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Question 4 - 2000, Paper 1

A 36 week pregnant woman is involved in a car crash and suffers fractures to her left femur and tibia and left ribs 4-8. What are the cardiorespiratory changes in normal pregnancy? 
How do they effect her response to these injuries?

College Answer

This question had two  parts. Lists would suffice. For example: (a) Cardiorespiratory changes include:
•  Increased blood, plasma and Rd cell volume from 6 weeks. maximal at 28 to 32 weeks 
•   Increased cardiac output (33% by 10 weeks.to 40-50'/o by 28 to 32 weeks) 
•   Decreased blood pressure due to low SVR 
•   Susceptibility to aorto-caval compression develops during second trimester (maximal at 36- 
38 weeks) 
•  Cardiac hypertrophy with increased wall thickness and chamber volume. 
•   Left axis deviation, horizontal heart 
•  Hb decreased due to relative haemodilution 
•   Upper respiratory tract oedema and capillary engorgement 
•   Increased minute volume, respiratory rate, V, lV, RR. Chronic respiratory allcalosis 
•   Decreased  FRC, RV, TLC, AWR

(b) The clinical effects on her response to the injury include: 
•   Larger blood volume allows blood loss to be relatively better tolerated 
•  Susceptible to supine hypotension 
•    Susceptible to basal atelectasis and hypoxia 
•  Difficult intubation 
•  High Vand low FRC means that hypoxia and hypercarbia develop rapidly with airway 
obstruction. apnoea etc

Discussion

This question forms a part of the "manage this pregnant trauma patient" spectrum of fellowship questions. For a general reference, one is directed to Question 3 from the first paper of 2007 (Outline the special considerations involved in the care of a pregnant patient involved in multi-trauma.). That answer also covers section (b) of the current question ("How do they effect her response to these injuries?")

The management of the pregnant poly-trauma patient is discussed elsewhere. The answer prepared for Question 3 from the first paper of 2007 is very similar: "Outline the special considerations involved in the care of a pregnant patient involved in multi-trauma.".

In summary:

Airway changes

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

Respiratory changes

  • 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 

Circulatory changes

  • 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

Electrolyte and endocrine changes

  • 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

Renal changes

  • 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

Gastrointestinal and nutritional changes

  • Nausea and vomiting: in 50-90%. 
  • Oesophageal sphincter tone is decreased (aspiration is more likely)
  • There is increased intragastric pressure due to upward displacement
  • Gastric emptying is delayed, and is virtually non-existant during labour
  • Thiamine supplementation is important, because prolonged hyperemesis can result in vitamin deficiency.
  • Abdominal compartment pressure measurements are going to be wildly inaccurate.
  • There is insulin resistance, particularly later in pregnancy
  • Metabolic fuel use favours lipolysis, preserving the glucose and amino acids for use by the foetus.
  • Protein catabolism is decreased
  • There is a peak of calcium demand in the third trimester

Specific features of the cardiorespiratory changes in pregnancy can be found on the page dedicated to this topic. In brief summary, they are as follows:

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  
pH increases to 740-7.47
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  
Circulatory Changes in Pregnancy
Heart rate Increased (from 75 to 85-90)
Stroke volume Increased (from 65ml to 80-90ml)
Cardiac output Increased (from 5L/min to 7L/min)
Blood pressure Decreased
   
Systemic vascular resistance Decreased
Pulmonary vascular resistance Decreased
Pulmonary artery wedge pressure Unchanged
Blood volume Increased by 50%
CVP Unchanged
Renal blood flow Increased by 30-80%
Resting oxygen consumption Increased by 20-30%
Colloid oncotic pressure Decreased


 

References

Critical Care Medicine has dedicated an entire supplement to the influence of pregnancy in critical care: Volume 33 Supplement 10 October 2005 - pg. S247-S397

 

Additionally, UpToDate has an excellent summary for the paying customer.

 

Hunter, Stewart, and Stephen C. Robson. "Adaptation of the maternal heart in pregnancy." British heart journal 68.6 (1992): 540.

 

Metcalfe, James, and Kent Ueland. "Maternal cardiovascular adjustments to pregnancy." Progress in cardiovascular diseases 16.4 (1974): 363-374.

Question 1c - 2003, Paper 2

You are called to see a 39 year old female driver in the Emergency Department who has been brought in by ambulance after a motor vehicle crash (head on collision). She is eight months pregnant (first pregnancy), and is complaining of abdominal pain.

(c)        Please discuss the expected physiological changes associated with pregnancy and how they would impact on her management.

College Answer

Multiple factors: consider the following:

Cardiovascular: vasodilated state with lower baseline BP, higher baseline HR, and higher cardiac output. Masking of initial hypovolaemia, risking foetal circulation, best monitored by foetal heart rate. Large intra-abdominal mass (uterus) puts patient at risk of supine hypotensive syndrome: need to displace uterus or position in left lateral position.

Respiratory: diagphragms pushed up, decreased FRC (need to insert ICCs higher); respiratory alkalosis (expected CO2 30, with HCO3 20): need to keep in mind when assessing blood gases and if ventilating patient. Swollen airway, larger breasts: intubation often difficult.

Gastrointestinal: decreased gastric emptying, and weakened lower oesophageal sphincter: increased risk of aspiration.

Haematological: hypercoagulable state, risk of Rh incompatibility with foetus: potential for Rhesus isoimmunisation.

Foetus: benefits from supplemental oxygen; avoid tetracyclines, quinalones, NSAIDs (premature ductal closure), etc.

Discussion

The management of the pregnant poly-trauma patient is discussed elsewhere. The answer prepared for Question 3 from the first paper of 2007 is very similar: "Outline the special considerations involved in the care of a pregnant patient involved in multi-trauma.".

In summary:

Airway changes

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

Respiratory changes

  • 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 

Circulatory changes

  • 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

Electrolyte and endocrine changes

  • 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

Renal changes

  • 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

Gastrointestinal and nutritional changes

  • Nausea and vomiting: in 50-90%. 
  • Oesophageal sphincter tone is decreased (aspiration is more likely)
  • There is increased intragastric pressure due to upward displacement
  • Gastric emptying is delayed, and is virtually non-existant during labour
  • Thiamine supplementation is important, because prolonged hyperemesis can result in vitamin deficiency.
  • Abdominal compartment pressure measurements are going to be wildly inaccurate.
  • There is insulin resistance, particularly later in pregnancy
  • Metabolic fuel use favours lipolysis, preserving the glucose and amino acids for use by the foetus.
  • Protein catabolism is decreased
  • There is a peak of calcium demand in the third trimester

References

Oh's Intensive Care manual: Chapter 64   (pp. 684) General  obstetric  emergencies by Winnie  TP  Wan  and  Tony  Gin

 

Soar, Jasmeet, et al. "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution." Resuscitation 81.10 (2010): 1400-1433.

 

Mattox, Kenneth L., and Laura Goetzl. "Trauma in pregnancy." Critical care medicine 33.10 (2005): S385-S389.

 

DROST, THOMAS F., et al. "Major trauma in pregnant women: maternal/fetal outcome." Journal of Trauma-Injury, Infection, and Critical Care 30.5 (1990): 574-578.

Question 18 - 2006, Paper 1

A 35 year old woman with pre-eclampsia at 38 weeks gestation  is transferred to ICU post lower segment Caesarean section under general anaesthesia (performed because of failure to progress in labour).  Blood gases, electrolytes  and  full blood count  post extubation are as follows:

Normal values

Barometric pressure

760mm Hg

FiO2

0.5

pH

7.31

7.35-7.45

pO2

150mm Hg

pCO2

42 mm Hg

35-45

HCO3-

20.3mmol/L

21-30

Standard base excess

-5.0mmol/L

Sodium

137mmol/L

135 -145

Potassium

4.3mmol/L

3.2 - 4.5

Chloride

106mmol/L

100 -110

Haemoglobin

110g/L

125 - 165

WCC

19.8x 109/L

4.0 - 11.0

Neutrophils

17.3x 109/L

1.8 - 7.5

Lymphocytes

1.8x 109/L

1.5 - 4.0

Describe and  explain  the acid-base  status.   

Calculate  and  interpret the A-a gradient.

What is the likely significance of the anaemia  and leucocytosis?

College Answer

The intention of this question is to test the candidates’ understanding of some important normal alterations in physiology due to pregnancy, and how this affects our interpretation of common ICU
data.


Acid-base status: Acute respiratory acidosis. Anion gap normal. At 38 weeks pregnancy the normal PaCO2 is <30 mm Hg with a compensatory reduction in bicarbonate. The blood gases therefore indicate acute CO2 retention, probably due to pain and narcotics. In the non-pregnant state these values would indicate an uncompensated normal anion gap metabolic acidosis. However these data must be interpreted in the light of the normal changes of pregnancy.


A-a gradient: There is a raised A-a gradient of 154 mm Hg, suggesting shunt and/or V/Q mismatch. Potential explanations are the loss of FRC after abdominal surgery, segmental collapse or consolidation, or aspiration.


Anaemia and leucocytosis: The mild anaemia is physiological in pregnancy, and the neutrophil leucocytosis is a normal feature during labour and early post-partum. This lady has been in labour prior to Caesarean section.


Sixteen out of twenty-six candidates passed this question.

Discussion

This question is virtually identical to Question 9.2 from the second paper of 2011.

Whatever the reason, one identical question has been placed in the acid base disorders section, and another in the O&G section.

In this incarnation of the discussion section, I will focus on the normal changes which take place during pregnancy.

In summary:

  • 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 

There is a mild respiratory acidosis. The normal CO2 of late pregnancy is around 30mmHg, which is generally sustained with a bicarbonate of 20. In this scenario the bicarbonate has not changed, and the CO2 is elevated by 12mmHg. The use of the standard equation yields an expected pH of 7.304 for this change in CO2- very close to the measured pH (7.31), so there really is no metabolic acid-base disturbance at all.

The anion gap is normal if you calculate it without the potassium. It is 15.3 with potassium included, trivially elevated (by 3.3).

References

Oh's Intensive Care manual:

Chapter 64   (pp. 684) General  obstetric  emergencies by Winnie  TP  Wan  and  Tony  Gin

Chapter 65   (pp. 692) Severe  pre-existing  disease  in  pregnancy by Jeremy  P  Campbell  and  Steve  M  Yentis

 

Carlin, Andrew, and Zarko Alfirevic. "Physiological changes of pregnancy and monitoring." Best Practice & Research Clinical Obstetrics & Gynaecology 22.5 (2008): 801-823.

 

Chesnutt, Asha N. "Physiology of normal pregnancy." Critical care clinics 20.4 (2004): 609-615.

 

Silversides, Candice K., and Jack M. Colman. "Physiological changes in pregnancy." Heart Disease in Pregnancy 2 (2007): 7-16.

Question 12 - 2006, Paper 2

List the likely causes of sudden respiratory distress in a woman in labour, who has no previous history of cardiac or respiratory disease. List 2 cardinal clinical features for each of these conditions.

College Answer

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)       Other causes as in the non-pregnant patient

Discussion

The college has actually only asked for two causes.

The list of causes generated by the college, however, is impressive.

1) Amniotic fluid embolism

Two features: DIC and right heart failure with cyanosis

2) Pulmonary embolism

Two features: increased A-a gradient and right heart strain on ECG

The belowmentioned article gives a list which looks a little like this:

  • preeclampsia
  • tocolytic therapy resulting in pulmonary oedema
  • blood transfusion reaction
  • sepsis
  • aspiration
  • fluid overload

The college would add:

  • peripartum cardiomyopathy
  • air embolism
  • pneumomediastinum

To this list, I would add:

  • High epidural with motor block of respiratory muscles
  • Excessive peripartum opiate use

In general:

Acute Respiratory Failure in Pregnancy
Cause Cardinal features and brief discussion
High epidural/spinal block
  • Abnormal (diaphragmatic) respiratory movements
  • Flaccid paralysis of the extremities
  • Otherwise preserved consciousness
  • Predominantly hypercapneic respiratory failure
Amniotic fluid embolism
  • Clinical evidence of right heart failure
  • Petechial rash
  • DIC
  • Seizures
  • Haemodynamic compromise
Pre-eclampsia leading to pulmonary oedema
  • Severe hypertension
  • Clinical features of pre-eclampsia, eg. proteinuria
Tocolytic-associated pulmonary oedema
  • Improves with the withdrawal of tocolytics
  • Associated with tachycardia
Peripartum cardiomyopathy
  • TTE evidence of LV dilatation and decreased LVEF (by definition, under 45%)
  • Displaced apex beat
  • Audible S3
Air embolism
Pneumomediastinum
(also known as Hamman's syndrome)
  • Follows a Valsalva manoeuvre during the second stage of labour
  • Typically, associated with pneumothorax;
    more rarely associated with an oesophageal rupture
  • Neck and facial crepitus (surgical emphysema)
  • Impressive CXR and CT features
  • A "mediastinal crunch" may be heard on auscultation, also known as "Hamman's Sign" and more familiar from the examination of cardiothoracic ICU patients who have just returned from a CABG. It is a fine crackle heard in synchrony with the heart beat.
Accidental magnesium overdose
  • Depressed or absent reflexes, flaccid paralysis
  • Clinical features of hypermagnesaemia
  • Historically, pre-eclampsia or eclampsia
  • Usually, associated with the use of premixed bags of MgSO4
Causes which are not unique to pregnancy, but which commonly co-exist with pregnancy
Sepsis
Peripartum opiate use
  • Predominantly hypercapneic respiratory failure
  • Clinical features of opiate toxidrome (pinpoint pupils, etc)
PE
  • Clinical features of right heart failure
  • Hypoxia, tachypnoea, tachycardia
  • Characteristic ECG changes (S1 Q3 T3, right heart strain)
Fluid overload
  • Historically, vigorous fluid resuscitation
  • Clinically, evidence of peripheral oedema
Aspiration
  • Auscultation findings consistent with aspiration
  • Characteristic CXR appearance
  • A history of vomiting or decreased level of consciousness (eg. seizures)
Transfusion reaction
  • History of recent large volume blood transfusion 
  • Usually, this is a TACO as opposed to TRALI
  • Haemolysis and haemoglobinuria may be present if this was really incorrectly crossmatched blood

References

Karetzky, Monroe, and Maria Ramirez. "Acute respiratory failure in pregnancy: an analysis of 19 cases." Medicine 77.1 (1998): 41-49. - this is a bit of a "royal sampler" of different causes of respiratory failure.

Oh's Intensive Care manual:

Chapter 64   (pp. 684) General  obstetric  emergencies by Winnie  TP  Wan  and  Tony  Gin

Chapter 65   (pp. 692) Severe  pre-existing  disease  in  pregnancy by Jeremy  P  Campbell  and  Steve  M  Yentis

Lapinsky, Stephen E. "Acute respiratory failure in pregnancy." Obstetric Medicine: The Medicine of Pregnancy 8.3 (2015): 126-132.

Samanta, Sukhen, J. Wig, and A. K. Baronia. "How safe is the prone position in acute respiratory distress syndrome at late pregnancy?." (2014).

Rubal, Bernard J., et al. "The'mill-wheel'murmur and computed tomography of intracardiac air emboli." Journal of the American Association for Laboratory Animal Science 48.3 (2009): 300-302.

Lifschultz, Barry D., and Edmund R. Donoghue. "Air embolism during intercourse in pregnancy." Journal of Forensic Science 28.4 (1983): 1021-1022.

Balkan, M. Erkan, and Göknur Alver. "Spontaneous pneumomediastinum in 3rd trimester of pregnancy." Annals of thoracic and cardiovascular surgery 12.5 (2006): 362.

Jain, Vikyath. "Acute respiratory distress syndrome, Respiratory failure, Pregnancy." ACUTE RESPIRATORY DISTRESS SYNDROME IN PREGNANCY 7540 (2015).

Robinson, Julian N., et al. "Inhaled nitric oxide therapy in pregnancy complicated by pulmonary hypertension." American journal of obstetrics and gynecology 180.4 (1999): 1045-1046.

Question 27 - 2007, Paper 2

With respect to pregnancy,

a)  indicate how the following variables change in the third trimester (either increase or decrease or no change)

Variable

Direction of change

Systolic blood pressure

 

Diastolic blood pressure

 

Heart rate

 

Blood volume

 

Haematocrit

 

Tidal volume

 

pH

 

PCO2

PO2

Bicarbonate

b)  List 4 conditions specific to pregnancy which may result in right or left heart failure or both.

c) Outline the major differences in approach to cardiopulmonary resuscitation in pregnancy as compared to the non pregnant adult.

College Answer

a)  indicate how the following variables change in the third trimester (either increase or decrease or no change)

Variable

Direction of change

Systolic blood pressure

Decrease

Diastolic blood pressure

Decrease

Heart rate

Increase

Blood volume

Increase

Haematocrit

Mild decrease

Tidal volume

Increase

pH

No change

PCO2

Decrease

PO2

Increase

Bicarbonate

Decrease

b)  List 4 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

c) Outline the major differences in approach to cardiopulmonary resuscitation in pregnancy as compared to the non pregnant adult.

1) CPR in left lateral position
2) Consideration of emergency Caesar

Discussion

This question closely resembles Question 16 from the second paper of 2010.

In summary:

a)

Question a) specifically refers to Table 64.1 on page 685. A summary of the normal physiological changes in pregnancy can be found elsewhere.

b) is perfect as a list. Amniotic fluid embolism actually causes right heart failure at first, and then turns into LV failure. In fact, it would be even more perfect as a table:

This works best as a table. In fact, in Sliwa et al (2010) there is an even better table (Table 3. p.772)

Left-dominant Right-dominant
  • Pre-eclampsia
  • Eclampsia
  • Tocolytic therapy
  • Peripartum cardiomyopathy
  • Pituitary apoplexy
    (Sheehan's syndrome)
  • Worsening of pre-existing
    rheumatic MR
  • Pre-existing idiopathic dilated cardiomyopathy (IDC) unmasked by pregnancy
  • Massive PE
  • Aminotic fluid embolism
  • Worsening of pre-existing rheumatic TR

Potentially bi-ventricular:

  • Pre-existing unrecognized congenital heart disease
  • Pregnancy-associated myocardial infarction

c) is well discussed in the chapter on cardiac arrest in the pregnant patient. In short:

Keep in mind the following alternative causes of arrest:

  • Amniotic fluid embolism
  • Hypertensive disorder of pregnancy (with ensuing cardiac failure)
  • Seizures (with ensuing hypoxia and arrest)
  • Haemorrhage from liver rupture
  • Haemorrhage from uterine rupture

Issues which complicate the pregnant arrest and peri-arrest scenario:

  • Difficult intubation
  • Increased risk of aspiration (the stomach just doent't empty)
  • Venous return is impaired by the gravid uterus
  • Systemic oxygen consumption is increased
  • Cardiac output and circulating volume are greater; decompensation occurs later.

