Firdaini 1740312092

Atika Shalhi 1110311003

Critical Care Management Of Adult

Traumatic Brain Injury
dr. Hj. Liliriawati Ananta Kahar, Sp.An, KIC
 CHAPTER 1
INTRODUCTION
 INTRODUCTION
Traumatic brain injury (TBI)
• Often results in death, disability, and also mental disability.
• Incidence TBI in the United States recorded more than 1,500 cases
per year, 10% cause death and 20% cause disability.

TBI is divided into two:

Primary brain injury

• by the direct mechanical forces which occur at the time of the
traumatic impact to the brain tissue.

Secondary brain injury

• caused by dysautoregulation of brain vessels and blood–brain barrier
(BBB)

(Batubara, 2016)
 (Kuroda , 2016)

INTRODUCTION
The central mechanisms of Complications
dysregulation after brain • Pneumonia, sepsis, or
injury may contribute to the multiple organ
development and dysfunction syndrome
progression of
extracerebral organ
dysfunction

Neurocritical care after

The trauma-induced
severe TBI has therefore
catecholamine surge
been refined to focus not
affects systemic organs
only on secondary brain
and contributes to organ
injury but also on systemic
damage
organ damage
 INTRODUCTION
Neurocritical care
• Intensive care provided to patients with severe neurological and
neurosurgical conditions.
• Provides comprehensive medical and specialized neurological
support for patients with life-threatening neurological diseases by
integrating and balancing the management of both the brain and the
body.
Intensive care management of patients with severe TBI is a dynamic
process
• Starts in the pre-hospital period, at the scene of the accident. During
the early stages of hospital care, the patients may be managed in
variety of locations including emergency department,the radiology
department, and the operating room before they are admitted to the
Intensive Care Unit(ICU)

(Haddad, 2012)
 CHAPTER 2
LITTERATTURE REVIEW
 LITTERATTURE REVIEW
Neurocritical care (NCC)

• rapidly growing subspecialty of critical care medicine that

focusses on the evaluation, diagnosis,and management of
patients with acute life-threatening central nervous system
diseases.
• Provided to patients with severe neurological and
neurosurgical conditions.
• Neurocritical care provides comprehensive medical and
specialized neurological support for patients with life-
threatening neurological diseases by integrating and
balancing the management of both the brain and the body.
(Sekhon, 2017)
(Kinoshita , 2016)
 LITTERATTURE REVIEW

Severe traumatic brain injury (TBI)

• defined as a post-resuscitation Glasgow Coma

Scale score of 8 or lower, has high rates of
mortality, disability and is a major
socioeconomic burden

(Puntis, 2017)
LITTERATTURE REVIEW

Regulatory systems of the brain

• Brain has several mechanisms for regulating pressure and volume.

• To maintain a continuous cerebral blood flow (CBF) and adequate oxygen
supply, despite changes in both systemic arterial pressure (SAP) and cerebral
metabolic requirement.
• The key mechanism is the change in cerebrovascular resistance through
vasoconstriction and dilatation.
• Cerebral pressure reactivity is one of the critical systems in cerebral
autoregulation and allows smooth vascular muscle response to changes in
SAP.
• Under physiological conditions, an increase in SAP caused by a compensatory
vasoconstriction will lead to increased cerebrovascular resistance, thus
keeping the CBF constant
(Kinoshita,2016)
 LITTERATTURE REVIEW(Regulatory systems of the brain)

•Maintain a constant CBF between mean arterial pressures (MAP) of 60 and 160 mmHg.
•When the autoregulation mechanism fails and the BBB is also disrupted, the CBF becomes dependent on SAP, resulting in a
critical condition for the injured brain.
•Accidental changes in SAP can cause severe and linear changes in CBF that lead to harmful and irreversible conditions, such
as hypoperfusion (brain ischemia) or hyperperfusion (e.g., hyperemia). These may lead to an irreversible and catastrophic
increase in ICP (Kinoshita , 2016)
 Vasodilatation & Vasocontriction Cascade of the Brain

