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Chapter 6 Admission emergencies

David T Y. Liu, Mentors: Khaled Ismail, Mark Kilby

CHAPTER CONTENTS

Management of imminent delivery with or without fetal compromise 35
Specific problems 36
Cord presentation or prolapse 36
Cord presentation 36
Cord prolapse 36
Major obstetric haemorrhage 37
Management 37
Antepartum haemorrhage 37
Important points to remember about vaginal bleeding in pregnancy 38
General guidelines for management 38
Placental separation (abruption) 38
Diagnosis 38
Management 39
Placenta praevia 40
Grading of placenta praevia 40
Management 40
Fits 40
Eclampsia 41
Guidelines for management 41
Suspected fetal death 43
Cardiac arrest and cardiopulmonary resuscitation in the obstetric woman 43
Myocardial infarction 43
Management 43

When emergencies occur a well-rehearsed approach facilitates efficient teamwork and ensures that all correct steps are taken. Availability of clear, updated protocols is crucial for immediate management by staff on the labour ward.

Training protocols or drills for staff (doctors, midwives, anaesthetists, paediatricians and theatre assistants) are encouraged for improving performance and outcome in emergencies.

MANAGEMENT OF IMMINENT DELIVERY WITH OR WITHOUT FETAL COMPROMISE

The following procedures should be adopted if delivery is imminent.

Determine at once whether vaginal delivery is feasible and safe.
Reassurance. These women are often agitated and distressed on admission to hospital. Reassurance and supportive care are necessary. Discourage pushing until vaginal examination is performed.
Transfer the woman to the delivery room if vaginal delivery is safe. If fetal distress is present, expedite delivery and anticipate the need for neonatal resuscitation.
If there is indication for or need for recurrent caesarean section proceed to immediate delivery by caesarean section. For uncomplicated cephalic presentation when the fetal head is on the perineum a short period of close observation is acceptable, but anticipate assisted delivery if there is delay or onset of compromise.
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SPECIFIC PROBLEMS

Cord presentation or prolapse

Always confirm gestational age before planning any further management.

Cord presentation

This occurs when the cord is in front of the presenting part of the fetus behind intact membranes. When the membranes are not ruptured, palpate through them with the tip of the fingers to exclude the presence of pulsation due to cord presentation or vasa praevia (Figure 6.1a). The diagnosis can also be made using ultrasound and colour flow Doppler, and is useful in circumstances such as an unstable breech presentation. Variable fetal heart rate decelerations may be evident.

image

Figure 6.1 (a) Cord presentation and (b) cord prolapse.

Management

Cord presentation during labour and before full cervical dilatation necessitates delivery by caesarean section.
If the cervix is fully dilated, the presenting part is below the ischial spines and the pelvis is adequate, rupture the membranes, displace the cord and deliver by forceps or ventouse.

Cord prolapse

Following membrane rupture the cord may prolapse through the cervix, may remain in the vagina or be expelled through the introitus (Figure 6.1b).

Cord prolapse occurs in approximately 0.2% of all births.

Risk factors for cord prolapse

Amniotomy.
Low birth weight (<2.5 kg).
Premature birth/preterm prelabour rupture of membranes.
Malpresentations/(flexed or footling, breech).
Second twin.
High presenting part/disproportions/placenta praevia grade I or II.
Polyhydramnios and uncontrolled rupture of membranes.
Anencephaly and other congenital malformations with a potential for cephalopelvic disproportion.
Long cord or abnormal cord insertion.

Points to remember in management

Figure 6.2 presents an algorithm for management of cord prolapse.

image

Figure 6.2 Steps in the management of cord prolapse.