Manually displace the uterus to the left (off the aorta and vena cava)

  • Manually displace the uterus to the left (off the aorta and vena cava)
  • Add a left lateral tilt (the ideal angle is unknown, and is thought to be between 15° and 30°)
  • Biaxillary defibrillator pad placement
  • Prepare for an emergency perimortem caesarian.

To the college answer  I might add that the emergency caesarian should be considered after 4 minutes of CPR, as per the ILCOR guidelines. The weirdly specific 27° pelvis tilt mentioned by the college can get you reaching for a protractor. It probably comes from the old AHA guidelines (these days the guideline-makers for the ECC and AHA no longer recommend the left lateral tilt (see the 2015 AHA update and the 2015 ECC guidelines).A left lateral tilt may compromise effective CPR, but is still recommended by the ARC Guideline 11.10  (2011) "Special Circumstances". Presumably, once the ARC get around to it, their guidelines will fall in line with international consensus. The 27° figure comes from Rees and Willis (1998), who got physicians to perform CPR on specially modified mannequins at different degrees of tilt. The authors found that the 27 degrees was the  angle at which safe positioning and compression efficacy were at optimal compromise. Chest compression force was not too badly affected (80% of the force of compressions with the patient in a supine position), and the patient was unlikely to roll off the bed at this angle.

References

Einav, Sharon, Nechama Kaufman, and Hen Y. Sela. "Maternal cardiac arrest and perimortem caesarean delivery: evidence or expert-based?." Resuscitation 83.10 (2012): 1191-1200.

Morris Jr, John A., et al. "Infant survival after cesarean section for trauma." Annals of surgery 223.5 (1996): 481.

Beckett, V. A., P. Sharpe, and M. Knight. "CAPS—A UKOSS STUDY OF CARDIAC ARREST IN PREGNANCY AND THE USE OF PERI-MORTEM CAESAREAN SECTION. IMPLICATIONS FOR THE EMERGENCY DEPARTMENT." Emergency Medicine Journal 32.12 (2015): 995-995.

Elkady, A. A. "Peri-mortem Caesarean Section Delivery: A Literature Review and Comprehensive Overview." Enliven: Gynecol Obstet 2.3 (2015): 005.

Campbell, Tabitha A., and Tracy G. Sanson. "Cardiac arrest and pregnancy." Journal of emergencies, trauma, and shock 2.1 (2009): 34.

Katz, Vern L., Deborah J. Dotters, and William Droegemueller. "Perimortem cesarean delivery." Obstetrics & Gynecology 68.4 (1986): 571-576.

Manner, Richard L. "Court-Ordered Surgery for the Protection of a Viable Fetus:, 247 6a. 8b, 274 SE 2d 457 (1981)." (1982).

Question 9.1 - 2008, Paper 1

A 34 year old lady who is 34 weeks pregnant presents with acute onset epigastric pain. The plasma biochemistry and the haematology report are provided.

Test

Normal Range

Sodium           138 mmol/L

135-145

Potassium        4.4 mmol/L

3.2-4.5

Chloride         102 mmol/L

100-110

Bicarbonate      27 mmol/L

17-28

Anion Gap        9 mmol/L

5-15

Creatinine       66 micromol/L

50-100

Urea             4.3 mmol/L

1.0-5.0

Tot Protein      76 H g/L

55-75

Albumin          36 g/L

28-38

Calcium          2.35 mmol/L

2.00-2.50

Ca Alb Cor       2.53 H mmol/L

2.00-2.50

Phosphate        1.03 mmol/L

0.7-1.4

Magnesium        0.8 mmol/L

0.7-1.0

Glucose          4.7 mmol/L

3.6-7.7

CK Total         71 U/L

<160

LD               748 H U/L

100-200

AST              241 H U/L

10-45

ALT              189 H U/L

5-45

GGT              45 U/L

10-70

ALP              185 H U/L

65-180

Bilirubin Total        40 micromol/L

<20

WCC              12.4 ^9/L
Hb               88 g/L
Plat             64L x10^9/L

4.0-15.0
110-160
150-400

1. What is the most likely diagnosis?

2. What 2 additional tests will support your diagnosis?

3. List 4 treatment options

College Answer

1. What is the most likely diagnosis? HELLP

2. What 2 additional tests will support your diagnosis?

Haptoglobins : low
Blood film showing evidence of hemolysis

3. List 4 treatment options

  • Delivery of baby
  • Steroids
  • Antihypertensives
  • Magnesium sulphate
  • Plasma exchange

Discussion

1) This is HELLP syndrome. The platelets are low, the LDH is high, and there is raised bilirubin.

2) a blood film, reticulocyte count and serum haptoglobin would support this diagnosis

3) There is no specific management strategy for HELLP; delivery of the baby is the only "curative" procedure. Contrary to the college answer, neither plasma exchange nor corticosteroids have been show to improve maternal morbidity or mortality.

HELLP is discussed at lengths elsewhere.

References

Question 18.3 - 2008, Paper 2

You are called to the Emergency Department to review a nulliparous 28 year old woman. She is currently 35 weeks pregnant, and has presented with 72 hours of nausea  and vomiting accompanied by epigastric and right upper quadrant pain. On examination she was jaundiced, confused and had a blood pressure of 120/70. Laboratory results from a venous blood taken on arrival are shown below:

Venous Blood

Value

Reference range

Na+

138

135 -145 mmol/L

K+

3.8

3.2-4.5 mmol/L

Urea

15

3.0-8.0 mmol/L

Creatinine

245

50-100 micromol/L

Albumin

30

33-40g/L

Glucose

2.5

3.0-7.8mmol/L

Bilirubin (total)

142

<20micromol/L

ALP

293

32-156 U/L

AST

99

<31U/L

ALT

88

<34U/L

GGT

67

<38U/L

LDH

180

110-250U/L

Uric acid

0.72

0.15-0.5 mmol/L

APTT

45

36-38 sec

INR

2.8

<1.2

Platelets

123

150-450x109/L

List 3 likely differential diagnoses for the above history and laboratory data

College Answer

List 3 likely differential diagnoses for the above history and laboratory data

A number of differentials are possible however in the third trimester in a nulliparous woman the three main considerations are:
•    Acute fatty liver of pregnancy ( AFLP):
•    HELLP (Haemolysis, elevated liver enzymes and low platelets) Syndrome:
•    Pre eclampsia with hepatic involvement.

Other considerations are: (these are not the cause of severe hepatic failure in pregnancy and so will attract fewer marks if mentioned without the first three)
•    Intrahepatic Cholestasis of Pregnancy:
•    Viral hepatitis: The commonest cause of jaundice in pregnancy. May occur at any time. The ALT and AST would be expected to be greatly elevated (>500-
1000U/L). DIC is rare.

Discussion

Yes, the model answer lists at least 5 differentials, but the question asked for only "3 likely differential diagnoses".

Thus, one would be forced to mention the following:

  • HELLP (but LDH is not elevated)
  • Acute fatty liver of pregnancy
  • HUS-TTP (the renal function is wildly deranged)

Elaboration upon these syndromes is carried out in the discussion of Question 6 from the first paper of 2010.

In too mich detail, here are the causes of acute liver failure in pregnancy:

Acute Liver Failure in Pregnancy
Cause Diagnostic features Notes and management options
Causes of liver failure which are unrelated to pregnancy
Drug-induced hepatitis
  • Paracetamol level
  • N-acetylcysteine crosses the placenta and has a protective effect in the foetus (Horowitz et al, 1997)
Shock, haemorrhage
  • Ultrasound: structurally normal liver
  • The LFT derangement which follows resuscitation for severe postpartum haemorrhage
  • Should improve after the shock state has resolved
Decompensation of pre-existing liver disease
  • Ultrasound: cirrhosis
  • Risk of preterm delivery and peripartum complications is increased (Aggarwal et al, 1999)
  • Normal management of the cirrhotic patient applies
Causes of liver failure which are exacerbated by pregnancy
Viral hepatitis
  • Hep B and C serology
  • Most common cause of LFT derangement in pregnancy
  • B and C are the most common
  • usually, BP is normal (in contrast with HELLP)
  • Ribavirin is contraindicated (a teratogen)
  • Other antiviral drugs may still be useful to decrease the viral load preior to delivery (to protect the baby from vertical transmission)
Portal vein thrombosis
  • Ultrasound: portal vein occlusion on Doppler
  • Due to hypercoagulable state of pregnancy
  • Heparin infusion is the standard of care 
  • Generally, TIPS procedure is too technically difficult in pregnancy - but that is another option
Hepatic venous thrombosis
  • Ultrasound: hepatic vein occlusion on Doppler
Cholecystitis
  • Ultrasound: thickened gall bladder wall, stones
  • LFTs: cholestatic picture
  • Conservative antibiotic therapy is best
  • Non-emergency surgery has better outcomes, i.e. it pays to delay until the acute flare has passed (Casey et al, 1996)
Pregnancy-related causes of liver failure
Hyperemesis gravidarum
  • LFTs: "transaminitis"
  • Unlike the others, this is a feature mainly of the first trimester
  • It is associated with raised transaminases, as opposed to liver failure per se - synthetic function is preserved (Outlaw et al, 2000)
  • Antiemetics and supportive care are the only options
Intrahepatic cholestasis of pregnancy (icterus gravidarum)
  • History of jaundice and pruritis
  • LFTs: cholestatic picture
  • Ultrasound: gall bladder looks normal
  • Pruritis is usually the patient's greatest concern. Can be managed with ursodeoxycholic acid.
  • Resolves rapidly with delivery
  • Will occur again in the next pregnancy in 60%
Pre-eclampsia
  • LFT derangement is due to fibrin deposition and endothelial dysfunction in the sinusoids.
  • Typically, this is also not "liver failure" but rather an LFt derangement of unclear significance (Munazza et al, 2013)
  • Standard therapy applies: antihypertensives, magnesium sulfate, and urgent delivery
HELLP
  • Thrombocytopenia
  • Low haptoglobin
  • Raised LDH,
  • Uncojugated bilirubin
  • Blood film features of haemolysis
  • See the local chapter.
  • Delivery is the treatment
  • Some authors recommend corticosteroids (Guntupalli et al, 2005) but only as a means of helping foetal lung maturation
  • Thrombocytopenia and LFT derangement will continue for up to 48 hours postpartum
  • Standard therapy applies: antihypertensives, magnesium sulfate, urgent delivery, correction of coagulopathy
Acute fatty liver of pregnancy
  • Presents with abdominal pain, vomiting, hypoglycaemia, coagulopathy
  • Characteristic ultrasound findings of the liver parenchyma
  • 18% maternal mortality, 2% foetal mortality (Guntupalli et al, 2005)
  • Liver failure is present, not just LFT derangement
  • Delivery fixes everything, as in HELLP
  • Fulminant liver failure may be present by then, and liver transplant may be the only option
Acute hepatic rupture
  • Ultrasound: haematoma
  • Haemodynamic instability and haemorrhagic shock
  • Abdominal pain (RUQ)
  • Haemoperitoneum
  • Maternal mortality is around 30% (Manas et al, 1985
  • If it has not ruptured (i.e. only a subcapsular haematoma) then conservative management and urgent dleivery are probably safe
  • Surgical packing and/or angioembolisation may be the only options
Other causes of febrile jaundiced coma with thrombocytopenia
TTP/HUS
  • Pentad: thrombocytopenia, microangiopathic haemolytic anemia, neurologic abnormalities, renal failure, and fever. See local chapter.
  • Low ADAMTS-13 levels are found. 
  • The SAQs often give a picture which could be consistent with TTP. It actually does occur often in pregnancy and the postpartum period (McMinn et al, 2001)
  • "How is this not HELLP?" one might ask. Well:
    • HELLP is never in the first trimester
    • HELLP always resolves following delivery
  • I.e. if after delivery the abnormalities persist, plasmapheresis becomes a serious option.
Sepsis with DIC
  • Bacteraemia
  • Haemodynamic instability, hypotension
  • blood film (for HELLP, TTP, HUS)
  • Septic screen (for sepsis)
  • Quantitiative D-dimer (for DIC)
  • formal LFTs (for HELLP)
  • ADAMTS13 (for TTP)
  • Urinary protein (for pre-eclampsia)
  • Ammonia level (for encephalopathy of acute fatty liver of pregnancy)
  • Liver ultrasound (for fatty liver of pregnancy, as well as to exclude liver rupture)

References

Question 1 - 2008, Paper 2

A 35 year old female is 39 weeks pregnant. Her pregnancy has been complicated by hypertension and  proteinuria. Her blood  pressure is 160/120 mm  Hg. You are called to the labour ward when she suffers a generalised (“grand mal”)  convulsion. Outline  your overall plan of management.

College Answer

Initial management
ABC
Left side
Terminate the seizure
a.   Diazepam 5-10mg or Mg 4g IV up to 8 g
Monitors / investigations

Management of Hypertension
Hydrallazine
Labetalol
(Other  agents  are  acceptable  –  late  in  pregnancy  –  increasing  trend  to  use
“mainstream” agents)

Treatment of convulsions
MgSO4 bolus followed by maintenance MgSO4
(Shown to be more effective than phenytoin or diazepam in preventing recurrent seizures)
Addition of Benzodiazepine / Barbiturate if recurrent seizures despite MgSO4

Planning for delivery
Brief period of resuscitation once seizures controlled

Post partum management
Continue anti-convulsants until patient improves (diuresis, fall in BP)

Discussion

This question closely resembles Question 23 from the first paper of of 2011. 

Also, that's not how you spell hydralazine.

Anyway, the management should look like this:

  • Attention to the ABCS, with management of life-threatening problems simultanous with a rapid focused examination and a brief history.
  • Airway:
    • Assess the need for airway support in context of post-ictal unconscious state
    • Weigh benefits of intubation against risks in context of the known airway access problems associated with pregnancy
  • Breathing/ventilation
    • Assess oxygenation and briefly examine for aspiration
    • High flow oxygen via NRBM if patient is not in need of immediate intubation
  • Circulatory support
    • Assess cardiovascular stability
      • left lateral 30° tilt if hypotensive
    • Access with widebore cannula
  • Immediate investigations:
    • FBC - looking for thrombocytopenia
    • LFTs - looking for HELLP, hepatic encephalopathy
    • EUC - looking for hyponatremia
    • CMP
    • Coags
    • Antiepileptic drug levels, if relevant
    • CT brain, if the patient fails to awaken
  • Specific management
    • Antihypertensives:
      • labetalol, nifedipine or hydralazine are of equivalent benefit
      • methyldopa and sodium nitroprusside are second line agents
    • Antiepileptic therapy:
      • Loading dose of magnesium sulfate, followed by an infusion, aiming at a serum level of 2.0-3.5mmol/L
      • Diazepam and phenytoin can be considered if seziures are refractory
    • Arrange for a consultation with the obstetrician regarding the safety and practicality of immediate delivery.

References

Heres an article by Baha  Sibai, who came up with the Tennessee classification for the HELLP syndrome:

Sibai, Baha M. "Diagnosis, prevention, and management of eclampsia."Obstetrics & Gynecology 105.2 (2005): 402-410.

Question 18 - 2009, paper 1

Outline the challenges specifically associated with the management of a pregnant patient with status asthmaticus.

College Answer

1) Pregnancy can worsen asthma – pulmonary congestion, reflux disease, low FRC

2) Because of reduced respiratory reserve, decompensation can be rapid

3) Need to be aware of the changes in blood gas reference values

4) Medications –
a) Steroids – potential malformations in the fetus if used in the first trimester – cleft lip

b) Beta 2 agonists- risk of tocolytic pulmonary oedema - delay in onset of labour

5) Sedation of the ventilated pregnant patient

Benzodiazepines – floppy infant syndrome

Opiates- fetal respiratory depression
If need for prolonged paralysis – risk of arthrogyphosis in the fetus

6) IPPV –
High risk intubation
Avoid nasal intubation
High pressures may reflect raised intraabdominal pressures

7) Maternal hypercapnia – reduces uteroplacental blood flow
Also shifts oxyHb dissociation curve in the fetus to the right, thus impairing fetal oxygenation – fetal monitoring essential
Long term maternal hypoxia associated with IUGR

8) NIV – may be difficult with increased risk of aspiration

9) Positioning of patient issues – Risk of aortocaval compression

Discussion

The management of the pregnant asthmatic in the ICU is dealt with elsewhere.

To approach it systematically:

Main issues in pregnancy which complicate asthma:

  • More reflux, thus more exacerbations
  • More allergic exacerbations, particularly in the last trimester
  • Less capacity to compensate, thus more frequent presentations
  • They are already tachypnoeic, with a mild respiratory alkalosis, which can confuse their presentation.
  • The preload is already decreased by uterine compression of the vena cava, let alone the intrinsic PEEP.
  • Prolonged maternal hypoxia is associated with intrauterine growth retardation.
  • There is a greatly increased risk of pre-term delivery with poorly controlled asthma

Airway control:

  • Needs to be accomplished by an expert

Ventilation:

  • Cautious use of NIV (aspiration risk)
  • Cautious use of permissive hypercapnea
  • Cautious use of beta agonists (tocolytic effects)
  • avoid hypoxia (foetal growth retardation)
  • may benefit from BAl or heliox

Circulatory support:

  • Assure normovolemia
  • Avoid adrenaline
  • Position patient into a 30° left tilt

Neuromuscular blockade:

  • only in emergency, and only for short periods

Specific management:

  • constant foetal monitoring
  • may need to organise for a caesarian to protect the foetus from hypoxia.

Avoid harmful strategies:

References

Bakhireva, Ludmila N., et al. "Asthma control during pregnancy and the risk of preterm delivery or impaired fetal growth." Annals of Allergy, Asthma & Immunology 101.2 (2008): 137-143.

Schatz, Michael, and Mitchell P. Dombrowski. "Asthma in pregnancy." New England Journal of Medicine 360.18 (2009): 1862-1869.

Question 14 - 2009, Paper 2

14.1     Outline briefly the difficulties associated with the diagnosis of sepsis during pregnancy and labour.

14.2     List the leading causes of sepsis in pregnant patients.

14.3     What are the common pathogens  encountered in pregnancy related sepsis?

14.4     List 2 antibiotics contraindicated during pregnancy.

College Answer

14.1     Outline briefly the difficulties associated with the diagnosis of sepsis during pregnancy and labour.

Applying SIRS criteria to pregnancy may be problematic as there is:

1)  Leukocytosis
2)  Body temperature is raised during pregnancy and labour
3)  Tachycardia and tachypnoea are seen during normal labour

14.2     List the leading causes of sepsis in pregnant patients.

1)  Pyelonephritis
2)  Chorioamnionits
3)  Septic abortion
4)  Episiotomy infections
5)  Necrotising fasciitis
6)  Septic thrombophlebitis
7)  Aspiration pneumonia

14.3     What are the common pathogens  encountered in pregnancy related sepsis?

Gram negative more common than Gram positive agents
E.Coli one of the common pathogens
Can also be polymicrobial – E.coli, Klebsiella

14.4     List 2 antibiotics contraindicated during pregnancy.

Tetracyclines
Chloramphenicol

Discussion

a) Outline briefly the difficulties associated with the diagnosis of sepsis during late pregnancy and labour.

