ARDS IN TRAUMATIC BRAIN

INJURY
BY DR. PIYUSH GIRDHAR
• TBI is an important cause of mortality and
morbidity worldwide which gets further
complicated by lung complications and ARDS
concomitantly.

• MV related challenges in patients with

combined acute brain injury and lung injury
are what we are going to explore here forth
• We will discuss the use of ventilator strategy
such as protective ventilation, high PEEP,
prone positioning, RMs as well as techniques
which at present are used for rescue in ARDS
(ECMO)
• Most of the lung protective ventilatory
strategies ( low TV, Plateau pressure limiting,
Permissive hypercapnia, prone positioning,
high PEEP and RMs) are associated with
increased risk of ICH
• There are tight interactions between
cerebral and respiratory dynamics so
MV can have effect on cerebral
perfusion and represent a potential
burden for iatrogenic secondary
brain damage
• MAIN TARGETS OF TBI PATIENTS
(Recent published BTF guidelines):
–To avoid hypoxia and cerebral hypo-
perfusion
–Prevent hypoxic secondary insults
through maintenance of adequate CPP
and cerebral oxygen delivery
• When concomitance of TBI and
ARDS occurs the ventilatory
management can be very challenging
as ventilatory targets are often in
conflict in these 2 pathologies
• RMs, prone positioning and use of high PEEP
can improve pulmonary gas exchange and
respiratory mechanics by reducing V/Q
mismatch, opening collapsed alveoli, reducing
intra- pulmonary shunts however, they may
cause Intracranial HTN by impairing jugular
venous outflow and decreasing cerebral
venous return to right heart
 VENTILATORY TARGETS
1) PaO2
• Hypoxaemia: Significant secondary insult with TBI
and associated with poor outcome
Recent guideline from IMPACT study database
recommend avoidance of PaO2 less than 60 in
TBI since hypoxeamia results in decreased
cerebral oxygen delivery causing cerebral
vasodilatation and increase in ICP but ARDS NET
target PaO2 of 55- 80 which might be low to be
safely applied to all patients with TBI
2) PaCo2 and TV :
Low TV and permissive hypercapnia of ARDS
NET strategy is associated with cerebral
vasodilatation and raise in ICP
• Grubb et al demonstrated that cerebral blood
volume is linearly related to PaCO2. Therefore,
in TBI patients the standard of care is to
ventilate to low normocapnia (PaCo2- 33 to
37) but this maybe a challenge in ARDS
• So, we need to find a balance between CO2
control and Lung protection, PaCO2 values
should be set case by case according to ICP.
• Moreover, multi model brain monitoring such
as Micro dialysis catheters or brain
parenchymal O2 electrodes may allow
intensivist’s to tolerate a higher PaCO2, if
cerebral metabolism remains intact
3) PEEP
• The use of PEEP has been considered very
controversial in TBI patients, because the
raised mean intra-thoracic pressure related to
PEEP can reduce cerebral venous return and
consequently increase ICP. Also, the optimal
level of PEEP is still uncertain in ARDS
patients.
• At present, therefore, the use of PEEP to treat
ARDS may be appropriate in TBI patients,
provided that MAP is maintained and a strict
close attention needs to be paid to any
changes in CPP [cerebral perfusion pressure]
and ICP. When a decision of increasing PEEP in
a TBI patient is made, it is necessary to ensure
MAP stability and a close monitoring of
cerebral parameters, mainly ICP and CPP,
according to the article
4) RMs:
Are useful strategies able to improve oxygenation,
alveolar recruitment, and optimize ventilation-
perfusion mismatch .However, RMs can have
dangerous effect on ICP, as they can cause a
significant elevation of ICP in patients with
altered cerebral auto-regulation, by impairing
jugular blood outflow and increasing intra-
thoracic pressure, central venous pressure (CVP)
and impeding cerebral venous return to the right
atrium
• Nemer et al. studied the effects of RMs in a
RCT including patients with SAH and TBI who
developed ARDS and found that pressure
control recruitment maneuver doesn’t impair
ICP or CPP, while it improves oxygenation .
This suggests that RMs can be used with
caution in patients with TBI, ensuring
hemodynamic stability and a close monitoring
of cerebral parameters.
5) Prone Positioning :
Prone ventilation is known to improve
PaO2/FiO2 ratio in ARDS. In TBI patients
however there are serious concerns over the
effect on ICP of prone positioning and also
technical difficulties can be present, such as
risks of removal or displacements of ICP Bolt
