90774117 aims-of-obstetric-critical-care-management

2
Aims of obstetric critical care management
Laura Claire Price* BSc, MBChB, MRCA, MRCP
SpR Respiratory and Intensive Care Medicine
Adult ICU, St George’s Hospital, London, UK
Andrew Slack MBBS, MRCP
SpR Renal and Intensive Care Medicine
Adult ICU, Kings College Hospital, London, UK
Catherine Nelson-Piercy MA, FRCP, FRCOG
Consultant Obstetric Physician
Directorate Office, North Wing, St Thomas’ Hospital, London, UK
The aims of critical care management are broad. Critical illness in pregnancy is especially perti-
nent as the patient is usually young and previously fit, and management decisions must also
consider the fetus. Assessment must consider the normal physiological changes of pregnancy,
which may complicate diagnosis of disease and scoring levels of severity. Pregnant women
may present with any medical or surgical problem, as well as specific pathologies unique to preg-
nancy that may be life threatening, including pre-eclampsia and hypertension, thromboembolic
disease and massive obstetric haemorrhage. There are also increasing numbers of pregnancies
in those with high-risk medical conditions such as cardiac disease. As numbers are small and
clinical trials in pregnancy are not practical, management in most cases relies on general inten-
sive care principles extrapolated from the non-pregnant population. This chapter will outline the
aims of management in an organ-system-based approach, focusing on important general princi-
ples of critical care management with considerations for the pregnant and puerperal patient.
Key words: pregnancy; high risk; complications; pre-eclampsia; postpartum haemorrhage;
thromboembolism; intensive care; critical care.
GENERAL OVERVIEW
Maternal mortality is fortunately rare in the UK, with 13.95 maternal deaths per
100 000 deliveries in 2003–2005.1
However, despite modern-day advances in care,
* Corresponding author. Tel.: þ44 2074311250; Fax: +44 2084584505.
E-mail address: lauracprice@hotmail.com (L.C. Price).
1521-6934/$ - see front matter ª 2008 Elsevier Ltd. All rights reserved.
Best Practice & Research Clinical Obstetrics and Gynaecology
Vol. 22, No. 5, pp. 775–799, 2008
doi:10.1016/j.bpobgyn.2008.06.001
available online at http://www.sciencedirect.com

this figure has remained static over the last few decades, and this may relate to a higher
number of high-risk pregnancies progressing to term.2
Worldwide, maternal mortality
is greater with 55–920 maternal deaths per 100 000 live births3
, with the highest rates
in sub-Saharan Africa. The most common reasons for intensive care unit (ICU) admis-
sions in the UK are pre-eclampsia, sepsis and haemorrhage.4
Overall, 0.9% of pregnant
women require ICU admission in the UK, comparable to US figures.5
The most
common cause of maternal death on ICU is acute respiratory distress syndrome
(ARDS). UK maternal mortality could be improved with prompt recognition of critical
illness, earlier use of critical care facilities and earlier senior involvement. Perinatal
mortality rates are up to 20–25% depending on the underlying maternal diagnosis.
The assessment and management of obstetric admissions to critical care can be chal-
lenging, with unique disease states and physiological changes seen. These changes occur
in all major systems and persist for up to 6 weeks post partum. In 50–80% of cases, preg-
nant women require ICU admission due to a direct obstetric cause; the remainder relate
to medical causes. There may be diseases specific to pregnancy (massive obstetric hae-
morrhage, amniotic fluid embolism, pre-eclampsia, peripartum cardiomyopathy); an in-
creased susceptibility to certain diseases due to pregnancy (venous thromboembolism,
urinary tract infection, varicella pneumonia); pre-existing disease exacerbation (asthma,
cardiac disease); or incidental diseases during pregnancy (e.g. diabetic ketoacidosis). The
requirement for critical care support for one or more organ failures usually results from
the development of a multisystem disorder such as shock, ARDS or sepsis.
The aim of critical care management in any population is to ensure adequate oxygen
delivery and tissue perfusion. There are specific conditions requiring attention in preg-
nancy, and this review will consider general ICU principles and these with reference to
obstetric physiology. The altered maternal physiology should be considered during
each stage of assessment, resuscitation, monitoring, use of pharmacological therapies,
and single or multiple organ support. Young, previously healthy patients often show
relative compensation in critical illness. The signs of sepsis and haemorrhage are often
masked initially and abnormal signs may overlap normal signs of pregnancy. Some signs
always indicate abnormality, including tachypnoea and metabolic acidosis. Obstetric
and medical staff should be trained in the recognition of critical illness in this popula-
tion as the disease processes can follow a rapid and fulminant course.
The effects on fetal perfusion are dependent on placental perfusion and oxygen
delivery, both reflecting maternal wellbeing. The fetus is adapted to living in a relatively
hypoxic environment with the oxygen dissociation curve shifted to the left, high
haematocrit and high cardiac output (CO). Despite this, small changes in maternal
homeostasis may have an adverse effect on the fetus. If the mother does become crit-
ically ill, premature delivery may be indicated with the associated neonatal complica-
tions of respiratory distress syndrome, jaundice, intracranial haemorrhage and
necrotizing enterocolitis.
AIMS OF ORGAN SUPPORT IN CRITICAL CARE
General supportive care
Immediate resuscitation is the primary aim in the management of any critically ill pa-
tient, with systematic assessment of deranged physiology using an organ-based
systematic approach. This is generic, irrespective of the underlying pathology, and is
followed by more specific diagnostic consideration when the patient is more stable.
776 L. C. Price et al

Appropriate investigations and procedures are then carried out, depending on the
clinical history and examination. It is important not to withhold or delay useful inves-
tigations because the patient is pregnant.
The gestational age and condition of the fetus must always be considered, as well
as the effects of any drugs or procedures on the fetus. The obstetric team should
perform a fetal scan to assess viability. Often if the mother is or has been critically
ill, the fetus may have succumbed. Once this is established, liaison with obstetrics
to deliver the baby will usually improve maternal physiology, although delivery itself
is associated with significant temporary haemodynamic demands and changes. If the
fetus is viable, the advisability of delivery needs a multidisciplinary discussion balancing
the fetal risks of prematurity versus any maternal benefits from delivery. The moth-
er’s health should be the priority. The fetus is at significant risk if the mother is se-
riously ill, particularly if she is acidotic, and regular fetal monitoring is appropriate.
Fetal management primarily involves maternal resuscitation, maintaining adequate pla-
cental oxygenation and perfusion. Delivery may be indicated in some settings of se-
vere maternal illness such as cardiac arrest, severe asthma, acute fatty liver of
pregnancy or pre-eclampsia, or with fetal distress. When considering the timing of
delivery, the effects of drugs on fetal physiology and the requirement for neonatal re-
suscitation should be considered. Drugs are classed according to the risk of fetal ef-
fects into Category A (no fetal risk) to Category D (fetal risk), and Category X
(contra-indicated). The maternal volume of distribution is increased and glomerular
filtration rate (GFR) is elevated in pregnancy, so higher doses are needed for drugs
with renal elimination. Sedative effects on fetal respiratory function should be antic-
ipated, although polarized agents such as neuromuscular blocking agents do not cross
the placenta.
Critical care involves intensive monitoring and physiological support for patients
with life-threatening but potentially reversible conditions. Patients should be managed
in either an ICU (Level 3) or high-dependency (Level 2) setting. Level 3 usually involves
patients with multi-organ failure and/or requiring mechanical ventilation, while Level 2
involves non-invasive ventilation (NIV), renal replacement therapy or intensive
monitoring.
Early involvement and planning should involve all members of the multidisciplinary
team. This includes obstetricians, midwives, physicians (obstetric physicians if avail-
able), intensivists, anaesthetists, haematologists, paediatricians and neonatologists.
Elective ICU beds should be booked for certain patients such as those with significant
cardiac disease undergoing elective caesarean section.
Early recognition of critical illness is essential. There is good evidence that early
intervention in the first 6 h of severe sepsis influences survival. Ideally, early warning
scoring systems adapted to pregnancy physiology should be implemented on obstetric
wards to identify patients at an early stage. ICU care can often be commenced in the
operating theatre or emergency department (ED) prior to transfer to the ICU to
avoid delays, and stabilization and elective intubation may be necessary prior to
transfer.
Aims should also include adherence to recent developments in critical care prac-
tice including the Surviving Sepsis Campaign guidelines6
, considered use of activated
protein C7
, insulin therapy to maintain normoglycaemia8
, corticosteroids in septic
shock9
, lung protective ventilatory strategies in ARDS management, and early
goal-directed therapy for severe sepsis and septic shock.10
Although not written
with the obstetric patient in mind, most aspects of management should not differ
dramatically.
Aims of obstetric critical care management 777