Anticipate in the presence of risk factors.
Note suspicious or abnormal cardiotocographic changes.
Inform the woman of the situation and the need for urgency (if fetus is alive).
If fetal demise is suspected confirm by scan and manage as for stillbirth. It has been reported that fetal activity could be visualised in cases of inaudible fetal heart tones and absent cord pulsation.
Check the presence of pulsation, replace the cord in the warmth of the vagina and determine dilatation of the cervix.
Maternal oxygen, intravenous access and group and save.
Deliver by forceps or ventouse if cervix is fully dilated and vaginal delivery is considered to be safe.
If the cervix is not fully dilated, displace the presenting part of the fetus away from the cervix with examining digits to prevent cord compression (most effective). This manoeuvre is made easier if the mother is placed in Trendelenburg’s or knee-chest position. Some authors advocate a temporary measure by inserting a number 16 Foley catheter to fill the bladder with 500 ml of saline using a standard infusion set. Bladder filling raises the presenting part of the fetus away from the cord. (Digital elevation of presenting part is more effective.)
Avoid handling the cord because this will cause spasm of the vessels and fetal bradycardia.
Request assistance and organise a theatre for caesarean section if vaginal delivery is not considered safe. Fetal resuscitation is often required.

Major obstetric haemorrhage

Haemorrhage remains one of the leading causes of maternal mortality in the world. It is the leading cause of maternal mortality in developing countries.
It is defined as the loss of more than 500 ml of blood, either antepartum or postpartum.
Accurate measurement of blood loss is difficult hence a definition based on volume alone has shortcomings. Tachycardia (>120 beats per minute), hypotension (systolic below 100 mmHg), peripheral vasoconstriction and decreased urine output are important signs.
Underestimation of blood loss may delay steps to prepare for or prevent further bleeding. Check haemoglobin and haematocrit levels as objective guides to blood loss.

Management

Clear guidelines must be available for haemorrhage. These will include details for contact of senior obstetric staff, anaesthetists and haematologist.
Adequate tissue perfusion is essential to preserve organ function.
Hypotension-mediated endothelial damage may trigger disseminated intravascular coagulation (DIC).
Basic resuscitation includes:
Minimising effects of aortocaval compression (left lateral tilt or wedging 5–15°).
Administering a high concentration of oxygen to the woman regardless of her oxygen saturation.
Assess Airway and Breathing effort. Intubation may be indicated if the mother has depressed conscious level due to hypotension (near arrest scenario).
Establish two 14 G intravenous lines and take 20 ml of blood for diagnostic test (full blood count, urea and electrolytes, coagulation screen and cross matching).
Maintain the Circulation by normal/saline or Hartmann’s solutions and colloid until blood is available.
Monitor pulse, blood pressure (direct or indirect), respiratory rate, oxygen saturation, urine output and fluid balance.
Central venous pressure monitoring is recommended. Use antecubital fossa and long line, as safer when coagulopathy threatens. Fluid warmers and high pressure infusers are helpful in these situations. If CVP is more than 5 mmHg maintenance fluid volume is sufficient.
Delegate one member of staff to record time, drugs given and fluids used.
Identify and treat the cause of bleeding.
A well-drilled multidisciplinary team of anaesthetists, haematologists, and maternity staff will achieve best results. Observe in high-dependency unit after resuscitation.

Box 6.1 gives details of blood component therapy.

Box 6.1 Blood component therapy

O negative blood should be available on the delivery suite. This carries a small risk of sensitisation to ‘c’ antigen.
Full infection screen is necessary for fresh whole blood.
After 48 hours storage, platelet numbers and function of important clotting factors (V and VIII) are reduced.
Full cross-match of blood may take up to an hour.
Fresh frozen plasma (FFP) is separated from whole blood within 6 hours of donation and stored for up to 1 year at −20 °C to −30 °C. FFP provides all necessary clotting factors. Give 1 unit after 8 units of rapidly transfused blood. Use coagulation screen as guide.
Cryoprecipitate contains more fibrinogen than FFP but lacks antithrombin III (coagulation inhibitor), which is depleted in obstetric related coagulopathies. Cryoprecipitate is useful for hypofibrinogenaemia.
Platelet packs have a limited shelf life of 5 days and should be given through a platelet filter. Rarely indicated above a platelet count of 50 × 109/l.
In the presence of maternal antibodies, blood should be cross-matched before onset of labour or caesarean section.
Use blood warming equipment.

