Antenatal complications Flashcards
Uncomplicated nausea and vomiting in prengancy
affects 80% of women
Typically week 8-14
10% of pregnancies will have continued n+v beyond 20w until birth
Definition of hyperemesis gravidarum
Severe, intractable vomiting in pregnancy that results in inability to maintain hydration orally, metabolic disturbance, and admission to hospital for parenteral hydration
Prevalence of hyperemesis gravidarum
Occurs in less than 1% of pregnancies
Pathogenesis of hyperemesis gravidarum
Hormonal (hCG and oestrogen)
Mechanical (red LOS tone, gastric peristalsis and gastric emptying)
?Emotional
Complications of hyperemesis gravidarum
Hyponatremia Hypokalemia Metabolic hypochloraemic alkalosis Ketonuria Raised haematocrit Increased specific gravity of urine Wernicke's encephalopathy
Investigations if suspecting hyperemesis gravidarum
Urinalysis and MCS Stool culture EUC BGL (if diabetic) LFTs TFTs (?thyrotoxicosis) Serum amylase (?pancreatitis) Ultrasound (?ongoing pregnancy, multiple, molar) Abdominal erect and supine x-rays (?bowel obs)
Management of hyperemesis gravidarum
IV hydration if required (0.9% Na + K or Hartmann’s)
Glucose and vitamins (esp. thiamine) if prolonged vomiting
- administer thiamine first to prevent Wernickes
Dietary modification (small frequent low-fat meals, early when hungry)
Alternative (acupuncture, Ginger, multivitamins[B6])
Pharmacologic
Antiemetics for use in Hyperemesis gravidarum
Metoclopramide 10mg TDS
Doxylamine 25mg nocte
Promethazine 25mg BD (sedation)
Prochlorperazine 25mg suppository 1-2/day
Ondansetron 4-8mg oral or IV (if IV rehydration, thiamine and electrolyte correction)
Corticosteroids if refractory
Complication of use of corticosteroids in first trimester of pregnancy
Increased risk of oral clefting
Definition of oligohydramnios
An amniotic fluid volume that is less than expected for gestational age
Causes of oligohydramnios
Placental (3)
- abruption
- twin-twin transfusion
- placental thrombosis/ischaemia
Foetal (6)
- Chromosomal abnormalities
- congenital abnormalities (esp if impairs urine production e.g. renal obstruction)
- Growth restriction (blood flow redirected away from kidneys)
- intrauterine foetal demise
- post-term pregnancy
- ruptured foetal membranes
Maternal (7)
- Medical:
- chronic HTN
- collagen vascular disease
- nephropathy
- thrombophilia
- Obstetric:
- Preeclampsia
- medications:
- ACE-inhibitors
- NSAIDsNormal daily foetal urine production
800-1200mL/day
Normal volume swallowed by foetus per day
500-1000mL/day
Normal measurements of amniotic fluid
Deepest volume pocket (DVP) 2-8cm
Amniotic fluid index (sum of 4 quadrant DVP) 5-25
Measurement of oligohydramnios in multiple pregnancy
Single deepest pocket (SDP) under 2cm
Components of biophysical profile (5)
Foetal HR Foetal breathing movements Foetal activity/gross body movement Foetal muscle tone Qualitative AFI
Management of oligohydramnios
Identify cause (history, USS)
+/- Increase amniotic fluid
Serial USS to monitor AFI and foetal growth (weekly, 4-weekly respectively)
+Non-stress testing +/- Biophysical profile
Likely to require early delivery
Indications to increase amniotic fluid volume in oligohydramnios
Improve detection of foetal anomalies
Facilitate cephalic version
Prevent foetal sequelae
Methods to increase amniotic fluid volume in oligohydramnios
Amnioinfusion
Maternal hydration
Foetal membrane sealants (if leaking PPROM)
Commonest causes for severe polyhydramnios
Foetal anomalies (particularly trisomy 21)
Maternal and idiopathic factors are more often associated with milder cases
Incidence of polyhydramnios
1-2% of pregnancies
What syndrome is suggested by IUGR plus polyhydramnios
Trisomy 18
Causes of polyhydramnios
Foetal (33%) - Chromosomal anomalies - CNS: ancephaly, hydrocephalus - GI: oesophageal atresia/TOF, facial clefts (impaired swallowing) - Neuromuscular condition inhibiting swallowing Maternal: - Type 1 DM (disordered transchorionic flow) Maternal-foetal - Chorioangioimas - Multiple gestation - Foetal hydrops Idiopathic (40%)