Haemodynamic management
The aims of cardiovascular support in any setting are to maintain adequate cardiac out-
put (CO) and blood pressure (BP). There is a 20% increase in maternal oxygen de-
mand in pregnancy; CO increases by 30–50% due to an increase in stroke volume
and heart rate, and BP is reduced by 5–10 mm Hg by mid-pregnancy. There is no
change in central venous pressure (CVP) or pulmonary artery wedge pressure
(PAWP) as systemic and pulmonary vascular resistance are both reduced.11
These hae-
modynamic changes begin as early as 8 weeks, and gradually return to normal 2–12
weeks post partum.12
The supine hypotension syndrome is an important consideration after 24 weeks. It
relates to compression of the inferior vena cava by the gravid uterus, and can lead to
a dramatic drop in preload, leading to a 25–30% drop in CO, severe hypotension and
bradycardia. It can be reduced by positioning in a lateral tilt although a full left lateral
position is sometimes required.
The most significant cardiovascular challenge occurs at birth. Up to 500 mL of
blood is autotransfused back into the circulation following relief of aortocaval
compression by the fetoplacental unit aortocaval compression by the fetoplacental
unit and contraction of the uterus, and CO may increase by up to 80% of preterm
baseline. These fluid shifts are especially challenging in parturients with cardiac disease,
who should be monitored for 72 h post partum.13
Shock
Cardiovascular support may be required in states of circulatory shock. In shock,
reduced tissue oxygenation leads to anaerobic metabolism, reflected by an increased
serum lactate and reduced maternal central venous oxygen saturations (SvO2). This
will affect fetal oxygenation despite adaptation to a relatively hypoxic environment.
Lactate levels >2 mmol/L indicate tissue hypoxia except in settings with poor
lactate clearance such as liver failure. Serial measurements are useful, for example,
in septic shock (Table 1).14
The most common causes of shock in the obstetric population are major haemor-
rhage and sepsis. When reversible causes have been controlled, support of the
Table 1. Types of shock.
Type of shock Pathophysiology Cardiac
output
Systematic
vascular
resistance
Examples of causes
Hypovolaemia Loss of circulating
volume
Low High Massive haemorrhage, diabetic
ketoacidosis, burns
Distributive Pathological
vasodilatation
High/low Low Sepsis, liver failure, pancreatitis,
anaphylaxis
Cardiogenic Severe pump failure Low High Cardiomyopathy, valvular dysfunction
Obstructive Obstruction to
cardiac output
Low High Pulmonary embolism, amniotic fluid
embolus, tamponade
Neurogenic Loss of sympathetic
outflow if lesion
above T6
Low Low Spinal trauma, intracranial haemorrhage

cardiovascular system may involve fluid administration, correction of heart rate and
rhythm disorders, the use of vasoactive agents, thrombolysis, pacemakers, ventilatory
support and mechanical devices. Invasive or non-invasive haemodynamic monitoring is
an important tool. Techniques may be invasive (lithium dilution pulsed contour analysis
and the pulmonary artery catheter), semi-invasive (oesophageal Doppler) or non-inva-
sive (echocardiography).
Fluids
Fluid administration is an important part of most resuscitation scenarios, aiming to
improve microvascular blood flow by increasing plasma volume, and improve CO by
the Frank-Starling mechanism.15
However, the use of fluids in obstetrics should be
more cautious than in the non-obstetric setting. Even in a normal pregnancy, colloid
oncotic pressure (COP) is reduced by 14% (from 20.8 to 18 mm Hg).16
This reduction
in COP, when combined with any condition predisposing to either increased capillary
leak (e.g. in pre-eclampsia and many critical illness states) or raised left atrial pressure,
can relatively easily lead to pulmonary oedema.17
It is not thought to be as common as
this suggests, because pulmonary lymphatic drainage is increased in pregnancy.
The choice of fluid used will depend on the setting. In major haemorrhage, replace-
ment is needed with blood products. Otherwise, the choice between crystalloid and
colloid remains under debate. Excessive use of normal saline leads to hyperchloraemic
acidosis18
, and Hartmann’s solution is currently the most ‘physiological’ crystalloid in
use. Colloids remain in the intravascular compartment for longer. Overall, the choice
will depend on the underlying diagnosis, local availability, the evaluation of the content
of each fluid type, and the benefits and complications of each (see Table 2).19
The concept of a fluid challenge requires haemodynamic monitoring to assess
volume responsiveness to a set volume of fluid.20
Following this, a 20% rise in stroke
volume suggests intravascular depletion, and sufficient intravascular volume is sug-
gested when the rise is sustained. Small rises or a fall in the stroke volume suggest fluid
overload as the myocardium is stretched ‘over the Starling curve’. Obstetric patients
are best managed with a neutral or even negative fluid balance, as the development of
acute prerenal failure is usually reversible if recognised and treated early, compared
with the potential risks of non-cardiogenic pulmonary oedema or ARDS.
Table 2. Fluid composition.
Fluid Ionic content (mmol/L) pH Complications
Normal saline
(NaCl 0.9%)
Naþ
154, ClÀ
154 5.0 Hyperchloraemic acidosis
5% dextrose Nil 4.0 Hyponatraemia, oedema
Hartmann’s
(compound Na lactate)
Naþ
131, Kþ
5, ClÀ
111,
Ca2þ
2, HCO3
-
29
6.5 Fluid overload
(with all fluids), Kþ
may
accumulate
Gelofusin Naþ
154, Kþ
0.4, ClÀ
154,
Ca2þ
0.4
7.4 Allergy (<0.1%),
hyperchloraemia
Albumin 4.5% Naþ
150, Kþ
2, ClÀ
120 7.4 Transfusion reactions,
TRALI
TRALI, transfusion-related lung injury.

