP or amniotic fluid volume assessment within 24 hours. Continue with daily FM counting.
      • Atypical/abnormal NST: further testing (BPP ± contraction stress test and assessment of amniotic fluid volume) should be performed asap
  • Gestational age – Fetal movements are perceived by women regularly after 24 weeks in a constant fashion. Most studies initiated fetal movements at 28-32 weeks. In extremely early gestational age, iatrogenic preterm delivery may have grave consequences. Therefore, fetal movement counting should not be encouraged prior to viability and possibly should start at 26-32 weeks based on the facilities available.
  • Non-perception of fetal movements – Women perceived 87-90% of fetal movements. A small percentage of women do not perceive fetal movements. Fetal movement counting can not be used in these women. Perception may improve with looking at movements during ultrasound scanning.
  • Optimal time for testing – Fetal movements were found to be increased at evening time.
  • Position – Fetal movements are perceived best when lying down.
  • Activity Maternal exercise was not shown to alter fetal activity.
  • Food – Most studies did not show an increase of movements following food or glucose.
  • Smoking – Smoking reduces fetal movements temporarily by increasing carboxyhemoglobin levels and reducing fetal blood flow.
  • Drug effect – Most drugs have no effect on fetal movements. Depressant drugs and narcotics may reduce fetal movements. Notably, antenatal corticosteroids may have the same effect for two days.
  • Anxiety and stress – Fetal movement counting does not increase maternal stress or anxieties.
  • Optimally, the technique for fetal movement counting is performed with the woman concentrating on the movements and in a reclined (not supine) position.
Non-Stress Test
  • Antepartum non-stress testing may be considered when risk factors for adverse perinatal outcome are present.
  • In the presence of a normal non-stress test, usual fetal movement patterns, and absence of suspected oligohydramnios, it is NOT necessary to conduct a BPP or contraction stress test.
  • A normal NST be classified and documented by an appropriately trained and designated individual asap, (ideally < 24 h). For atypical or abnormal non-stress tests, the nurse should inform the attending physician (or primary care provider) at the time that the classification is apparent. An abnormal non-stress test should be viewed by the attending physician (or primary care provider) and documented immediately.
  • The acceleration is 15 beats/minute above the baseline, and the acceleration lasts 15 seconds and < 2 minutes from the onset to return to baseline.
    • Before 32 wk GA, accelerations are defined as having an acme 10 beats/min above the baseline with a duration of 10 seconds from onset to the return to baseline.
    • Prolonged acceleration is 2 minutes and < 10 minutes in duration. Acceleration of 10 minutes is a baseline change.
  • Classification of variability
    • Undetectable Absent
    • 5 bpm Minimal
    • 6 to 25 bpm Moderate
    • 25 bpm Marked
  • Variable decelerationis – abrupt decrease in the FHR with the onset of the deceleration to the nadir of less than 30 seconds. The deceleration should be at least 15 beats below the baseline, lasting for at least 15 seconds, but less than 2 minutes in duration.
    • a response of the FHR to cord compression
  • Complicated variable decelerations may be indicative of fetal hypoxia:
    • Deceleration to less than 70 bpm lasting more than 60 seconds
    • Loss of variability in the baseline FHR and in the trough of the deceleration
    • Biphasic deceleration
    • Prolonged secondary acceleration (post deceleration smooth overshoot of more than 20 bpm increase and/or lasting more than 20 seconds)
    • Slow return to baseline
    • Continuation of baseline rate at a lower level than prior to the deceleration
    • Presence of fetal tachycardia or bradycardia
  • Late deceleration is a visually apparent gradual decrease in the FHR and return to baseline with the onset of the deceleration to the nadir of greater than 30 seconds. The
    onset, nadir, and recovery of the deceleration occur after the beginning, peak, and ending of the contraction, respectively.

    • Associate with uteroplacental insufficiency and imply some degree of hypoxia
  • Early deceleration is a gradual decrease in the FHR (defined as onset of deceleration to nadir ≥ 30 seconds) and return to baseline associated with uterine contraction:
    • The onset, nadir, and recovery of the decelerations coincide with the beginning, peak, and ending of the contraction, respectively.
    • They are associated with fetal head compression

8 In a patient presenting with dystocia (prolonged dilatation, failure of descent):

a) Diagnose the problem.