Problems of the obsolete definition of sepsis and SIRS:

  • Neutrophilia is normal in pregnancy
  • Inflammatory markers are normally slightly elevated
  • The patient is normally slightly tachycardic, and may be slightly hypotensive, with a decreased SVRI. The circulation is normally hyperdynamic. They appear to be in early stages of vasodilated shock at the best of times.
  • Tachypnoea is normal in pregnancy and labour (chronic respiratory alkalosis)
  • The whole process of labour tends to obscure the findings one would normally associate with sepsis.
  • Then, suddenly, they collapse (as they tend to compensate right up until the last minute, and then drop everything, given their increased susceptibility to lipopolysaccharide)

Other problems (stolen from the LITFL entry on this topic)

  • Pneumonia may masquerade as the normal shortness of breath in pregnancy
  • Abdominal pain due to visceral pathology may masquerade as contractions (or - more  confusingly - may co-present with labour)
  • Appendicitis may be more difficult to diagnose, as the gravid uterus gets in the way of palpation.
  • Nausea, vomiting, constipation - all of these may be routine for the pregnant woman, and a bowel obstruction may present disastrously late (eg. this case report by Khan et al, 2012).
  • Abdominal pathology may be impossible to image, as everybody is going to freak out about the radiation exposure associated with a CT abdo/pelvis. This is in fact quite irrational, as the risks to a late-term foetus are quite small  (Chen et al, 2008). Instead, people should think about the foetal risk associated with remaining inside the septic abdomen of a critically ill mother whose source control is compromised by indecision about imaging. (In case anybody is interested, the dose from such a CT will total about 5 rads, which maxes out the recommended safe total foetal cumulative dose of 5-10 rads).
  • Urinary sepsis may be asymptomatic (urinary frequency is pretty normal)

b) List the leading causes of sepsis in pregnant patients.

  • Chorioamnionitis
  • Urinary tract infections
  • Pyelonephritis
  • Endometritis
  • Septic abortion

also...

  • Episiotomy infections
  • Necrotising fasciitis of the ceasarian wound
  • Septic thrombophlebitis - especially pelvic vein thrombophlebitis
  • Aspiration pneumonia
  • Acute pyelonephritis
  • Retained products of conception
    • Septic abortion
    • Conservative management of placenta accreta or percreta
  • Neglected chorioamnionitis or endomyometritis
    • Uterine microabscess or necrotizing myometritis
    • Gas gangrene
    • Pelvic abscess
  • Unrecognized or inadequately treated necrotizing fasciitis
    • Abdominal incision
    • Episiotomy
    • Perineal laceration
  • Bacterial pneumonia
  • Bacterial examples
    • Staphylococcus
    • Pneumococcus
    • Mycoplasma
    • Legionella
  • Viral pneumonia
    • Influenza
    • H1N1
    • Herpes
    • Varicella
  • Intraperitoneal etiology (nonobstetric)
    • Ruptured appendix or acute appendicitis
    • Bowel infarction
    • Acute cholecystitis
    • Necrotizing pancreatitis

c) What are the common pathogens encountered in pregnancy-related sepsis?

Oh's Manual quotes the following bugs:

To this, the Sanford Guide adds a few:

  • Enterobacteriaceae
  • Chlamydia trachomatis
  • Ureaplasma urealyticum

(these are specific to chorioamnionitis and septic abortion)

d) List two antibiotics contra-indicated during pregnancy.

 The full list:

Antibiotics which are contraindicated in pregnancy or lactation, and Why
Contraindicated antibiotics Why
Aminoglycosides in high doses Increased uptake by neonatal kidney leads to increased nephrotoxicity (but apparently gentamicin is still relativey safe)
Streptomycin 8th cranial nerve damage 
Sulfonamides Kernicterus in the newborn due to displacement of bilirubin off albumin, particularly if used shortly before birth. The specific culprit is sulfamethoxazole. Trimpethoprim appears to be relatively safer.
Tetracyclines Tetracyclines have nightmarish dental and bony effects.  In fact, these drugs are contraindicated from 16th week of gestation all the way until the 7th year of extrauterine life.
Quinolones Quinolones cause birth defects (though it seems fluoroquinolones are safe, and it was really mainly nalidixic acid that was the culprit).
Rifampicin Seems to be somewhat teratogenic, mainly in animal studies (spina bifida and impaired osteogenesis seem to be the major consequences)- but in humans one may overlook this if rifampicin is strongly indicated (eg. treatment of lifethreatening tuberculosis)
Fusidic acid Like sulfonamides, causes displacement of bilirubin by competing with it for albumin binding
Chloramphenicol This "Grey baby syndrome" is the consequence of disrupted mitochondrial function, when chloramphenicol metabolites interfere with the electron transport chain. Foetal failure to properly metabolise chloraphenicol by glucourinidation seems to be to blame.
Azole antifungals Teratigenic and embryotoxic. The specific dangerous ones are ketoconazole  fluconazole and voriconazole, earning a D classification. 
Echinocandins Hard to discuss humans in the absence of real data, but in animals using normal treatment doses caspofungin and anidulafungin cause skeletal abnormalities, reduction of litter size, ossification and rib malformations.
Flucytosine Embryotoxic and in fact abortificant in the first trimester, which is hardly surprising given that its main metabolite is 5-fluorouracil
Albendazole Teratogenic and embryotoxic. If the pregnant lady has some sort of hideous helminthic parasitosis which cannot wait until after delivery, ivermectin is probably a safer alternative
Foscarnet Seems to be teratogenic in animals, but if your CV infection is so severe and resistant that you've failed primary therapy, the chances are that your foetus is already significantly damaged by congenital CMV.

The college answer for Question 3.1 from the first paper of 2014 also lists nitrofurantoin, isoniazid and macrolides as drugs which are relatively contraindicated. This in fact, is not true:

 

References

Oh's Intensive Care manual: Chapter 64   (pp. 684) General  obstetric  emergencies by Winnie  TP  Wan  and  Tony  Gin

Fernandez-Perez, Evans R., et al. "Sepsis during pregnancy." Critical care medicine 33.10 (2005): S286-S293.

van Dillen, Jeroen, et al. "Maternal sepsis: epidemiology, etiology and outcome." Current opinion in infectious diseases 23.3 (2010): 249-254.

Demers, P., et al. "Effects of tetracyclines on skeletal growth and dentition. A report by the Nutrition Committee of the Canadian Paediatric Society."Canadian Medical Association Journal 99.17 (1968): 849.

Bar-Oz, Benjamin, et al. "The safety of quinolones—a meta-analysis of pregnancy outcomes." European Journal of Obstetrics & Gynecology and Reproductive Biology 143.2 (2009): 75-78.

Erić, Mirela, and Ana Sabo. "Teratogenicity of antibacterial agents.Collegium antropologicum 32.3 (2008): 919-925.

 

Question 6 - 2010, Paper 1

A  20  year  old  primi-gravida   presents  at  37  weeks  gestation  with  jaundice, headache,  blurred vision and hypertension  (140/90mmHg).  The antenatal  period was otherwise unremarkable. She is febrile, drowsy, pale, icteric and has pedal oedema. The uterus is palpated as for a full term pregnancy with a normal CTG trace. Examination is otherwise normal.

The following are her early blood results:

Hb*

80 G/L

(115-160)

Platelets*

52 x 109/L

(140-400)

INR*

1.8

(0.9-1.3)

APTT*

55 seconds

(25-38)

LDH*

654 U/L

(110-250)

Fibrinogen*

1.0 G/L

(1.5-4.0)

Total Bilirubin*

51µmol/L

(<20)

Urea*

30 mmol/L

(3-8)

Creatinine*

298 µmol/L

(70-120)

Potassium*

5.1 mmol/L

(3.2-4.5)

(a) List 4 likely differential diagnoses for this clinical presentation.

(b) What other investigations would you order for this patient and why?

(c) List the important management interventions for each of your differential diagnoses.

College Answer

(a) List 4 likely differential diagnoses for this clinical presentation.

•     Pre-eclampsia
•    HELLP Syndrome
•    Sepsis with DIC
•     HUS-TTP
•    Acute fatty liver of pregnancy

(b) What other investigations would you order for this patient and why?

•  Transaminases (full liver function tests) Assessment of HELLP

•  Peripheral blood film smear
Evidence of haemolysis or MAHA

•  Reticulocyte count, haptoglobins, conjugated/unconjugated bilirubin
Haemolysis screen

•  Blood, sputum, urine and vaginal swab for MC&S Septic screen

•  Urinalysis – protein, WBCs, RBCs, casts
Evidence of infection or proteinuria (pre-eclampsia)

•  Renal tract ultrasound
Rule out obstruction

(c) List the important management interventions for each of your differential diagnoses.

a.  Pre-eclampsia
i.  Deliver baby

ii.  Control BP
iii.  Hydralazine, beta blockers
iv.  SNP/GTN if intravenous agent required.

v.  Prevention of seizures
vi.  Magnesium sulphate

b.  HELLP Syndrome
i.  Deliver baby
ii.  Regular monitoring of platelet count and liver function
iii. Supportive measures whilst observing in HDU for dangerous complications  – hepatic haemorrhage/rupture,  progressive  renal failure, pulmonary oedema.

c.  Sepsis with DIC
i.  Timely delivery of baby in consultation with obstetrician.

ii.  Early broad spectrum antibiotics.
iii.  Cardiovascular support – adequate volume resuscitation and establish a MAP > 65mmHg.

d.  HUS-TTP
i.  Deliver the baby.
ii.  Fresh frozen plasma
iii.  Therapeutic plasma exchange

iv.  Corticosteroid therapy
v.  Monoclonal antibody  therapy – Rituximab

e.  Acute fatty liver of pregnancy
i.       Timely delivery of baby once mother stabilised

ii.      Correction of DIC
iii.       Supportive therapy
iv.      Monitoring      and     treatment     of     complications     post     delivery     eg pancreatitis
v.      Consideration for liver transplantation in with irreversible severe liver
failure despite delivery and aggressive supportive care

Discussion

One cannot add very much to this question.

One also cannot help but notice that it closely resembles Question 28 from the second paper of 2013.The question has been slightly altered, but otherwise it is exactly the same.

(a) List 4 likely differential diagnoses for this clinical presentation.

Pre-eclampsia is present - on the basis of the hypertension

  • HELLP (grade 1)- because of the combination of thrombocytopenia and deranged LFTs
  • TTP-HUS - on the basis of thrombocytopenia and renal failure
  • Sepsis and DIC - on the basis of fever, thrombocytopenia and low fibrinogen
  • Acute fatty liver of pregnancy - on the basis of LFT derangement and coagulopathy

(b) What other investigations would you order for this patient and why?

  • blood film (for HELLP, TTP, HUS)
  • Septic screen (for sepsis)
  • Quantitiative D-dimer (for DIC)
  • formal LFTs (for HELLP)
  • ADAMTS13 (for TTP)
  • Urinary protein (for pre-eclampsia)
  • Ammonia level (for encephalopathy of acute fatty liver of pregnancy)
  • Liver ultrasound (for fatty liver of pregnancy, as well as to exclude liver rupture)

(c) List the important management interventions for each of your differential diagnoses.

For all of them, expeditious delivery of the baby.

For all of them, correction of coagulopathy

For all of them, supportive measures and observation in critical care environment

For pre-eclampsia, standard management as routine

For HELLP, no specific management

For sepsis, IV antibiotics

For TTP, plasma exchange

For acute fatty liver of pregnancy, nothing specific until they need a transplant.

References

Brief summaries with references:

Pre-eclampsia and eclampsia

HELLP syndrome

The UpToDate links for the college's differentials are here:

Oh's Intensive Care manual: Chapter 63   (pp. 677) Preeclampsia  and  eclampsia by Wai  Ka  Ming  and  Tony  Gin

RCOG Guidelines for the management of severe pre-eclampsia/eclampsia (2006)

Haram, Kjell, Einar Svendsen, and Ulrich Abildgaard. "The HELLP syndrome: clinical issues and management. A review." BMC pregnancy and childbirth 9.1 (2009): 8.

Geary, Michael. "The HELLP syndrome." BJOG: An International Journal of Obstetrics & Gynaecology 104.8 (1997): 887-891.

 

Question 16 - 2010, Paper 2

With respect to pregnancy.

a.       Indicate  how  the  following  variables  change  in  the  third  trimester  (either increase or decrease or no change).

Variable

Direction of Change

Systolic Blood Pressure

 

Diastolic Blood Pressure

 

Heart Rate

 

Blood Volume

 

Haematocrit

 

Tidal Volume

 

pH

 

PCO2

 

PO2

 

Bicarbonate

 

b.  List  4 conditions  specific  to pregnancy  which  may result  in right  or left heart failure or both.

c.   Outline the major differences in approach to cardiopulmonary  resuscitation in pregnancy as compared to the non-pregnant adult.

College Answer

a.       Indicate  how  the  following  variables  change  in  the  third  trimester  (either increase or decrease or no change).

Variable

Direction of Change

Systolic Blood Pressure

Decrease

Diastolic Blood Pressure

Decrease

Heart Rate

Increase

Blood Volume

Increase

Haematocrit

Mild decrease

Tidal Volume

Increase

pH

No change

PCO2

Decrease

PO2

Increase

Bicarbonate

Decrease

b.  List  4 conditions  specific  to pregnancy  which  may result  in right  or left heart failure or both.

•  Peripartum cardiomyopathy
•  Amniotic fluid embolism
•   Pre-eclampsia 
•  Tocolytic pulmonary oedema
•  Pulmonary thromboembolism

c.   Outline the major differences in approach to cardiopulmonary  resuscitation in pregnancy as compared to the non-pregnant adult.

•    CPR in left lateral position (27 degree tilt)
•    Consideration for emergency caesarian section
•    Hands slightly higher on sternum for chest compressions
•    Additional personnel / equipment for emergency c-section and neonatal resuscitation

Discussion

This entire question draws heavily from Oh's Intensive Care manual: Chapter 64   (pp. 684) General  obstetric  emergencies by Winnie  TP  Wan  and  Tony  Gin,

Question a) specifically refers to Table 64.1 on page 685. A summary of the normal physiological changes in pregnancy can be found elsewhere.

In summary:

a)

Question a) specifically refers to Table 64.1 on page 685. A summary of the normal physiological changes in pregnancy can be found elsewhere.

b) is perfect as a list. Amniotic fluid embolism actually causes right heart failure at first, and then turns into LV failure. In fact, it would be even more perfect as a table:

This works best as a table. In fact, in Sliwa et al (2010) there is an even better table (Table 3. p.772)

Left-dominant Right-dominant
  • Pre-eclampsia
  • Eclampsia
  • Tocolytic therapy
  • Peripartum cardiomyopathy
  • Pituitary apoplexy
    (Sheehan's syndrome)
  • Worsening of pre-existing
    rheumatic MR
  • Pre-existing idiopathic dilated cardiomyopathy (IDC) unmasked by pregnancy
  • Massive PE
  • Aminotic fluid embolism
  • Worsening of pre-existing rheumatic TR

Potentially bi-ventricular:

  • Pre-existing unrecognized congenital heart disease
  • Pregnancy-associated myocardial infarction

c) is well discussed in the chapter on cardiac arrest in the pregnant patient. In short:

Keep in mind the following alternative causes of arrest:

  • Amniotic fluid embolism
  • Hypertensive disorder of pregnancy (with ensuing cardiac failure)
  • Seizures (with ensuing hypoxia and arrest)
  • Haemorrhage from liver rupture
  • Haemorrhage from uterine rupture

Issues which complicate the pregnant arrest and peri-arrest scenario:

  • Difficult intubation
  • Increased risk of aspiration (the stomach just doent't empty)
  • Venous return is impaired by the gravid uterus
  • Systemic oxygen consumption is increased
  • Cardiac output and circulating volume are greater; decompensation occurs later.

Manually displace the uterus to the left (off the aorta and vena cava)

  • Manually displace the uterus to the left (off the aorta and vena cava)
  • Add a left lateral tilt (the ideal angle is unknown, and is thought to be between 15° and 30°)
  • Biaxillary defibrillator pad placement
  • Prepare for an emergency perimortem caesarian.

b) is perfect as a list. Amniotic fluid embolism actually causes right heart failure at first, and then turns into LV failure

To (c) I might add that the emergency caesarian should be considered after 4 minutes of CPR, as per the ILCOR guidelines. The weirdly specific 27° pelvis tilt mentioned by the college can get you reaching for a protractor. It probably comes from the old AHA guidelines (these days the guideline-makers for the ECC and AHA no longer recommend the left lateral tilt (see the 2015 AHA update and the 2015 ECC guidelines).A left lateral tilt may compromise effective CPR, but is still recommended by the ARC Guideline 11.10  (2011) "Special Circumstances". Presumably, once the ARC get around to it, their guidelines will fall in line with international consensus. The 27° figure comes from Rees and Willis (1998), who got physicians to perform CPR on specially modified mannequins at different degrees of tilt. The authors found that the 27 degrees was the angle at which safe positioning and compression efficacy were at optimal compromise. Chest compression force was not too badly affected (80% of the force of compressions with the patient in a supine position), and the patient was unlikely to roll off the bed at this angle.

References

Oh's Intensive Care manual: Chapter 64   (pp. 684) General  obstetric  emergencies by Winnie  TP  Wan  and  Tony  Gin

ARC Guideline 11.10  (2011) "Special Circumstances". 

the 2015 AHA update:

2015 ECC guidelines:

Rees, G. A. D., and B. A. Willis. "Resuscitation in late pregnancy."Anaesthesia 43.5 (1988): 347-349.

Question 26 - 2010, Paper 2

You are called to assess a 38 year old female with respiratory failure in the Emergency  Department.  This  is  her  first  pregnancy  and  she  is  28  weeks pregnant   after  several   attempts   at  IVF.  She  is  positive  for  Swine-Origin Influenza Virus (H1N1).

Arterial blood gas on a FiO2 of 0.8 shows:

  • pH  7.31 
  • pCO2  48 mm Hg
  • pO55 mm Hg
  • Bicarbonate 18 mmol/L

Evaluation of the foetal heart reveals significant bradycardia.

a)  Outline the specific challenges in this case that distinguish it from a similar illness in a previously healthy 38 year old male.

b)  Outline your specific approach to the management of this case.