Furthermore, the appropriate management of oliguria in these patients is not neces-
sarily a fluid challenge, as discussed further in the renal section.
Cardiac failure
Cardiac failure may be primarily left sided with pulmonary oedema, right sided with ev-
idence of hepatic and renal congestion, or biventricular. Reversible causes such as coro-
nary ischaemia or pulmonary embolism should be managed as appropriate. Non-invasive
continuous positive airways pressure (CPAP) is averyeffective treatment forcardiogenic
pulmonary oedema21,22
, and will increase CO, reduce left ventricular afterload, increase
functional residual capacity (FRC) and respiratory mechanics, and reduce work of
breathing. Invasive ventilation may be needed if the woman is severely acidotic, hypercap-
nic, hypotensive or has very poor left ventricular function.23
Vasodilator therapy is im-
portant, and both glyceryl trinitrate (GTN) and hydralazine are safe in pregnancy.
Loop diuretics are used to reduce pulmonary congestion, although they may reduce
CO and uteroplacental perfusion if hypovolaemic. If inotropes are needed, dobutamine
is safe in pregnancy. Newer inotropes such as levosimendan may improve arterioventric-
ular coupling24
, although there are only case reports of use in pregnancy in peripartum
cardiomyopathy.25
Mechanical devices to augment CO such as ventricular assist devices
and intra-aortic balloon pumps may be required.
Vasoactive agents
Heart rate and rhythm disorders are corrected in the usual way according to resusci-
tation council guidelines. Most supraventricular tachycardias and ventricular ectopics
require no drug therapy in pregnancy, and vagal manouevres such as carotid sinus
massage should be tried first in paroxysmal supraventricular tachycardia. Atrial fibril-
lation should be restored to sinus rhythm in pregnancy with electrical cardioversion,
or rate controlled with digoxin or cardioselective beta-blockers. Replacement of
potassium and magnesium may be required, then chemical or electrical cardioversion
as appropriate, or use of specific anti-arrhythmic agents. Cardioselective beta-
blockers, diltiazem, verapamil and adenosine are safe; however, amiodarone should
be avoided as it can inhibit fetal thyroid function.26
Vasopressors areoften used for hypotension in the setting of obstetric regional anaes-
thesia. Ephedrine may lead to maternal tachycardia due to its chronotropic effects on the
cardiac beta-1 receptor and reduced fetal pH, although it is less likely to cause uteropla-
cental vasoconstriction. Phenylephrine, an alpha-1 adrenergic agonist and powerful arte-
riolar constrictor, causes less fetal acidosis although it may reduce maternal heart rate
and therefore CO.27
If inotropes or more powerful vasopressors are required in an
ICU setting, the effects on uteroplacental perfusion should be considered, and CO mon-
itoring is useful. The choice of agent will depend on the mean arterial pressure (MAP),
CO and systematic vascular resistance (SVR), and should follow appropriate fluid resus-
citation. In the setting of vasodilatory shock with low SVR and high CO (sepsis, liver fail-
ure), sympathomimetic vasopressors such as norepinephrine are used. Vasopressin has
been used in some settings such as resistant septic shock and cardiac arrest28
, but re-
duced blood flow to some organs may occur29
so it should be reserved for ‘salvage’ ther-
apy.30
In cardiogenic shock, increased inotropy from beta-1 agonism may be useful using
dobutamine (and epinephrine with added vasoconstrictive effects). Inodilators are useful
when low CO occurs with vasoconstriction (high SVR), with agents including milrinone
and the calcium-sensitizer levosimendan (Table 3).24

Hypertension
Hypertension complicates 12% of pregnancies31
and may be classified into pre-eclampsia,
gestational hypertension, chronic essential hypertension and malignant hypertension
presenting in pregnancy. The overall management strategy of pre-eclampsia with deliv-
ery as a prime goal is discussed in detail elsewhere. There is no single ideal anti-hy-
pertensive regime used for acute severe hypertension in pregnancy, and most units
have their own protocol. Intravenous hydralazine and labetalol are equally effective
but labetalol is preferred as it has fewer side effects.32
Sodium nitroprusside is an ef-
fective vasodilator, and is therefore a good choice if pulmonary oedema is present,
and its short half-life is useful when titrating the dose. However, toxicity may occur
with cyanide or thiocyanate accumulation, usually in those with renal failure and if
treated for more than 24 h. GTN is useful and safe for short-term use, although
mainly as a venodilator as it has little effectiveness in hypertensive emergencies
and so is not usually a first-line agent, and problems result with tachyphylaxis. Oral
nifedipine, doxasocin and alpha-methyldopa are oral options. Angiotensin-converting
enzyme inhibitors are teratogenic33
and are therefore contra-indicated, although they
may be life-saving in some cases of malignant hypertension including scleroderma.
Respiratory management
The overall aim of respiratory management is to maintain gas exchange. This encom-
passes airway management, administering oxygen therapy and ensuring adequate
Table 3. Vasoactive agents.
Use if Clinical example Important side effects
Vasopressors
Less potent
Ephedrine Low SVR Spinal/epidural/general
anaesthetic-induced
vasodilatation
All have effects on
UP perfusionPhenylephrine
Metaraminol
More potent
Noradrenaline Low SVR with
shock unresponsive
to fluid challenge
Septic shock Lowers UP perfusion;
digital necrosisVasopressin
Inotropes
Inoconstrictor
Adrenaline Low CO
þ low SVR
Septic shock Lactic acidosis
Inodilators
Milrinone Low CO
þ high SVR
Cardiogenic shock Hypotension, dose prolonged
in renal failure (milrinone)Levosimendan
Variable
Dobutamine Low CO Sometimes combined
with a vasoconstrictor
in some shock settings,
or used alone in
cardiogenic shock
Variable effects on blood
pressure (dobutamine)
Tachycardia (dopexamine)
Dopexamine Low CO with poor
splanchnic
perfusion
CO, cardiac output; SVR, systematic vascular resistance; UP, uteroplacental.

ventilation (CO2 clearance). These general principles are as for the non-pregnant
population, with added considerations of the physiological changes, including the left
lateral tilt in positioning, and the need in later pregnancy to consider a delivery
plan. It is important to remember that oxygen delivery to the tissues and effective
CO2 removal involves the heart and circulation as well as the lungs. Oxygen delivery
to the tissues involves a cascade of processes depending on alveolar oxygen concen-
tration, oxygen transfer, haemoglobin and the oxygen dissociation curve, then diffusion
from capillary blood into mitochondria along a concentration gradient. Defects can
occur at any of these levels.
The differential diagnosis of primary respiratory failure in pregnancy is broad, and
the changes in respiratory physiology should be remembered in assessment and
management. Erect partial pressure of oxygen (PaO2) increases by the end of the first
trimester, and falls during each of the following trimesters. This is due to an increased
arteriovenous oxygen difference as oxygen consumption increases above CO with the
advancement of pregnancy. After mid-gestation, PaO2 is <13.1 kPa in supine patients
due to airway closing capacity being above FRC, and also from aortocaval compres-
sion. The reduced FRC and greater oxygen consumption make episodes of desatura-
tion more rapid. Adequate fetal oxygenation requires a maternal paO2 > 9.2 kPa,
corresponding to a maternal arterial oxygen saturations (SaO2) > 95%34
; much higher
than the saturations usually tolerated outside pregnancy.
It is important to consider the normal progressive respiratory alkalosis when con-
sidering respiratory management, as ventilation requirements may change depending
on the stage of pregnancy. In severe asthma, a ‘normal’ partial pressure of CO2
(pCO2) of 4–5.5 kPa is usually a warning of impending respiratory failure. In pregnancy,
this is, in fact, relative hypercapnia as the usual upper limit in pregnancy is 3.5 kPa. The
effects of pCO2 on fetal wellbeing are not clear, although they are likely to be detri-
mental with acidosis leading to reduced ability of fetal haemoglobin to bind oxygen.
A diffusion gradient of approximately 1.3 kPa is needed for placental pCO2 clear-
ance35
, and high maternal levels may interfere with this. A maternal pCO2 target of
<5.9 kPa or pH >7.30 has therefore been suggested36
, avoiding hypercapnia (Table 4).
Upper airway
Airway management may be challenging in obstetric practice. There are changes in ma-
ternal anatomy with increased upper airway oedema, especially in pre-eclampsia where
fluid retention enlarges the tongue and makes identification of airway landmarks more
Table 4. Causes of respiratory failure in pregnancy.
Pulmonary causes
Asthma, severe pneumonia, pleural effusion, pneumothorax, pulmonary haemorrhage, interstitial
lung disease, exacerbation of underlying respiratory disease (e.g. cystic fibrosis, chronic obstructive
pulmonary disease, bronchiectasis, pulmonary hypertension), atypical infection (including human
immunodeficiency virus), respiratory muscle myopathies (hypercapnic respiratory failure)
Acute respiratory distress syndrome (ARDS) and acute lung injury (see later)
Cardiac causes
Cardiogenic pulmonary oedema, e.g. peripartum cardiomyopathy, mitral stenosis
Iatrogenic fluid overload
Tocolytic pulmonary oedema (rare now with alternatives to beta-sympathomimetics)

