Pregnancy Complications Flashcards
Spontaneous Miscarriage: definition
TERMINATION/LOSS of PREGNANCY BEFORE 24 WEEKS GESTATION
Spontaneous Miscarriage: classification
Threatened = BLEEDING from GRAVID UTERUS BEFORE 24 WEEKS GESTATION + VIABLE FOETUS + NO EVIDENCE of CERVICAL DILATION
Inevitable = CERVIX BEGUN to DILATE
Incomplete = PARTIAL EXPULSION of PRODUCTS of CONCEPTION
Complete = COMPLETE EXPULSION of POC
Septic = following incomplete miscarriage - RISK of ASCENDING INFECTION INTO UTERUS, can spread throughout pelvis
Missed = FOETUS DIES, UTERUS MAKES NO ATTEMPT to EXPEL POC
Spontaneous Miscarriage: aetiology
- ABNORMAL CONCEPTUS = CHROMOSOMAL, GENETIC, STRUCTURAL
- UTERINE ABNORMALITY = CONGENITAL, FIBROIDS
- CERVICAL INCOMPETENCE = PRIMARY, SECONDARY (i.e. following cervical trauma - dilation of cervix, cone biopsy rx, surgery, tears during vaginal delivery - doesn’t heal v. well)○ Cervix opens prematurely w/ absent/minimal uterine activity & pregnancy expelled
- MATERNAL = INCREASING AGE, DIABETES, THYROID DISEASE, SLE, ACUTE MATERNAL ILLNESS
- UNKNOWN
Ectopic Pregnancy: management
- CONSERVATIVE + BLOOD/FLUID (blood loss)
- MEDICAL = METHOTREXATE (when giving methotrexate - measure βHCG lvls to ensure it’s falling; also monitor closely in case it bursts)
- SURGICAL = SALPINGECTOMY, SALPINGOTOMY for few indications○ Mostly by LAPAROSCOPY
○ e.g. for when V. SORE, WORRIED IT MAY RUPTURE
○ OVARY LEFT BEHIND - otherwise early menopause
Ectopic Pregnancy: investigations/diagnosis
- USS = NO INTRAUTERINE GESTATION SAC, may see ADNEXAL MASS, FLUID in POUCH of DOUGLAS
- FBC (blood loss) + CROSS-MATCH & TYPE
- SERUM βHCG lvls = may need to SERIALLY TRACK LVLS OVER 48HR INTERVALS - NORMAL EARLY INTRAUTERINE PREGNANCY βHCG lvls will INCREASE by ≥ 66%○ Looking for SUBOPTIMAL INCREASE
Looking for SUBOPTIMAL INCREASE
Ectopic Pregnancy: definition
PREGNANCY IMPLANTED OUTW/ UTERINE CAVITY e.g. fallopian tube, cervix, peritoneum
Ectopic Pregnancy: risk factors
- ENDOMETRIOSIS
- PELVIC INFLAMMATORY DISEASE e.g. chlamydia, gonorrhoea
- PREVIOUS TUBAL SURGERY (or instrumentation)
- PREVIOUS ECTOPIC
- ASSISTED CONCEPTION
- COPPER IUD
Ectopic Pregnancy: presentation
- PERIOD of AMENORRHOEA (w/ +VE PREGNANCY TEST) - may say they’ve had a missed period
- ± VAGINAL BLEEDING/DISCOMFORT
- ± ABDOMINAL PAIN
- ± GI/URINARY SYMPTOMS - ECTOPIC can PRESS ON BLADDER/BOWEL
Antepartum Haemorrhage: definition
HAEMORRHAGE from GENITAL TRACT > 24 WEEK GESTATION + < DELIVERY of BABY
Antepartum Haemorrhage: aetiology
Placenta praevia: PLACENTA ATTACHED to LOWER SEGMENT of UTERUS
Placental abruption: PLACENTA STARTING to SEPARATE from UTERINE WALL BEFORE BIRTH of BABY
• Ass. w/ RETROPLACENTAL CLOT
APH of unknown origin: incl. HAEMORRHAGE where OTHER CAUSES COMPLETELY EXCLUDED
Local lesions of genital tract: incl. those from CERVIX & VAGINA e.g.