College Answer

a)  Outline the specific challenges in this case that distinguish it from a similar illness in a previously healthy 38 year old male.

•    Precious pregnancy in older, primiparous patient.
•    Known high incidence of morbidity and mortality in mother and foetus with H1N1
Influenza infection with severe CAP.
•    Requirement to work closely with specialist obstetric team and rationalising potentially conflicting priorities eg. timing of delivery of foetus.

•    Anatomical and Physiological considerations during pregnancy- elevated diaphragm and decreased FRC, decreased chest wall compliance, increased risk of aspiration during intubation, pressure of gravid uterus on IVC (and aorta) decreasing venous return (and increasing afterload) in the supine position.

•    Maintaining effective foeto-placental circulation while optimising maternal outcome.
•    Safety of various drugs in pregnancy eg. anti-virals, sedatives.
•    History of severe asthma complicating current episode of severe CAP likely to make ventilatory strategy more complex.

•    Importance of keeping family members well informed of considerations and likelihood of poor foetal outcome as priority will be given to mother’s survival.

b)  Outline your specific approach to the management of this case.

Immediate- 
•    Clinical scenario described requires rapid resuscitation.
•    Airway- Secure early, rapid sequence induction. Anticipate difficult airway (ensure help and difficult airway equipment available.
•    Breathing- Ventilate with protective lung strategy.  Example of Settings – SIMV/PC, FiO2-1.0 PC to achieve Tidal Volumes of 6-8ml/kg, Low rate- 6-8/min I:E ratio 1:3-4 to allow adequate expiratory time, PEEP 10-15cm titrated to oxygenation. Close monitoring with regular blood gas evaluation. Tolerate hypercapnia (although not ideal for foetus) if poorly compliant lungs. Position at least 30 degrees head-up to optimise respiratory mechanics. Sedate heavily to minimise oxygen consumption. Neuromuscular blockade if required to facilitate ventilation.

•    Circulation-. Fluid resuscitate (likely to be volume depleted) to clinical endpoints, vasoconstrictors to maintain perfusion pressure (eg MAP>60mmHg). Assessment of cardiac output if unstable haemodynamics with these measures (eg. echocardiogram, PiCCO, PA catheter, ScVO2)- High cardiac output expected due to
pregnancy and infection. Inotropes if cardiac output low. Position slightly left lateral to relieve IVC compression.

•    Early specialist obstetric evaluation to determine foetal condition, position of placenta and risk versus benefit of delivery of foetus may need to be considered carefully taking into consideration maternal and foetal factors.

Discussion

If we trim the psychosocial fat away from the lean physiology, there are several considerations in the management of this ARDS patient

Specific challenges:

  • Decreased FRC and chest wall compliance
  • ARDS management cannot use "permissive hypercapnea" as the fetal hemoglobin will decrease in its affinity for oxygen, thus CO2 should be kept no higher than 45mmHg. The second part of the college answer mentions this. An article commenting on one author's experience suggests that the intensivist should ignore this, as making attempts to increase minute ventilation will overload the right heart.
  • Must avoid hypoxia in order to maintain foetal wellbeing (already bradycardic, thus likely already hypoxic)
  • Need to monitor foetus closely, deliver when permissible by foetal survival
  • Safety of various drugs in pregnancy

Major pregnancy-related limiting factors which complicate the management of ARDS are as follows:

  • Intubation will be difficult, for well-known reasons.
  • Need to maintain normoxia to maintain a satisfactory foetal oxygen transfer gradient
  • Cannot tolerate permissive hypercapnea as this runs the risk of foetal acidosis. Foetal hemoglobin will decrease in its affinity for oxygen, thus CO2 should be kept no higher than 45mmHg. The second part of the college answer to Question 26 from the second paper of 2010 mentions this. An article commenting on one author's experience suggests that the intensivist should ignore this, as making attempts to increase minute ventilation will overload the right heart.
  • Pressures will be high: the gravid uterus contributes to decreased respiratory compliance
  • Prone ventilation will be difficult,  because of the belly.  However it is not completely off the table:  see this case report by Samanta et al (2014) who safely ventilated a third-trimester patient with H1N1.
  • Sustained paralysis is out of the question because of the risks to the foetus (arthrogryposis)
  • Pulmonary vasodilators are still available, including nitric oxide - though there is no experience in pregnant ARDS,  only in pulmonary hypertension as in Robinson et al (1999).

Thus, a management strategy mentioning all the important points would resemble the following list:

Airway:

  • Prepare for intubation with optimal senior ICU/anaesthetic expertise 
  • Expect a difficult airway and greatly decreased reserve

Ventilation:

  • Ensure normoxia by using a higher FiO2 target (minimum saturation 95%)
  • Aim for normocapnea,  CO2  no higher than 45mmHg
  • Rely on sedation to relax the respiratory muscles; sustained NMJ blockade is out of the question
  • Consider inhaled nitric oxide or prostacycline to improve V/Q matching
  • If these measures fail, the next option will be determined by local level of experience in prone ventilation or ECMO. Both will be risky and difficult to manage.

Circulation:

  • Ensure good central venous filling; high ventilator pressures may give rise to haemodynamic instability in the volume-depleted woman
  • Nurse the patient in alternating left and right recovery position (this may also improve V-Q matching)

Sedation

  • Avoid long-acting opiates and benzodiazepines to protect the foetal respiratoryt drive

Foetal wellbeing:

  • Continuous CTG monitoring
  • Early O&G/neonatology involvement
  • Preparation of the foetal lung for delivery with steroids

Social issues:

  • Maternal in-hospital mortality may be in the realm of 45%. Foetal mortality is more difficult to estimate. Family need to be aware of this.

References

Langenegger, Eduard, et al. "Severe acute respiratory infection with influenza A (H1N1) during pregnancy." SAMJ: South African Medical Journal 99.10 (2009): 713-716.

Oh's Intensive Care manual:

Chapter 64   (pp. 684) General  obstetric  emergencies by Winnie  TP  Wan  and  Tony  Gin

Chapter 65   (pp. 692) Severe  pre-existing  disease  in  pregnancy by Jeremy  P  Campbell  and  Steve  M  Yentis

Lapinsky, Stephen E. "Acute respiratory failure in pregnancy." Obstetric Medicine: The Medicine of Pregnancy 8.3 (2015): 126-132.

Samanta, Sukhen, J. Wig, and A. K. Baronia. "How safe is the prone position in acute respiratory distress syndrome at late pregnancy?." (2014).

Rubal, Bernard J., et al. "The'mill-wheel'murmur and computed tomography of intracardiac air emboli." Journal of the American Association for Laboratory Animal Science 48.3 (2009): 300-302.

Lifschultz, Barry D., and Edmund R. Donoghue. "Air embolism during intercourse in pregnancy." Journal of Forensic Science 28.4 (1983): 1021-1022.

Balkan, M. Erkan, and Göknur Alver. "Spontaneous pneumomediastinum in 3rd trimester of pregnancy." Annals of thoracic and cardiovascular surgery 12.5 (2006): 362.

Jain, Vikyath. "Acute respiratory distress syndrome, Respiratory failure, Pregnancy." ACUTE RESPIRATORY DISTRESS SYNDROME IN PREGNANCY 7540 (2015).

Robinson, Julian N., et al. "Inhaled nitric oxide therapy in pregnancy complicated by pulmonary hypertension." American journal of obstetrics and gynecology 180.4 (1999): 1045-1046.

Question 23 - 2011, Paper 1

A  35  year  old  female  is  39  weeks  pregnant.   Her  pregnancy   has  been complicated  by hypertension  and proteinuria.  Her blood pressure  is 160/120 mm Hg. You are called  to the labour  ward when  she suffers  a generalised (“grand mal”) convulsion.

Outline your overall plan of management.

College Answer

Initial management
ABC – ensure patent airway, oxygen via reservoir mask or bag-valve-mask  assembly and
support ventilation as needed
Left lateral tilt
Terminate the seizure
Diazepam 5-10mg or Mg 4g IV up to 8 g
Monitors / investigations

Management of Hypertension
Hydrallazine
Labetalol
(Other agents are acceptable – late in pregnancy – increasing trend to use “mainstream”
agents)

Treatment of convulsions
MgSO4 bolus followed by maintenance MgSO4
(Shown to be more effective than phenytoin or diazepam in preventing recurrent seizures) Addition of Benzodiazepine / Barbiturate if recurrent seizures despite MgSO4

Planning for delivery
Brief period of resuscitation once seizures controlled.

Post partum management
Continue anti-convulsants until patient improves (diuresis, fall in BP).

Discussion

This patient was having what can be described as "severe preeclampsia". The seizure pushes her over into the eclampsia territory.

Consequently, the management should look like this:

  • Attention to the ABCS, with management of life-threatening problems simultanous with a rapid focused examination and a brief history.
  • Airway:
    • Assess the need for airway support in context of post-ictal unconscious state
    • Weigh benefits of intubation against risks in context of the known airway access problems associated with pregnancy
  • Breathing/ventilation
    • Assess oxygenation and briefly examine for aspiration
    • High flow oxygen via NRBM if patient is not in need of immediate intubation
  • Circulatory support
    • Assess cardiovascular stability
      • left lateral 30° tilt if hypotensive
    • Access with widebore cannula
  • Immediate investigations:
    • FBC - looking for thrombocytopenia
    • LFTs - looking for HELLP, hepatic encephalopathy
    • EUC - looking for hyponatremia
    • CMP
    • Coags
    • Antiepileptic drug levels, if relevant
    • CT brain, if the patient fails to awaken
  • Specific management
    • Antihypertensives:
      • labetalol, nifedipine or hydralazine are of equivalent benefit
      • methyldopa and sodium nitroprusside are second line agents
    • Antiepileptic therapy:
      • Loading dose of magnesium sulfate, followed by an infusion, aiming at a serum level of 2.0-3.5mmol/L
      • Diazepam and phenytoin can be considered if seziures are refractory
    • Arrange for a consultation with the obstetrician regarding the safety and practicality of immediate delivery.

References

Heres an article by Baha  Sibai, who came up with the Tennessee classification for the HELLP syndrome:

Sibai, Baha M. "Diagnosis, prevention, and management of eclampsia."Obstetrics & Gynecology 105.2 (2005): 402-410.

Question 20 - 2012, Paper 1

A 40-year-old woman who is 34 weeks pregnant, presents to hospital following a generalised tonic/clonic seizure lasting 5 minutes.

  • List 6 differential diagnoses
  • Briefly discuss the indications for an urgent CT scan in this patient
  • List the reasons why pregnant patients may experience worsening of seizure controlList the consequences of seizures on perinatal morbidity and mortality 

College Answer

  • Differential diagnoses
    • Eclampsia
    • Idiopathic epilepsy including non-compliance, or subtherapeutic anticonvulsant levels
    • Intracerebral haemorrhage – including, venous thrombosis
    • Infection – meningitis, encephalitis
    • Space occupying lesion – abscess, tumour
    • Metabolic disorders – hypoglycaemia, hyponatremia
    • Hepatic encephalopathy- fatty liver of pregnancy
    • Hypertensive encephalopathy
    • Cerebral vasculitis.
    • Use of elicit drugs – Amphetamines, Cocaine
    • Reversible posterior leukoencephalopathy syndrome
  • Indications for CT scan
    • It is probably unnecessary in those with a clear diagnosis (e.g. known epilepsy or being treated for pregnancy induced hypertension), and who wake quickly without focal neurological deficit.
    • In patients without a clear cause for the seizure, and in particular those who are at risk for focal intracranial pathology (ie. Persistent altered level of consciousness and focal neurological signs) a CT scan may be warranted with appropriate shielding of the baby
    • It may be indicated imaging is thought warranted and urgent MRI is unavailable or not feasible (patient unstable)
  • Seizure control in pregnancy
    • Psychological stress
    • Altered Vd
    • Increased hepatic metabolism
    • Poor compliance because of fears of teratogenecity
    • Sleep deprivation
  • Seizures and perinatal morbidity and mortality
      • Risk of fetal hypoxia and acidosis
      • Fetal intracranial haemorrhage
      • Stillbirth
      • Fetal bradycardia
      • Neonatal haemorrhagic disorder secondary to deficient Vit K dependent clotting factors induced by AEDs
      • Maternal death
      • Maternal trauma leading to premature rupture of membranes, placental abruption, fetal death

Discussion

Organised into a familiar patern, the differentials for seizures in pregnancy look like this:

  • Stroke, cerebral aneurysm, eclampsia, sinus thrombosis
  • Menignitis / encephalitis
  • Intracranial neoplasm
  • Cocaine toxicity, poor antiepileptic drug compliance
  • SLE encephalitis, CNS vasculitis
  • Traumatic injury in context of coagulopathy or thrombocytopenia
  • Hepatic encephalopathy, hypoglycaemia, hyponatremia

As far as the CT goes... When would you expose a pregnant woman to radiation?

  • Failure to wake up after the seizure
  • Focal neurological signs
  • No obvious extracranial (eg. metabolic) cause for the seizure
  • Suspicion of intracranial hypertension

In any case, this authoritative body states that


" Teratogenesis is not a major concern after diagnostic CT studies of the pelvis in pregnancy, because the radiation dose is generally too low to cause such effects."

Reasons an epileptic might have more seziures during pregnancy:

  • Poor compliance
  • Anxiety regarding teratogenicity, and cessation of drugs on those grounds
  • Increased clearance of the drug
  • Increased volume of distribution
  • Stress and sleep deprivation

Weirdly, progensterone has an antiepileptic effect, and its levels are wildly elevated in pregnancy

Consequences to the foetus:

References

 

Beach, Robert L., and Peter W. Kaplan. "Seizures in pregnancy: diagnosis and management." International review of neurobiology 83 (2008): 259-271.

Walker, S. P., M. Permezel, and S. F. Berkovic. "The management of epilepsy in pregnancy." BJOG: An International Journal of Obstetrics & Gynaecology116.6 (2009): 758-767.

Chen, Yi-Hua, et al. "Affect of seizures during gestation on pregnancy outcomes in women with epilepsy." Archives of neurology 66.8 (2009): 979-984.

Otani, Koichi. "Risk factors for the increased seizure frequency during pregnancy and puerperium." Psychiatry and Clinical Neurosciences 39.1 (1985): 33-42.

Teramo, K., et al. "Fetal heart rate during a maternal grand mal epileptic seizure." Journal of Perinatal Medicine-Official Journal of the WAPM 7.1 (1979): 3-6.

LaJoie, Josiane, and Solomon L. Moshé. "Effects of seizures and their treatment on fetal brain." Epilepsia 45.s8 (2004): 48-52.

Klein, Pave, and Andrew G. Herzog. "Hormonal effects on epilepsy in women."Epilepsia 39.s8 (1998): S9-S16.

Question 21.1 - 2012, Paper 2

A 28-year-old 35-week pregnant woman presents to the Emergency Department with acute onset epigastric pain. The biochemical profile and haematology report are as follows:

Parameter

Result

Normal Range

Sodium

138 mmol/L

135 – 145

Potassium

4.4 mmol/L

3.2 –4.5

Chloride

102 mmol/L

100 – 110

Bicarbonate

27 mmol/L

22 – 27

Urea

4.3 mmol/L

3.0–8.0

Creatinine

0.07 mmol/L

0.07 – 0.12

Calcium

2.35 mmol/L

2.15 – 2.6

Corrected Calcium

2.53 mmol/L

2.15 – 2.8

Phosphate

2.75 mmol/L*

0.7 –1.4

Magnesium

0.8 mmol/L

0.7 –1.0

Glucose

4.7 mmol/L

3.6 –7.7

Albumin

36 G/L

33 – 47

CK

71 U/L

<160

Total Bilirubin

40 micromol/L*

4 – 20

GGT

45 U/L

0 – 50

ALP

185 U/L*

40 – 110

LDH

748 U/L*

110 – 250

AST

241 U/L*

<40

ALT

189 U/L*

<40

Haemoglobin

88 G/L*

110 – 160

White Cell Count

12.4 x 109/L

4.0 –15.0

Platelets

64 x 109/L*

150 – 400

  • What is the most likely diagnosis?
  • Give two additional tests that would support your diagnosis

College Answer

  • HELLP syndrome
  • Haptoglobins – low
  • Blood film showing evidence of haemolysis

Discussion

The diagnosis and management of HELLP syndrome is well covered elsewhere.

The things to look for:

  • Blood film shows fragmented RBCS - schistocytes
  • There is a raised reticulocyte count
  • The unconjugated bilirubin fraction increases
  • The haptoglobin decreases (as haptoglobin/hemoglobin complexes are removed)

Thus, one would order the following tests:

  • Blood film
  • Reticulocyte count
  • Unconjugated fraction of bilirubin
  • Haptoglobin

References

 

Oh's Intensive Care manual: Chapter 63   (pp. 677) Preeclampsia  and  eclampsia by Wai  Ka  Ming  and  Tony  Gin

Haram, Kjell, Einar Svendsen, and Ulrich Abildgaard. "The HELLP syndrome: clinical issues and management. A review." BMC pregnancy and childbirth 9.1 (2009): 8.

Question 28 - 2013, paper 2

A 20-year-old primigravida presents at 37 weeks gestation with jaundice, headache, blurred vision and hypertension (140/90 mmHg). The antenatal period was otherwise unremarkable. She is febrile, drowsy, pale, icteric and has pedal oedema. The uterus is palpated as for a full term pregnancy with a normal CTG trace. Examination is otherwise normal.