difficult.37
Any neck or face oedema in a woman with pre-eclampsia should forewarn
of a likely difficult intubation.38
These patients may even develop stridor and may have
difficult extubations.39
Airway oedema in pre-eclampsia can even lead to obstructive
sleep apnoea.37
Sleep-disordered breathing is probably underdiagnosed in pregnancy40
and may have adverse fetal effects.41
Obesity is more common and correlates with dif-
ficult intubations42
, instrumental deliveries, a higher incidence of postpartum haemor-
rhage43
, and an even greater incidence of gastric acid aspiration during general
anaesthesia.44
The upper airway in pregnancy is prone to contact bleeding with any
airway manipulation. This mucosal swelling leads to a smaller laryngeal inlet. Any air-
way intervention should involve a skilled anaesthetist with a fluent difficult/failed intu-
bation drill.
Ventilation
The aims of ventilation are to oxygenate, ventilate and relieve the work of breathing. In
pregnancy, ventilation can be problematic. As in the non-pregnant patient, ventilation
may be invasive, through an endotracheal tube or tracheotomy, or non-invasive,
through a tightly fitting facemask. NIV may exert CPAP or bi-level positive airway pres-
sure (BiPAP). CPAP is the application of a constant positive end-expiratory pressure,
called ‘positive end-expiratory pressure’ in the invasively ventilated patient. Non-inva-
sive CPAP differs from BiPAP in several ways. BiPAP enables spontaneous breathing
over two pressure levels, and is therefore more effective at clearing CO2, hence its
use in hypercapnic respiratory failure. CPAP circuits can deliver a higher fractional in-
spired oxygen concentration (FiO2) and can be humidified, and the FiO2 can be mea-
sured accurately. With BiPAP, FiO2 is not measured accurately, oxygen is entrained in
L/min, the circuit tolerates leaks, and the delivered FiO2 is dependent on the inspira-
tory flow rate.
Non-invasive ventilation. The evidence for acute NIV is well established in the treatment
of hypercapnic respiratory failure in chronic obstructive pulmonary disease, where it
reduces the need for intubation in mildly acidotic patients.45
There is also good evi-
dence for NIV in cardiogenic pulmonary oedema and in immunocompromised states.
It has physiological benefit in other causes of respiratory failure, but should be used in
a controlled, monitored setting as a trial of therapy. Patients should be awake with
good respiratory drive, haemodynamically stable and without excessive respiratory se-
cretions. Those with more marked acidosis (pH <7.25) should be considered for ear-
lier invasive ventilation. There is less evidence for its use in other causes of
hypoxaemic respiratory failure, but it has been used in asthma, pneumonia, ARDS
and others including postoperative cases.46
There is little evidence for its use in the
obstetric population, although it has been used in sleep-disordered breathing during
pregnancy.40
NIV cannot therefore be currently recommended except as a closely
monitored trial of therapy in selected obstetric patients, in an ICU setting. Further-
more, there is a theoretical even greater risk of gastric acid aspiration with the gastric
distention that occurs with NIV.
Invasive ventilation. Invasive ventilatory support may be necessary in primary respira-
tory failure, when a trial of NIV fails, in severe acidosis, and with reduced levels of con-
sciousness and respiratory drive. The overall management of a ventilated obstetric
patient is similar to the non-pregnant population. This includes adequate thrombopro-
phylaxis, enteral feeding, sedation breaks and weaning techniques. Spontaneous

breathing modes are preferred to maintain respiratory muscle strength, but increased
sedation and paralysis may be needed to optimize ventilation.47
Gastric acid suppress-
ion therapy should be routine, especially with the increased risk of gastric acid aspira-
tion in these patients.
It is important to prevent ventilator-associated pneumonia (VAP), thought to follow
bacterial colonization of the upper respiratory tract. Diagnosis based on clinical crite-
ria has poor specificity, and microbiological samples are used including direct bron-
choalveolar lavage48
, protected specimen brush49
or non-invasive endotracheal
aspiration. Biomarkers such as C-reactive protein and procalcitonin50
can be useful,
although they are probably less specific in the obstetric population. Methods to pre-
vent VAP include nursing ventilated patients head-up, avoiding re-intubation and min-
imizing changes in ventilator circuits.51
Strategies for weaning from mechanical ventilation, including the use of weaning
protocols52
, are no different to the non-obstetric population. Percutaneous tracheos-
tomy insertion may be indicated early in patients requiring prolonged ventilation53
,
bearing in mind that the upper airway in any parturient is more oedematous and prone
to contact bleeding.
Acute respiratory distress syndrome
Acute lung injury and ARDS are a disease spectrum with many underlying causes. The
diagnosis is based on three factors: the presence of pulmonary oedema; evidence of
poor oxygenation; and clinical, echo or direct evidence of normal left atrial pressure
to exclude a cardiogenic cause of pulmonary oedema.54
The extent of poor oxygen-
ation is based on a ‘P:F’ ratio of PaO2 to FiO2. For example, breathing air (FiO2 0.21),
the normal range of PaO2 would be 13–17 kPa, giving a P:F ratio of 72 kPa. With
ARDS, the FiO2 may be 0.8 and the PaO2 only 15 kPa, giving a P:F ratio of 18.7 kPa
(or 142 mm Hg), hence indicating poor oxygenation. It is always important to note
the FiO2 when measuring blood gases for this reason (Table 5).
Any pathology causing inflammation-induced injury to the alveolar–capillary inter-
face can lead to ARDS. There is no suggestion that it is more common in pregnancy,
but it may be the end result in several ‘obstetric’ diseases. Maternal mortality may be
35–60% with higher mortality post partum, and morbidity often persisting after recov-
ery in survivors (Table 6).36
Ventilatory strategies in ARDS are similar to the non-pregnant patient with consid-
eration of the normal progressive respiratory alkalosis and the effects of hypoxia, hy-
percapnia and acidosis on the fetus. Invasive ventilation is often necessary, and is
thought to contribute to a syndrome of lung injury itself. There has recently been
a drive towards a ‘lung protective’ ventilation strategy to reduce the need for invasive
ventilation. The components of iatrogenic ventilator-associated lung injury include
those due to excess airway pressure (barotrauma55
), too high tidal volumes (volu-
trauma56
), airway collapse (atelectrauma9
) and local inflammation (biotrauma57
). The
Table 5. Definitions of acute respiratory distress syndrome (ARDS) and acute lung injury (ALI).54
Bilateral chest X-ray infiltrates
P/F ratio < 26 kPa (ARDS) or <39 kPa (ALI)
Pulmonary artery wedge pressure <18 mm Hg (or 2.4 kPa)