* CERVICAL EROSIONS & POLYPS * Occasionally CERVICAL CANCER * TRICHOMONAS/THRUSH INFECTION W/I VAGINA can occasionally cause BLOOD-STAINED DISCHARGE
Vasa praevia - rare but serious: usually SMALL BLOOD LOSS due to RUPTURE of FOETAL VESSEL W/I FOETAL MEMBRANES
• FOETAL BLOOD LOSS - NOT MATERNAL BLOOD LOSS = EFFECT ON FOETUS can be CATASTROPHIC
Placenta Praevia: presentation
Symptoms:
• PAINLESS PV BLEEDING = AMOUNT of BLOOD LOSS CORRELATES to CLINICAL PICTURE (e.g. when measuring pulse, BP)
○ Bleeding due to placental separation as lower uterine segment forms + cervix effaces (cervical thinning) ○ Blood loss occurs from venous sinuses in lower segment ○ VARIABLE AMOUNT of BLOOD LOSS = MINOR - LIFE-THREATENING
- FOETAL MALPRESENTATION e.g. on USS
- INCIDENTAL FINDING e.g. on USS
Signs:
- MATERNAL CONDITION CORRELATES w/ AMOUNT of PV BLEEDING
- SOFT, NON-TENDER UTERUS ± FOETAL MALPRESENTATION
Placenta Praevia: investigations/diagnosis
- NO VAGINAL EXAMINATION - can trigger even bigger bleed
- USS = LOCATE PLACENTAL SITE - more accurate for anterior placenta praevias
- MRI = more accurate as can identify internal cervical os, not widely available - use if USS inconclusive
Placenta Praevia: definition
ALL/PART of PLACENTA IMPLANTS IN LOWER UTERINE SEGMENT
Placenta Praevia: prognosis
PPH RISK - uterus cannot contract ~ lower segment
Placenta Praevia: risk factors
- MULTIPAROUS WOMEN
- MULTIPLE PREGNANCIES - increased placental mass
- PREVIOUS CAESARIAN SECTION - scars over that area
Placenta Praevia: classification
Grade 1 = placenta encroaches on lower segments but not internal cervical os
Grade 2 = placenta reaches internal cervical os
Grade 3 = placenta eccentrically covers os
Grade 4 = central placenta praevia
Placental Abruption: presentation
Symptoms:
- PAIN - SEVERE + ABDOMINAL
- VAGINAL BLEEDING - may be MINIMAL, VARYING AMOUNTS from small to severe
- INCREASED UTERINE ACTIVITY
Signs:
- LONGITUDINAL FOETAL LIE w/ PRESENTING PART FIXED IN PELVIS
- INCREASED UTERINE TONE + poss. UTERINE CONTRACTIONS
- WHEN PALPATING = PAINFUL + V. IRRITABLE
Placental Abruption: investigations/diagnosis
• CLINICAL DIAGNOSIS + CARDIOTOCOGRAPHY for FOETAL DISTRESS
Placental Abruption: management
- DEPENDS on AMOUNT of BLEEDING, GENERAL CONDITION of MOTHER & BABY, GESTATION
- VARIES = EXPECTANT TREATMENT - ATTEMPTING VAGINAL DELIVERY - IMMEDIATE CAESARIAN SECTION○ SMALL = CAN STOP
○ CLOSE to TERM = DELIVER
○ PRE-TERM = WAIT if poss.