• Cerebral autoregulatory mechanism, the maximum cerebral vasoconstriction response would drive the
vascular mechanism to minimize the cerebral blood volume (CBV).
• Many factors can initiate the vasodilation and vasoconstriction cascades, including SAP, systemic blood
volume, blood viscosity, oxygen delivery/metabolism, hypo/ hypercapnia, and pharmacologic agents
• ICP normally ranges approximately between 60 and 70 mmHg (Kinoshita , 2016)
 LITTERATTURE REVIEW
Hyperemia after Traumatic Brain Injury
• Associated with elevated CBV and a drop in distal cerebrovascular
resistance and frequently observed as “luxury perfusion”
• Dysfunctional pressure or volume autoregulation may elicit
hyperemia that is associated with intracranial hypertension and an
unfavorable outcome.
• hyperemia combines with BBB disruption, capillary leakage in the
dilated vascular bed may cause a brain edema to occur.
• In the latter process, increased CBF and CBV due to vessel dilation
with BBB disruption may lead to aggravated vascular engorgement
and brain edema, ultimately leading to “malignant brain swelling,”
the development of irreversible intracranial hypertension.
• If the vasoconstriction cascade is intact and responding normally,
hyperventilation therapy has been proposed to reduce PaCO2 levels,
which might be effective for treating brain swelling.
Kinoshita,2016)
Intracranial effects
Intracranial
bleeding and
cerebral
oedema

Direct increased
cerebral intracranial
ischaemia
structural pressure
damage (ICP)

Impair
cerebral
perfusion

Kinoshita,2016)
Intracranial effects

(Puntis, 2017)
 Systemic effects
Catecholamines released
following TBI can cause
neurogenic pulmonary oedema
and myocardial ischaemia.
Cardiogenic pulmonary oedema
and non-haemorrhagic systemic
hypotension occur infrequently
after TBI, but are associated
with high mortality.
Catecholamine-induced
myocyte dysfunction and
inflammatory responses can
lead to the neurogenic stunned
myocardium syndrome.
In response to injury, neurones
and glial cells produce pro
inflammatory cytokines
generating local and systemic
inflammatory responses.
Cardiac injury characterized by
ECG changes, elevated cardiac
troponin and a spectrum of
ventricular dysfunction in the
absence of coronary ischaemia.
Endocrine and electrolyte
abnormalities, particularly
disturbances of sodium and
glucose homeostasis,
hypothalamicpituitary- adrenal
axis dysfunction and secondary
adrenal insufficiency,
Puntis, 2017)
LITTERATTURE REVIEW
Initial Evaluation

• All patients who present with suspected TBI should undergo a

rapid primary and secondary survey with thorough evaluation :
• airway, breathing, circulation
• Airway patency and adequate oxygenation and ventilation are
paramount to avoiding secondary brain injury. The patient’s
cervical spine should be immobilized until cervical spine injury
is ruled out.
• Urgent intubation to secure the patient’s airway should be
considered in any patient who presents with a GCS < 8 or in those
who are unable to protect their airway. Intravenous access should be
rapidly established
• Bedside glucose testing should be performed in all unconscious
patients and hypoglycemia rapidly treated if present
Puntis,2017)
LITTERATTURE REVIEW
Initial Evaluation

• Thiamine (100 mg) should be administered in patients at risk

for nutritional deficience.
• Bedside glucose testing should be performed in all
unconscious patients and hypoglycemia rapidly treated if
present
• If opioid toxicity is suspected, naloxone 0.4 mg IV should be
administered and repeated as necessary, up to 4 mg
• If definitive neurosurgical care cannot be provided at theinitial
presenting institution, transfer to a higher level of care should
be facilitated in a rapid fashion to preserve the “Golden Hour”
and optimize the patient’s outcome
Puntis,2017)
LITTERATTURE REVIEW
Critical care management

• Once the severely head-injured patient has been transferred

to the ICU, the management consists of the provision of
high quality general care and various strategies aimed at
maintaining hemostasis with:6
• Stabilization of the patient, if still unstable
• Prevention of intracranial hypertension
• Maintenance of an adequate and stable cerebral
perfusion pressure (CPP)
• Avoidance of systemic, secondary brain insults (SBI)
• Optimization of cerebral hemodynamic and oxygenation
Puntis,2017)
Critical care management

(Kuroda,2016)
LITTERATTURE REVIEW

Cardiovascular and respiratory support

• Hypotonic solutions can worsen cerebral oedema

and shouldbe avoided.
• Vasopressors may be required to maintain cerebral
perfusion in the presence of adequate filling, and
norepinephrine is widely used. Non-invasive
cardiac output monitoring can be useful to
optimize fluid status.