Antepartum haemorrhage

This is vaginal bleeding after a gestational age of 24 weeks.
Bleeding is due to:
placental abruption or separation of the placenta, which is normally situated in the upper uterine segment
placental praevia or separation of the abnormally situated placenta which lies in or encroaches onto the lower uterine segment
non-placental causes secondary to trauma, infection or neoplasms
vasa praevia. Bleeding is associated with rupture of blood vessels in the fetal membranes. Fetal blood is lost. Abnormal cord insertion or succenturiate placenta is commonly found. The Apt test can be used if bleeding of fetal origin is suspected. The basis of this test is that fetal haemoglobin is alkaline stable, whereas adult haemoglobin is not.
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Important points to remember about vaginal bleeding in pregnancy

A show is diagnosed only when blood-stained mucus is noted, usually in association with contractions. Presence of pure blood is not a show.
A high presenting part or malpresentation on abdominal examination may be due to placenta praevia (irrespective of an early pregnancy ultrasound scan).
A tense contracted tender uterus is one of the signs of placental abruption.
Vaginal examination is contraindicated until placenta praevia is excluded.
The fetus can contribute to the bleeding hence the real risk of exsanguination.
Bleeding is often more extensive than that observed.
Increased uterine activity can produce or follow placental separation.
Anti-D for rhesus negative mothers – use Kleihauer’s test.
Anticipate postpartum haemorrhage.
Ultrasound scan may detect retroplacental collection of blood.
Placental damage and thromboplastin release can cause coagulation defect.

General guidelines for management

1. Apply general rule for resuscitation (Airway, Breathing and Circulation +2)
2. Ensure intravenous access (at least 16 G, preferably 14 G).
3. Perform full blood count, group and cross-match blood (number of units required depends on amount of bleeding).
4. Exclude placenta praevia by ultrasound scan. Check fetal viability.
5. Perform speculum examination (if no placenta praevia) to exclude local causes for bleeding.
6. Take vaginal swab to screen for infection.
7. Commence cardiotocography to assess fetal wellbeing. Further placental separation can occur. Do not stop monitoring too early.
8. Note presence or absence of uterine activity.
9. Clot lysis suggest activation of fibrinolytic system. Correct coagulopathy (present in up to 30%) before caesarean section.
10. Epidural anaesthesia is contraindicated if the mother is hypotensive or coagulopathy is present.
11. Consider peritoneal and abdominal wound, drain if oozing is present.
12. Keep uterus contracted by intravenous oxytocin (Syntocinon) infusion after delivery to prevent postpartum haemorrhage.
13. A neonatologist must attend delivery. Fetal blood loss (asphyxia pallida) will require urgent resuscitation.

Note: Modify guidelines for degree of antepartum haemorrhage.

Placental separation (abruption)

Presentation depends on the amount of bleeding (Table 6.1).

Table 6.1 Placental separation: presentation and consequences

image

Diagnosis

A careful history should be taken to define obstetric complications, the site of pain and if coitus had taken place.
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Exclude differential diagnosis.
If pain is not localised to the placental site concealed haemorrhage is less likely.
Note the presence of uterine activity.
Ultrasound examination is helpful for assessing fetal wellbeing, placental localisation and identifying retroplacental haematoma.
A negative scan does not exclude the diagnosis of abruption.
Major placental separation produces the classic picture of shock, a rock-hard uterus, coagulation defects and fetal death (in 50% of cases).
Uterine tenderness and rigidity may be absent if the placenta is posterior.
Haematuria may be present.
There is an association with pre-eclampsia (2%).