Dystocia

  • In the active phase of the first stage: > 4 hours of < 0.5cm / hr dilation or No cervical dilatation over 2 hours1
  • In the 2nd stage: > 1 hour with no descent during active pushing.
    • Ok to rest if no urge to push up to 1hr – no evidence that a prolonged passive second stage with poor contractions is harmful to the fetus.
    • ‘Time limits’ should be initiated when contractions are adequate and active pushing commences.
  • Prolonged 2nd stage:
    • Nullipara – lack of  progress for 3 hr with epidural or 2hr w/o epidural
    • Parous – lack of progress for 2 hr with epidural or 1hr w/o epidural
    • close attention to CTX strength and progress is necessary
    • 3 Common causes: uterine inertia, fetal malposition, CPD
    • A prolonged second stage in obstructed labor with adequate contractions is harmful.
Etiology: 4Ps
  • Powers – ineffective CTX
  • Passenger – fetal size, altitude, position, anomalies
  • Passage: cephalopelvic disproportion (CPD), soft tissue factors (tumours, full bladder/ rectum, vaginal septum)
  • Psyche: pain and anxiety

Prevention:

  • Labor preparation
  • Continuous emotional support during labor
  • Careful labor assessment (consider a partogram)
  • Use of appropriate analgesia
  • For women with epidural analgesia, if inadequate labor progress is suspected, early ARM and oxytocin  for uterine inertia

Tx:

  • Ensuring adequate maternal hydration
  • Considering therapeutic rest with analgesia if the woman is exhausted
  • Amniotomy:
    • indicated to accelerate labor that is not progressing adequately
    • it is necessary to ensure that the fetal head is well-applied to the cervix (not ballottable) to minimize the risk of cord prolapse
  • Oxytocin augmentation – need IV, EFM, & possible epidural
    • to start with a low dose, use low dose increments, and make dosage increments at 30 minute intervals
      • initial dose 1-2 mU/min and increase by 1-2 mU/min Q30min; usual dose 8-12 mU/min
    • Adverse effects:
      • xs uterine activity could cause fetal compromise / uterine rupture, prevented by correcting the dose
      • ADH effect: water intoxication, prevented by limit free water
      • Vasodilatation: hypotension, prevented by avoiding IV bolus
      • Contraction strength depends on the dose of oxytocin & uterine sensitivity to oxytocin
  • If clinical assessment of contraction strength inadequate, considering IUPC
  • Cesarean section if other interventions have failed

First stage:
  1. latent phase: infrequent and irregular contractions, slow, cervical dilatation to 3-4cm and effacement
  2. Active phase:
    • rapid cervical dilatation (null 1.2cm/h, multip 1.5cm/h), maximal slope of friedman curve
    • contractions approx q2-3mins last 45-60sec, strongest at fundus, weakest at lower segment
    • Women in active labour should receive continuous close support from an appropriately trained person. Intensive fetal surveillance by intermittent auscultation or electronic fetal monitoring requires the continuous presence of nursing or midwifery staff. One-to-one care of the woman is recommended
    • There is no justification for the restriction of fluids and food in labor for low-risk women
Healthy women at term in labour in the absence of risk factors for adverse perinatal outcome
  • Admission fetal heart tracings are not recommended for , as there is no evident benefit.
  • Intermittent auscultation Q15-30min in active phase and Q5min in 2nd stage; compared with EFM, IA has lower intervention rates without evidence of compromising neonatal outcome.
  • Intermittent auscultation may be used to monitor the fetus when epidural analgesia is used during labour, provided that a protocol is in place for frequent intermittent auscultation assessment (e.g., every 5 minutes for 30 minutes after epidural initiation and after bolus top-ups as long as maternal vital signs are normal).
Women with risk factors for adverse perinatal outcome.
  • Admission fetal heart tracings are recommended
  • Electronic fetal monitoring is recommended for pregnancies at risk of adverse perinatal outcome. (II-A)
  • When a normal tracing is identified, it may be appropriate to interrupt the EFM for up to 30 minutes to facilitate periods of ambulation, bathing, or position change, providing that
    • (1) the maternal-fetal condition is stable and
    • (2) if oxytocin is being administered, the infusion rate is not increased.
  • Digital fetal scalp stimulation is recommended in response to atypical electronic fetal heart tracings. (II-B)
    • In the absence of a positive acceleratory response with digital fetal scalp stimulation, Fetal scalp blood sampling is recommended when available
    • If fetal scalp blood sampling is not available, consideration should be given to prompt delivery, depending upon the overall clinical situation