Causes of foetal hydrops
Anaemia (thalassaemia, virus, ABO incompatibility)
Congestive heart failure
Infection (TORCH, syphilis, varicella)
Obstructed lymphatic flow
Red. plasma oncotic pressure (liver disease, nephropathy)
Metabolic storage disease
Thoracic abnormalities (e.g. chylothorax, diaphragmatic hernia)
AV and venous malformations
GI malformations
GU malformations
Twin gestation (twin-twin transfusion syndrome)
Clinical features of polyhydramnios
Uterine size large for dates
FLUID THRILL
Mother may experience SOB, uterine irritability and contractions, abdominal discomfort
Ultrasonographic findings of polyhydramnios
Single deepest pocket greater than 8cm
AFI greater than 24 cm
Management options of polyhydramnios
Antepartum foetal monitoring Nonstress test + biophysical profile every 1-2 weeks until 37 weeks (more often if severe) Amnioreduction if severe and symptomatic Indomethacin Generally induce labour early
Indomethacin use in polyhydramnios (dose, side effects, contraindications)
25mg orally QID (works in 2-3d)
S/E: nausea, reflux, gastritis, vomiting, platelet dysfunction
Foetal A/E: constriction of ductus arteriosus, necrotising enterocolitis, intraventricular haemorrhage
Contraindicated after 32 weeks (risk of closure of ductus)
Mechanism of action of indomethacin in polyhydramnios
Stimulates foetal ADH secretion - antidiuretic response in kidneys + reduced renal blood flow - reduced foetal urine production
Prognosis of polyhydramnios
Increased risk of perinatal mortality (2- to 5- fold)
Many IDIOPATHIC cases resolve spontaneously
Complications related to polyhydramnios
Maternal respiratory compromise Preterm labour, PPROM, preterm delivery Foetal malposition Macrosomia Umbilical cord prolapse Placental abruption upon rupture of membranes Postpartum uterine atony - PPH
Definition of IUGR
A foetal weight below the 10th percentile for gestational age
- typically if following normal growth trajectory, normal Doppler of umbilical artery and normal amniotic fluid volume, likely to be constitutional SGA
Categories of IUGR
Symmetric: body and head growth reduced
- begins in EARLY gestation
- usually INTRINSIC factors (chromosomal, congenital)
Asymmetric (head-sparing): usually just reduced weight(AC) with normal length and head
- begins in late SECOND or THIRD trimesters
- Due to reductions in foetal nutrients - limited fat storage but enough to allow continued brain growth
Maternal causes of IUGR (9)
Severe starvation
Hypoxaemia
Haematologic/immunologic causing thrombosis
Medical or obstetric conditions associated with vasculopathy (PET, nephropathy, vascular disease)
TORCH, malaria
Substance abuse
Toxin exposure (warfarin, AEDs, folic acid antagonists)
High altitude
Demographic (rage, age, size, previous SGA)
Placental causes of IUGR (9)
Abnormal uteroplacental vasculature Chronic inflammatory lesions Abruption Thrombophilia related pathology Gross structural anomalies (single umbi art, velamentous insertion, haemangioma) Infarction Tumour Villous placentitis Confined placental mosaicism
Diagnosis of IUGR
Ultrasound showing estimated foetal weight OR abdominal circumference below 10th percentile for gestational age
In which pregnancies are SFH measurements unsuitable/inaccurate
Large fibroids
High maternal BMI
Intentional weight loss while pregnant (e.g. post-bariatric surgery)
Polyhydramnios/oligohydramnios
Foetal causes of IUGR (6)
Chromosomal anomalies
Genetic syndromes (E.g. Russel-Silver, dwarfism, Bloom)
Major congenital anomalies (congenital heart disease)
Multiple gestation
Metabolic disorders
Investigations to consider in IUGR
FTS for T21 Early USS - dating, NT Uterine artery Doppler (19-23 weeks) Later USS: EFW, AC, AFV, BPPP, umbilical art Doppler, placental/uterine/foetal abnormalities Amniocentesis if high risk TORCH screen
Definition of preeclampsia
A multisystem disorder characterised by the new onset of hypertension + proteinuria OR end-organ dysfunction after 20 weeks of gestation in a previously normotensive woman