Management

This is governed by the amount of bleeding, whether bleeding continues, the status both of the mother and fetus, the gestational age of the pregnancy and previous obstetric history.

Placental abruption can occur at any gestational age. Follow the general guidelines of management of antepartum haemorrhage. Placental abruption is usually treated actively by delivery, by caesarean section if the fetus is alive and viable but vaginally if the fetus is dead. Close monitoring throughout labour is essential. Caesarean section might be required if labour is prolonged to decrease the risk of severe coagulopathy.

Severity of bleeding is a useful guide for management.

Mild bleeding

Admit and observe after instituting general procedures.
If the woman is in labour and the fetus is mature, rupture the membranes to check the state of liquor and provide access to the fetus for direct fetal heart rate monitoring.
Close observation is mandatory. This includes extended cardiotocography if conservative management is adopted. Further placental separation can occur.

Moderate bleeding

Replace blood loss.
Carry out coagulation screen and correct defects.
Rupture the membranes, administer oxytocics if labour is delayed.
Perform caesarean section for fetal distress. Coagulation defects must first be excluded.
An indwelling drain for the abdomen and wound after caesarean section is advised.
An experienced obstetrician and anaesthetist are required.
Ensure strict fluid balance and monitor the renal output (>20 ml/h).
Epidural anaesthesia is contraindicated if the mother is hypotensive or there is evidence of coagulopathy (up to 30%).
Presence of pre-eclampsia requires close watch for blood pressure fluctuations, renal shut down and electrolyte disturbances. These women are best observed on the labour ward until clinically stable.
Keep uterus contracted by intravenous Syntocinon infusion after delivery.
A neonatologist must attend delivery. Fetal blood loss (asphyxia pallida) will require urgent resuscitation.

Severe bleeding

See Major obstetric haemorrhage above.

Fetal death is usual. The aim is to resuscitate and evacuate the uterus.
Correct coagulation defects.
Blood transfusion is required.
Control fluid replacement by use of a central line (exclude coagulopathy).
Rupture the membranes and encourage labour.
Watch closely for blood pressure changes and onset of coagulopathy.
Labour usually supervenes or follows Syntocinon infusion. If not, caesarean section is justified if condition is stable, the cervix is unfavourable and there is no coagulation defect. Delay allows further decompensation of the situation and risks onset of coagulopathy.
Keep uterus contracted after delivery to prevent risk of postpartum haemorrhage. The Couvelaire uterus may not contract well.
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Placenta praevia

This describes a placenta inserted partially or wholly in the lower uterine segment.
Characteristically presents with unprovoked painless bleeding. Occasionally, bleeding may be provoked by sexual intercourse. Note evidence of uterine activity.
It is discovered following clinical or ultrasound examination. Unstable lie or high presenting part should alert to this condition. Transvaginal scanning is safe and more accurate.

Grading of placenta praevia

Not clinically useful for predicting severity of antepartum haemorrhage.

I. The placenta is in the lower uterine segment but the placental edge does not reach the internal os.
II. The lower edge of the placenta reaches but does not cover the internal os.
III. The placenta covers the internal os asymmetrically.
IV. The placenta covers the internal os symmetrically.

Management

Management depends on the gestational age, the amount of blood loss, fetal position and the placental site (in cases of minor placenta praevia).