The following are her early blood results:

Parameter

Patient Value

Normal Adult Range

Hb

80 G/L*

115 – 160

Platelets

52 x 109/L*

140 – 400

International Normalised Ratio

1.8*

0.9 – 1.3

Activated Partial Thromboplastin Time

55 seconds*

25 – 38

Lactate Dehydrogenase

654 U/L*

110 – 250

Fibrinogen

1.0 G/L*

1.5 – 4.0

Total Bilirubin

51 micromol/L*

< 20

Urea

30 mmol/L*

3 – 8

Creatinine

298 micromol/L*

70 – 120

Potassium

5.1 mmol/L*

3.2 – 4.5

a) List four likely diagnoses for this clinical presentation.

b) For each of your differential diagnoses:

  1. List the important management interventions.
  2. List one additional diagnostic test.

College Answer

a)

  • Pre-eclampsia
  • HELLP Syndrome
  • Sepsis with DIC
  • HUS-TTP
  • Acute fatty liver of pregnancy

b) 
Pre-eclampsia

  • Deliver baby
  • Control BP
    • Hydralazine, beta blockers
    • SNP/GTN if intravenous agent required.
  • Prevention of seizures
  • Magnesium sulphate
  • Urinalysis – protein, WBCs, RBCs, casts 
  • Evidence of infection or proteinuria (pre-eclampsia) 
  • Renal US

HELLP Syndrome

  • Deliver baby
  • Regular monitoring of platelet count and liver function
  • Supportive measures whilst observing in HDU for dangerous complications
    • hepatic haemorrhage/rupture, progressive renal failure, pulmonary oedema.
  • Peripheral blood film smear 
  • Reticulocyte count, haptoglobins, conjugated/unconjugated bilirubin 
  • Haemolysis screen 
  • Full liver function tests

Sepsis with DIC

  • Timely delivery of baby in consultation with obstetrician.
  • Early broad-spectrum antibiotics.
  • Cardiovascular support – adequate volume resuscitation and establish MAP > 65mmHg.
  • Blood, sputum, urine and vaginal swab for MC&S 
  • Septic screen

HUS-TTP

  • Deliver the baby.
  • Fresh frozen plasma
  • Therapeutic plasma exchange
  • Corticosteroid therapy
  • Monoclonal antibody therapy – Rituximab
  • Evidence of haemolysis or MAHA 
  • Reticulocyte count, haptoglobins, conjugated/unconjugated bilirubin 
  • Haemolysis screen 
  • ADAMTS 13

Acute fatty liver of pregnancy

  • Timely delivery of baby once mother stabilised
  • Correction of DIC
  • Supportive therapy
  • Monitoring and treatment of complications post delivery e.g. pancreatitis
  • Consideration for liver transplantation in with irreversible severe liver failure despite delivery and aggressive supportive care
  • Full set liver function tests 
  • BSL 
  • Liver US
  • Evidence of haemolysis or MAHA 
  • Reticulocyte count, haptoglobins, conjugated/unconjugated bilirubin 
  • Haemolysis screen

Discussion

This question closely resembles Question 6 from the first paper of 2010.

The college has yielded five differentials, each of which deserve a whole chapter dedicated to them.

There is little to add to the sufficently detailed yet concise college answer.

One must remember that in most of these conditions, the key step is to deliver the baby.

The one critical investigations for each differential would be...

  • Pre-eclampsia - urinary protein
  • HELLP Syndrome - hemolytic screen
  • Sepsis with DIC - septic screen
  • HUS-TTP - ADAMTS13 test
  • Acute fatty liver of pregnancy - ultrasound to rule out hepatic rupture 

A more complete list:

Acute Liver Failure in Pregnancy
Cause Diagnostic features Notes and management options
Causes of liver failure which are unrelated to pregnancy
Drug-induced hepatitis
  • Paracetamol level
  • N-acetylcysteine crosses the placenta and has a protective effect in the foetus (Horowitz et al, 1997)
Shock, haemorrhage
  • Ultrasound: structurally normal liver
  • The LFT derangement which follows resuscitation for severe postpartum haemorrhage
  • Should improve after the shock state has resolved
Decompensation of pre-existing liver disease
  • Ultrasound: cirrhosis
  • Risk of preterm delivery and peripartum complications is increased (Aggarwal et al, 1999)
  • Normal management of the cirrhotic patient applies
Causes of liver failure which are exacerbated by pregnancy
Viral hepatitis
  • Hep B and C serology
  • Most common cause of LFT derangement in pregnancy
  • B and C are the most common
  • usually, BP is normal (in contrast with HELLP)
  • Ribavirin is contraindicated (a teratogen)
  • Other antiviral drugs may still be useful to decrease the viral load preior to delivery (to protect the baby from vertical transmission)
Portal vein thrombosis
  • Ultrasound: portal vein occlusion on Doppler
  • Due to hypercoagulable state of pregnancy
  • Heparin infusion is the standard of care 
  • Generally, TIPS procedure is too technically difficult in pregnancy - but that is another option
Hepatic venous thrombosis
  • Ultrasound: hepatic vein occlusion on Doppler
Cholecystitis
  • Ultrasound: thickened gall bladder wall, stones
  • LFTs: cholestatic picture
  • Conservative antibiotic therapy is best
  • Non-emergency surgery has better outcomes, i.e. it pays to delay until the acute flare has passed (Casey et al, 1996)
Pregnancy-related causes of liver failure
Hyperemesis gravidarum
  • LFTs: "transaminitis"
  • Unlike the others, this is a feature mainly of the first trimester
  • It is associated with raised transaminases, as opposed to liver failure per se - synthetic function is preserved (Outlaw et al, 2000)
  • Antiemetics and supportive care are the only options
Intrahepatic cholestasis of pregnancy (icterus gravidarum)
  • History of jaundice and pruritis
  • LFTs: cholestatic picture
  • Ultrasound: gall bladder looks normal
  • Pruritis is usually the patient's greatest concern. Can be managed with ursodeoxycholic acid.
  • Resolves rapidly with delivery
  • Will occur again in the next pregnancy in 60%
Pre-eclampsia
  • LFT derangement is due to fibrin deposition and endothelial dysfunction in the sinusoids.
  • Typically, this is also not "liver failure" but rather an LFt derangement of unclear significance (Munazza et al, 2013)
  • Standard therapy applies: antihypertensives, magnesium sulfate, and urgent delivery
HELLP
  • Thrombocytopenia
  • Low haptoglobin
  • Raised LDH,
  • Uncojugated bilirubin
  • Blood film features of haemolysis
  • See the local chapter.
  • Delivery is the treatment
  • Some authors recommend corticosteroids (Guntupalli et al, 2005) but only as a means of helping foetal lung maturation
  • Thrombocytopenia and LFT derangement will continue for up to 48 hours postpartum
  • Standard therapy applies: antihypertensives, magnesium sulfate, urgent delivery, correction of coagulopathy
Acute fatty liver of pregnancy
  • Presents with abdominal pain, vomiting, hypoglycaemia, coagulopathy
  • Characteristic ultrasound findings of the liver parenchyma
  • 18% maternal mortality, 2% foetal mortality (Guntupalli et al, 2005)
  • Liver failure is present, not just LFT derangement
  • Delivery fixes everything, as in HELLP
  • Fulminant liver failure may be present by then, and liver transplant may be the only option
Acute hepatic rupture
  • Ultrasound: haematoma
  • Haemodynamic instability and haemorrhagic shock
  • Abdominal pain (RUQ)
  • Haemoperitoneum
  • Maternal mortality is around 30% (Manas et al, 1985
  • If it has not ruptured (i.e. only a subcapsular haematoma) then conservative management and urgent dleivery are probably safe
  • Surgical packing and/or angioembolisation may be the only options
Other causes of febrile jaundiced coma with thrombocytopenia
TTP/HUS
  • Pentad: thrombocytopenia, microangiopathic haemolytic anemia, neurologic abnormalities, renal failure, and fever. See local chapter.
  • Low ADAMTS-13 levels are found. 
  • The SAQs often give a picture which could be consistent with TTP. It actually does occur often in pregnancy and the postpartum period (McMinn et al, 2001)
  • "How is this not HELLP?" one might ask. Well:
    • HELLP is never in the first trimester
    • HELLP always resolves following delivery
  • I.e. if after delivery the abnormalities persist, plasmapheresis becomes a serious option.
Sepsis with DIC
  • Bacteraemia
  • Haemodynamic instability, hypotension

References

The UpToDate links for the college's differentials are here:

Question 3.1 - 2014, Paper 1

a) Outline briefly the difficulties associated with the diagnosis of sepsis during late pregnancy and labour.

b) List the leading causes of sepsis in pregnant patients.

c) What are the common pathogens encountered in pregnancy-related sepsis?

d) List two antibiotics contra-indicated during pregnancy.

College Answer

a) Applying SIRS criteria to pregnancy may be problematic as there is:
1. Leukocytosis
2. Body temperature is raised during pregnancy and labour
3. Tachycardia and tachypnoea are seen during normal labour

b)
1. Pyelonephritis
2. Chorioamnionits
3. Septic abortion
4. Episiotomy infections
5. Necrotising fasciitis
6. Septic thrombophlebitis
7. Aspiration pneumonia

c)
1. Gram negative more common than Gram positive agents
2. E.Coli
3. Group B Streptococcus
4. Can also be polymicrobial – E.coli, Klebsiella

d)
1. Tetracyclines
2. Chloramphenicol
3. Aminoglycosides
4. Metronidazole
5. Sulphonamides
6. Trimethoprim
7. Fluoroquinolones
8. Some macrolides
9. Nitrofurantoin
10. Isoniazid

Note: Some antibiotics in the above list are relatively rather than absolutely contra-indicated. The list is not exclusive and candidates giving other valid choices were given credit.

Discussion

a) Outline briefly the difficulties associated with the diagnosis of sepsis during late pregnancy and labour.

Problems of the obsolete definition of sepsis and SIRS:

  • Neutrophilia is normal in pregnancy
  • Inflammatory markers are normally slightly elevated
  • The patient is normally slightly tachycardic, and may be slightly hypotensive, with a decreased SVRI. The circulation is normally hyperdynamic. They appear to be in early stages of vasodilated shock at the best of times.
  • Tachypnoea is normal in pregnancy and labour (chronic respiratory alkalosis)
  • The whole process of labour tends to obscure the findings one would normally associate with sepsis.
  • Then, suddenly, they collapse (as they tend to compensate right up until the last minute, and then drop everything, given their increased susceptibility to lipopolysaccharide)

Other problems (stolen from the LITFL entry on this topic)

  • Pneumonia may masquerade as the normal shortness of breath in pregnancy
  • Abdominal pain due to visceral pathology may masquerade as contractions (or - more  confusingly - may co-present with labour)
  • Appendicitis may be more difficult to diagnose, as the gravid uterus gets in the way of palpation.
  • Nausea, vomiting, constipation - all of these may be routine for the pregnant woman, and a bowel obstruction may present disastrously late (eg. this case report by Khan et al, 2012).
  • Abdominal pathology may be impossible to image, as everybody is going to freak out about the radiation exposure associated with a CT abdo/pelvis. This is in fact quite irrational, as the risks to a late-term foetus are quite small  (Chen et al, 2008). Instead, people should think about the foetal risk associated with remaining inside the septic abdomen of a critically ill mother whose source control is compromised by indecision about imaging. (In case anybody is interested, the dose from such a CT will total about 5 rads, which maxes out the recommended safe total foetal cumulative dose of 5-10 rads).
  • Urinary sepsis may be asymptomatic (urinary frequency is pretty normal)

b) List the leading causes of sepsis in pregnant patients.

  • Chorioamnionitis
  • Urinary tract infections
  • Pyelonephritis
  • Endometritis
  • Septic abortion

also...

  • Episiotomy infections
  • Necrotising fasciitis of the ceasarian wound
  • Septic thrombophlebitis - especially pelvic vein thrombophlebitis
  • Aspiration pneumonia
  • Acute pyelonephritis
  • Retained products of conception
    • Septic abortion
    • Conservative management of placenta accreta or percreta
  • Neglected chorioamnionitis or endomyometritis
    • Uterine microabscess or necrotizing myometritis
    • Gas gangrene
    • Pelvic abscess
  • Unrecognized or inadequately treated necrotizing fasciitis
    • Abdominal incision
    • Episiotomy
    • Perineal laceration
  • Bacterial pneumonia
  • Bacterial examples
    • Staphylococcus
    • Pneumococcus
    • Mycoplasma
    • Legionella
  • Viral pneumonia
    • Influenza
    • H1N1
    • Herpes
    • Varicella
  • Intraperitoneal etiology (nonobstetric)
    • Ruptured appendix or acute appendicitis
    • Bowel infarction
    • Acute cholecystitis
    • Necrotizing pancreatitis

c) What are the common pathogens encountered in pregnancy-related sepsis?

Oh's Manual quotes the following bugs:

To this, the Sanford Guide adds a few:

  • Enterobacteriaceae
  • Chlamydia trachomatis
  • Ureaplasma urealyticum

(these are specific to chorioamnionitis and septic abortion)

d) List two antibiotics contra-indicated during pregnancy.

 The full list:

Antibiotics which are contraindicated in pregnancy or lactation, and Why
Contraindicated antibiotics Why
Aminoglycosides in high doses Increased uptake by neonatal kidney leads to increased nephrotoxicity (but apparently gentamicin is still relativey safe)
Streptomycin 8th cranial nerve damage 
Sulfonamides Kernicterus in the newborn due to displacement of bilirubin off albumin, particularly if used shortly before birth. The specific culprit is sulfamethoxazole. Trimpethoprim appears to be relatively safer.
Tetracyclines Tetracyclines have nightmarish dental and bony effects.  In fact, these drugs are contraindicated from 16th week of gestation all the way until the 7th year of extrauterine life.
Quinolones Quinolones cause birth defects (though it seems fluoroquinolones are safe, and it was really mainly nalidixic acid that was the culprit).
Rifampicin Seems to be somewhat teratogenic, mainly in animal studies (spina bifida and impaired osteogenesis seem to be the major consequences)- but in humans one may overlook this if rifampicin is strongly indicated (eg. treatment of lifethreatening tuberculosis)
Fusidic acid Like sulfonamides, causes displacement of bilirubin by competing with it for albumin binding
Chloramphenicol This "Grey baby syndrome" is the consequence of disrupted mitochondrial function, when chloramphenicol metabolites interfere with the electron transport chain. Foetal failure to properly metabolise chloraphenicol by glucourinidation seems to be to blame.
Azole antifungals Teratigenic and embryotoxic. The specific dangerous ones are ketoconazole  fluconazole and voriconazole, earning a D classification. 
Echinocandins Hard to discuss humans in the absence of real data, but in animals using normal treatment doses caspofungin and anidulafungin cause skeletal abnormalities, reduction of litter size, ossification and rib malformations.
Flucytosine Embryotoxic and in fact abortificant in the first trimester, which is hardly surprising given that its main metabolite is 5-fluorouracil
Albendazole Teratogenic and embryotoxic. If the pregnant lady has some sort of hideous helminthic parasitosis which cannot wait until after delivery, ivermectin is probably a safer alternative
Foscarnet Seems to be teratogenic in animals, but if your CV infection is so severe and resistant that you've failed primary therapy, the chances are that your foetus is already significantly damaged by congenital CMV.

The college answer for Question 3.1 from the first paper of 2014 also lists nitrofurantoin, isoniazid and macrolides as drugs which are relatively contraindicated. This in fact, is not true:

References

Oh's Intensive Care manual:

Chapter 64   (pp. 684) General  obstetric  emergencies by Winnie  TP  Wan  and  Tony  Gin

Chapter 65   (pp. 692) Severe  pre-existing  disease  in  pregnancy by Jeremy  P  Campbell  and  Steve  M  Yentis

Fernandez-Perez, Evans R., et al. "Sepsis during pregnancy." Critical care medicine 33.10 (2005): S286-S293.

Barton, John R., and Baha M. Sibai. "Severe sepsis and septic shock in pregnancy." Obstetrics & Gynecology 120.3 (2012): 689-706.

van Dillen, Jeroen, et al. "Maternal sepsis: epidemiology, etiology and outcome." Current opinion in infectious diseases 23.3 (2010): 249-254.

Khan, Muhammad R., and Sameer ur Rehman. "Sigmoid volvulus in pregnancy and puerperium: a surgical and obstetric catastrophe. Report of a case and review of the world literature." World Journal of Emergency Surgery 7.1 (2012): 1.

Demers, P., et al. "Effects of tetracyclines on skeletal growth and dentition. A report by the Nutrition Committee of the Canadian Paediatric Society."Canadian Medical Association Journal 99.17 (1968): 849.

Bar-Oz, Benjamin, et al. "The safety of quinolones—a meta-analysis of pregnancy outcomes." European Journal of Obstetrics & Gynecology and Reproductive Biology 143.2 (2009): 75-78.

Erić, Mirela, and Ana Sabo. "Teratogenicity of antibacterial agents.Collegium antropologicum 32.3 (2008): 919-925.

Chen, Morie M., et al. "Guidelines for computed tomography and magnetic resonance imaging use during pregnancy and lactation." Obstetrics & Gynecology 112.2, Part 1 (2008): 333-340.

Mylonas, Ioannis. "Antibiotic chemotherapy during pregnancy and lactation period: aspects for consideration." Archives of gynecology and obstetrics 283.1 (2011): 7-18.

Pilmis, Benoît, et al. "Antifungal drugs during pregnancy: an updated review." Journal of Antimicrobial Chemotherapy (2014): dku355.

David, S. Ben, et al. "The safety of nitrofurantoin during the first trimester of pregnancy: meta‐analysis." Fundamental & clinical pharmacology 9.5 (1995): 503-507.

Lin, Kueiyu Joshua, et al. "Safety of macrolides during pregnancy." American journal of obstetrics and gynecology 208.3 (2013): 221-e1.

Bar-Oz, Benjamin, et al. "Pregnancy outcome after gestational exposure to the new macrolides: a prospective multi-center observational study." European Journal of Obstetrics & Gynecology and Reproductive Biology 141.1 (2008): 31-34.

Ormerod, P. "Tuberculosis in pregnancy and the puerperium." Thorax 56.6 (2001): 494-499.

Question 19 - 2014, paper 2

A 26-year-old female presents from home confused with a low-grade fever. Her blood pressure is 160/100 mmHg. She has no gross motor deficits on neurological examination.

Ten days prior to this presentation, she had induction of labour and delivery of a still-born foetus, at 32 weeks gestation, complicated by disseminated intravascular coagulation. She had been on labetalol for pregnancy-induced hypertension.

Her discharge medications included paracetamol, tramadol and a selective serotonin reuptake inhibitor. She has a six-year history of uncomplicated Hepatitis C infection.

a) List the differential diagnoses for her confusion and temperature.

b) Outline your approach to establishing the diagnosis.