(Thomas,2017)
LITTERATTURE REVIEW
Hemodynamic care

• Hemodynamic management for patients with TBI has been

discussed at length CPP management is one of the critical
strategies that focuses on pressure response During CPP
management with norepin-ephrine for increasing MAP, the risk
of hyperemia could be reduced if pressure autoregulation is
preserved.
• While there is no standard regimen for patients in
hemorrhagic shock with TBI complications, the goal of fluid
resuscitation for these patients is 60 mmHg of CPP or greater,
or if CPP of patients with severe TBI is measurable, the target
systolic SAP is 90–100 mmHg in-stead of achieving normal SAP

(Puntis,2016)
LITTERATTURE REVIEW
Analgesia and sedation

• Adequate sedation is a key component of the management of

severe TBI to control ICP and reduce cerebral metabolic
demand and tolerance of the injured brain to ischaemia.
• Propofol is widely used because it effectively reduces ICP and
allows rapidly titratable sedation levels. The infusion rate
should not exceed 4 mg/kg/hour
• midazolam is often added to minimize total propofol dose.
• Analgesia is usually provided with paracetamol and infusion of
opioids such as fentanyl. Neuromuscular blocking agents
should not be used routinely but reserved for patients with
refractory.
(Puntis,2016)
Monitoring CBF and metabolism balance
– Jugular bulb oxygen saturation (SjO2) provides information
on global cerebral oxygen delivery and metabolism, which
is used for detecting cerebral hypoperfusion,
hyperperfusion, or secondary ischemic brain injury
– The normal SjO2 level is approximately 60 %. SjO2 values
under 50 % is considered to be cerebrally ische-mic when
accompanied by low CBF or/and CPP.

– High SjO2 values may reflect hyperemia (higher CBF and

dilatation of blood vessels; increased CBV) or severe
metabolic depression due to severe brain damage.

(Puntis,2016)
Monitoring CBF and metabolism balance
• Continuous SjO2 monitoring is effective for detecting
cere-bral ischemia after TBI.

• SjO2 monitoring is most commonly used for severely

brain-injured patients to de-tect post-injury brain
ischemia and to monitor the effi-cacy of mannitol
injection or hyperventilation therapy.

• If hyperventilation becomes excessive, cerebral

vasocon-striction will occur and ultimately lead to
further aggra-vation of cerebral perfusion of the
already injured brain (reduced CPP that leads to brain
ischemia).

(Puntis,2016)
Monitoring CBF and metabolism balance
• CPP can be boosted by infusing fluids or by administer-ing
mannitol (as a volume expander) or vasopressors, with a
subsequent vasoconstriction of brain blood vessels.

• Finally, ICP can be lowered as a result of reduced CBV

after vasoconstriction. Above the upper autoregulated
limit, hyperperfusion may be a risk for hyperemia.

• Conversely, a drop in SAP at the lower limit for

autoregulation response may reduce CPP and cause brain
ischemia. Increased ICP levels may lead to further
reductions in CPP

(Puntis,2016)
 CHAPTER 3
CLONCLUSION
CLONCLUSION
• Responses in the injured brain through many mecha-nisms that lead
to secondary brain injuries.
• Arterial hypotension, hypertension, or excess hyperventilation
intended to reduce ICP in patients with damaged auto-regulation
response also lead to secondary brain injury and critical brain
conditions after TBI that are associated with a poor outcome.
• The central dysregulation mecha-nisms after brain injury could
contribute to the develop-ment and progression of extracerebral
organ dysfunction by promoting systemic inflammation that may
cause medical complications
• Neurocritical care after severe TBI has therefore been refined to
focus not only on sec-ondary brain injury but also on systemic organ
damage after excitation of sympathetic nerves following stress
reactions.
(Puntis,2016)
TERIMA KASIH

(Puntis,2016)