Apply the general guidelines for antepartum haemorrhage.
Consider expectant management if the gestational age is less than 37 weeks when bleeding is mild. Close observation is mandatory.
It is safer to avoid tocolytics in cases of antepartum haemorrhage. However, in a tertiary setting for selected situations prolonged gestation can be achieved with no increase in mortality or morbidity.
Ensure cross-matched blood is available at all times.
For moderate bleeding after 36 completed weeks or if bleeding is severe or continues after 24 weeks, caesarean section should be performed. Additional cross-matched blood must be available. A senior obstetrician and anaesthetist should be available to assist or advise especially where placentation is anterior. Placenta praevia, particularly in women with a previous uterine scar, may be associated with uncontrollable uterine haemorrhage at delivery and caesarean hysterectomy may be necessary. A consultant must be in attendance.
Remember placenta accreta in an anterior placenta with a previous caesarean section scar.
Examination in theatre is acceptable when diagnosis is uncertain or when there is a grade I anterior placenta praevia (see Box 6.2).
Choice of anaesthetic technique must be made by the anaesthetist.
Placenta accreta, increta and percreta: there is a strong association between these abnormal placentations and placenta praevia and presence of a uterine (caesarean section) scar. Ultrasound scanning and magnetic resonance imaging can forewarn. Apply drill for massive haemorrhage. Consider hysterectomy early rather than late.

Box 6.2 Examination in theatre: requirements

Blood must be available in theatre.
No fetal distress.
Prepare the woman for caesarean section.
Lithotomy position.
Palpate around fornices. Interposing placenta distant present parts.
Locate the cervix and examine with a single digit in enlarging circles. The placenta has a spongy feel.
Brisk bleeding indicates the need for immediate delivery.

For grade I anterior placenta praevia, rupture the membranes and attempt vaginal delivery. Close surveillance is mandatory. All other grades of placenta praevia necessitate caesarean section.

Fits

Pregnancy can aggravate an existing tendency to fits (epilepsy), or convulsions can complicate pre-eclampsia (eclampsia). The presence of hypertension, proteinuria and generalised oedema and past history of epilepsy are important points that need to be considered in this situation. Close monitoring of the woman’s condition, the fetus (by cardiotocography) and laboratory results (e.g. blood count, urea, electrolytes, clotting screen and liver function) are mandatory.

Two-thirds of eclampsia occur before and a third after delivery, sometimes 3 or more days post partum (12%). Eclampsia is associated with up to 14% direct maternal deaths in the UK (Confidential Enquiries into Maternal Deaths in the United Kingdom 2004).

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Eclampsia

Prevention and anticipation are important measures. Note symptoms (hyper-reflexion, clonus, headaches, photophobia, epigastric pain, flashing lights) elevated transaminases, creatinine, urea, proteinuria (>1 g/24 h or 3 plus) platelets below 100 × 109/l or prolonged clotting times.

Guidelines for management

Clear, written management protocols for severe pre-eclampsia should guide initial and ongoing treatment in hospital.
Established intravenous access and inserted bladder catheter.
Stop/prevent fitting. Give intravenous magnesium sulphate (4 g over 15 minutes).
Reduce blood pressure. Give hydralazine/labetalol/nifedipine. (Care should be taken when combining magnesium sulphate and nifedipine. This combination is best avoided (calcium chelator and calcium blocker).) Both drugs can have a synergistic effect which can cause significant hypotension.
Management protocols should recognise the need to avoid very high systolic blood pressures associated with the risk of intracerebral haemorrhage.
Automated blood pressure recording systems can systematically underestimate blood pressure in pre-eclampsia, to a serious degree.
Anticipate complications. Review the woman frequently and monitor closely in a high-dependency unit with senior staff involvement.
Deliver the baby. There is no place for continuing the pregnancy if eclampsia occurs. Consider induction of labour or caesarean section. A major complication is fetal or maternal mortality.
There should be early engagement of consultant obstetricians and intensive care specialists in the care of women with severe pre-eclampsia.
Ensure detailed documentation of drugs, fluids and observations.