principles of a protective ventilation strategy in ARDS are to minimize airway pres-
sures and to tolerate a higher pCO2. There are, however, fetal effects of hypercapnia
and acidosis, so this ‘permissive hypercapnia’ is not recommended in the obstetric pa-
tient. Furthermore, the low tidal volumes desired in ARDS in a non-obstetric patient
may not be sufficient for the higher ventilatory requirements needed in pregnancy. In
fact, higher tidal volumes and plateau pressures than usual may actually be necessary
for this reason, and higher SaO2 and pO2 targets are recommended. As in any setting,
positive end-expiratory pressure is useful to prevent end-expiratory lung collapse, and
can improve recruitment and oxygenation of alveolar units. These effects may be offset
by negative effects on cardiac filling with reduced systemic BP, exaggerated with intra-
vascular fluid depletion.
Renal support
The incidence of acute renal failure (ARF) in pregnancy has reduced over time in both
developed (1–2.8%) and developing (10–15%) countries with improvements in obstet-
ric care, especially a reduction in septic abortions.58
The World Health Organization
has estimated that one in eight pregnancy-related deaths in the developing world are
the result of unsafe abortions and about 8% of these deaths are due to ARF.59
The diagnosis of ARF is complex with over 30 definitions of ARF in the literature.
The RIFLE criteria were developed to provide a uniform means of classifying ARF;
these have been modified recently and the term ‘acute kidney injury’ (AKI) has
been introduced to encompass all causes of ARF. The classification is based on changes
in serum creatinine and/or urine output over a 48-h period.60
It is easy to apply clin-
ically, and importantly highlights the requirement of repeated testing of serum creat-
inine and the close monitoring of urine output in any patient with suspected or at risk
of ARF.
Obstructive uropathy must always be excluded, and this can be difficult in preg-
nancy due to physiological hydronephrosis, therefore an early ultrasound can provide
an invaluable baseline reference for the future when obstructive uropathy is suspected.
Progesterone-induced ureteric smooth muscle relaxation plus compression by the
gravid uterus leads to ureteric and renopelviceal dilatation. There is greater hydro-
nephrosis on the right side due to physiological engorgement of the right ovarian
vein and dextrorotation of the uterus.
Early recognition and treatment of AKI saves nephrons and prevents further decline
in glomerular filtration rate (GFR). Serum creatinine concentration is a poor marker of
GFR because it does not rise appreciably until GFR has fallen significantly. From the
first trimester of pregnancy until term, there are significant increases in renal blood
Table 6. Causes of acute respiratory distress syndrome in pregnancy.
Causes specific to pregnancy
Massive haemorrhage, pre-eclampsia (especially with fluid overload), sepsis (due to chorioamnionitis,
endometritis, pyelonephritis), amniotic fluid embolism, trophoblastic embolism, gastric acid
aspiration
Other causes
Sepsis (other causes), pneumonia, transfusion-related acute lung injury, trauma, inhalational injury,
burns, near-drowning, acute pancreatitis etc.

flow (50–85%) and GFR (40–65%); consequently, there is a parallel decline in the se-
rum creatinine concentration. Therefore, small changes in the serum creatinine con-
centration can represent a significant deterioration in GFR. The calculation of
estimated GFR using the modification of diet in renal disease study (MDRD) equation
is not recommended in pregnancy as it overestimates GFR.
Aetiology
Conventionally, the major causes of AKI are grouped into three general categories:
prerenal; intrinsic renal; and obstructive causes. This holds true in pregnancy, but
most importantly includes the placenta-driven diseases including pre-eclampsia and
HELLP (haemolysis–elevated liver enzymes–low platelets) syndrome (Table 7).
Urinary electrolyte measurements are rarely helpful clinically as they are unreliable
in distinguishing between prerenal failure and acute tubular necrosis, and they do not
affect management. It is useful to quantify the degree and change in proteinuria, which
requires repeated random urine samples for protein:creatinine ratio measurement.
This method has been validated in hypertensive and non-hypertensive pregnant
patients and is comparable to 24-h collections.61
Management of acute kidney injury
The mainstay of treatment in ARF is aimed at minimizing damage to surviving nephrons
whilst providing support until the kidney recovers. This includes the removal of tubu-
lar toxins, specific treatment of glomerular diseases and restoration of the circulation.
Haemodynamic monitoring using clinical and invasive methods guides volume resusci-
tation and the use of vasopressors with the goal of improving perfusion pressure and
urine output (>0.5–1 mL/kg/h). Failure to achieve this goal will usually become appar-
ent at an early stage, and persistent oliguria will eventually lead to volume derange-
ments. Oliguria can be converted to a non-oliguric state by using diuretics and low-
dose dopamine, liberating valuable time prior to commencing renal replacement ther-
apy. There is, however, little evidence to suggest that these two agents improve renal
recovery times; ultimately, this depends on the number of remaining functional neph-
rons increasing their filtration to maintain GFR. In the postpartum patient, oliguria may
Table 7. Aetiology of acute kidney injury.
Pre renal Intrinsic renal Post renal
Hypovolaemia
(e.g. sepsis, haemorrhage)
Inflammatory
(eg anti-GBM (glomerular basement membrane)
disease, ANCA-associated GN, SLE)
Urolithiasis
Low cardiac output states
(e.g. heart failure)
Thrombotic
[e.g. DIC, thrombotic micro-angiopathy
(TTP, HUS), antiphospholipid syndrome]
Blood clot
Pre-eclampsia and
HELLP syndrome
Interstitial nephritis (e.g. infections, drugs),
pre-eclampsia and HELLP syndrome
Urethral stricture
ANCA, antineutrophil cytoplasmic antibody; GBM, glomerular basement membrane; GN, glomerulone-
phritis; SLE, systemic lupus erythematosus; DIC, disseminated intravascular coagulation; TTP, thrombo-
cytopenic purpura; HUS, haemolytic uraemia syndrome; HELLP, haemolysis–elevated liver enzymes–low
platelets.

be normal, and, as described above, inappropriate intravenous fluids can precipitate
iatrogenic pulmonary oedema. Lower targets for urine output are therefore
appropriate.
Metabolic derangements are an important aspect of AKI management. Hyperkalae-
mia is best managed by limiting potassium input, augmenting elimination with diuretics,
and promoting cellular uptake with insulin and glucose boluses. Severe acidosis (pH
<7.2) may require treatment with sodium bicarbonate, although avoiding hypernatrae-
mia and excessive volume expansion. The intracellular acidosis that follows should be
remembered, although it is not a problem if the spontaneously breathing patient is able
to ‘blow off’ the CO2 or if the patient is being adequately mechanically ventilated.
The indications for renal replacement therapy are the same in pregnancy as for the
general population, but it is rarely required (<1 in 10 000–15 000 pregnancies). There
is no clear evidence guiding dialysis dose prescription in AKI. Pregnant chronic dialysis
patients achieve better fetal outcomes at higher dialysis doses (usually >20 h/week)
compared with the standard regimen of 4 h thrice weekly.62
GFR is higher in preg-
nancy so the goal should be to avoid under-dialysing these patients. The aim is for
more frequent and longer dialysis sessions if using haemodialysis, and in the ICU
setting, continuous haemofiltration should be >35 mL/kg/h.
Hypothalamic pituitary adrenal function in critical illness
Hypothalamic pituitary adrenal function during critical illness is important and has
been shown to affect outcome in septic patients.63
Adrenergic receptor desensitiza-
tion has been demonstrated with a reduction in alpha- and beta-adrenergic receptors.
Steroids have been shown to help resensitize these receptors.
The evaluation of adrenal function during critical illness is controversial. Adrenal func-
tion should still be tested, but commencement of steroid therapy should not be withheld
until results are available.64
Currently, testing relies on random and low-dose Synacthen-
stimulated serum total cortisol levels. In sepsis, adrenal insufficiency is likely when base-
line cortisol levels are <10 mg/dL or the change in cortisol is <9 mg/dL, and unlikely when
the Synacthen-stimulated cortisol level is !44 mg/dL or the change in cortisol is
!16.8 mg/dL.9
Free cortisol or salivary cortisol when they become available will be
more useful. Plasma aldosterone and renin level are useful when primary adrenal disease
is suspected, but pregnancy-specific normal ranges must be used.
When suspected, glucocorticoid doses should be physiological with either a contin-
uous infusion of hydrocortisone or 4–6-hourly boluses with a daily dose 200 mg.
This regimen should be discontinued once there has been clinical improvement.
Such patients may include those requiring >24 h or an increasing dose of vasopres-
sors, or those with diseases such as meningococcaemia.
Neurological management
Neurological support aims to relieve pain and anxiety. Sedation is usually required for
mechanical ventilation and invasive procedures. Agents include analgesics (paraceta-
mol, opioids) and sedative-anxiolytics (benzodiazepines, propofol, haloperidol and clo-
nidine). These are all used as needed, with consideration given to the implications on
the fetus. Intubation and some modes of ventilation may also require neuromuscular
blockade. Daily sedation breaks are recommended to allow a circadian sleep–wake cy-
cle and to re-assess neurology in these patients. Very agitated patients may need