College Answer

a)

Pregnancy related: Eclampsia / preeclampsia / HELLP, Posterior reversible encephalopathy
syndrome (PRES), Hypertensive encephalopathy

Primary neurological: Infection (meningitis / encephalitis), cerebral venous thrombosis, seizure
disorder, other cerebro-vascular

Metabolic: Sodium (hypo/hyper), Glucose (hypo/hyper), Renal failure, Liver failure (HCV /
Paracetamol / Antidepressants),

Drugs: Accidental / intentional overdose, drug reactions (serotonin syndrome)

b)
History: Collateral, Pregnancy issues, Ongoing blood loss, bleeding / bruising, drug ingestions, mood
/ affect, headaches

Examination: BP, uterine size / discharge, oedema, meningism, neurological (tone, reflexes,
symmetry), chronic liver disease

Investigations:
FBC: Bleeding, platelets, WCC
UEC: urea / creatinine, Na, Ca, glucose
Coagulation: DIC, INR for CLD
LFT / Ammonia: hepatic encephalopathy, drug reactions ABG: hypoxia / hypercardia
Urinary drug screen / paracetamol level
Sepsis Screen, CT head +/- LP

Discussion

This works better if it is presented in the form of a table

Differential Diagnosis
of Unconsciousness and Fever
in the Pregnant Patient
Causes Investigations

Vascular causes:

  • Cerebral venous sinus thrombosis
  • PRES, hypertensive encephalopathy
  • Subarachnoid haemorrhage
  • CT brain +/- CT angiogram (venogram)
  • MRI brain

Infectious causes:

  • Meningitis 
  • Encephalitis without meningism
  • Neurological sequelae of systemic infection, eg. septic encephalopathy
  • Inflammatory markers
  • Blood cultures
  • Antenatal history, (i.e. thinking about Group A  streptococci)
  • LP, CSF microscopy and culture
  • CT brain to rule out brain abscess

Drug-related causes:

  • Paracetamol overdose with hepatic encephalopathy
  • Serotonin syndrome
  • Tramadol overdose
  • Overdose (or, just real party-style dosing) of recreational drugs
  • History  of drug abuse
  • Examination findings consistent with IVDU
  • Clinical features of  a recognisable toxidrome, eg. opiate, or classicl features of serotonin syndrome
  • Paracetamol level
  • CK, urinary myoglobin

Intrinsic neurological cause

  • Worsening of seizure disorder, associated with pregnancy (i.e. non-convulsive status epilepticus)
  • History of epilepsy
  • History or typical seizure control measures and compliance with them

Autoimmune causes

  • SLE-related Cerebral vasculitis
  • "Vasculitic screen" -ANA, ENA, ANCA, etc
  • CTA or MRA with contrast
  • ESR

Traumatic or environmental causes

  • Traumatic brain injury due to accident or non-accidental trauma 
  • Hypothermia or hyperthermia
  • History of domestic violence
  • History of exposure to the elements (eg. known to be homeless)
  • Clinical features consistent with non-accidental injury, eg. brusing at varying stages of evolution 

Endocrine and metabolic causes:

  • Hypoadrenalism
  • Hypothyroidism
  • Hepatic encephalopathy
  • Uremic encephalopathy
  • Wernicke's encephalopathy
  • Hyper or hyponatremia
  • Hyper or hypoglycamia
  • Numerous others!
  • Random cortisol
  • Short syncathen test
  • TFTs, free T3 and T4
  • EUC and CMP - for renal function and sodium
  • BSl, ketones, serum osmolality (HONK, hypoglycaemia)
  • Red cell transketolase (thiamine deficiency)
  • LFTs (acute hepatitis)
  • Coags (chornic hepatitis - synthetic function)
  • Ammonia level (hepatic encephalopathy, valproate overdose)
  • ABG (hypoxia, hypercapnea, acidosis of other causes)

Differentials specific to pregnancy:

  • Eclampsia or preeclampsia
  • HELLP
  • Historic details of antenatal care, eg. has anybody tested for proteinuria

References

Oh's Intensive Care manual: Chapter 63   (pp. 677) Preeclampsia  and  eclampsia by Wai  Ka  Ming  and  Tony  Gin

RCOG Guidelines for the management of severe pre-eclampsia/eclampsia (2006)

Duckitt, Kirsten, and Deborah Harrington. "Risk factors for pre-eclampsia at antenatal booking: systematic review of controlled studies." Bmj 330.7491 (2005): 565.

Lorquet, Sophie, et al. "Aetiology and physiopathology of preeclampsia and related forms." Acta Clinica Belgica 65.4 (2010): 237-241.

Young, Brett C., Richard J. Levine, and S. Ananth Karumanchi. "Pathogenesis of preeclampsia." Annual Review of Pathological Mechanical Disease 5 (2010): 173-192.

Altman, D., et al. "Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial."Lancet 359.9321 (2002): 1877-1890.

Beach, Robert L., and Peter W. Kaplan. "Seizures in pregnancy: diagnosis and management." International review of neurobiology 83 (2008): 259-271.

Walker, S. P., M. Permezel, and S. F. Berkovic. "The management of epilepsy in pregnancy." BJOG: An International Journal of Obstetrics & Gynaecology116.6 (2009): 758-767.

Chen, Yi-Hua, et al. "Affect of seizures during gestation on pregnancy outcomes in women with epilepsy." Archives of neurology 66.8 (2009): 979-984.

Otani, Koichi. "Risk factors for the increased seizure frequency during pregnancy and puerperium." Psychiatry and Clinical Neurosciences 39.1 (1985): 33-42.

Teramo, K., et al. "Fetal heart rate during a maternal grand mal epileptic seizure." Journal of Perinatal Medicine-Official Journal of the WAPM 7.1 (1979): 3-6.

LaJoie, Josiane, and Solomon L. Moshé. "Effects of seizures and their treatment on fetal brain." Epilepsia 45.s8 (2004): 48-52.

Klein, Pave, and Andrew G. Herzog. "Hormonal effects on epilepsy in women."Epilepsia 39.s8 (1998): S9-S16.

Vajda, Frank JE, et al. "Seizure control in antiepileptic drug‐treated pregnancy." Epilepsia 49.1 (2008): 172-176.

Question 30.2 - 2016, Paper 2

A 30-year-old female who is 34 weeks pregnant (G1PO) has presented with nausea and vomiting for 3 days with right upper quadrant pain. On examination she is confused, jaundiced with a blood pressure of 120/70 mmHg.

The following are results from a venous blood sample taken on admission:

Parameter

Patient Value

Normal Adult Range

Sodium

138 mmol/L

135 - 145

Potassium

3.8 mmol/L

3.5 - 5.0

Urea

15.0 mmol/L*

3.0 - 8.0

Creatinine

245 µmol/L*

45 - 90

Albumin

30 q/L*

33 - 40

Glucose

2.5 mmol/L*

3.0 - 7.8

Bilirubin (total)

142 umol/L*

< 20

Alkaline phosphatase

293 U/L*

30 - 110

Aspartate  aminotransferase

99 U/L*

< 31

Alanine  aminotransferase

88 U/L*

< 34

y-Glutamyl  transferase

67 U/L*

< 40

Lactate  dehydrogenase

180 U/L

110 - 250

Uric acid

0.72 mmol/L*

0.15 - 0.50

Activated partial thromboplastin time

45 sec*

36 - 38

International normalised ratio

2.8*

0.9 - 1.3

Platelets

123 x 109/L*

150 - 450

List three likely differential diagnoses for the above clinical picture. (30% marks)

College answer

  • Acute fatty liver of pregnancy (AFLP): 
  • HELLP (Haemolysis, elevated liver enzymes and low platelets) Syndrome: 
  • Pre-eclampsia with hepatic involvement 
  • Viral hepatitis – commonest cause of jaundice in pregnancy 
  • ALT and AST would be expected to be greatly elevated (>500 – 1000 U/L) and DIC is rare
  • Intrahepatic Cholestasis of Pregnancy 

 
Additional Examiners‟'Comments: 
Many candidates did not complete part 2. 

 

Discussion

The abnormalities are:

  • Confusion
  • RUQ pain
  • Renal failure
  • Hypoglycaemia
  • Raised bilirubin
  • Raised LFTs - no specific pattern
  • Raised urate
  • Coagulopathy (both APTT and INR)
  • Thrombocytopenia, which is mild

Thus, this is pre-eclampsia, or something along the spectrum between pre-eclampsia and HELLP syndrome. A distant third possibility is TTP-HUS, but the LDH is within the normal range, which means that there is probably no haemolysis.

Thus, the differentials might include

  • Pre-eclampsia
  • HELLP
  • TTP/HUS
  • Acute fatty liver of pregnancy

Such things are usually best described in the form of a table. Good articles inform the discussion, most notably the article by Guntupalli et al from the 2005 special pregnancy issue of Critical Care Medicine.

Acute Liver Failure in Pregnancy
Cause Diagnostic features Notes and management options
Causes of liver failure which are unrelated to pregnancy
Drug-induced hepatitis
  • Paracetamol level 
  • N-acetylcysteine crosses the placenta and has a protective effect in the foetus (Horowitz et al, 1997)
Shock, haemorrhage
  • Ultrasound: structurally normal liver
  • The LFT derangement which follows resuscitation for severe postpartum haemorrhage
  • Should improve after the shock state has resolved
Decompensation of pre-existing liver disease
  • Ultrasound: cirrhosis
  • Risk of preterm delivery and peripartum complications is increased (Aggarwal et al, 1999)
  • Normal management of the cirrhotic patient applies
Causes of liver failure which are exacerbated by pregnancy
Viral hepatitis
  • Hep B and C serology
  • Most common cause of LFT derangement in pregnancy
  • B and C are the most common
  • usually, BP is normal (in contrast with HELLP)
  • Ribavirin is contraindicated (a teratogen)
  • Other antiviral drugs may still be useful to decrease the viral load preior to delivery (to protect the baby from vertical transmission)
Portal vein thrombosis
  • Ultrasound: portal vein occlusion on Doppler
  • Due to hypercoagulable state of pregnancy
  • Heparin infusion is the standard of care 
  • Generally, TIPS procedure is too technically difficult in pregnancy - but that is another option
Hepatic venous thrombosis
  • Ultrasound: hepatic vein occlusion on Doppler
Cholecystitis
  • Ultrasound: thickened gall bladder wall, stones
  • LFTs: cholestatic picture
  • Conservative antibiotic therapy is best
  • Non-emergency surgery has better outcomes, i.e. it pays to delay until the acute flare has passed (Casey et al, 1996)
Pregnancy-related causes of liver failure
Hyperemesis gravidarum
  • LFTs: "transaminitis"
  • Unlike the others, this is a feature mainly of the first trimester
  • It is associated with raised transaminases, as opposed to liver failure per se - synthetic function is preserved (Outlaw et al, 2000)
  • Antiemetics and supportive care are the only options
Intrahepatic cholestasis of pregnancy (icterus gravidarum)
  • History of jaundice and pruritis
  • LFTs: cholestatic picture
  • Ultrasound: gall bladder looks normal
  • Pruritis is usually the patient's greatest concern. Can be managed with ursodeoxycholic acid.
  • Resolves rapidly with delivery
  • Will occur again in the next pregnancy in 60%
Pre-eclampsia
  • LFT derangement is due to fibrin deposition and endothelial dysfunction in the sinusoids.
  • Typically, this is also not "liver failure" but rather an LFt derangement of unclear significance (Munazza et al, 2013)
  • Standard therapy applies: antihypertensives, magnesium sulfate, and urgent delivery
HELLP
  • Thrombocytopenia
  • Low haptoglobin
  • Raised LDH,
  • Uncojugated bilirubin
  • Blood film features of haemolysis
  • See the local chapter.
  • Delivery is the treatment
  • Some authors recommend corticosteroids (Guntupalli et al, 2005) but only as a means of helping foetal lung maturation
  • Thrombocytopenia and LFT derangement will continue for up to 48 hours postpartum
  • Standard therapy applies: antihypertensives, magnesium sulfate, urgent delivery, correction of coagulopathy
Acute fatty liver of pregnancy
  • Presents with abdominal pain, vomiting, hypoglycaemia, coagulopathy
  • Characteristic ultrasound findings of the liver parenchyma
  • 18% maternal mortality, 2% foetal mortality (Guntupalli et al, 2005)
  • Liver failure is present, not just LFT derangement
  • Delivery fixes everything, as in HELLP
  • Fulminant liver failure may be present by then, and liver transplant may be the only option
Acute hepatic rupture
  • Ultrasound: haematoma
  • Haemodynamic instability and haemorrhagic shock
  • Abdominal pain (RUQ)
  • Haemoperitoneum
  • Maternal mortality is around 30% (Manas et al, 1985
  • If it has not ruptured (i.e. only a subcapsular haematoma) then conservative management and urgent dleivery are probably safe
  • Surgical packing and/or angioembolisation may be the only options
Other causes of febrile jaundiced coma with thrombocytopenia
TTP/HUS
  • Pentad: thrombocytopenia, microangiopathic haemolytic anemia, neurologic abnormalities, renal failure, and fever. See local chapter.
  • Low ADAMTS-13 levels are found. 
  • The SAQs often give a picture which could be consistent with TTP. It actually does occur often in pregnancy and the postpartum period (McMinn et al, 2001)
  • "How is this not HELLP?" one might ask. Well:
    • HELLP is never in the first trimester
    • HELLP always resolves following delivery
  • I.e. if after delivery the abnormalities persist, plasmapheresis becomes a serious option.
Sepsis with DIC
  • Bacteraemia
  • Haemodynamic instability, hypotension

References

Oh's Intensive Care manual:

Chapter 64   (pp. 684) General  obstetric  emergencies by Winnie  TP  Wan  and  Tony  Gin

Chapter 65   (pp. 692) Severe  pre-existing  disease  in  pregnancy by Jeremy  P  Campbell  and  Steve  M  Yentis

Pandey, Chandra Kant, et al. "Acute liver failure in pregnancy: Challenges and management." Indian journal of anaesthesia 59.3 (2015): 144.

Sahai, Shweta, and Ravi Kiran. "Acute liver failure in pregnancy: Causative and prognostic factors." Saudi journal of gastroenterology: official journal of the Saudi Gastroenterology Association 21.1 (2015): 30.

Guntupalli, Saketh R., and Jay Steingrub. "Hepatic disease and pregnancy: an overview of diagnosis and management." Critical care medicine 33.10 (2005): S332-S339.

Aggarwal, Neelam, et al. "Pregnancy and cirrhosis of the liver." Australian and New Zealand journal of obstetrics and gynaecology 39.4 (1999): 503-506.

Horowitz, Rivka S., et al. "Placental transfer of N-acetylcysteine following human maternal acetaminophen toxicity." Journal of Toxicology: Clinical Toxicology 35.5 (1997): 447-451.

Outlaw, William M., Jamal A. Ibdah, and Kenneth L. Koch. "Hyperemesis Gravidarum and Maternal Liver Disease." (2000).

Munazza, Bibi, et al. "Liver function tests in preeclampsia." J Ayub Med Coll Abbottabad 23.4 (2011): 3-5.

Manas, Kenneth J., et al. "Hepatic hemorrhage without rupture in preeclampsia." New England Journal of Medicine 312.7 (1985): 424-426.

Kang, Yun Dan. "Portal Vein Thrombosis during Pregnancy." Korean Journal of Perinatology 26.3 (2015): 245-249.

Casey, Brian M., and Susan M. Cox. "Cholecystitis in pregnancy." Infectious diseases in obstetrics and gynecology 4.5 (1996): 303-309.

McMinn, Johnny R., and James N. George. "Evaluation of women with clinically suspected thrombotic thrombocytopenic purpura‐hemolytic uremic syndrome during pregnancy." Journal of clinical apheresis 16.4 (2001): 202-209.

Question 9.3 - 2017, Paper 1

With respect to the coagulation status of a third trimester pregnant patient compared to that in the nonpregnant state, indicate the change you would anticipate for each test listed below:

Platelet count

Factor V, Vll, 'X, X levels

Fibrinogen level

Protein S level

(20% marks)

College answer

a) Platelet count: Decrease

b) Factors V, VII, IX, X level: Increase

c) Fibrinogen level: Increase

d) Protein S level: Decrease

Discussion

The overall trend in pregnancy is towards hypercoagulability. In the third trimester, coagulation activity is about double that of normal. The best source to read further is probably the 2003 article by Katarina Bremme.

In brief:

  • Platelet count decreases, particularly in late pregnancy
    • Normal pregnancy is associated with a degree of enhanced platelet destruction which is compensated for by increased production
    • The destruction takes place in the uteroplacental circulation
  • Factors VII, VIII, IX, X, XII and von Willebrand factor increase significantly
    • Factor VII may increase as much as tenfold.
  • Factor XI decreases down to 60–70% of the non-pregnant value
  • Factors II and V do not change much in pregnancy (Factor V seems to decrease slightly, down to 82% of the normal level)
  • Fibrinogen levels increase throughout pregnancy
  • Protein S levels decrease progressively during pregnancy
  • Protein C activity is unaffected by pregnancy
  • Plasma fibrinolytic activity decreases throughout pregnancy, but returns to normal within one hour of delivery. This is due to synthesis of plasminogen activator inhibitor-1 and -2 by the placenta

References

Bremme, Katarina A. "Haemostatic changes in pregnancy." Best practice & research Clinical haematology 16.2 (2003): 153-168.

Question 28 - 2017, Paper 1

This question relates to the critically ill obstetric patient.

a) List the diagnostic criteria for peri-partum cardiomyopathy. (30%marks)

With respect to amniotic fluid embolism (AFE):

i.  List six important risk factors.(30% marks)

ii. Outline the important clinical features.(40% marks)

 

College answer

a)
• 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. The latter 
may be characterized as an LV ejection fraction < 45%, fractional shortening < 30%, or 
both, with or without an LV end-diastolic dimension 2.7 cm/m2 body surface area. (This 
level of detail not expected)

b)
i. List six important risk factors 
• 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

ii. Outline the important clinical features of amniotic fluid embolism 
• The onset of the symptoms and signs of amniotic fluid embolism syndrome 
(AFES) most commonly occurs during labour and delivery, or immediately 
postpartum
• Non-specific symptoms – chills, nausea, vomiting, agitation
• Hypotension due to cardiogenic shock
• Hypoxemia and respiratory failure
• Disseminated intravascular coagulation
• Coma or seizures

Discussion

a)

In actual fact there are several competing definitions, of which the college offers one which is probably the least vague. Here is a table from  the ESC statement (Sliwa et al, 2010)

definitions of peripartum cardiomyopathy




     
  •  

Characteristic features of peripartum cardiomyopathy (also from Sliwa et al):

  • It is usually a postpartum process: only 9% present antepartum. NHL-BIOR definition calls it PPCM if it is one month before or five months after delivery, but the ESC people felt this (totally arbitrary) timeframe would lead to underdiagnosis.
  • There is mainly LV dysfunction
  • The LV is usually dilated (if it is dilated beyond 60mm, the chances of recovery are small)
  • It usually gets better: An estimated 23%-54% of patients show complete recovery of their systolic function within 6 months.

b)

To mix up the college answer with an article by Knight et al (2012)

  • Precipitous or tumultuous labour.
  • Ethnic minority background
  • Emergency delivery
  • Smoking during pregnancy
  • Diabetes
  • Socioeconomic disadvantage
  • Age over 35 (what the college describes as "advanced maternal age", otherwise known as "checkout time" )
  • 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

Cardinal clinical features:

  • Shock
  • Hypoxia
  • Altered mental status
  • DIC

Other associated features are listed by Moore et al (2005):

  • Seizures
  • Confusion
  • Agitation
  • Foetal distress
  • Fever
  • Rigors
  • Nausea / vomiting
  • Headache

References

Moore, Jason, and Marie R. Baldisseri. "Amniotic fluid embolism." Critical care medicine 33.10 (2005): S279-S285.

Meyer, JR "Embolia pulmonar amnio caseosa". Brasil Medico. 1926; 2:301. 

