Journal of Neonatal Nursing (2015) 21, 161e167

www.elsevier.com/jneo

CASE HISTORY

Meconium aspiration syndrome and

persistent pulmonary hypertension
of the newborn
Fiona Brooke-Vincent, HND, Bsc Critical care, Bsc (Hons)
Midwifery
Available online 6 June 2015

KEYWORDS Abstract The focus of this article will be to critically assess the nursing care pro-
Hypercapnia; vided to an infant, “James”, with meconium stained aspiration (MAS) and persistent
Hypoxia; pulmonary hypertension (PPHN) with particular regard to James’s hypercapnia,
Hypotension; hypoxia, tachypnoea, low mean systemic blood pressure (BP), low pre and post
Ventilation/perfusion ductal oxygen saturations and cool extremities. The hypercapnia, hypoxia and ta-
mismatch; chypnoea and underlying physiological mechanisms will be related to the patho-
Persistent pulmonary physiology of MAS, and the low mean systemic BP, oxygen saturations and cool
hypertension; extremities will be related to the PPHN. Knowledge of the underlying physiological
Meconium aspiration mechanisms which will then be used to discuss the nursing care provided, and the
syndrome; impact it had on James’s condition. The overarching aim of nursing care was to
Respiratory acidosis; reduce James’s need for respiratory support and return his blood gases to normal.
Continuous positive The interventions that supported this such as positioning, fluid balance and comfort
airway pressure; measures will be looked at in more detail. Other aspects, including drugs that were
Developmental care; used will also be discussed.
Prone position ª 2015 Neonatal Nurses Association. Published by Elsevier Ltd. All rights reserved.

Case study presented to hospital in spontaneous labour with

A pseudonym, James, has been used in order to
protect the identity and confidentiality of the baby
and his family (Nursing Midwifery Council, 2015).
James was born at 40 þ 1 weeks. His mother had
E-mail address: fionabv@hotmail.co.uk.
meconium stained liquor and reduced fetal
movements. A fetal tachycardia, maternal tachy-
cardia and maternal pyrexia, combined with a
suspicious cardiotocography resulted in a decision
to expedite delivery via forceps. James had a
shoulder dystocia and was delivered through thick
meconium. His mother did not receive intrapartum

http://dx.doi.org/10.1016/j.jnn.2015.05.002
1355-1841/ª 2015 Neonatal Nurses Association. Published by Elsevier Ltd. All rights reserved.
162
antibiotics e for unknown reasons. At birth James
was centrally cyanosed with poor tone and
required stimulation, airway management, oxygen
via a facemask and Continuous Positive Airway
Pressure (CPAP). (Resuscitation Council UK, 2010).
His apgar scores were 3, 7 and 9. He was then
transferred to the Neonatal Intensive Care Unit
(NICU) for ongoing respiratory support, observa-
tion and partial septic screen.
James became tachypnoeic and developed an
oxygen requirement of 100% FiO2. His blood gases
showed hypercapnia, hypoxia (see Table 1 below)
and his mean systemic blood pressure (BP) was
low. James had cool extremities. A diagnosis of
meconium aspiration syndrome (MAS) was made
which was presumed to have resulted in secondary
persistent pulmonary hypertension (PPHN). A de-
cision was made not to intubate and mechanically
ventilate but to continue with CPAP and to grad-
ually attempt to reduce the amount of FiO2
depending on his clinical condition. His ongoing
care included CPAP, oxygen, full cardiac and res-
piratory monitoring (including regular blood gases)
with non invasive blood pressure checks, nursed
prone in an incubator, intravenous fluids, intrave-
nous antibiotics and minimal handling.
James’s x-ray showed wet streaky lungs consis-
tent with MAS. An echocardiogram was not carried
out so the diagnosis of PPHN was not confirmed.
Over the course of twelve hours his blood gases
became more normal and his FiO2 was reduced to
21%. James’s c-reactive protein came back as less
than one.