sedation if intensive monitoring and treatment is required. ICU delirium is common
and difficult to manage.65
Investigations for coma would be as in the non-pregnant population with computed
tomography þ/À magnetic resonance imaging, blood tests including cultures, lumbar
puncture if considering meningitis, encephalitis or demyelination, and urine for toxico-
logical screening (Table 8). Electroencephalography can be useful to assess metabolic
coma and non-convulsive status, and hypoxic brain injury. Antidotes such as naloxone
and flumazenil may be needed but with consideration of the risk of precipitating sei-
zures and fetal effects. Cases of poisoning or overdose should be discussed with
the local poisons unit.
For those with known epilepsy, the risk of seizures increases at the time of deliv-
ery. For women at high risk for intrapartum seizures, intravenous phenytoin or rectal
carbamazepine can be given pre-emptively. In pre-eclampsia, the development of sei-
zures defines eclampsia, and this is prevented and treated with magnesium sulphate.
There are many other causes of seizures in pregnancy (including conditions listed in
Table 8) as well as others including thrombotic thrombocytopaenic purpura) and ini-
tial management focuses on resuscitation with control of fitting. Metabolic abnormal-
ities including hypoglycaemia and hypocalcaemia should be corrected and intravenous
magnesium sulphate given, even without known pre-eclampsia; eclampsia may present
de novo. Further seizure management is with lorazepam or diazepam, then loading
with intravenous phenytoin (20 mg/kg). Status epilepticus (seizures lasting >30 min
or multiple seizures without regaining consciousness) is managed as outside preg-
nancy, remembering the teratogenic effects of anticonvulsants during the first trimes-
ter, and fetal respiratory effects if peripartum.
The use of mild therapeutic hypothermia following cardiac arrest is a fairly recent
treatment concept that followed two large multicentre randomized controlled trials
published in 2002.66,67
It involves active cooling to 32–34

C when return of sponta-
neous circulation (ROSC) follows a ventricular fibrillation or ventricular tachycardia
out-of-hospital arrest. The proposed mechanism is a reduction in cerebral metabolic
rate which, with less free radical production and intracellular acidosis, is neuroprotec-
tive.68
However, adverse events including arrhythmias, coagulopathy, immunoparesis,
and abnormal blood glucose and acid–base control may occur, and its use in pregnancy
has not been reported to date.
Table 8. Causes of coma or collapse in pregnancy.
Intracerebral haemorrhage: arteriovenous malformation (AVM), Berry aneurysm, pre-eclampsia,
hypertension
Subarachnoid haemorrhage
Trauma: extradural or subdural haematoma
Prolonged hypotension or hypoxia
Embolic or ischaemic stroke, venous sinus thrombosis
Pituitary apoplexy
Brain structural abnormality, e.g. tumour
Infection: abscess, meningitis, encephalitis, septic encephalopathy
Demyelination
Metabolic: hypoglycaemia, hyponatraemia, acid-base disorders, rare causes (e.g. carbamyltransferase
deficiency)
Severe depression

Neurological intensive care
The principles of neurological intensive care management are similar to the non-preg-
nant setting, with prevention of secondary brain injury following an initial insult. The
aetiology of most brain insults can be subdivided into those causing coma and those
leading to traumatic brain injury (TBI); the leading cause of mortality in young people.
Severe cases of TBI are best managed in major hospitals with neurosurgical and
neuro-intensive care facilities.69
Management is as for the non-pregnant woman using
the airways, breathing, circulation (ABC) approach (and cervical spine control) and
consideration for the fetus; immediate delivery may be indicated. Intubation and
ventilation is indicated when the Glasgow Coma Scale score is 8/15, or drops by
2 points, or earlier depending on the pathology and management plan. In trauma,
the secondary survey is essential in order not to miss other life-threatening
injuries.70
Prevention of secondary brain injury entails maintaining cerebral perfusion pres-
sure (CPP) and normoglycaemia, and preventing complications such as infection.
CPP depends on the pressure difference between MAP and intracranial pressure
(ICP) within the rigid box that is the cranium (CPP ¼ MAP-ICP). ICP is usually
10 mm Hg; an ICP 20 mm Hg may distort cerebral architecture, reduce cerebral
blood flow and lead to ischaemia and oedema. It is important to maintain MAP 80–
90 mm Hg to maintain CPP in the non-obstetric population, and this target may be
lower in pregnancy.
Cerebral oedema may occur in TBI or other metabolic causes of coma due to dis-
ruption of the blood–brain barrier, impaired mitochondrial ability to maintain normal
ionic cellular gradients, and ischaemia. ICP monitoring may be indicated, as the com-
plication if left untreated is increasing pressure leading to coning and brain death. ICP
monitoring may be indicated and depends on local practice. Initial management for
raised ICP is sedation, mannitol, moderate hyperventilation and cerebrospinal fluid
drainage. Further therapies include profound hyperventilation, barbiturate coma and
surgical decompression. In the obstetric patient, the effects of further hypocapnia
are not clear. The diagnosis of brain death is no different to the non-pregnant patient,
with considerations for perimortem caesarean section for fetal survival.71
Somatic
support of a pregnant women following brain death is rare72
, and organ support to
preserve the fetoplacental unit must consider the predictable physiological changes
that occur following brain death. These include haemodynamic instability from the ex-
cessive sympathetic discharge, panhypopituitarism, hypothermia, poor nutrition and
infectious complications.71
Haematological management
Haematological disorders are relatively common in pregnancy. Pregnancy is a thrombo-
philic state with increased levels of most procoagulants that prevent excessive mater-
nal blood loss at the time of delivery. This and the reduction in venous flow due to the
gravid uterus leads to a five-fold increased risk of venous thromboembolism during
and immediately following pregnancy73
, and is even higher in the puepurium.74
Preven-
tion of venous thromboembolic events is therefore especially relevant in obstetrics.
Prophylaxis with low-molecular-weight heparin (LMWH) or low-dose unfractionated
heparin, and the use of a mechanical intermittent compression device or compression
stockings is essential. The anticoagulant dose of LMWH is increased as glomerular fil-
tration is elevated; for example, the dose of enoxaparin is 1 mg/kg bd, reverting to the

usual 1.5 mg/kg od dose following delivery.75
The prophylactic subcutaneous dose is
40 mg/day in a normal-sized woman.
Anaemia is common in critical illness for many reasons. Blood transfusion targets in
the non-pregnant population are 7 g/dL, except in those with cardiac disease who
are kept 8 g/dL.76
Pregnancy targets should be similar, bearing in mind normal phys-
iological anaemia.
Disseminated intravascular coagulation (DIC) is an acquired coagulopathy that
follows a trigger of generalized coagulation activity. Other causes of coagulopathy
are outlined in Table 9. In DIC, further consumption of platelets, clotting factors
and fibrin occurs, leading to a cycle of continuing bleeding and consumption of clot-
ting components. In pregnancy, it should be anticipated from some of the associ-
ated conditions such as massive obstetric haemorrhage (especially placental
abruption with direct exposure to fetal material), pre-eclampsia, retained fetal prod-
ucts and amniotic fluid embolism. Sepsis is the most common overall cause in any
ICU population, and other causes include transfusion reactions, trauma and drugs.
Diagnosis is based on deranged clotting in an appropriate clinical setting with low
fibrinogen and elevated fibrinogen breakdown products (FDPs) or D dimer levels.
Management is similar to that of major obstetric haemorrhage with prompt resus-
citation and fluid replacement, with identification and treatment of the underlying
cause. Blood products need to be given as soon as available including packed red
cells, fresh frozen plasma, cryoprecipitate and platelets. Recent developments in-
clude recombinant activated factor VIIa (NovoSeven), originally used for haemo-
philia and factor VII deficiency. It has been used for intractable blood loss and
fulminant disseminated intravascular coagulation as it induces short-term local hae-
mostasis. It has been used (off licence) with life-saving results in cases of massive
obstetric haemorrhage.77
NUTRITION AND GASTROINTESTINAL MANAGEMENT
Nutrition in pregnancy is important for the development of a healthy baby. The
gastrointestinal system is the portal through which macro- and micronutrients enter
Table 9. Causes of coagulopathy in pregnancy.
Obstetric causes Non-obstetric causes
DIC due to placental abruption,
placenta praevia, massive obstetric
haemorrhage, amniotic fluid embolus
DIC due to any other causes including
sepsis, trauma, incompatible transfusion reaction
Thrombocytopenia, e.g. HELLP syndrome,
TTP
Thrombocytopenia, e.g. ITP, sepsis, alcohol
Liver failure due to acute
fatty liver of pregnancy
Liver failure due to alcohol, paracetamol overdose etc.
Bone marrow failure due to effects of
shock (many causes)
Bone marrow failure or infiltration (many causes)
Pre-existing, e.g. haemophilia
Iatrogenic Hypothermia
DIC, disseminated intravascular coagulation; TTP, thrombocytopenic purpura; HELLP, haemolysis–
elevated liver enzymes–low platelets; ITP idiopathic thrombocytopaenic purpura.