HELLP syndrome
Haemolysis, Elevated Liver enzymes, Low Platelets
Gestational hypertension definition
hypertension without proteinuria or other signs of preeclampsia that develops after 20 weeks of gestation and resolves by 12 weeks postpartum
Potential complications of preeclampsia/eclampsia
Placental abruption Acute kidney injury Cerebral haemorrhage (STROKE) Hepatic failure or rupture Pulmonary oedema Disseminated intravascular coagulation
Risk factors predisposing to preeclampsia
Past history of PET
Nulliparity
Family history of preeclampsia in first degree relative
Twin pregnancy
Advanced maternal age (over 40)
Pre-existing: DM, HTN, ANTIPHOSPHOLIPID ANTIBODIES, overweight BMI
Women who smoke have a LOWER risk of preeclampsia than non-smokers
Clinical presentation of PET
After 20w GA (usually after 34)
- new development of HTN
- Proteinuria
- persistent/severe headache (non-responsive to OTC analgesia)
- Visual abnormalities
- sudden and rapid weight gain
- oedema of hands and face
- upper abdo/epigastric pain
- nausea, vomiting
- dyspnoea, retrosternal chest pain
- altered mental status
Pre-eclampsia prior to 20 weeks gestation is usually associated with what type of pregnancy
complete or partial molar pregnancy
Criteria for diagnosis of PET
Systolic BP higher than 140 OR DBP higher than 90
AND
- proteinuria 0.3g in 24h OR ACR 0.3
OR
- signs of end-organ dysfunciton (thrombocytopaenia, raised creatinine, raised transaminases)
Mechanism of thrombocytopaenia in PET
microangiopathic endothelial injury and activation - platelet and fibrin thrombi - accelerated platelet consumption
Incidence of women with PET who develop eclampsia
2%
Management of PET
Severe disease: indicates delivery
When to initiate delivery is based on GA, severity of disease, and maternal and foetal condition
- 37GA+ are delivered
- Serious maternal end-organ dysfunciton or indeterminate tests of foetal health may indicate delivery at any age
- if mother and foetus are stable, close monitoring with conservative approach
Definition of a heterotopic pregnancy
An ectopic pregnancy plus an intrauterine pregnancy concomitantly
Name for a pregnancy with both ectopic and intrauterine pregnancies
Heterotopic pregnancy
Incidence of ectopic pregnancy
2%
Subsequent risk:
after 1: 10-15% chance of another
after 2: 25-65% chance of another
Risk factors for ectopic pregnancy
Previous ectopic PID Tubal surgery (e.g. sterilisation or reversal) IVF Smoking Age 35+ Multiple sexual partners
IUCD (50% risk of ectopy if becomes pregnancy as prevents normal plantation in endometrial cavity but not from occuring in tubes)
Incidence of heterotopic pregnancy
Uncommon in general population (1/4000)
VERY common in IVF cycles - 1%
Most common sites for ectopic pregnancy
85% in ampulla (S-bend) portion of tube
5% in other areas of tube
Uncommon locations:
- ovary
- tubal interstitium (cornual pregnancy)
- cervical
- LSCS scar
- Abdominal
Presentation of ectopic pregnancy
Amenorrhoea
Pain (RIF or shoulder-tip secondary to intra-abdominal haemorrhage)
+/- PV bleeding (usually light spotting)
+ve pregnancy test
Tachycardia and hypotension if perforated
Confirmation of ectopic pregnancy
Serial b-hCG rising at slower rate than normal (less than doubling every 2-3 days)
Correlation of single hCG with USS
- ?obvious gestational sac and embryo in extrauterine site
- inability to identify gestational sac and embryo in uterus
Management of ectopic pregnancy
GOLD STANDARD: surgery Laparoscopic slapingectomy (removal of fallopian tube)
Salpingotomy - removal of pregnancy without removal of rest of tube - no increased fertility afterwards compared to salpingectomy
Follow up to ensure pregnancy not persistent
Medical:
- Prostaglandin or hypertonic saline direct tubal injection
- MTX by IM injection
- may be better option if multiple adhesions in abdo (e.g. Crohn’s disease, multiple past laparotomies)
Expectant management if appears to have miscarried?