Magnesium sulphate

This drug is used for seizure prophylaxis. This is the current drug of choice in eclampsia (dispensed in 50% W/V solutions with 1 g in 2 ml).
There must be a protocol for magnesium sulphate administration.
After the loading dose (4–5 g given slowly over 15–20 minutes) infuse 1–2 g/h for maintenance (20 ml magnesium sulphate in 250 ml normal saline at 50 ml/h).
Adjust therapeutic levels by increasing or decreasing infusion.
Infusion should be continued for 24 hours. Post partum ensure tendon reflex is present, note urine output (should be 30 ml/h or 100 ml/4 h).
The first sign of toxicity is loss of the knee reflex. Check serum magnesium levels 1 hour after loading dose and then every 6 hours to ensure therapeutic levels of 2–3 mmol/l.
Calcium gluconate 10% intravenously is given as antidote (require 10–20 ml).
Continuous monitoring of oxygen saturation is required.
Magnesium sulphate increases sensitivity to muscle relaxants (non-depolarising). Reduce infusion if blood pressure <110/70 mmHg and respiratory rate is below 16 per minute.
Use clinical findings as guide to duration of infusion.
If fits continue give diazepam 5 mg/min (up to 20 mg) intravenously.

Fluid balance

Insert an indwelling urinary catheter and keep a strict input/output chart with hourly running totals. Aim for 100 ml/h total fluid input.
Maintenance fluids should be given as crystalloid (85 ml/h). Beware of fluid overload.
Colloids may be required prior to vasodilatation (with epidural anaesthesia).
Diuretics are only indicated for women with confirmed pulmonary oedema.
Central venous pressure monitoring might be required.
Oliguria (urine output <30 ml/h persists) follows renal vessel spasms, renal failure precipitated by haemorrhage and hypotension or fluid deficit. Check urea, creatinine and electrolytes (test by 200 ml bolus of crystalloid over 30 minutes and review urinary output).
Total fluid intake should not exceed 2.5 l over 24 hours. Colloids can be used with caution for fluid challenges (200 ml) if the urine output is decreased.
Furosemide is used for pulmonary oedema, in the presence of overhydration, particularly with heart failure or with impending renal failure.

Antihypertensives (see Box 6.3 and Box 6.4)

A blood pressure of 160 mmHg systolic over 110 mgHg diastolic requires urgent treatment to prevent cerebral haemorrhage. Aim for a diastolic of 90–95 mmHg to ensure adequate placental perfusion. Monitor maternal blood pressure (5–10 minutes intervals) and fetal heart rate (cardiotocography).

Box 6.3 Hydralazine treatment

Mode of action

Direct acting vasodilator
Can cause sodium and fluid retention
Plasma half life 2–3 hours

Contraindications

Known hypersensitivity
Systemic lupus erythematosus
Tachycardia
High output state (thyrotoxicosis)
Aortic or mitral stenosis
Isolated right ventricular failure due to pulmonary hypertension

Cautions

Renal impairment
Ischaemic heart disease
Surgery can exaggerate hypertension

Side effects

Tachycardia, palpitations, flushing hypotension, anginal symptoms, oedema, heart failure
Headache dizziness, peripheral neuritis, hyper-reflexion
Arthralgia rash
Proteinuria, increased plasma creatinine, haematuria, renal failure
Gastrointestinal disturbances, abnormal liver function
Agitation, anxiety
Dyspnoea

Compatibility

Incompatible with dextrose
Use following magnesium sulphate or other anti-hypertensives can cause precipitous fall in blood pressure

Acute treatment

5 mg by slow (1 mg/min) intravenous bolus (up to 10 mg)
Check blood pressure (BP) every 5 minutes for 30 minutes, or until BP is stable at <100 mmHg diastolic, then every 15 minutes for further 60 minutes
Repeat bolus if blood pressure is not controlled after 30 minutes

Maintenance

40 mg hydralazine in 40 ml 0.9% saline (via syringe pump) giving 1000 μg/ml solution

Start 40 μg/min (2.4ml/h)
30min 80 μg/min (4.8ml/h)
60min 120 μg/min (7.2ml/h)
90min 160 μg/min (9.6ml/h)

Do not increase if pulse is >140 or if target BP is reached. Reduction by 10–20 μg/min every 30 minutes.