the body. Proteins, fats and complex carbohydrates are digested, and vitamins, min-
erals and water are absorbed across the gut mucosa. In pregnancy, there is an in-
creased requirement for zinc, folate and vitamin B12 in the first trimester, and
calories in the second and third trimester. Nutritional support is required to meet
the increased metabolic demand and limited nutritional reserve during critical illness.
However, despite extensive research, many areas in this field of critical care medicine
remain controversial, due to a lack of well-controlled randomized trials.
The availability of functioning small bowel is vital and should prompt early feeding,
preferably via the enteral route. Enteral nutrition is cheap and safe, but can be com-
plicated by aspiration and poor gastric emptying, which results in poor absorption and
under-feeding. Increased progesterone levels in pregnancy cause smooth muscle relax-
ation. This results in an increased likelihood of aspiration and constipation due to the
reduced oesophageal sphincter tone and bowel peristalsis. Aspiration can be pre-
vented by a 45

head-tilt position and confirming the nasogastric tube placement ra-
diologically. Good absorption of feed often requires the use of prokinetic agents to
promote gastric emptying when residual gastric volumes are high, and laxatives and
enemas to prevent constipation. If poor absorption is a problem, drugs given via the
nasogastric tube should also be considered to be poorly absorbed, and prompt con-
version to the intravenous route should be instituted. Some drugs require enteral feed
to be discontinued to ensure good uptake and effective absorption, such as the anti-
convulsive drug phenytoin.
Protocols have been developed and are implemented by nurses to ensure that ad-
equate enteral nutrition is delivered early and effectively. The failure to deliver 25% of
a patient’s calculated calorific requirement has been shown to result in increased mor-
tality and infection rates.78
Protocol-directed regimens have been shown to reduce the
incidence of under-feeding; however, it remains a significant problem for many patients
due to frequent and often avoidable interruptions.
Total caloric requirements can be either estimated or calculated, and are often es-
timated at 25–35 kcal/kg/day. Calculations are required at extremes of weight and per-
formed by dieticians. The recommended nutritional requirements of a septic patient
are 25 total kcal/kg/day, given in three forms: protein 1.3–2.0 g/kg/day; glucose
30–70% of non-protein calories; and lipids 15–30% of non-protein calories.
The H2 receptor blocker ranitidine is used as prophylaxis against stress ulceration;
there is no evidence to suggest that proton pump inhibitors are superior.79
The Na-
tional Institute for Health and Clinical Excellence recommends that parenteral nutri-
tion should be limited to 50% of the calculated calorific requirement, and it has
been shown to be less harmful than first thought. It is useful when the small bowel
is being rested or not functioning for prolonged periods. Glycaemic control has also
been shown to affect outcome in sepsis, and the Surviving Sepsis Campaign guidelines
advise controlling blood glucose 8.3 mmol/L. This should be achieved using insulin
infusions and close monitoring of blood glucose.8
Micronutrients and electrolytes, e.g. magnesium, iron, copper, zinc and selenium,
are necessary in small amounts. Phosphate is important since it is required for normal
metabolic processes resulting in the formation of ATP. Hypophosphataemia results in
reduced contractility of skeletal muscles including respiratory muscles, which can lead
to difficulties weaning from ventilatory support. Other micronutrients include fat-sol-
uble (vitamins A, carotene) and water-soluble vitamins (vitamins B, C, D and E). The
precise requirements for specific vitamins remain unclear, although several studies
have shown extremely low circulating concentrations. In pregnancy, the supplementa-
tion of folate should be continued.

Early goal-directed therapy
Haemodynamic goal-directed therapy (GDT) was first used in sepsis and has since
been introduced in the peri-operative care setting, targeting oxygen delivery as the
‘goal’. Original studies of sepsis in the late 1980s noted that survivors of sepsis had
supranormal levels of oxygen delivery (DO2) compared with controls.80
However, tar-
geting high DO2 levels did not initially appear to improve outcome.81
It became appar-
ent from a meta-analysis of all the optimization trials that the timing of such
interventions was crucial82
where the earlier interventions did in fact reduce mortality.
There are evidently two phases to sepsis. The early phase is characterized by low ox-
ygen delivery, high lactate and low SvO2 levels. This phase is associated with high mor-
bidity and mortality if left untreated, but may be reversible if targeted early.83
In
comparison, the later phase of ‘established’ sepsis is more hyperdynamic with a higher
SvO2, CO and DO2 (Table 10).84
This early work led to a landmark study of sepsis before admission to ICU. Rivers
et al studied patients with severe sepsis and septic shock over 6 h following presenta-
tion to the emergency department (ED).10
Patients with systemic inflammatory re-
sponse syndrome criteria and BP 90 mm Hg or serum lactate 4 mmol/L were
randomized to standard ED care or the early GDT protocol with continuous central
venous oxygen saturations (ScvO2) monitoring with goals as follows: CVP 8–
12 mm Hg, MAP 65 mm Hg, urine output (UO) 0.5 mL/kg/h, ScvO2 70% (or
SvO2 65%). If the ScvO2 was below target, protocolized manouevres were under-
taken to increase DO2. These included fluid boluses, giving packed cells to increase
haematocrit 30% and using vasopressors or inotropes. The other important feature
in the trial was the use of antibiotics within 1 h. The overall results from the early
GDT protocol indicted a significant mortality benefit (30.5% for early GDT vs
46.5% for standard care). The important message from this is that survival in sepsis
does appear to be influenced by the care in the first few hours, and that sepsis appears
to have an early reversible phase. It has revolutionized the importance of early diag-
nosis and accessibility to critical care facilities for patients admitted with septic shock
and severe sepsis. This principle has been extrapolated to the peri-operative care of
patients.85
Cardiopulmonary resuscitation in pregnancy
Cardiac arrests in pregnancy are fortunately rare, occurring in approximately one in
30 000 late pregnancies. They are less likely to have a primary cardiac cause compared
Table 10. Definitions of sepsis syndromes.83
Infection The inflammatory response to invasion of micro-organisms into normally sterile
host tissue
SIRS Response to a variety of clinical insults with more than two of: temperature 36

C
or 38

C; pulse 90 beats/min, respiratory rate 20/min; white cell count 12 or 4
Sepsis The systemic response to infection with more than two of the above SIRS criteria
Severe
sepsis
Sepsis with organ dysfunction, hypoperfusion or hypotension
(systolic blood pressure 40 mm Hg below baseline)
Septic shock Sepsis with hypotension despite adequate fluid resuscitation
SIRS, systemic inflammatory response syndrome.