○ TOCOLYSIS = SLOWS DOWN LABOUR SHORT-TERM, not for long-term use, allows for steroids to be given
○ STEROIDS = STIMULATES FOETAL LUNG DEVELOPMENT (2 DOSES IM)
- VARIES = EXPECTANT TREATMENT - ATTEMPTING VAGINAL DELIVERY - IMMEDIATE CAESARIAN SECTION○ SMALL = CAN STOP
Placental Abruption: definition
HAEMORRHAGE resulting from PREMATURE PLACENTA SEPARATION BEFORE BIRTH of BABY
Placental Abruption: risk factors
- PRE-ECLAMPSIA/CHRONIC HYPERTENSION
- MULTIPLE PREGNANCY
- POLYHYDRAMNIOS
- SMOKING, INCREASING AGE, PARITY
- PREVIOUS ABRUPTION
- TRAUMA DURING PREGNANCY
- COCAINE - vasoconstrictor
Placental Abruption: classification
Revealed = MAJOR HAEMORRHAGE APPARENT EXTERNALLY as BLEED ESCAPES THROUGH CERVICAL OS
Concealed = HAEMORRHAGE occurs BWTN PLACENTA & UTERINE WALL
* UTERINE CONTENTS INCREASE IN VOL. + FUNDAL HEIGHT LARGER than what would be consistent for gestation * Sometimes = BLOOD PENETRATES UTERINE WALL + UTERUS APPEARS BRUISED - COUVELAIRE/BLUE UTERUS, UTERUS DOESN’T CONTRACT WELL
Mixed = CONCEALED + REVEALED HAEMORRHAGE - vaginal bleeding + retroplacental clot both present
Pre-term Labour: definition
ONSET of LABOUR < 37 COMPLETED WEEKS GESTATION (259 DAYS)
* 32 - 36 WEEKS = MILDLY PRE-TERM * 28 - 32 WEEKS = V. PRE-TERM * 24 - 28 WEEKS = EXTREMELY PRE-TERM
Pre-term Labour: neonatal complications
- RESPIRATORY DISTRESS SYNDROME
- INTRAVENTRICULAR HAEMORRHAGE
- CEREBRAL PALSY
- NUTRITION
- TEMP. CONTROL
- JAUNDICE
- INFECTIONS
- VISUAL IMPAIRMENT
- HEARING LOSS
Pre-term Labour: aetiology
• SPONTANEOUS/INDUCED (IATROGENIC)
Pre-term Labour: risk factors
- MULTIPLE PREGNANCY
- POLYHYDRAMNIOS
- APH
- PLACENTAL ABRUPTION
- PRE-ECLAMPSIA
- INFECTION e.g. UTI
- PRE-LABOUR PREMATURE RUPTURE of MEMBRANES
MAJORITY = IDIOPATHIC
Pre-term Labour: management
- DIAGNOSIS = CONTRACTIONS w/ EVIDENCE of CERVICAL CHANGE on VAGINAL EXAMINATION
- CONSIDER POSS. CAUSE = ABRUPTION, INFECTION
< 24 - 26 weeks - v. poor prognosis, decisions made in discussion w/ parents + neonatologists (if out of specialised neonatal unit - not poss.)
cases considered viable - TOCOLYSIS (for steroids, transfer to NICU facility), aim for vaginal delivery
Hypertensive Disorders: types
Chronic HTN: at booking/before 20weeks gestation
- MILD HTN = 140 - 149 / 90 - 99
- MODERATE HTN = 150 - 159 / 100 - 109
- SEVERE HTN = ≥ 160 / ≥ 110
Gestational HTN:
• same as above but appears after 20weeks gestation
Pre-eclampsia:
- NEW HYPERTENSION > 20 WEEKS + SIGNIFICANT PROTEINURIA
- AUTOMATED REAGENT STRIP URINE PROTEIN ESTIMATE > 1+
- SPOT URINARY PROTEIN : CREATININE RATIO > 30 mg/mmol
- 24HRS URINE PROTEIN COLLECTION > 300 mg/day
Essential/Chronic HTN: management
• Ideally CARE OPTIMISED PRE-PREGNANCY
○ CHANGE ANTI-HYPERTENSIVE DRUGS if INDICATED e.g. § ACEI (Ramipril/Enalapril cause birth defects, impaired growth, renal defects) § ARB (Losartan, Candesartan) § ANTI-DIURETICS - stop diuretics as they interfere w/ plasma vol. § LOWER DIETARY SODIUM • AIM TO KEEP BP < 150/100 = LABETOLOL, NIFEDIPINE, METHYLDOPA * MONITOR for SUPERIMPOSED PRE-ECLAMPSIA * MONITOR FOETAL GROWTH - growth can be restricted * HIGHER INCIDENCE of PLACENTAL ABRUPTION