Prolonged use (more than 24 hours) of hydralazine results in tachycardia and loss of antihypertensive effect. If required consider adding a β-blocker.

Box 6.4 Labetalol treatment

Cautions

Asthma
Heart failure
Cardiogenic shock
Atrio-ventricular block

Side effects

Postural hypotension
Tiredness, weakness, headache, rashes, scalp tingling
Difficulty in micturition
Epigastric pain
Nausea, vomiting
Rarely lichenoid rash

Oral therapy

200 mg oral loading then 200 mg oral three times daily
Increase to a maximum of 600 mg four times daily

Intravenous therapy

Acute: bolus dose for acute therapy, 10–20 mg intravenously slowly (5–10 min), effective within 5 minutes and lasts for 6 hours (repeat if needed to maximum of 100 mg)
Intravenous infusion solution: 5 mg/ml (200 mg in 40 ml) as alternative to repeat bolus

Set a target BP. Increase infusion as stated until target BP is reached

Start at 20 mg/h (=4 ml/h)

At 30min 40mg/h
At 60min 80mg/h
At 90min 160mg/h

To reduce, decrease by 10 mg/h every 30 min as required. Convert to oral therapy by giving 200 mg orally 1 hour prior to stopping infusion, followed by 200 mg three times daily.

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Suspected fetal death

Any mother presenting with diminished fetal movements must be examined at once.

Check for fetal heart rate.
Reassure mother if the fetal heart is heard. Obtain a 30-minute external cardiotocographic trace of the fetal heart for inspection.
Discharge if the antenatal history suggests no cause for concern. Admit and investigate if obstetric complications are present.
Perform ultrasound scan if fetal heart is not heard. If fetal death is confirmed after ultrasound scan as a double check, inform the woman and partner immediately. Transfer to a quiet room for natural expression of grief. Discuss openly possible reasons for the tragedy but protect them from any feeling of guilt.
At a convenient time discuss the proposed course of further action.
Suppress lactation.
Counsel the couple about the different levels of post-mortem examination (see Box 23.2).
Provide administrative support and aid to parents for registration of the stillbirth.
Provide a follow-up appointment for further counselling when results such as post-mortem findings are available.

Cardiac arrest and cardiopulmonary resuscitation in the obstetric woman

Cardiac arrest in late pregnancy or during delivery is a rare event. It usually accompanies major complications (e.g. amniotic fluid embolism). The physiological changes in late pregnancy often hamper effective cardiopulmonary efforts.
Some causes include:
total spinal anaesthetic
local anaesthetic toxicity from unintentional intravascular injection
trauma
pulmonary embolism
amniotic fluid embolism.
Physiological changes in pregnancy relevant to cardiopulmonary resuscitation (CPR) include:
women become hypoxic more readily (20% decrease in their functional residual capacity and 20% increase in their resting oxygen consumption)
the enlarged uterus can decrease compliance during controlled ventilation
aortocaval compression in the supine position necessitate lateral tilt.
Tilt the uterus to the left side. A member of the team should be instructed to act as a ‘human wedge’ by kneeling down (both knees). The woman is placed across the wedge of the bent knees.
CPR should begin immediately after establishing airway. Follow advanced cardiac life support programme.
If CPR is not successful after 5 minutes, caesarean delivery must be performed.
CPR should be continued throughout the procedure.

Myocardial infarction

Myocardial infarction associated with labour or need for delivery is not a common situation (6.2 per 100 000 maternities). In pregnancy the majority of infarcts are transmural involving the anterior rather than posterior myocardium. The cause is usually coronary artery thrombosis where pre-existing arteriosclerosis or aneurysm of the artery may exist. Coronary artery spasm is also a possibility. Haemodynamic changes during labour and delivery more often precipitate myocardial infarcts in the primigravida in the postpartum period whereas infarct in multigravid mothers is usually an antepartum event. Maternal mortality (7.3%) and fetal mortality is high.