Introduction
Meconium aspiration syndrome
Meconium aspiration syndrome (MAS) is defined as
respiratory distress with changes on x-ray, unex-
plained by any other underlying pathology, and
accompanied by meconium stained amniotic fluid
(MSAF) at (like James), or prior to, delivery
(Stenson and Smith, 2012). MSAF is associated with
Table 1 Normal values taken from Boxwell (2010).
pH pCO2 pO2 Base cHCO-3 Sodium
(kPA) (kPA) excess (mmol/l) (mmol/l)
(mmol/l)
Normal 7.3 to 7.4 4.5 to 6.0 8.0 to 12 7 to þ3 18 to 25 135 to 146 0.5 to 2.0 30 to 55 30 to 60
Values
James’s 7.23 8.1 5.68 11.3 15.5
values
F. Brooke-Vincent
fetal hypoxia although Monen et al. (2014) suggest
that, as it occurs in 30e40% of post term de-
liveries, it maybe a physiological consequence of
foetal maturation. Of that number up to 10% go on
to develop MAS (Edwards et al., 2013). Supple-
mental oxygen is the main therapy, although
approximately one third of affected infants will
require mechanical ventilation (Dargaville, 2012).
James required CPAP to improve his lung function
and gaseous exchange.
Persistent pulmonary hypertension
Persistent pulmonary hypertension (PPHN) is a
failure of the fetal circulation to adapt to extra-
uterine life. It is characterised by a high pulmonary
vascular resistance (PVR) and can sometimes be
associated with a low systemic vascular resistance
(SVR) (Nair and Lakshminrusimha, 2014) and should
be suspected when the baby’s oxygen requirement
is out of proportion to the level of pulmonary dis-
ease (Bendapudi et al., 2015). It affects 2 in 1000
live births, and is associated mostly with term or
near term infants (Nair and Lakshminrusimha,
2014). Mortality remains at 10%. PPHN is associ-
ated with MAS, pneumonia, sepsis, pulmonary hy-
poplasia, congenital diaphragmatic hernia, and
maladaptation of the pulmonary vascular bed both
in utero and ex utero (Nair and Lakshminrusimha,
2014; Teixeire-Mendonca and Henriques-Coelho,
2013). Treatment strategies include respiratory
support, which for James was CPAP, but for more
severe PPHN high frequency ventilation, surfac-
tant and pulmonary vasodilators such as nitric
oxide may be required.
MAS, hypercapnia, hypoxia and tachypnoea
Fetal distress leads to fetal hypoxia at which point
the fetus passes meconium resulting in meconium
stained fluid (MSAF). Meconium is inhaled, and
causes hypoxia in infants in three ways e airway
obstruction, chemical pneumonitis, and surfactant
dysfunction (Mokra and Calkovska, 2013). Meco-
nium blocks the airways and can lead to gas
Lactate Systemic Respiratory Oxygen
(mmol/l) BP mean rate per saturations
(mmHg) minute in air (%)
➢95
132.9 3.9 28 70 40 to 50
Meconium aspiration syndrome
trapping due to the ball-valve effect where air can
get into the lungs but not out, hyperinflation and
increased risk of air leaks. This will reduce gaseous
exchange resulting in hypercapnia and hypoxia and
tachypnoea as seen with James.
Chemical pneumonitis invokes a powerful in-
flammatory response mediated by neutrophils and
macrophages and exacerbated by the presence of
pro-inflammatory substances in meconium such as
interleukin 8 and phospholipase A2 (Stenson and
Smith, 2012). Inflammation in the pulmonary
vasculature increases the distance gases have to
diffuse in order to be exchanged which also results
in hypercapnia hypoxia and tachypnoea.
MAS causes surfactant dysfunction in several
ways (Mokra and Calkovska, 2013; Stenson and
Smith, 2012) e it interferes with the adsorption
of phospholipids and their ability to form a film,
destroys the fibrillary structure, decreases the
concentration of surface proteins SP-A and SP-B so
reducing lateral stability, and is toxic to type II
pneumocytes cells where surfactant is produced.
Surfactant dysfunction increases surface tension in
the alveoli which meant an increase in James’s
work of breathing, increasing his adeno-
triphosphate (ATP) requirement and therefore
oxygen requirements. The increased surface ten-
sion as a result of surfactant dysfunction meant
that higher pressures were required to ventilate
him and improve his gaseous exchange.
James’s initial blood gas showed a low pH, hy-
percapnia, indicating a respiratory acidosis (Casey,
2013) and hypoxia. Increased carbon dioxide (CO2)
in the plasma leads to increased production of
carbonic acid and hydrogen ions (Hþ) (Goel and
Calvert, 2011) as shown below:
CO2 þ H2O/H2CO3%H þ þHCO3
Chemoreceptors in James’s aorta, carotid ar-
tery and medulla detected the increase in
hydrogen ions and increased his respiratory rate in
order to remove the excess CO2 e hence his
tachypnoea. The hypoxia leads to anaerobic
glycolysis, of which a waste product is lactic acid,
resulting in a metabolic acidosis (Casey, 2013) e
again, as shown in James’s blood gas.
