Obstetrics Flashcards
In third trimester pregnancy what happens to;
Platelet count
Factor V, Vll, ‘X, X levels
Fibrinogen level
Protein S level
Platelet count: Decrease
Factors V, VII, IX, X level: Increase
Fibrinogen level: Increase
Protein S level: Decrease
diagnostic criteria for peri-partum cardiomyopathy
- Onset of heart failure in the last month of pregnancy or within 5 months post-partum
- Absence of an identifiable cause of heart failure
- Absence of recognizable heart disease prior to the last month of pregnancy
- LV systolic dysfunction demonstrated by classical echocardiographic criteria.
important risk factors for amniotic fluid embolism
- Precipitous or tumultuous labour.
- Advanced maternal age.
- Caesarean and instrumental delivery.
- Placenta previa and abruption.
- Grand multi-parity (≥5 live births or stillbirths),
- Cervical lacerations.
- Foetal distress.
- Eclampsia.
- Medical induction of labour.
- Polyhydramnios
Leading causes of sepsis in pregnancy
- Pyelonephritis
- Chorioamnionits
- Septic abortion
- Episiotomy infections
- Necrotising fasciitis
- Septic thrombophlebitis
- Aspiration pneumonia
Antibiotics contraindicated in pregnancy
- Tetracyclines
- Chloramphenicol
- Aminoglycosides
- Metronidazole
- Sulphonamides
- Trimethoprim
- Fluoroquinolones
- Some macrolides
- Nitrofurantoin
- Isoniazid
Causes of Acute Liver Failure in Pregnancy
unrelated to pregnancy
- drug overdose
- shock/haemorrhage
- Decompensation of pre-existing liver disease
Related to pregnancy -
- Intrahepatic cholestasis of pregnancy (icterus gravidarum)
- PET
- HELLP
- Acute fatty liver of pregnancy- abdominal pain, vomiting, hypoglycaemia, coagulopathy, Ix with liver USS, 18% maternal mortality
- acute hepatic rupture
Exacerbated by pregnancy -
- viral hepatitis
- Portal vein thrombosis
- hepatic vein thrombosis
- cholecystitis
Other causes of febrile jaundiced coma with thrombocytopenia
- TTP/HUS
- sepsis with DIC
Ix to preform to confirm HELLP
Blood film
Reticulocyte count
Unconjugated fraction of bilirubin
Haptoglobin
conditions specific to pregnancy which may result in right or left heart failure or both.
Peripartum cardiomyopathy Pulmonary thromboembolism Amniotic fluid embolism Preclampsia Tocolytic pulmonary oedema
Causes of sudden onset anaphlyaxis in labour in women with no cardioresp Hx
a) Venous thromboembolism with PE: (Signs of DVT, Rt. Heart failure, ECG, CTPA)
b) Amniotic fluid embolus: Hemodynamic collapse with seizures, DIC
c) Pulm oedema secondary to pre-eclampsia: HT, proteinuria
d) Tocolytic pulmonary oedema: Tocolytic administration, rapid improvement
e) Aspiration pneumonitis – classic features
f) Peripartum cardiomyopathy: cardiomegaly, S3
g) Air embolism: Hypotension, cardiac mill wheel murmur
h) Pneumomediastinum: occurs during delivery
i) anaplhyaxis
j) accidental Mg OD
K) high epidural
Acid base changes of pregnancy
pH increases to 7.40-7.47 PaCO2 decreases to 30 mmHg PaO2 increases to 105 mmHg HCO3- decreases to 20 mmol/L Maternal 2,3-DPG increases p50 remains the same because of alkalosis
Airway changes in pregnany
Bag-mask ventilation becomes more difficult:
- The nasal mucosa is engorged, which means there is greater resistance to flow
- The upper airway mucosa is oedematous
- There has been weight gain
Laryngoscopy becomes more difficult:
- Upper airway oedema
- Breast enlargement
- The Mallampatti grade changes during pregnancy, largely because of oedema of the pharynx, and due to weight gain. It gets even worse with labour.
Less time is available for intubation:
- Decreased FRC, less time to intubate
- Increased oxygen consumption, less time to intubate
Intubation is more risky
- Increased risk of aspiration, decreased stomach emptying
Circulatory changes in pregnancy
Cardiac output increases (from 5L/min to 7L/min)
Stroke volume increases (from 65ml to 80-90ml)
Heart rate increases (from 75 to 85-90)
Systemic vascular resistance decreases (down by as much as 40%) - in fact, the vascular system becomes fairly refractory to the effects of vasoconstrictors such as angiotensin and vasopressin
The IVC is compressed by the gravid uterus in the supine position, decreasing the preload
Blood pressure decreases (and is lowest in the second trimester)
Pulmonary vascular resistance decreases
Pulmonary artery wedge pressure remains unchanged
Blood volume is increased by 50%
CVP remains unchanged
Colloid oncotic pressure decreases
Oxygen consumption increases by 20% during pregnancy
Renal changes in pregnancy
Renal blood flow increases: the renal arteries are also affected by the fall in SVRI, and this is mediated by relaxin (which influences endothelial nitric oxide production).
GFR increases by as much as 85%
Urea and creatinine decrease because of this
Kidneys become enlarged; the renal pelvis dilates and there is a “physiological hydronephrosis” - more so on the right because the right ureter crosses iliac and ovarian vessels at an angle. This predisposes to pyelonephritis
Tubular resorption of urate and glucose decreases
Respiratory changes in pregnancy
The diaphragm is pushed up by 4cm
Tidal volume increases by ~ 30-50%
Respiratory rate increases to 15-17
Minute volume increases by 20-50%.
Chest wall compliance decreases
Lung compliance remains the same
FRC decreases during pregnancy, due to compression of the diaphragm by the gravid uterus.
pH increases to 7.40-7.47
PaCO2 decreases to 30 mmHg
PaO2 increases to 105 mmHg
HCO3- decreases to 20 mmol/L
Maternal 2,3-DPG increases
p50 remains the same because of alkalosis
Electrolyte and endocrine changes in pregnancy
Vasopressin release increases;
- Thus, there is water retention
- A hypervolemic hypoosmolar state develops
In response to a decreased SVR, aldosterone release is increased. This is the major contributor to the 50% circulating volume expansion
There is a relative iodine deficiency (the foetus is stealing it all)
Cortisol secretion is increased, which has implications for all those people who still do random cortisol levels on their patients
