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Reproductive System > Pregnancy Complications > Flashcards

Pregnancy Complications Flashcards

1
Q

Spontaneous Miscarriage: definition

A

TERMINATION/LOSS of PREGNANCY BEFORE 24 WEEKS GESTATION

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2
Q

Spontaneous Miscarriage: classification

A

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

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3
Q

Spontaneous Miscarriage: aetiology

A
  • 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
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4
Q

Ectopic Pregnancy: management

A
  • 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
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5
Q

Ectopic Pregnancy: investigations/diagnosis

A
  • 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
    • SERUM PROGESTERONE lvls = w/ VIABLE IU PREGNANCY - HIGH LVLS > 25ng/mL (or > 50?)

Looking for SUBOPTIMAL INCREASE

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6
Q

Ectopic Pregnancy: definition

A

PREGNANCY IMPLANTED OUTW/ UTERINE CAVITY e.g. fallopian tube, cervix, peritoneum

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7
Q

Ectopic Pregnancy: risk factors

A
  • ENDOMETRIOSIS
    • PELVIC INFLAMMATORY DISEASE e.g. chlamydia, gonorrhoea
    • PREVIOUS TUBAL SURGERY (or instrumentation)
    • PREVIOUS ECTOPIC
    • ASSISTED CONCEPTION
    • COPPER IUD
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8
Q

Ectopic Pregnancy: presentation

A
  • 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
    • PYREXIA (SEPTIC)
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9
Q

Antepartum Haemorrhage: definition

A

HAEMORRHAGE from GENITAL TRACT > 24 WEEK GESTATION + < DELIVERY of BABY

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10
Q

Antepartum Haemorrhage: aetiology

A

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 &amp; 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
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11
Q

Placenta Praevia: presentation

A

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
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12
Q

Placenta Praevia: investigations/diagnosis

A
  • 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
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13
Q

Placenta Praevia: definition

A

ALL/PART of PLACENTA IMPLANTS IN LOWER UTERINE SEGMENT

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14
Q

Placenta Praevia: prognosis

A

PPH RISK - uterus cannot contract ~ lower segment

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15
Q

Placenta Praevia: risk factors

A
  • MULTIPAROUS WOMEN
    • MULTIPLE PREGNANCIES - increased placental mass
    • PREVIOUS CAESARIAN SECTION - scars over that area
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16
Q

Placenta Praevia: classification

A

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

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17
Q

Placental Abruption: presentation

A

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
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18
Q

Placental Abruption: investigations/diagnosis

A

• CLINICAL DIAGNOSIS + CARDIOTOCOGRAPHY for FOETAL DISTRESS

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19
Q

Placental Abruption: management

A
  • 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)
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20
Q

Placental Abruption: definition

A

HAEMORRHAGE resulting from PREMATURE PLACENTA SEPARATION BEFORE BIRTH of BABY

21
Q

Placental Abruption: risk factors

A
  • PRE-ECLAMPSIA/CHRONIC HYPERTENSION
    • MULTIPLE PREGNANCY
    • POLYHYDRAMNIOS
    • SMOKING, INCREASING AGE, PARITY
    • PREVIOUS ABRUPTION
    • TRAUMA DURING PREGNANCY
    • COCAINE - vasoconstrictor
22
Q

Placental Abruption: classification

A

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

23
Q

Pre-term Labour: definition

A

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
24
Q

Pre-term Labour: neonatal complications

A
  • RESPIRATORY DISTRESS SYNDROME
    • INTRAVENTRICULAR HAEMORRHAGE
    • CEREBRAL PALSY
    • NUTRITION
    • TEMP. CONTROL
    • JAUNDICE
    • INFECTIONS
    • VISUAL IMPAIRMENT
    • HEARING LOSS
25
Q

Pre-term Labour: aetiology

A

• SPONTANEOUS/INDUCED (IATROGENIC)

26
Q

Pre-term Labour: risk factors

A
  • MULTIPLE PREGNANCY
    • POLYHYDRAMNIOS
    • APH
    • PLACENTAL ABRUPTION
    • PRE-ECLAMPSIA
    • INFECTION e.g. UTI
    • PRE-LABOUR PREMATURE RUPTURE of MEMBRANES

MAJORITY = IDIOPATHIC

27
Q

Pre-term Labour: management

A
  • 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

28
Q

Hypertensive Disorders: types

A

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
29
Q

Essential/Chronic HTN: management

A

• 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
30
Q

Pre-eclampsia: complications

A

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

31
Q

Pre-eclampsia: management

A
  • 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

32
Q

Pre-eclampsia: pathophysiology

A
  • IMMUNOLOGICAL
    • GENETIC PREDISPOSITION○ 2ndary invasion of maternal spiral arterioles by trophoblasts impaired - REDUCED PLACENTAL PERFUSION
      ○ Imbalance bwtn vasodilators & vasoconstrictors in pregnancy (prostocyclin/thromboxane)
33
Q

Pre-eclampsia: risk factors

A
  • 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
34
Q

Pre-eclampsia: definition

A
  1. MILD HT on 2 OCCASIONS > 4HRS APART/MODERATE - SEVERE HT
    1. PROTEINURIA > 300mgms/24hrs (protein urine > +; protein creatinine ratio > 30 mgms/mmol)

MULTI-SYSTEM MULTI-ORGAN DISORDER = RENAL, LIVER, VASCULAR, CEREBRAL, PULMONARY

35
Q

Pre-eclampsia: presentation of severe PET

A

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

36
Q

Pre-existing DM: effects on mother, foetus, neonate

A

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

37
Q

Pre-existing DM: pathophysiology

A

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
38
Q

Pre-existing DM: effects on mother, foetus, neonate

A

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

39
Q

Pre-existing DM: management

A

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
40
Q

Pre-existing DM: management

A

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
41
Q

Gestational DM: risk factors

A
  • 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
42
Q

Gestational DM: screening

A

• 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

43
Q

Gestational DM: management

A
  • 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
44
Q

VTE: risks increased during pregnancy because

A

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

45
Q

VTE: risk factors

A
  • 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
46
Q

VTE: management

A

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

47
Q

VTE: presentation

A

DVT = calf pain, increased girth of affected leg/unilateral leg swelling, calf muscle tenderness

PE = SOB, pain on breathing, cough, tachycardia, hypoxia, pleural rub

48
Q

VTE: investigations/diagnosis

A
  • ECG
    • BLOOD GASES
    • DOPPLER
    • V/Q LUNG SCAN
    • CTPA

Reproductive System (16 decks)

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