Pre-eclampsia: complications
Maternal:
• ECLAMPSIA = SEIZURES (only if poorly controlled pre-eclampsia; postpartum > antepartum > intrapartum)
• SEVERE HT = CEREBRAL HAEMORRHAGE, STROKE
• HELLP (HAEMOLYSIS, ELEVATED LIVER ENZYMES, LOW PLATELETS)
• DIC (DISSEMINATED INTRAVASCULAR COAGULATION) - uses all coagulation factors & platelets - risk of BLEEDING
• CVD
• RENAL FAILURE
• PULMONARY OEDEMA, CARDIAC FAILURE - less fluid in intravascular space as fluid is distributed elsewhere - in the extravascular 3rd space, causing pulmonary oedema, puffy hands & feet
Foetal:
• IMPAIRED PLACENTAL PERFUSION = IUGR, FOETAL DISTRESS, PREMATURITY, INCREASE POST-NATAL MORTALITY
Pre-eclampsia: management
- ONLY CURE = DELIVERY of BABY & PLACENTA (if severe - may have to deliver pre-term)
- Consider INDUCTION of LABOUR (stable woman)/C-SECTION (unstable woman) if MATERNAL or FOETAL CONDITION DETERIORATES - IRRESPECTIVE of GESTATION
- PET RISKS may CONTINUE INTO PUERPERIUM - CONTINUE MONITORING POST-DELIVERY (risk of seizures persists a little after birth)
Conservative: for foetal maturity
• CLOSE OBSERVATION of CLINICAL SIGNS + INVESTIGATIONS
- ANTI-HYPERTENSIVES - LABETOLOL, METHYLDOPA, NIFEDIPINE
- STEROIDS for FOETAL LUNG MATURITY if GESTATION < 36 WEEKS
Seizures/impending seizures:
• MAGNESIUM SULPHATE BOLUS + IV INFUSION
- BP CONTROL - IV LABETOLOL, HYDRALAZINE (if > 160/110)
- AVOID FLUID OVERLOAD - aim for 80 mL/hr fluid intake; can go into cardiac failure
PET prophylaxis:
• LOW DOSE ASPIRIN from 12 WEEKS - DELIVERY
• HIGHER RISK of HTN in LATER LIFE
Pre-eclampsia: pathophysiology
- IMMUNOLOGICAL
- GENETIC PREDISPOSITION○ 2ndary invasion of maternal spiral arterioles by trophoblasts impaired - REDUCED PLACENTAL PERFUSION
○ Imbalance bwtn vasodilators & vasoconstrictors in pregnancy (prostocyclin/thromboxane)
- GENETIC PREDISPOSITION○ 2ndary invasion of maternal spiral arterioles by trophoblasts impaired - REDUCED PLACENTAL PERFUSION
Pre-eclampsia: risk factors
- 1ST PREGNANCY
- EXTREMES of MATERNAL AGE
- PRE-ECLAMPSIA in PREVIOUS PREGNANCY - esp. if severe PET, delivery < 34weeks, IUGR baby, IUD, abruption
- PREGNANCY INTERVAL > 10YRS - body treats next pregnancy as if it’s the first baby
- BMI > 35
- FHx of PET
- MULTIPLE PREGNANCY
- UNDERLYING MATERNAL DISORDERS○ CHRONIC HT
○ PRE-EXISTING RENAL DISEASE, PRE-EXISTING DM
○ AUTOIMMUNE DISORDERS e.g. antiphospholipid antibodies, SLE
Pre-eclampsia: definition
- MILD HT on 2 OCCASIONS > 4HRS APART/MODERATE - SEVERE HT
- PROTEINURIA > 300mgms/24hrs (protein urine > +; protein creatinine ratio > 30 mgms/mmol)
MULTI-SYSTEM MULTI-ORGAN DISORDER = RENAL, LIVER, VASCULAR, CEREBRAL, PULMONARY
Pre-eclampsia: presentation of severe PET
Presentation:
HEADACHE, BLURRED VISION, EPIGASTRIC PAIN, PAIN BELOW RIBS, VOMITING, SUDDEN SWELLING of HANDS, FACE, LEGS
Biochemical abnormalities:
RAISED LIVER ENZYMES, BILIRUBIN if HELLP present