Management

Note risk factors for myocardial infarction, e.g. longstanding hypertension, family history, hypercholesterolaemia.
Intensive care requires a multidisciplinary team of cardiologists, anaesthetists and obstetricians.
Vaginal delivery if considered appropriate requires close monitoring of fetus with cardiotocography and continuous electrocardiographic surveillance of the woman; epidural anaesthesia to reduce pain and thus the adverse effects of catecholamines release and appreciation of effects associated with haemodynamic changes. Ergometrine should not be used. Oxytocin reduces coronary blood flow when levels exceed 4 mm/L.
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Elective caesarean section should be considered for myocardial infarction at term to allow better control of the situation and haemodynamic changes.

References

Confidential Enquiries into Maternal Deaths in the United Kingdom. Why Mothers Die. The Sixth Report of Confidential Enquiries into Maternal Deaths in the United Kingdom 2000–2002. London: CEMACH, 2004.

Bibliography

Altman D, Carolli G, Duley L, et al. Do women with pre-eclampsia, and their babies benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet 2002;. 2002;359:1877-1890.

Andra H, James MD, Margaret G, et al. Acute myocardial infarction in pregnancy. A United States population based study. Circulation. 2006;113:1564-1571.

Baldwin KJ, Johanson RB, Anthony J. The acute management of severe hypertensive illness in pregnancy. O’Brien S, editor. The Yearbook of Obstetrics and Gynaecology, 5. London: RCOG Press. 1997:233-245.

Besinger RE, Moniak CN, Paskiewicz LS, et al. The effect of tocolytic use in the management of symptomatic placenta praevia. American Journal of Obstetrics and Gynecology. 1995;172:1770-1778.

Caspi E, Lotan Y, Schreyer P. Prolapse of the cord: reduction of perinatal mortality by bladder instillation and caesarean section. Israel Journal of Medical Sciences. 1983;19:541-545.

Chetty RM, Moodley J. Umbilical cord prolapse. South African Medical Journal. 1980;57:128-129.

Cortis BS, Gensini GG. Can the risks of myocardial infarction in pregnancy be reduced?. Cardiovascular Diseases. 1977;4:49.

Driscoll JA, Sadan O, Van Gelderen CJ, et al. Cord prolapse: can we save more babies? Case reports. British Journal of Obstetrics and Gynaecology. 1987;94:594-595.

Duley L, Henderson-Smart D. Drugs for treatment of very high blood pressure during pregnancy. In: The Cochrane Library, Issue 2. Oxford: Update software; 2001.

Hankin GDU, Wendel GDJr, Leveno KJ, et al. Myocardial infarction during pregnancy: A review. Obstetrics and Gynecology. 1985;65:139-146.

Ladner HE, Danielsen B, Gilbert WM. Acute myocardial infarction in pregnancy and the puerperium: a population based study. Obstetrics and Gynecology. 2005;105:480-484.

Leerentveld RA, Gilberts EC, Arnold MJ, et al. Accuracy and safety of transvaginal sonographic placental localisation. Obstetrics and Gynecology. 1990;76:759-762. 1990

Johanson RJ, Cox C, Grady K, et al. Managing Obstetric Emergencies and Trauma: The MOET Course Manual. London: RCOG Press, 2003.

Royal College of Obstetricians and Gynaecologists. Placenta praevia: Diagnosis and management. In: Guideline No 27. London: RCOG; 2001.

Towers CV, Pircon RA, Heppard M. Is tocolysis safe in the management of third trimester bleeding?. American Journal of Obstetrics and Gynecology. 1999;180:1572-1578.

Tucker D, Liu DTY, Ramoutar P. Myocardial infarction at term: a case report to consider management options. British Journal of Obstetrics and Gynaecology. 1996;6:522-524.

Vago T. Prolapse of the umbilical cord. A method of management. American Journal of Obstetrics and Gynecology. 1970;107:967-969.