Definition of antepartum haemorrhage
Vaginal bleeding associated with intrauterine pregnancy from 24 weeks gestation until the onset of labour
Risk factors of antepartum haemorrhage
Domestic violence Previous C-section Male gender of foetus Previous placenta praevia or abruption Cocaine Smoking in pregnancy
Potential causes for antepartum haemorrhage
Vulva/vaginal trauma, inflammation
Cervix: (may be provoked by sex) ectropion, carcinoma, effacement in labour
Placental (praevia, abruption, vasa praevia)
Uterine rupture
Unexplained (most common)
Most common causes for antepartum haemorrhage
Placental abruption (30%) Placenta praevia (20%) Labour
Uterine rupture, vasa praevia are rare causes
Definition of placenta praevia
Defined as a placenta encroaching on the lower segment, with the lower segment arbitratily defined on ultrasound as extending 5cm from the internal os
Prevalence of placenta praevia
0.35-0.5%
Complications of placenta praevia
Antepartum haemorrhage Intrapartum haemorrhage Postpartum haemorrhage Need of transfusion Maternal mortality Neonatal mortality Recurrence Increased risk of other pregnancy complications (malpresentation, placenta accreta, preterm labour and PROM, IUGR, vasa praevia and velementous insertion)
Risk factors for placenta praevia
Previous placenta praevia Older maternal age Previous C-section Multiple gestation Multiparity Infertility treatment Previous abortion Previous intrauterine surgery Maternal smoking, cocaine Male foetus Non-white race
Grading of placenta praevia
I: encroaches on lower segment - MINOR
II: reaches margin of internal os - MINOR
III: partially covers internal os - MAJOR
IV: Completely covers internal os - MAJOR
Presentation of placenta praevia (not diagnosed on antenatal scans)
Painless vaginal bleeding after 20 weeks gestation (60% after 30 weeks)
+/- uterine contractions
Management of placenta praevia discovered at morphology scan
Follow up transvaginal USS at 32 weeks,
If placental edge still less than 2cm from internal os, follow-up at 36 weeks
Reducing risk of bleeding in woman with known placenta praevia
Avoid vaginal intercourse after 20 weeks gestation
Reduce overall physical activity in third trimester
Seek immediate attentino if contractions or bleeding occur
Management of asymptomatic woman with confirmed placenta praevia in late pregnancy
Elective delivery at 38-39 weeks
Management of acutely bleeding placenta praevia
Achieve/maintain haemodynamic stability in mother
Determine if C-section indicated
- non-reassuring FHR
- life-threatening refractory haemorrhage
- significant vaginal bleeding after 24 weeks
Indications for c-section delivery in woman with low-lying placenta
Placenta less than 20mm from internal os
Definition of placental abruption
Bleeding at the decidual-placental interface that causes partial or total placental detachment prior to the delivery of the foetus after 20 weeks gestation
Incidence of placental abruption
less than 1% of pregnancies
Common gestation at which placental abruption occurs
40-60% before 37 weeks
15% before 32 weeks
Risk factors for placental abruption
Severe maternal trauma Uterine abnormalities Cocaine and cigarettes Polyhydramnios (occurs at SROM) HTN, PET or eclampsia PROM Chorioamnionitis Previous PET IUGR or abruption Advanced maternal age Multiparity Male sex
Presentation of acute placental abruption
Acute onset vaginal bleeding + abdominal/back pain + contractions
Contractions typically high frequency, low amplitude
Couvelaire uterus (firm, rigid and tender uterus during and between contractions)
Presentation of concealed placental abruption
Preterm labour with no or scant bleeding
10-20% of women with abruption
Investigations in placental abruption
USS - only sensitive in 25-50%
CBE, biochem, renal function
Blood type and crossmatch
Coagulation studies
Fibrinogen (best correlation with severity of bleeding - initial levels less than 200mg/dL predict severe PPH)
D-dimer, fibrin degradation products (evidence of acute DIC)
Kleihauer-Betke test (foetal bleeding)
Complications of placental abruption
PPH
Excessive blood loss and DIC (end organ failure, hypovolaemic shock, peripartum hysterectomy, need for blood transfusion)
Emergency C-section
Recurrence
Perinatal morbidity and mortality (hypoxaemia, asphyxia, low birth weight, preterm)
IUGR (with chronic abruption)
Management of abruption
ABCs, stabilise mother
Indications for delivery:
- severe abruption at any gestational age OR
- non-severe abruption at less than 36 weeks
Vaginal if mother stable and FHR reassuring
Emergency C-section if:
- mother unstable or FHR non-reassuring and vaginal delivery not imminent
- vaginal delivery contraindicated (e.g. malpresentation)
- failure to progress with vaginal delivery
Non-severe less than 36 weeks: close monitoring or deliver if risk of developing sudden severe abruption
Delivery of further pregnancies before 37 weeks
Antihypertensives used in pre-eclampsia
Labetalol
Methyldopa
Nifedipine (FAST-ACTING - often not available in rural sites)
Role of antihypertensives in pre-eclampsia
Reduces maternal end organ failure and stroke
No reduction in risk of eclampsia progression
No change in outcomes for foetus