with cardiac arrests outside pregnancy. The most common reason for syncope is the
supine hypotension syndrome, and management of patients in the left lateral position
is essential. Other common causes of cardiac arrest in pregnancy are shown in Table 11.
The concept of a ‘chain of survival’ with basic and advanced life support is as impor-
tant in pregnancy as in the general population. It includes early recognition and call for
help, early cardiopulmonary resuscitation (CPR), early defibrillation and postresuscita-
tion care. The structured ABC, airway-breathing-circulation approach in cardiac arrest
underpins the principles of basic and advanced life support with the goal of establishing
a spontaneous return of circulation.
CPR in pregnancy is complicated by both physiological and physical changes that are
well established late in pregnancy. They affect the quality of CPR that can be delivered,
and increase the possibility of complications. Each component is considered below, in-
cluding the important differences in pregnancy.
Airway
Simple airway manoeuvres remain the same as for the general population. Difficult intu-
bations are more common and effective pre-oxygenation is essential. Insertion of an ad-
vanced airway at an earlier stage and with a 0.5–1 mm smaller endotracheal tube is
recommended. The short obese neck and full breasts make insertion of the laryngoscope
more problematic. Short-handled laryngoscopes, blades mounted greater than 90

and
dismountable blades first inserted into the mouth can all help to overcome these difficul-
ties. A laryngeal mask airway may be needed in cases of failed intubation, although cricoid
pressure should be released and re-applied after insertion and inflation of the mask.
Breathing
Mouth-to-mouth and bag and mask ventilation should be performed without a pillow
and the head fully extended. Ventilation can be hampered by flared ribs, raised dia-
phragm, reduced chest compliance and difficulties seeing the chest rise. These along
with greater oxygen demand and reduced FRC lead to rapid desaturation with inade-
quate ventilation. The problems of ventilation can be compounded by aspiration,
which is more likely in late pregnancy due to the incompetent gastro-oesophageal
sphincter and raised intragastric pressure.
Circulation
Femoral intravenous access for resuscitation drugs is not advised, as central maternal
delivery will not occur until the fetus is delivered. Chest compressions should be
Table 11. Causes of cardiac arrest in pregnancy.
Obstetric causes Non-obstetric causes
Pulmonary embolism Trauma
Amniotic fluid embolism Septic shock
Massive blood loss Drug overdose
Complications of pre-eclampsia
(and magnesium toxicity)
Acute myocardial infarction
Severe asthma
Uterine inversion Local anaesthetic toxicity
Aortic dissection Failed intubation, high spinal block

performed at the standard rate of 100/min and a ratio of 30:2. Hands should be po-
sitioned further up the sternum because abdominal contents are displaced upwards
by the gravid uterus. The patient must be rolled into the left lateral position. This
should be up to 30

or there is a tendency to roll into the full lateral position. This
angle is ideal for effective chest compression, and aids displacing the uterus off the in-
ferior vena cava. This manouevre, along with raising the patient’s legs, will improve ve-
nous return. One technique to achieve this is the ‘human wedge’, whereby the patient
is tilted on to a rescuer’s knees to provide a stable position for CPR.
Defibrillation and drug administration is similar in pregnancy as for the general pop-
ulation. Defibrillation will not deliver significant current to the fetus, but any fetal mon-
itoring electrodes must be removed. Adhesive defibrillation pads have removed the
difficulties of applying the paddles in the correct position, normally affected by the
full breasts and left lateral position adopted. Excessive magnesium sulphate used to
treat and prevent eclampsia can contribute to cardiac arrest. Empiric calcium should
be given and can be life saving.
Perimortem caesarean section
Failure to achieve ROSC after 5 min of CPR should prompt consideration of perimor-
tem delivery. This should be considered by the team leader at the onset of cardiac ar-
rest. The greatest chance of infant survival is in pregnancies 24 weeks of gestation as
neonatal resuscitation can commence. It is obviously an aggressive procedure, but in-
fant and maternal survival may depend on it. In pregnancies 20 weeks, emptying the
uterus after this will improve CO by 60–80% of prepregnancy levels, allowing venous
return and improving chances of ROSC, improving maternal and fetal outcome. Car-
diac compressions are also more effective after delivery.86
In pregnancies 20 weeks,
the gravid uterus is unlikely to have detrimental compressive effects. In pregnancies
23 weeks, infant survival is unlikely; if done, it should be for maternal survival.
Between 1975 and 2000, there were 56 postmortem caesarean deliveries with six
neurologically normal surviving infants (survival rate 10.7%). Eight infants were deliv-
ered alive but died in the neonatal period. Of the 40 perimortem deliveries, 25 sur-
vived neurologically intact (survival rate 62.5%).87
Post-resuscitation care
ROSC is an important step in resuscitation, but this must be followed by meticulous
postresuscitation care to increase the chance of a return to normal cerebral function.
It focuses on the re-assessment of ABCDE to ensure good oxygenation, stable cardiac
rhythm and BP. Once established, the patient can be transferred to a critical care area
for ongoing postresuscitation care.
SUMMARY
It is important to understand the aims of managing critically ill obstetric patients in
many areas of clinical medicine, surgery and anaesthesia. The most common reasons
for UK obstetric ICU admissions are pre-eclampsia, sepsis and haemorrhage. The ma-
ternal physiological differences make a significant impact on the assessment and man-
agement, and must be considered at all times, especially the supine hypotension
syndrome in positioning and resuscitation scenarios. Additional considerations are
for fetal wellbeing and appropriateness for delivery, which may be life saving for the

mother. The developments and trials in critical care medicine over the last 50 years
have not included obstetric patients specifically. However, with the changes in mater-
nal physiology borne in mind, there are no reasons why the principles should differ
greatly. When considering haemodynamic management, the requirement for a high
maternal CO should be remembered. The low colloid oncotic pressure leads to an
increased tendency to develop iatrogenic pulmonary oedema, and several obstetric pa-
thologies tend to increase alveolar capillary permeability, compounding the problem.
Oliguria post delivery, especially in pre-eclampsia, should not usually be managed
with a fluid challenge. Airway management may be challenging with altered anatomy
Practice points
General supportive care
immediate resuscitation of the mother is paramount for maternal and fetal
survival
consider fetal age at an early stage; monitoring/assessment and delivery if
indicated
early identification of warning signs of critical illness
always plan in advance with the multidisciplinary team, where possible, such as
booking an ICU bed for expected high-risk deliveries
Haemodynamic management
remember the supine hypotension syndrome
beware of iatrogenic pulmonary oedema with fluid challenges
labour is a high-risk time for cardiac patients, with fluid shifts for up to 72 h
post partum
Cardiopulmonary resuscitation
airway: pregnant women may be very difficult to intubate (need skilled anaes-
thetist). Need smaller endotracheal tube, short-handled laryngoscope blade
and ‘difficult intubation’ equipment
breathing: may be difficult to ventilate. Increased risk of gastric acid aspiration
circulation: always use lateral position to avoid the supine hypotension syn-
drome. CPR cycles and drugs given as outside pregnancy, remembering that
MgSO4 toxicity can lead to cardiac arrest (give empiric calcium intravenously)
perimortem caesarean section may be necessary and should be considered at
the start of CPR
Research agenda
more on the mechanism of ARDS in pre-eclampsia, and how to avoid iatro-
genic pulmonary oedema
ideal ventilatory targets throughout pregnancy
short-term effects of fetal hypoxia, hypercapnia and acidosis

and high oxygen consumption, and rapid oxygen desaturation may occur. Ventilatory
management may be difficult for this reason and higher pressures may be needed.
Some of the recommended ARDS ventilatory strategies are probably not appropriate
as fetal haemoglobin binds oxygen less well when acidotic. Overall, critical care man-
agement in obstetrics is mostly similar to a non-obstetric setting, applying the changes
in maternal and fetal physiology in each case. High-risk patients should be identified
early, with appropriate planning and involvement of the multidisciplinary team.
ACKNOWLEDGEMENTS
The authors would like to thank Dr John Dick, consultant anaesthetist, for his helpful
comments.
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