The hypoxia caused by the MAS leads to pul-
monary constriction resulting in a ventilation/
perfusion mismatch (Holme and Chetcuti, 2012)
where blood is shunted away from non ventilated
areas of the pulmonary vasculature. The ventila-
tion/perfusion mismatch in the pulmonary vascu-
lature will also prevent the Bohr Effect from
happening (McCance et al., 2010). The combina-
tion of hypoxia due to MAS, pulmonary
163
vasoconstriction and ventilation/perfusion
mismatch can trigger PPHN (Edwards et al., 2013).
Persistent pulmonary hypertension, low pre
and post ductal oxygen saturations, low
mean systemic BP and cool extremities
PPHN is a failure of fetal circulation to adapt to
extrauterine life and in James’s case was second-
ary to the hypoxia, hypercarbia and acidosis
caused by MAS (Cabral and Belik, 2013; Stayer and
Liu, 2010). Hypoxia in particular is implicated in
the development of PPHN (LaPointe and
Barrington, 2011). Hypoxia reduces nitric oxide
(NO) production by causing endothelial dysfunc-
tion and impairs the release of NO, disrupting the
conversion of cyclic guanyl triphosphate (cGTP) to
cyclic guanyl monophosphate (cGMP). As these
substances inhibit the influx of intracellular cal-
cium, reduced circulating amounts result in the
PVR remaining high (Bendapudi et al, 2015). The
increase in circulating vasoactive substances, due
to MAS, such as inflammatory tumour necrosis
factor, interleukin 6 and interleukin 10, which
favour contraction of smooth muscle fibres,
further increases the pulmonary vascular resis-
tance (LaPointe and Barrington, 2011).
The ventilation/perfusion mismatch, intra-
pulmonary and extrapulmonary shunting from right
to left across the foramen ovale and ductus arte-
riosus led to low oxygenation contributing to
James’s low pre and post ductal oxygen satura-
tions (Nair and Lakshminrusimha, 2014). PPHN
causes reduced pulmonary venous return, which
causes a drop in pressure in the left atrium, which
leads to an increase in right to left shunt across the
foramen ovale (Storme et al., 2013) and reduced
left ventricular output. This physiological mecha-
nism resulted in James’s low pre-ductal satura-
tions, a decrease in oxygen delivery to the tissues
and his low systemic BP (Paize and Turner, 2011).
The increase in right ventricular after load also
leads to low cardiac output and low systemic
pressure, contributing to James’s low mean sys-
temic BP (Storme et al., 2013). James’s blood
pressure was dependent on his systemic vascular
resistance (SVR) and cardiac output (CO), which in
turn was dependent on James’s heart rate (HR)
and stroke volume (SV) as demonstrated in the
equations below (Broom and Parry, 2012).
CO ¼ HR  SV
BP ¼ CO  SVR
164
The drop in systemic blood pressure was
detected by the baroreceptors in his carotid si-
nuses and aortic arch which then stimulated the
sympathetic nervous system to increase peripheral
resistance which increased SVR thus improving
James’s mean BP (Deho and Nadel, 2008). How-
ever, blood flow to his skin and extremities was
reduced causing him to have cool extremities, pale
skin and a temperature gap between his core and
toes. Reduction of blood flow to the peripheries
will reduce oxygen delivery and therefore a
reduction in oxidative phosphorylation and ATP
production, exacerbating the metabolic acidosis
(Morrison, 2006)
Interventions and nursing care
The overarching aim of nursing care was to reduce
James’s need for respiratory support and return his
blood gases to normal. The actions underpinning
this were to modify the macro and micro envi-
ronment so that James’s energy and thus oxygen
requirement was reduced. Within this, the targets
were to reverse his hypoxaemia, improve his pul-
monary perfusion, increase systemic BP and
maintain adequate oxygenation (Nicholls, 2012;
Sharma et al., 2011). Nicholls (2012) suggests
that the goal of nursing care should also to be to
minimise hypoxia and acidosis thus preventing the
downward spiral and progression of PPHN. With
this in mind the nursing care was focused on
keeping James as calm and comfortable as possible
in order to reduce his stress levels, minimise oxy-
gen requirement and return the paCO2, paO2,
tachypnoea, low pre and posts oxygen saturations,
cool extremities and low mean systemic BP to
normal.
Respiratory support was provided in the form of
CPAP although several authors suggest that me-
chanical ventilation is the appropriate manage-
ment for PPHN (Bendapudi et al, 2015; Sharma
et al., 2011; Storme et al., 2013). However, the
CPAP appeared to effectively improve his ventila-
tion and reduce his work of breathing thus
reducing his energy and oxygen requirement.