and drains and practical difficulties in
positioning neuromonitoring.
• there is no clear evidence to aid intensivists when
deciding whether or not proning a patient when
there is co-existence of ARDS and TBI; however, it
doesn’t seem unreasonable to attempt prone
ventilation when hypoxemia is refractory to
conventional ventilation." In addition, the article
says the effect of proning on ICP should be
observed in real continuous time, with additional
treatments for increased ICP or de-escalation to a
different ventilatory strategy if ICP increases too
much
6) ECMO:
It is another technique used for "rescue" in ARDS
in patients with TBI. Nowadays ECMO is feasible
only in a limited number of centers. Despite the
large number of complications associated with
this treatment (bleeding, hemorrhage, acquired
von-Willebrand disease during ECMO), it should
be considered as rescue therapy for management
of refractory respiratory failure even in trauma
patients.
• Technical improvement in ECMO devices and
full Heparin coated circuits have lead to
significant reduction in bleeding complications
7)ECCO2R :
The largest series of 90 patients demonstrated
improvement in oxygenation, reduction in
CO2 with the use of ECCO2R in ARDS patients
• There has been a small case series describing
ECCO2R in 5 patients with TBI where no
complication attributed to anticoagulation
was seen. However, because of small no. of
patients larger prospective trial are warranted
in neuro-critical patients
 CONCLUSION
• The lung and brain interaction poses important
challenges to ventilator management of patients
with TBI and ARDS. The beneficial effect of
protective lung ventilation and respiratory
strategies is well established both in intensive care
and in the operating room. However, the
application of these techniques on neurocritical
care patients is contrasting because of the specific
needs and ventilator targets in this group of
patients.
• Moreover, hemodynamic and general
management (including Hb target and fluid
balance) can be contrasting in this group of
patients. The use of cerebral multimodal
monitoring can be useful to assess cerebral
hemodynamic and to evaluate the effects of
ventilator strategies commonly used in ARDS
patients. It would be desirable a concomitant
cerebral and respiratory system monitoring in
these patients, mainly in the more severe ones, in
order to allow the best approach to these
patients and avoid complications.
• Further studies will be necessary to create
shared diagnostic and therapeutic guidelines
based on available evidence and that can
contribute to improve patients’ clinical
outcome.
 Neurogenic pulmonary edema
• NPE has been reported with a number of proposed
mechanisms. While the exact locations and circuits
involved in the central nervous system (CNS) have not
been clearly identified, this uncommon but potentially
life-threatening condition may occur in the setting of
acute, severe brain injuries including traumatic brain
injury, intracerebral hemorrhage (ICH), and even in
seizures.
• Sudden rise in intracranial pressure (ICP) such
as in SAH or ICH, hypothalamic involvement,
rapidly occurring sympathetic surge, increased
systemic vascular resistance (SVR) have all
been implicated in pathophysiology . Elevated
tone of venous circulation results in more
venous return. Increase in hydrostatic pressure
in the pulmonary vasculature may lead to
interstitial edema formation
• Complicating the picture further, elevation in SVR
raises afterload for the heart, which in turn can lead
to a similar pathophysiology as cardiogenic
pulmonary edema with worsening left ventricular
failure and further edema formation in the
pulmonary interstitial spaces. This entity is a
diagnosis of exclusion and requires ruling out
primary causes such as exacerbation of congestive
heart failure, aspiration pneumonia, pulmonary
contusion, and other disease processes that may
cause pulmonary edema formation.
• NPE has a characteristic, rapid formation of
edema typically occurring in a few hours after the
onset of CNS injury. Intracranial hypertension is
common and the treatment should focus on
promptly treating ICP and optimizing cerebral
perfusion pressure while addressing the
underlying brain injury. Since this is a
multisystem failure involving brain, heart, lungs
as well as the peripheral vasculature, care should
be given to ensure euvolemic state, support the
contractility and vascular tone, and resuscitate the
brain all simultaneously.