RAISED U+E, RAISED URATE
Haematological abnormalities:
LOW PLATELETS
LOW Hb, SIGNS of HAEMOLYSIS
DIC FEATURES
Pre-existing DM: effects on mother, foetus, neonate
Foetus:
• FOETAL CONGENITAL ABNORMALITIES e.g. CARDIAC ABNORMALITIES, SACRAL AGENESIS; esp. if high blood sugars at peri-conception
- MISCARRIAGE
- FOETAL MACROSOMIA, POLYHYDRAMNIOS
- OPERATIVE DELIVERY, SHOULDER DYSTOCIA - risk of Erb’s palsy
- STILLBIRTH, INCREASED PERINATAL MORTALITY
Mother:
• PRE-ECLAMPSIA
• WORSENING of MATERNAL NEPHROPATHY, RETINOPATHY, HYPOGLYCAEMIA, REDUCED AWARENESS of HYPOGLYCAEMIA - monitor eyes + kidney function
• INFECTIONS
Neonate:
• IMPAIRED LUNG MATURITY
• NEONATAL HYPOGLYCAEMIA
• JAUNDICE
Pre-existing DM: pathophysiology
INSULIN REQ. of MOTHER INCREASE = PLACENTAL HORMONES have an ANTI-INSULIN EFFECT so pt. needs more insulin
FOETAL HYPER-INSULINAEMIA OCCURS = increased maternal glucose crosses placenta + induces increased insulin production - foetal hyperinsulinaemia causes MACROSOMIA
• Post-delivery = baby no longer exposed to hyperglycaemic environment, but still produces too much insulin - increased risk of neonatal hypoglycaemic + respiratory distress - needs to be watched carefully
Pre-existing DM: effects on mother, foetus, neonate
Foetus:
• FOETAL CONGENITAL ABNORMALITIES e.g. CARDIAC ABNORMALITIES, SACRAL AGENESIS; esp. if high blood sugars at peri-conception
- MISCARRIAGE
- FOETAL MACROSOMIA, POLYHYDRAMNIOS
- OPERATIVE DELIVERY, SHOULDER DYSTOCIA - risk of Erb’s palsy
- STILLBIRTH, INCREASED PERINATAL MORTALITY
Mother:
• PRE-ECLAMPSIA
• WORSENING of MATERNAL NEPHROPATHY, RETINOPATHY, HYPOGLYCAEMIA, REDUCED AWARENESS of HYPOGLYCAEMIA - monitor eyes + kidney function
• INFECTIONS
Neonate:
• IMPAIRED LUNG MATURITY
• NEONATAL HYPOGLYCAEMIA
• JAUNDICE
Pre-existing DM: management
Pre-conception:
• BETTER GLYCAEMIC CONTROL - ideally BG ~ 4 - 7 mmol/L pre-conception + HbA1c < 6.5% (< 48 mmol/mol)
- FOLIC ACID (5mg - high dose)
- DIETARY ADVICE
- RETINAL + RENAL ASSESSMENT
During pregnancy:
• OPTIMISE GLUCOSE CONTROL - INSULIN REQ/ INCREASE
- Can CONTINUE ORAL ANTI-DIABETIC AGENTS (METFORMIN), may need to CHANGE to INSULIN for TIGHTER GLUCOSE CONTROL
- Make aware of HYPOGLYCAEMIA RISK - provide GLUCAGON INJECTIONS/CONC. GLUCOSE SOLN.
- HYPOGLYCAEMIA AWARNESS GOES AWAY - EDUCATION, SWEETS, GLUCAGON etc.
- Watch for KETONURIA/INFECTIONS - aggressively treat infection as can enter DKA v. quickly
- REPEAT RETINAL ASSESSMENTS - 28 + 34 WEEKS
- Watch FOETAL GROWTH
- OBSERVE for PET
Pre-existing DM: management
Pre-conception:
• BETTER GLYCAEMIC CONTROL - ideally BG ~ 4 - 7 mmol/L pre-conception + HbA1c < 6.5% (< 48 mmol/mol)
- FOLIC ACID (5mg - high dose)
- DIETARY ADVICE
- RETINAL + RENAL ASSESSMENT
During pregnancy:
• OPTIMISE GLUCOSE CONTROL - INSULIN REQ/ INCREASE
- Can CONTINUE ORAL ANTI-DIABETIC AGENTS (METFORMIN), may need to CHANGE to INSULIN for TIGHTER GLUCOSE CONTROL
- Make aware of HYPOGLYCAEMIA RISK - provide GLUCAGON INJECTIONS/CONC. GLUCOSE SOLN.