Management of abnormal fetal heart rate by intermittent auscultation

  • Auscultate FHR again following the next contraction to confirm characteristics
  • Assess potential causes: Check maternal pulse, BP, temperature
  • Perform a vaginal exam, as indicated
Interventions/Management
  • Attempt to eliminate or reduce the effects of the problem(s)/cause. Intervene to promote 4 physiologic goals:
    1. Improve uterine blood flow
    2. Improve umbilical blood flow
    3. Improve maternal/fetal oxygenation
    4. Decrease uterine activity
  • Reposition woman to increase uteroplacental perfusion or alleviate cord compression.
  • Correct maternal hypovolemia / HoTN, if present, by increasing IV fluids
  • Tachycardia
    • Rule out fever, dehydration, drug effect, prematurity
  • Bradycardia
    • Perform vaginal exam to assess for prolapsed cord or relieve cord compression
    • Administer oxygen at 8–10 L/min
  • Decelerations
    • Assess for passage of meconium
    • Administer oxygen at 8–10 L/min
  • Additional measures
    • Continue to auscultate FHR to clarify and document components of FHR
    • Consider initiation of electronic fetal monitoring (EFM)
  • If abnormal findings persist despite corrective measures, and ancillary tests are not available or desirable, expedited delivery should be considered

Second Stage: full cervical dilatation until delivery

  • Arrest of descent is no progress for >1hr
  • Prolonged if > 2 hrs (nuliparity), or >3hrs with epidural. For multips, this is >1hr and >2hrs(epidural).
  • No intervention strictly necessary with prolonged descent, if no fetal distress.
  • look for Cephlo-pelvic-disproportion, change position, fetal monitor and consider C/S if distress.

Third Stage: Delivery of placenta

  • Administer Oxytocin 10 IU IM x 1 routinely
  • prolonged if >30mins. If prolonged, may require manual extraction.
  • Signs of placental separation: gush of blood, lengthening of cord, uterus becomes globular, fundus rises

Cord Clamping

  • Delaying cord clamping by at least 60 seconds is preferred to clamping earlier in premature newborns (< 37 weeks’ gestation) since there is less intraventricular hemorrhage and less need for transfusion in those with late clamping
  • For term newborns, the possible increased risk of neonatal jaundice requiring phototherapy must be weighed against the physiological benefit of greater hemoglobin and iron levels up to 6 months of age conferred by delayed cord clamping

Fourth Stage: First hour post-partum

  • Monitor VS & bleeding, repair lacerations, ensure uterus is contracted (palpate uterus and monitor uterine bleeding)
  • Inspect placenta for completeness & umbilical cord for 2A + 1V
  • Ideally, cord blood sampling of both umbilical arterial and umbilical venous blood is recommended for ALL births, for quality assurance and improvement purposes. If only one sample is
    possible, it should preferably be arterial.
  • When risk factors for adverse perinatal outcome exist, or when intervention for fetal indications occurs, sampling of arterial and venous cord gases is strongly recommended.

3rd / 4th stages more dangerous to the mother (hemorrhage)


Obstetrical history and current pregnancy conditions associated with increased perinatal morbidity/mortality
  • Antenatal
    • Maternal
      • Hypertensive disorders of pregnancy
      • Morbid obesity, Pre-existing diabetes mellitus/Gestational diabetes
      • Antepartum hemorrhage, Maternal MVA/trauma
      • Maternal medical disease: cardiac, anemia, hyperthyroidism, vascular disease and renal disease
    • Fetal
      • Intrauterine growth restriction,  Prematurity, Oligohydramnios
      • Abnormal umbilical artery Doppler velocimetry
      • Isoimmunization
      • Multiple pregnancy, Breech presentation
  • Intrapartum
    • Maternal
      • Vaginal bleeding in labour
      • Intrauterine infection/chorioamnionitis, Prolonged membrane rupture 24 hours at term
      • Previous Caesarean section
      • Induced labour, Augmented labour, Hypertonic uterus
      • Preterm labour, Post-term pregnancy ( 42 weeks)
    • Fetal
      • Meconium staining of the amniotic fluid
      • Abnormal fetal heart rate on auscultation
Metabolic acidosis at birth
  • Hypoxic renal damage
  • Necrotizing enterocolitis
  • Intracranial hemorrhage
  • Seizures
  • Cerebral palsy
  • Neonatal encephalopathy

References:

 

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