James’s second blood gas showed that the hyper-
capnia was reducing, the PaO2 was rising and the
pH was less acidic indicating that the current
ventilation strategy was effective. His tachypnoea
was resolving. Dargaville (2012) suggests that the
discomfort associated with CPAP can exacerbate
PPHN to the point that intubation becomes
necessary. However, this was not necessary for
James. The fio2 was gradually reduced over 12 h to
21%, which, as oxygen use can cause oxidative
stress and alter vascular responses to endogenous
F. Brooke-Vincent
and exogenous nitric oxide (Teixeire-Mendonca
and Henriques-Coelho, 2013), is presumed to
have assisted with lowering the PVR and reversing
the PPHN.
James was nursed in a prone position in order to
optimise his oxygen saturations (Balaguer et al.,
2013). There are several explanations for how
prone positioning improved James’s oxygenation.
This position acts synergistically with positive end
expiratory pressure (PEEP) by redistributing lung
regional perfusion towards ventral regions
(Richard et al., 2008) and perfusion is more ho-
mogenous, minimizing ventilation/perfusion
mismatch so improving gaseous exchange in
James’s lungs (Balachandran et al., 2012). How-
ever, Elder et al. (2011) suggest that it is the sleep
state is the predominant influence on respiratory
variability rather than position, although it would
appear that the prone position enables infants to
achieve longer periods of quality sleep (Jarus
et al., 2011). Overall it could be suggested that
by nursing James in a prone position he was able to
self regulate himself, achieve better quality of
sleep and improve his ventilation thus reducing the
hypercapnia, improving oxygenation and resolving
his tachypnoea.
As the pulmonary vascular resistance reduced,
James’s systemic circulatory symptoms improved.
Whilst it is clear from his initial symptoms that
James was in compensated shock (Paize and
Turner, 2011), there is disagreement over what is
a normal systemic blood pressure for a neonate
which has implications for decisions regarding
management of hypotension. Broom and Parry
(2012) define hypotension as the mean blood
pressure below that of the infants’ gestational age
which means James’s mean systemic BP should
have been 40 mmHg. Conversely, Azhibekov et al.
(2014) argue that not only is the normal blood
pressure range unknown but that the blood pres-
sure value at which vital organs are compromised
and cerebral blood flow is impaired differs among
neonates of the same gestation. In addition there
is disagreement over what should be measured e
systolic blood pressure or mean blood pressure
(Gupta and Donn, 2014). Azhibekov et al. (2014) go
on to argue that, as blood pressure readings can be
misleading for a variety of reasons, haemodynamic
status should be evaluated by monitoring systemic,
organ and peripheral blood flow alongside BP
measurements, utilising high tech bedside assess-
ment such as functional echocardiography and
impedance electrical cardiometry. The authors
(Azhibekov et al., 2014) acknowledge the clinical
limitations of the technology. Furthermore it could
be argued that additional limitations are the cost
Meconium aspiration syndrome
of the equipment and lack of personnel with the
expertise to use it, as supported by Gupta and
Donn (2014). James’s haemodynamic status was
monitored by observing his mean blood pressure
non-invasively using the correct size BP cuff, and
monitoring his heart rate, capillary refill time
(CRT), skin colour and temperature, and urine
output.
In order to treat James’s shock appropriately it
was important to correctly identify the underlying
pathophysiology (Azhibekov et al., 2014; Gupta
and Donn, 2014). In James’s case it was felt that
his circulatory symptoms could be attributed to
the MAS and PPHN. He had already attempted to
improve his BP by increasing his SVR, so it was
decided to administer a fluid bolus with the aim of
increasing stroke volume and thus increasing his
cardiac output. It has also been suggested that
maintaining the mean systemic BP above the pul-
monary BP helps to reverse the right to left cardiac
shunting (Sharma et al., 2011). Maintenance fluids
were started at 50 ml per kg as per unit guidelines.
James’s mean systemic BP improved within mi-
nutes after the fluid bolus; however it took several
hours for his extremities to warm up indicating
that his SVR was reduced.
James’s pre and post ductal saturations were
monitored using oxygen saturation leads attached
to his left and right hands and lower limbs. A dif-
ference of 5% in saturations between the pre and
post ductal saturations is considered to be indica-
tive of PPHN (Bendapudi et al., 2015) although this
has been disputed (Rohan and Golombek, 2009;
Sharma et al., 2011). Although Boxwell (2010)
recommends measuring post ductal saturations
on the left hand, other authors suggest otherwise.