- HYPOGLYCAEMIA AWARNESS GOES AWAY - EDUCATION, SWEETS, GLUCAGON etc.
- Watch for KETONURIA/INFECTIONS - aggressively treat infection as can enter DKA v. quickly
- REPEAT RETINAL ASSESSMENTS - 28 + 34 WEEKS
- Watch FOETAL GROWTH
- OBSERVE for PET
Labour:
• LABOUR usually INDUCED 38 - 40 WEEKS, EARLIER if FOETAL/MATERNAL CONCERNS
- ELECTIVE C-SECTION if SIGNIFICANT FOETAL MACROSOMIA
- MAINTAIN BG in LABOUR w/ INSULIN-DEXTROSE INFUSION
- CONTINUOUS CTG FOETAL MONITORING in labour
- EARLY FEEDING of BABY - reduce neonatal hypoglycaemia
- RETURN to PRE-PREGNANCY REGIMEN of INSULIN POST-DELIVERY
Gestational DM: risk factors
- INCREASED BMI > 30
- PREVIOUS MACROSOMIC BABY > 4.5hg
- PREVIOUS GDM
- FHx of DIABETES
- WOMEN of HIGH RISK GROUPS for developing diabetes e.g. Asian origin
- POLYHYDRAMNIOS/BIG BABY in CURRENT PREGNANCY
- RECURRENT GLYCOSURIA in CURRENT PREGNANCY
Gestational DM: screening
• If risk factors present - offer HbA1c ESTIMATION at BOOKING
○ If > 6% (43 mmol/mol) = 75g OGTT done ○ If OGTT NORMAL = REPEAT OGTT at 24 - 28 weeks e.g. significant risk factor/s
Can also offer OGTT ~ 16 WEEKS + REPEAT at 28 WEEKS if SIGNIFICANT RISK FACTORS e.g. present GDM
Gestational DM: management
- CONTROL BG - DIET, METFORMIN/INSULIN if sugars remain high
- POST-DELIVERY - check OGTT 6 - 8 WEEKS POST-NATAL (should revert back to normal)
- YEARLY HbA1c CHECK/BLOOD SUGARS due to high risk of developing overt DM
VTE: risks increased during pregnancy because
HYPERCOAGULABLE STATE - protects mother against bleeding post-delivery
INCREASED STASIS - progesterone causes vasodilation, expanding uterus exerts pressure on vessels
VASCULAR DAMAGE at DELIVERY/C-SECTION
VTE: risk factors
- OLDER MOTHER, INCREASING PARITY
- INCREASED BMI, SMOKERS
- PWID
- PET
- DEHYDRATION - HYPEREMESIS
- DECREASED MOBILITY e.g. due to pelvic girdle pain
- INFECTIONS
- OPERATIVE DELIVERY, PROLOGED LABOUR
- HAEMORRHAGE, BLOOD LOSS > 2L
- PREVIOUS VTE - unexplained by other pre-disposing factors e.g. #, injury; those w/ THROMBOPHILIA (protein C, protein S, anti-thrombin III deficiencies), STRONG FHx of VTE
- SICKLE CELL DISEASE
VTE: management
Prophylaxis:
- TED STOCKINGS
- ADVICE regarding INCREASED MOBILITY, HYDRATION
- PROPHYLACTIC ANTI-COAGULATION w/ ≥ 3 RISK FACTORS
- May be 1 risk factor if significant
- May need to continue 6 weeks post-partum
Confirmed VTE: ANTI-COAGULATION
VTE: presentation
DVT = calf pain, increased girth of affected leg/unilateral leg swelling, calf muscle tenderness
PE = SOB, pain on breathing, cough, tachycardia, hypoxia, pleural rub
VTE: investigations/diagnosis
- ECG
- BLOOD GASES
- DOPPLER
- V/Q LUNG SCAN