Attwood, H. D. "The histological diagnosis of amniotic‐fluid embolism." The Journal of Pathology 76.1 (1958): 211-215.

Steiner, Paul E., and Clarence Chancelum Lushbaugh. "Maternal pulmonary embolism by amniotic fluid: as a cause of obstetric shock and unexpected deaths in obstetrics." Journal of the American Medical Association 117.15 (1941): 1245-1254.

Tuffnell, D. J. "United Kingdom amniotic fluid embolism register." BJOG: An International Journal of Obstetrics & Gynaecology 112.12 (2005): 1625-1629.

Conde-Agudelo, Agustín, and Roberto Romero. "Amniotic fluid embolism: an evidence-based review." American journal of obstetrics and gynecology 201.5 (2009): 445-e1.

Tamura, Naoaki, et al. "Amniotic fluid embolism: Pathophysiology from the perspective of pathology." Journal of Obstetrics and Gynaecology Research43.4 (2017): 627-632.

Sideris, Ioannis G., and Kypros H. Nicolaides. "Amniotic fluid pressure during pregnancy.Fetal diagnosis and therapy 5.2 (1990): 104-108.

Uyeno, Doko. "The physical properties and chemical composition of human amniotic fluid.Journal of Biological Chemistry 37.1 (1919): 77-103.

Lim, Y., et al. "Recombinant factor VIIa after amniotic fluid embolism and disseminated intravascular coagulopathy." International Journal of Gynecology & Obstetrics 87.2 (2004): 178-179.

Davies, Sharon. "Amniotic fluid embolism and isolated disseminated intravascular coagulation." Canadian Journal of Anesthesia 46.5 (1999): 456-459.

Kaneko, Yuhko, et al. "Continuous Hemodiafiltration for Disseminated Intrav ascular Coagulation and Shock due to Amniotic Fluid Embolism: Report of a Dramatic Response." Internal medicine 40.9 (2001): 945-947.

Awad, I. T., and G. D. Shorten. "Amniotic fluid embolism and isolated coagulopathy: atypical presentation of amniotic fluid embolism." European journal of anaesthesiology 18.6 (2001): 410-413.

Waters, Jonathan H., et al. "Amniotic fluid removal during cell salvage in the cesarean section patient.The Journal of the American Society of Anesthesiologists 92.6 (2000): 1531-1536.

Knight, Marian, et al. "Incidence and risk factors for amniotic-fluid embolism."Obstetrics & Gynecology 115.5 (2010): 910-917.

Knight, Marian, et al. "Amniotic fluid embolism incidence, risk factors and outcomes: a review and recommendations." BMC pregnancy and childbirth12.1 (2012): 7.

Question 17 - 2017, Paper 2

List the strategies available for the control of postpartum haemorrhage and give the advantages and disadvantages of each. 

College answer

Tx

Advantages 

Disadvantages

Physical – 

vigorous bi-manual massage

Immediate use, no specific equipment.

Only works in uterine atony Worsens traumatic injury

Pharmacological  

 Oxytocin (first line)

Simple, rapid action

Hypotension and tachycardia Risk on the CVS unstable pt with no haemorrhage control

 Ergometrine (second line)

Simple, rapid action

Hypertension, N&V

Vasospasm of the arteries in overdose-> gangrene, angina, ischaemia

Prostaglandin (third line)

Misoprostol PR 

Carboprost, IMI or intrauterine

Simple

B/Constriction, flushing 

Asthma is Contra Indic

May inc pulmonary shunting and maternal hypoxia

Surgical

Manual removal of placenta/retained products

Removes bleeding cause

Needs GA in theatre

Surgical repair Soft tissue trauma/artery ligation

Definitive Tx

Needs GA. 

Bakri Balloon +/- BT Cath

Immediate control

Infection risk

Not definitive Tx

Can mask ongoing bleeding.

Hysterectomy

Definitive Tx

fertility

Radiological

Selective embolisation of pelvic vessels

Balloon tamponade bilateral

fermoral arteries as a temporizing

measure

REBOA

May be definitive Can avoid hysterectomy

Only available in tertiary centres

Not suitable in catastrophic haemorrhage

Temporising measure 

Risk of ischeamia to pelvic organs

Maintain normal physiological milieu

Avoid acidosis

Not strictly a

May not be effective alone

Hypothermia

Hypocalcaemia

Correction of coagulopathy

control option but

will not allow normal haemostasis to occur if absent

Correction of coagulopathy may require product transfusion with attendant possible complications

Discussion

Advantages and disadvantages of Methods used to Control
Postpartum Haemorrhage
Method Advantages Disadvantages
Mechanical haemostasis methods

Uterine massage

  • Non-invasive
  • Requires zero training
  • Could be performed by the gravida herself
  • May assist in clot expulsion
  • Does not appear to have any harmful effects
  • May not be effective
  • Time-consuming and requires higher nursing workload
  • Lack of evidence regarding effect (WHO recommend against this practice and describe it as a time-wasting exercise) 

Bimanual compression

  • This is where you a fist
    in the vagina and a hand on the abdominal wall.
  • Effective to establish haemostasis.
  • Buys time for definitive management
  • Not exactly a long-term solution
  • All available evidence describing this technique is low quality. All society recommendations in support of it are weak recommendations.

Manual aortic compression

  • Effective to establish haemostasis
  • Buys time for definitive management
  • Only available intraoperatively
  • Not exactly a long-term solution
Pharmacological means of encouraging uterine contraction

Oxytocin

  • Synthetic analogue of endogenous hormone
  • Available widely, and cheap
  • Recommended universally in the management of the third stage of labour (Dahlke et al, 2015)
  • Fewer side-effects than ergometrine
  • Causes hypotension
  • Contraindicated in pre-eclampsia
  • Even though it's recommended as first  line by everyone, there are not randomised controlled trials which support its efficacy.

Ergometrine

  • Ergot alkaloid which increases uterine tone
  • Widely available
  • As prophylaxis, it is at least as effective as oxytocin
  • Causes vomiting, nausea, hypertension; more side-effects than oxytocin
  • Contraindicated in preeclampsia
  • May cause coronary vasospasm
  • May promote the retenion of the plancenta 

Carboprost

  • Synthetic prostaglandin analogue of PGF2α 
  • Increases uterine tone
  • May cause bronchospasm
  • No agreement as to when this should be used (i.e. no agreement as to where this drug belongs in line after the fisrt-line agents)

Misoprostol

  • Methyl ester synthetic analogue of  prostaglandin E1
  • High success rate if used with other uterotonic agents
  • Can be administered orally, sublingually, buccally, vaginally or rectally - by unskilled operators, in a resource poor setting
  • Not as effective as the other uterotonic agents (Tunçalp et al 2012)
  • Generally, only recommended as a co-uterotonic
  • Only indicated if other uterotonic agents are unavailable or are ineffective
Pharmacological measures to promote haemostasis

Tranexamic acid

  • Systemic antifibrinolytic
  • Inexpensive and requires minimal training to use
  • Can be added if uterotonics have been ineffective in controlling the bleeding
  • Supported by the WOMAN trial (Shakur et al, 2017)
  • Increased risk of VTE
  • Decreased seizure threshold

Factor VIIa

  • Expensive
  • May not be available
  • Thrombotic adverse event rate was 2.5% in on study
Surgical or radiological methods of haemostasis

Gause pack tamponade

  • "several yards of wide gauze placed inside the uterine cavity"
  • Acts by mechanical pressure effect as well as the prothrombotic effect of the fabric
  • May conceal haemorrhage
  • May encourage infection

Balloon tamponade

  • Provides more reliable tamponade than gauze packs
  • Includes a drainage channel to monitor blood loss
  • Can be inflated and deflated to test for re-bleeding
  • Inappropriate if there has been significant genital tract laceration
  • Uncomfortable
  • Invasive

Angio-embolisation

  • Minimally invasive means of devascularising the uterus
  • May be able to localise the precise territory from where blood loss is occuring
  • Radiation exposure is involved (not great for the breasts)
  • May not be available everywhere

Ligation of the uterine or common iliac artery

  • "stepwise uterine devascularisation" should terminate blood supply, preventing further bleeding
  • Apparently, this does not have any major adverse effects on fertility (Doumouchtsis et al, 2013)
  • Controls bleeding only in 50% of cases

Hysterectomy

  • May be a lifesaving step
  • High maternal morbidity
  • Fertility will obviously be affected
  • Bleeding may continue in spite of this procedure, because of coagulopathy
  • A more extensive procedure with risk of complications such as ureteric or bladder injury

For extra credit, the trainees were expected to mention the WOMAN trial (Shakur et al, 2017). Bleeding PPH patients were randomised to receive 1g of tranexamic acid (and another 1g if needed). A whopping 20,060 patients were enrolled. The difference in death from haemorrhage was 1.5% vs 1.9%, in favour of tranexamic acid by 0.4% of absolute risk reduction - a difference which only achieved statistical significance because the numbers were massive and because the sample size was increased by 5000 patients mid-study. The number needed to treat are 267. 

References

Oh's Manual, Chapter 64 ("General obstetric emergencies") by Winnie TP Wan and Tony Gin, p. 684

Mousa, Hatem A., et al. "Treatment for primary postpartum haemorrhage.The Cochrane Library (2014).

Oh's Manual, Chapter 64 ("General obstetric emergencies") by Winnie TP Wan and Tony Gin, p. 684

Mousa, Hatem A., et al. "Treatment for primary postpartum haemorrhage.The Cochrane Library (2014).

Tunçalp, Özge, G. Justus "Prostaglandins for preventing postpartum haemorrhage."Hofmeyr, and A. Metin Gülmezoglu. "Prostaglandins for preventing postpartum haemorrhage." Cochrane Database Syst Rev 8.8 (2012): CD000494.

Alfirevic, Zarko, et al. "Use of recombinant activated factor VII in primary postpartum hemorrhage: the Northern European registry 2000–2004." Obstetrics & Gynecology 110.6 (2007): 1270-1278.

Dahlke, Joshua D., et al. "Prevention and management of postpartum hemorrhage: a comparison of 4 national guidelines." American journal of obstetrics and gynecology 213.1 (2015): 76-e1.

Doumouchtsis, S. K., et al. "Menstrual and fertility outcomes following the surgical management of postpartum haemorrhage: a systematic review." BJOG: An International Journal of Obstetrics & Gynaecology 121.4 (2014): 382-388.

Smith, J., and H. A. Mousa. "Peripartum hysterectomy for primary postpartum haemorrhage: incidence and maternal morbidity." Journal of obstetrics and gynaecology 27.1 (2007): 44-47.

World Health Organization. WHO recommendations for the prevention and treatment of postpartum haemorrhage. World Health Organization, 2012.

Weeks, A. "The prevention and treatment of postpartum haemorrhage: what do we know, and where do we go to next?.BJOG: An International Journal of Obstetrics & Gynaecology122.2 (2015): 202-210.

Shakur et al  "Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial." The Lancet 389.10084 (2017): 2105-2116.

Question 20.1 - 2017, Paper 2

A 25-year-old female with a 5-day history of anorexia, nausea and vomiting presents to hospital after a convulsion and is transferred immediately to your ICU. She is G3P2 and 30/40 gestation.The following blood results are obtained: 

Parameter               Patient Value           Adult Normal Range
Fi02               0.28                      
pH               7.54*                 7.35 - 7.45
p02               87 mmHg (11.6 kPa)              
pC02               33.0 mmHg (4.4 kPa)*       35.0 - 45.0 (4.6 - 6.0)
Sp02               94%                      
Bicarbonate             28.0 mmol/L*             22.0 - 26.0
Base Excess             4.5 mmol/L*             -2.0 - +2.0
                                         
Sodium               127 mmol/L*             135 - 145
Potassium               2.3 mmol/L*             3.5 - 5.0
Chloride               84 mmol/L*             95 - 105
Glucose               4.8 mmol/L             3.5 - 6.0
Creatinine               354 µmol/L*             45 - 90  
Urea               29.0 mmol/L*             3.0 - 8.0
                                         
Haemoglobin             177 g/L*             120 - 160
White Cell Count             25.4 x 109/L*   j         4.0 - 11.0
Platelet count             29 x 109/L*   I         150 - 350
                                         
Prothrombin time             15.0 sec               12.0 - 16.5
INR               1.1                 0.9 - 1.3
APTT               28.0 sec               27.0 - 38.5
Fibrinogen               5.7 g/L*   ,           2.0 - 4.0
D-Dimer               16.8 mg/L* /           < 0.5    

Describe the important metabolic abnormalities and give one explanation for each.

(40% marks)

College answer

Describe the important abnormalities and give one explanation for each?                

  • Raised Aa gradient (aspiration, pneumonia, any plausible)
  • Metabolic alkalosis   -dehydration, vomiting                                       
  • Raised anion gap – sepsis, seizures, renal failure   
  • Respiratory alkalosis- pain, anxiety, post ictal                                                                       
  • Hypokalaemia, hyponatraemia : dehydration                                                 
  • AKI – sepsis, TTP, dehydration,eclampsia                                                     
  • Haemoconcentration – dehydration
  • Leucocytosis – sepsis
  • Thrombocytopenia –sepsis, TTP, HELLP       
  • Elevated fibrinogen, D-Dimer – sepsis

Discussion

Systematically:

  • The patient is alkalaemic. This pH is in excess of what would normally be expected in pregnancy
  • There is normoxia (PaO2 is satisfactory) but the A-a gradient is raised. 
  • The COis within normal limits for this stage in pregnancy
  • Oxygen saturation is lower than would be expected for this level of alkalosis (i.e. there is an unexplained right-shift of the oxyhaemoglobin dissociation curve).
  • Base excess and bicarbonate present a metabolic alkalosis. In pregnancy, one would conventionally expect to normally have a lower bicarbonate level because of the chronic respiratory alkalosis. Ergo, in this scenario, the metabolic alkalosis from vomiting and dehydration is even worse than it seems. 
  • The patient is hyponatremic, though it is not so severe as to produce the seizures. One possible explanation for this is the fluid overload and water retention related to the renal failure.
  • Potassium is severely depleted, which is likely related to the nausea and vomiting
  • The low chloride is due to the vomiting
  • The creatinine and urea are raised, indicating acute kidney injury
  • The haemoglobin is significantly higher than would be expected at this stage of pregnancy, which suggests significant dehydration
  • The white cell count is elevated, which may be a combination of haemoconcentration and infection
  • There is thrombocytopenia, consistent with HELLP - but it could also be consumptive, eg. in the context of thrombosis or something like TTP/HUS.
  • The coags are normal, which virtually excludes hepatic involvement 
  • The D-dimer is elevated, which might represent thrombosis and consumption (of particular interest would be cerebral venous sinus thrombosis).

References

Question 17 - 2018, Paper 2

Outline the causes and management of severe postpartum haemorrhage (PPH). 

College answer

Causes can be broken down into 4 main groups: the “4 T’s” 
Tone: uterine atony (most common) 
Trauma: Bleeding at surgical sites including episiotomy, genital tract laceration [vagina/cervix etc], uterine rupture 
Tissue: Retained tissue (placenta) and/or membranes  
Thrombin: Previously present or acquired maternal coagulation defect. Examples of acquired defects 
include those seen in severe pre-eclampsia, severe sepsis, amniotic fluid embolism, placental abruption or in the setting of massive transfusion.                          
                                              
Management can be broken down into initial resuscitation and specific treatment, with specific treatment having surgical and non-surgical modalities. Resuscitation and treatment should occur simultaneously. 
 

Resuscitation 
ABCDE approach. Assemble team (ICU/Anaesthesia/Obstetrics etc) 
Appropriate monitoring: ECG / NIBP / Arterial line / CVC if time or indication 
Large bore IV access x2 
Initial resuscitation with crystalloids / 4% albumin 
Activation of PPH protocol 
Activation of massive transfusion protocol / Use O neg blood (but likely to know blood group already and use group specific blood) early if no X matched blood available 
No specific Hb triggers for when to use blood, suggested after no more than 30mls/kg resusc fluids or evidence of ongoing bleeding 
Other products as required: NBA Obstetric guidelines suggest FFP 15mls/kg, platelets 1 pooled bag, cryoprecipitate 3-4g (8-10 bags): use local protocols if possible and involve specialist Haematologist. Keep fibrinogen >2.0 or replace if dropping (normal in pregnancy 4-6g/L: use cryoprecipitate or fibrinogen concentrate) Emphasis on early fibrinogen 
Viscoelastic tests 
Avoid hypothermia, hypocalcaemia and acidosis 
 
Non-Surgical Treatment 
Bimanual uterine compression 
Pharmacological Therapy (uterotonics): oxytocin, misoprostol, prostaglandin F2 alpha 
Tranexamic Acid (TXA): [the WOMAN trial showed a substantial mortality benefit if given within 3 hours] 
Balloon tamponade (Bakri balloon) 
Vaginal/Uterine packing 
Interventional Radiology: selective arterial embolization/balloon tamponade Consider Factor VIIa as rescue therapy 
 
Surgical treatment 
EUA: repair of lacerations / evacuation of retained placental fragments etc
Laparotomy: Uterine or iliac artery ligation, B-lynch brace suture 
Pelvic packing 
Aortic compression / X clamp 
Hysterectomy 
      
 

Discussion

Causes of PPH

It is not possible to add much to the (already comprehensive) list of causes offered by the model answer. 

  • Uterine atony
    • Prolonged labor
    • Polyhydramnios
    • Multiple gestations
    • Chorioamnionitis
    • Oxytocin augmentation of labor
  • Peripartum uterine trauma
    • Instrumental delivery
    • Surgical mishap
    • Laceration during labour (including episiotomy)
    • Uterine rupture
  • Postpartum retained products
    • Placenta 
    • Membranes
  • Coagulopathy
    • DIC
    • Amniotic fluid embolism
    • Sepsis 
    • Intrauterine foetal demise
    • HELP
    • Massive transfusion
  • Placental abnormality
    • Placenta previa
    • Placental abruption

Management of PPH

This structure and a lot of the components are borrowed from the RANZCOG statement C-Obs 43.

Resuscitation

  • A: either secure the airway if unprotected,  or prepare to do so with appropriate expertise (i.e. get an anaesthetist)
  • B: preoxygenate with high flow oxygen
  • C: establish IV access and give a fluid bolus; avoid hypothermia and use fluid warmers
  • D: reassure patient and ensure analgesia is adequate
  • E: correct ionised calcium (essential component of clotting); corrrect acidosis
  • F: monitor fluid resuscitation efficacy by observing urine output
  • G: fast the patient in preparation for surgery
  • H: correct coagulopathy and commence transfusion
    • Activate massive transfusion protocol: the college answer to Question 17 from the second paper of 2018 mentions the National Blood Authority's obstetric guidelines, which are endoresed by CICM. The guidelines recommend:
      • FFP: 15 mL/kg
      • platelets: 1 adult therapeutic dose
      • cryoprecipitate: 3–4 g
    • Fibrinogen is all-important- the same NBA guidelines recommend a fibrinogen level of > 2.0 as a therapeutic  target
    • Tranexamic acid is also known to be beneficial (WOMAN trial -Shakur et al, 2017) - to be given within 3 hours of haemorrhage
  • I: antibiotics are not routinely indicated for primary PPH outside of the scenario of septic abortion or endometritis. 