James’s post ductal saturations should have been
monitored on his lower limbs as the left hand is
considered to be pre-ductal (Ruegger et al., 2010).
However, this was further complicated by the fact
that James had a peripheral venous catheter (PVC)
in his right foot limiting the number of places that
could be used to monitor his post ductal
saturations.
James was started on intravenous antibiotics,
benzylpenicillin and gentamicin due to having
several risk factors for early onset sepsis (EOS)
(NICE, 2014). Severe respiratory distress such as
PPHN can sometimes be caused by Group B strep-
tococcus (Bedford Russell, 2015). The unit policy
at the time was to use the dose of 50 mg per kg for
benzylpenicillin despite advice to the contrary
from NICE (NICE, 2014). Penicillin and an amino-
glycoside provide excellent cover against most EOS
(Bedford Russell, 2015) and have a synergistic ef-
fect as penicillins increase bacterial permeability
165
to aminoglycosides (Pacifici, 2009). However
careful monitoring was required to ensure James
wasn’t given too high a dose of gentamicin, which
can damage the eighth cranial nerve and kidneys
(Pacifici, 2009). James’s blood results came back
as low risk for infection and so, as he had improved
clinically, the antibiotics were stopped after 48 h.
Minimal stimulation and clustering cares were
key to improving James’s condition (Nair and
Lakshminrusimha, 2014; Nicholls, 2012). The
stress response caused by handling and noxious
stimuli can lead to the release of catecholamines,
activating alpha-1 adrenoreceptors, which in-
creases PVR (Sharma et al, 2011; Stayer and Liu,
2010) and exacerbates PPHN potentially leading
to a pulmonary hypertensive crisis (Stayer and Liu,
2010). James was irritable on handling and became
distressed with an accompanying drop in oxygen
saturations which may have been due to cate-
cholamine release or a drop in airway pressure
resulting in decreased ventilation in his alveoli.
James’s cares were clustered as much as possible
as recommended (Hunt, 2008; Ludington-Hoe,
2013; Nicholls, 2012; Parry, 2011) in order to
reduce stimulation, however it was found that
grouping interventions together such as blood
sampling, blood pressure checks and nappy
changes caused James’s oxygen saturations to
drop. Therefore these interventions were baby-led
taking into account his sleep wake cycle (Altimer
et al., 2015). Kangaroo care is recommended
even for ventilated infants (Hunt, 2008; Ludington-
Hoe, 2013; Parry, 2011) but such was the severity
of James’s distress on handling, and desaturations
that it was decided, in partnership with his family,
not to try kangaroo care at that point (Gooding
et al., 2011; Staniszewska et al., 2012). Non-
nutritive sucking enabled James to self regulate
himself thus returning his observations such as
oxygen saturations, respiratory rate and heart rate
back to normal more quickly (Ludington-Hoe,
2013).
Noxious stimuli were further reduced by careful
planning and communication within the multidis-
ciplinary team about when blood samples were
taken from James and balancing this against the
need to know any changes in his blood gases (De
Lima and Carmo, 2010). James had pain relief
prior to the samples been taken so avoiding
adverse physiological responses to the noxious
stimuli. Slater et al. (2012) found a link between
painful procedures and oxidative stress thus
showing a clear link between pain and changes at
cellular level. However, their research was
focused on pre-term infants, rather than term in-
fants like James, which limits the transferability of
166
their research. Oral glucose was used as opposed
to oral sucrose of which the fructose component
has been found to inhibit adenosine triphosphate
(ATP) synthesis thus potentially reducing a neo-
nates modest ATP stores and increasing markers of
oxidative stress (Asmerom et al., 2013). A pain
assessment tool was not used despite been rec-
ommended in the literature (De Lima and Carmo,
2010; Parry, 2011) and this may be seen as a
deficit in the nursing care provided, as objective
pain scoring is considered essential for optimising
pain relief (De Lima and Carmo, 2010). However,
Scherman et al. (2014) suggest that guidelines and
assessment tools might not necessarily have the
desired impact on the daily work which means that
the use of guidelines and assessment tools might
not translate into better care and improved anal-
gesia for James.
James’s symptoms resolved over the first 18 h of
his life. A thorough understanding of the physio-
logical mechanisms underpinning his hypercapnia,
hypoxia, tachypnoea, low mean systemic BP, low
oxygen saturations and cool extremities was used
to inform the healthcare provided although as
discussed there were deficits and areas of care
that could be improved.
Funding
Nil.
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