Specific management

  • Uterine massage
  • Bimanual compression
  • Manual aortic compression
  • Oxytocin
  • Ergometrine
  • Carboprost
  • Misoprostol
  • Gause pack or balloon tamponade
  • Angioembolisation
  • Brace sutures
  • Ligation of the uterine artery
  • Hysterectomy

References

Oh's Manual, Chapter 64 ("General obstetric emergencies") by Winnie TP Wan and Tony Gin, p. 684

Mousa, Hatem A., et al. "Treatment for primary postpartum haemorrhage.The Cochrane Library (2014).

Tunçalp, Özge, G. Justus "Prostaglandins for preventing postpartum haemorrhage."Hofmeyr, and A. Metin Gülmezoglu. "Prostaglandins for preventing postpartum haemorrhage." Cochrane Database Syst Rev 8.8 (2012): CD000494.

Alfirevic, Zarko, et al. "Use of recombinant activated factor VII in primary postpartum hemorrhage: the Northern European registry 2000–2004." Obstetrics & Gynecology 110.6 (2007): 1270-1278.

Dahlke, Joshua D., et al. "Prevention and management of postpartum hemorrhage: a comparison of 4 national guidelines." American journal of obstetrics and gynecology 213.1 (2015): 76-e1.

Doumouchtsis, S. K., et al. "Menstrual and fertility outcomes following the surgical management of postpartum haemorrhage: a systematic review." BJOG: An International Journal of Obstetrics & Gynaecology 121.4 (2014): 382-388.

Smith, J., and H. A. Mousa. "Peripartum hysterectomy for primary postpartum haemorrhage: incidence and maternal morbidity." Journal of obstetrics and gynaecology 27.1 (2007): 44-47.

World Health Organization. WHO recommendations for the prevention and treatment of postpartum haemorrhage. World Health Organization, 2012.

Weeks, A. "The prevention and treatment of postpartum haemorrhage: what do we know, and where do we go to next?.BJOG: An International Journal of Obstetrics & Gynaecology122.2 (2015): 202-210.

Edhi, Muhammad Muzzammil, et al. "Post partum hemorrhage: causes and management.BMC research notes6.1 (2013): 236.

Sheiner, Eyal, et al. "Obstetric risk factors and outcome of pregnancies complicated with early postpartum hemorrhage: a population-based study." The Journal of Maternal-Fetal & Neonatal Medicine 18.3 (2005): 149-154.

Mousa, Hatem A., and Steven Walkinshaw. "Major postpartum haemorrhage.Current opinion in Obstetrics and Gynecology13.6 (2001): 595-603.

Mousa, Hatem A., et al. "Treatment for primary postpartum haemorrhage." Cochrane Database Syst Rev 2.2 (2014): CD003249.

Question 3 - 2020, Paper 2

With regard to severe post-partum haemorrhage (PPH):

a)    List the causes.    (20% marks)

b)    Outline the management.    (80% marks)
 

College answer

Not available.

Discussion

a) Causes of PPH

  • Uterine atony
    • Prolonged labor
    • Polyhydramnios
    • Multiple gestations
    • Chorioamnionitis
    • Oxytocin augmentation of labor
  • Peripartum uterine trauma
    • Instrumental delivery
    • Surgical mishap
    • Laceration during labour (including episiotomy)
    • Uterine rupture
  • Postpartum retained products
    • Placenta 
    • Membranes
  • Coagulopathy
    • DIC
    • Amniotic fluid embolism
    • Sepsis 
    • Intrauterine foetal demise
    • HELP
    • Massive transfusion
  • Placental abnormality
    • Placenta previa
    • Placental abruption

This structure and a lot of the components are borrowed from the RANZCOG statement C-Obs 43.

Resuscitation

  • A: either secure the airway if unprotected,  or prepare to do so with appropriate expertise (i.e. get an anaesthetist)
  • B: preoxygenate with high flow oxygen
  • C: establish IV access and give a fluid bolus; avoid hypothermia and use fluid warmers
  • D: reassure patient and ensure analgesia is adequate
  • E: correct ionised calcium (essential component of clotting); corrrect acidosis
  • F: monitor fluid resuscitation efficacy by observing urine output
  • G: fast the patient in preparation for surgery
  • H: correct coagulopathy and commence transfusion
    • Activate massive transfusion protocol: the college answer to Question 17 from the second paper of 2018 mentions the National Blood Authority's obstetric guidelines, which are endoresed by CICM. The guidelines recommend:
      • FFP: 15 mL/kg
      • platelets: 1 adult therapeutic dose
      • cryoprecipitate: 3–4 g
    • Fibrinogen is all-important- the same NBA guidelines recommend a fibrinogen level of > 2.0 as a therapeutic  target
    • Tranexamic acid is also known to be beneficial (WOMAN trial -Shakur et al, 2017) - to be given within 3 hours of haemorrhage
  • I: antibiotics are not routinely indicated for primary PPH outside of the scenario of septic abortion or endometritis. 

Specific management

  • Uterine massage
  • Bimanual compression
  • Manual aortic compression
  • Oxytocin
  • Ergometrine
  • Carboprost
  • Misoprostol
  • Gause pack or balloon tamponade
  • Angioembolisation
  • Brace sutures
  • Ligation of the uterine artery
  • Hysterectomy

References

Oh's Manual, Chapter 64 ("General obstetric emergencies") by Winnie TP Wan and Tony Gin, p. 684

Mousa, Hatem A., et al. "Treatment for primary postpartum haemorrhage.The Cochrane Library (2014).

Tunçalp, Özge, G. Justus "Prostaglandins for preventing postpartum haemorrhage."Hofmeyr, and A. Metin Gülmezoglu. "Prostaglandins for preventing postpartum haemorrhage." Cochrane Database Syst Rev 8.8 (2012): CD000494.

Alfirevic, Zarko, et al. "Use of recombinant activated factor VII in primary postpartum hemorrhage: the Northern European registry 2000–2004." Obstetrics & Gynecology 110.6 (2007): 1270-1278.

Dahlke, Joshua D., et al. "Prevention and management of postpartum hemorrhage: a comparison of 4 national guidelines." American journal of obstetrics and gynecology 213.1 (2015): 76-e1.

Doumouchtsis, S. K., et al. "Menstrual and fertility outcomes following the surgical management of postpartum haemorrhage: a systematic review." BJOG: An International Journal of Obstetrics & Gynaecology 121.4 (2014): 382-388.

Smith, J., and H. A. Mousa. "Peripartum hysterectomy for primary postpartum haemorrhage: incidence and maternal morbidity." Journal of obstetrics and gynaecology 27.1 (2007): 44-47.

World Health Organization. WHO recommendations for the prevention and treatment of postpartum haemorrhage. World Health Organization, 2012.

Weeks, A. "The prevention and treatment of postpartum haemorrhage: what do we know, and where do we go to next?.BJOG: An International Journal of Obstetrics & Gynaecology122.2 (2015): 202-210.

Edhi, Muhammad Muzzammil, et al. "Post partum hemorrhage: causes and management.BMC research notes6.1 (2013): 236.

Sheiner, Eyal, et al. "Obstetric risk factors and outcome of pregnancies complicated with early postpartum hemorrhage: a population-based study." The Journal of Maternal-Fetal & Neonatal Medicine 18.3 (2005): 149-154.

Mousa, Hatem A., and Steven Walkinshaw. "Major postpartum haemorrhage.Current opinion in Obstetrics and Gynecology13.6 (2001): 595-603.

Mousa, Hatem A., et al. "Treatment for primary postpartum haemorrhage." Cochrane Database Syst Rev 2.2 (2014): CD003249.

[Submit a comment or correctio

Question 22 - 2021, Paper 1

Outline the causes and management of severe postpartum haemorrhage (PPH).

College answer

Not available.

Discussion

This question is identical to Question 17 from the second paper of 2018, and is almost identical to the very similarly structured Question 3 from the second paper of 2020. Why they went back to the 2018 format is a mystery.

Causes of PPH

It is not possible to add much to the (already comprehensive) list of causes offered by the model answer. 

  • Uterine atony
    • Prolonged labor
    • Polyhydramnios
    • Multiple gestations
    • Chorioamnionitis
    • Oxytocin augmentation of labor
  • Peripartum uterine trauma
    • Instrumental delivery
    • Surgical mishap
    • Laceration during labour (including episiotomy)
    • Uterine rupture
  • Postpartum retained products
    • Placenta 
    • Membranes
  • Coagulopathy
    • DIC
    • Amniotic fluid embolism
    • Sepsis 
    • Intrauterine foetal demise
    • HELP
    • Massive transfusion
  • Placental abnormality
    • Placenta previa
    • Placental abruption

Management of PPH

This structure and a lot of the components are borrowed from the RANZCOG statement C-Obs 43.

Resuscitation

  • A: either secure the airway if unprotected,  or prepare to do so with appropriate expertise (i.e. get an anaesthetist)
  • B: preoxygenate with high flow oxygen
  • C: establish IV access and give a fluid bolus; avoid hypothermia and use fluid warmers
  • D: reassure patient and ensure analgesia is adequate
  • E: correct ionised calcium (essential component of clotting); corrrect acidosis
  • F: monitor fluid resuscitation efficacy by observing urine output
  • G: fast the patient in preparation for surgery
  • H: correct coagulopathy and commence transfusion
    • Activate massive transfusion protocol: the college answer to Question 17 from the second paper of 2018 mentions the National Blood Authority's obstetric guidelines, which are endoresed by CICM. The guidelines recommend:
      • FFP: 15 mL/kg
      • platelets: 1 adult therapeutic dose
      • cryoprecipitate: 3–4 g
    • Fibrinogen is all-important- the same NBA guidelines recommend a fibrinogen level of > 2.0 as a therapeutic  target
    • Tranexamic acid is also known to be beneficial (WOMAN trial -Shakur et al, 2017) - to be given within 3 hours of haemorrhage
  • I: antibiotics are not routinely indicated for primary PPH outside of the scenario of septic abortion or endometritis. 

Specific management

  • Uterine massage
  • Bimanual compression
  • Manual aortic compression
  • Oxytocin
  • Ergometrine
  • Carboprost
  • Misoprostol
  • Gause pack or balloon tamponade
  • Angioembolisation
  • Brace sutures
  • Ligation of the uterine artery
  • Hysterectomy

References

Oh's Manual, Chapter 64 ("General obstetric emergencies") by Winnie TP Wan and Tony Gin, p. 684

Mousa, Hatem A., et al. "Treatment for primary postpartum haemorrhage.The Cochrane Library (2014).

Tunçalp, Özge, G. Justus "Prostaglandins for preventing postpartum haemorrhage."Hofmeyr, and A. Metin Gülmezoglu. "Prostaglandins for preventing postpartum haemorrhage." Cochrane Database Syst Rev 8.8 (2012): CD000494.

Alfirevic, Zarko, et al. "Use of recombinant activated factor VII in primary postpartum hemorrhage: the Northern European registry 2000–2004." Obstetrics & Gynecology 110.6 (2007): 1270-1278.

Dahlke, Joshua D., et al. "Prevention and management of postpartum hemorrhage: a comparison of 4 national guidelines." American journal of obstetrics and gynecology 213.1 (2015): 76-e1.

Doumouchtsis, S. K., et al. "Menstrual and fertility outcomes following the surgical management of postpartum haemorrhage: a systematic review." BJOG: An International Journal of Obstetrics & Gynaecology 121.4 (2014): 382-388.

Smith, J., and H. A. Mousa. "Peripartum hysterectomy for primary postpartum haemorrhage: incidence and maternal morbidity." Journal of obstetrics and gynaecology 27.1 (2007): 44-47.

World Health Organization. WHO recommendations for the prevention and treatment of postpartum haemorrhage. World Health Organization, 2012.

Weeks, A. "The prevention and treatment of postpartum haemorrhage: what do we know, and where do we go to next?.BJOG: An International Journal of Obstetrics & Gynaecology122.2 (2015): 202-210.

Edhi, Muhammad Muzzammil, et al. "Post partum hemorrhage: causes and management.BMC research notes6.1 (2013): 236.

Sheiner, Eyal, et al. "Obstetric risk factors and outcome of pregnancies complicated with early postpartum hemorrhage: a population-based study." The Journal of Maternal-Fetal & Neonatal Medicine 18.3 (2005): 149-154.

Mousa, Hatem A., and Steven Walkinshaw. "Major postpartum haemorrhage.Current opinion in Obstetrics and Gynecology13.6 (2001): 595-603.

Mousa, Hatem A., et al. "Treatment for primary postpartum haemorrhage." Cochrane Database Syst Rev 2.2 (2014): CD003249.

Question 29.3 - 2021, Paper 1

A 25-year-old female with a 5-day history of anorexia, nausea and vomiting presents to hospital after a convulsion and is transferred immediately to your ICU. She is G3P2 and 30/40 gestation. The following blood results are obtained:

Parameter

Patient Value

Adult Normal Range

FiO2

0.28

pH

7.54*

7.35 – 7.45

PO2

87 mmHg (11.6 kPa)

PCO2

33.0 mmHg (4.4 kPa)*

35.0 – 45.0 (4.6 – 6.0)

SpO2

94%

Bicarbonate

28.0 mmol/L*

22.0 – 26.0

Base Excess

4.5 mmol/L*

-2.0 – +2.0

Sodium

127 mmol/L*

135 – 145

Potassium

2.3 mmol/L*

3.5 – 5.0

Chloride

84 mmol/L*

95 – 105

Glucose

4.8 mmol/L

3.5 – 6.0

Creatinine

354 µmol/L*

45 – 90

Urea

29.0 mmol/L*

3.0 – 8.0

Haemoglobin

177 g/L*

120 – 160

White Cell Count

25.4 x 109/L*

4.0 – 11.0

Platelet count

29 x 109/L*

150 – 350

Prothrombin time

15.0 sec

12.0 – 16.5

International normalised ratio (INR)

1.1

0.9 – 1.3

Activated partial thromboplastin time (APTT)

28.0 sec

27.0 – 38.5

Fibrinogen

5.7 g/L*

2.0 – 4.0

D-Dimer

16.8 mg/L*

< 0.5

a) Describe the important metabolic abnormalities and give one explanation for each.

(40% marks)

College answer

Not available.

Discussion

This question is identical to Question 20.1 from the second paper of 2017, except this time the examiners added the word "important" to "abnormalities", presumably because the last bunch of answers were filled with pointless trivial abnormalities. The reader is left to decide, which of the following list of problems fits that description, and invited to pick whichever ones seem important enough to write in the span of four minutes.

Systematically:

  • The patient is alkalaemic. This pH is in excess of what would normally be expected in pregnancy
  • There is normoxia (PaO2 is satisfactory) but the A-a gradient is raised. 
  • The COis within normal limits for this stage in pregnancy
  • Oxygen saturation is lower than would be expected for this level of alkalosis (i.e. there is an unexplained right-shift of the oxyhaemoglobin dissociation curve).
  • Base excess and bicarbonate present a metabolic alkalosis. In pregnancy, one would conventionally expect to normally have a lower bicarbonate level because of the chronic respiratory alkalosis. Ergo, in this scenario, the metabolic alkalosis from vomiting and dehydration is even worse than it seems. 
  • The patient is hyponatremic, though it is not so severe as to produce the seizures. One possible explanation for this is the fluid overload and water retention related to the renal failure.
  • Potassium is severely depleted, which is likely related to the nausea and vomiting
  • The low chloride is due to the vomiting
  • The creatinine and urea are raised, indicating acute kidney injury
  • The haemoglobin is significantly higher than would be expected at this stage of pregnancy, which suggests significant dehydration
  • The white cell count is elevated, which may be a combination of haemoconcentration and infection
  • There is thrombocytopenia, consistent with HELLP - but it could also be consumptive, eg. in the context of thrombosis or something like TTP/HUS.
  • The coags are normal, which virtually excludes hepatic involvement 
  • The D-dimer is elevated, which might represent thrombosis and consumption (of particular interest would be cerebral venous sinus thrombosis).

References

Question 15 - 2021, Paper 2

Regarding peri-partum cardiomyopathy (PPCM):

a)    Define peri-partum cardiomyopathy.    (20% marks)

b)    List five differential diagnoses.    (20% marks)

c)    Outline the management.    (60% marks)
 

College answer

Not available.

Discussion

a) Peripartum cardiomyopathy has some specific defining criteria:

  • Hear failure in the end of pregnancy, or in the following few months
  • No other explanation (diagnosis of exclusion)

This is from the ESC statement from 2010, and is probably enough for a sub-question worth only 20%  of the marks. If one wanted to write a little extra, a previous college answer holds clues to what the college examiners think is a good definition:

  • 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. The latter  may be characterized as an LV ejection fraction < 45%, fractional shortening < 30%, or both, with or without an LV end-diastolic dimension 2.7 cm/m2 body surface area.

This definition was generated by a panel of fourteen experts during a conference workshop (Pearson et al, 2000).

b) Five plausible differentials would include:

  • Massive PE
  • Amniotic fluid embolism
  • Worsening of pre-existing rheumatic MR or TR
  • Pre-eclampsia or eclampsia
  • Pre-existing unrecognized congenital heart disease, unmasked by the volume stress of pregnancy

c) Management is same as you would manage acute heart failure from any cause:

  • Management of preload
    • Diuretics, fluid restriction, venodilators
    • Maintenance of sinus rhythm and atrial systolic contribution
    • Pacing to maintain AV synchrony
  • Management of afterload
    • Left ventricle
      • Vasodilators
      • Beta-blockers
      • ACE-inhibitors are contraindicated in pregnancy
    • Right ventricle
      • Normoxia and normocapnea
      • Avoidance of excessive postive respiratory pressures
      • Pulmonary vasodilators
  • Management of contractility
    • Inotropes
      • Dobutamine
      • Milrinone
      • Levosimendan
    • Cardiac resychronisation
    • Supportive hormones and micronutrients (cortisol, insulin, calcium, glucagon, thyroxine, thiamine etc)
  • Cheating
    • Increase cardiac output by unnatural means:
      • IABP
      • LVAD
      • ECMO
      • Increase the pacemaker rate
  • Planning for delivery and the future:
    • Steroids to help foetal lung maturation, in case something happens
    • Instructions not to breastfeed (prolactin secretion can make PPCM worse)
    • Instructions to avoid getting pregnant again
    • Consider referral for transplant, if LV function fails to improve

References