Decompressive

Craniectomy
Elshurafa Mueen Zayed
DEPARTMENT OF ANESTHESIOLOGY AND REANIMATION
FACULTY OF MEDICINE UNIVERSITY OF SEBELAS MARET
Introduction

Raised intracranial pressure (ICP): common neurological complication in

critically ill children. High incidence, but few evaluated treatments of
intracranial hypertension.
Cerebral edema is a life-threatening condition that develops as a result of
an inflammatory reaction (cerebral trauma, massive cerebral infarction,
hemorrhages, abscess, tumor, allergy, sepsis, hypoxia, and other toxic or
metabolic factors)
Decompressive craniectomy (DC): removal of an area of skull to enhance
the potential volume of the intracranial compartment. It is commonly
accepted as a means of rapidly relieving intracranial hypertension
associated with a number of clinical conditions. Many studies show that DC
can significantly reduce mortality rate from 74.4% to 41.9% and improve
neurological outcome.
Literature Review
(Anatomy and Physiology of The Brain)

Figure 1. The Central Nervous System

Literature Review
(Anatomy and Physiology of The Brain)
Cerebrum
Divided into right and left hemispheres connected by corpus callosum
Each hemisphere divided into 4 lobes: frontal lobe, parietal lobe,
temporal lobe, and occipital lobe
The medial temporal lobe structures are considered by some to be part
of the so-called limbic lobe (Greeenstein et al., 2000)
The cerebrum is further divided into the telencephalon and
diencephalon. The telencephalon consists of the cortex, the
subcortical fibers, and the basal nuclei. The diencephalon mainly
consists of the thalamus and hypothalamus (Moore et al, 2010)
Literature Review
(Anatomy and Physiology of The Brain)
Cortex and subcortical fibers (Greeenstein et al., 2000)
Cortex has a slightly gray appearance (gray matter)
The cortex has a folded structure; gyrus, and groove between the folds is sulcus
Below the cortex are axons, which are long fibers that emanate from and connect
neurons. Axons are insulated by myelin, which increases the speed of conduction.
Myelin is what gives the white appearance (white matter)
Limbic system (Greeenstein et al., 2000)
A group of cortical and subcortical structures involved in memory formation and
emotional responses
Limbic structures: amygdala, hippocampus, fornix, mammillary bodies, cingulate
gyrus, and parahippocampal gyrus
The functional connections within the limbic system are best summarized by the
Papez circuit
Literature Review
(Anatomy and Physiology of The Brain)
Basal nuclei (ganglia) (Greeenstein et al., 2000)
The basal nuclei comprise the caudate nucleus, putamen, globus pallidus, subthalamic
nucleus, and substantia nigra
Integrated with the motor cortex, premotor cortex, and motor nuclei of the thalamus
and plays a crucial role in modulation of movements
The primary input to the basal nuclei is from the primary motor cortex and premotor
cortex (Brodmann areas 4 and 6) and consists primarily of the pyramidal cells in
cortical layer V. These excitatory projections lead primarily to the striatum.
Thalamus (Greeenstein et al., 2000)
Positioned between the brainstem and the telencephalon, the diencephalon is
composed of the thalamus, the epithalamus, the subthalamus, and the hypothalamus.
Serves as a relay station for ascending input to the cortex and receives information
from each of the cardinal senses (except smell)
Literature Review
(Anatomy and Physiology of The Brain)
Epithalamus
Epithalamus is made up of the habenula, the habenular commissure, the
posterior commissure, and the pineal gland
Subthalamus
Located between the midbrain and the thalamus,
Contains the subthalamic nucleus: the red nucleus, and the substantia nigra
Integrated with the basal nuclei and play a role in modulation of movement
Hypothalamus (Greeenstein et al., 2000)
Lie in the walls of the third ventricle anteriorly
Involved in mediating endocrine, autonomic, visceral, and homeostatic
functions
Literature Review
(Anatomy and Physiology of The Brain)
Cerebellum (Greeenstein et al., 2000)
Occupies the posterior fossa, dorsal to the pons and medulla and consists of 2
hemispheres, connected by vermis
Cerebellar cortex has 3 layers: molecular, Purkinje, and granular
4 deep cerebellar nuclei: the fastigial, globose, emboliform, and dentate nuclei
Involved in modulating motor control to enable precisely coordinated movements
Medulla oblongata (Greeenstein et al., 2000)
Ventrally, the pyramids and pyramidal decussation is visualized just below the pons.
These are the descending corticospinal tracts
Lateral to the pyramids, hypoglossal nerve exits the brainstem. Lateral to the hypoglossal
nerve is the inferior olive. Dorsolateral to the inferior olive are 9th and 10th cranial
nerves (glossopharyngeal and vagus) exit
Dorsally, there are gracile tubercles and cuneate tubercle that represent the nuclei
where sensory information from the dorsal columns is relayed onto thalamic projection
neurons
Literature Review
(Anatomy and Physiology of The Brain)
Pons (Greeenstein et al., 2000)
Located on superior to the medulla
Ventral surface characteristic: band of horizontal fibers
Dorsally, the pons forms the floor of the fourth ventricle.
Midbrain
The superiormost aspect of the brainstem
Ventrally, the midbrain appears as 2 bundles cerebral peduncles. Between
them, the third cranial nerve (oculomotor) can be seen exiting
The posterior aspect of the midbrain consists of superior and inferior
colliculi. The superior colliculi are involved in mediating the vestibulo-
ocular reflex, whereas the inferior colliculi are involved in sound
localization
Literature Review
(Anatomy and Physiology of The Brain)
Cranial nerves
(Greeenstein et al., 2000)
I: Olfactory nerve
VII: Thefacial nerve
VIII: The vestibulocochlear
nerve

II: The optic nerve

IX: The glossopharyngeal
nerve
III: The oculomotor nerve
X: Thevagus nerve
IV: The trochlear nerve
XI: The accessory nerve
V: Thetrigeminal nerve
XII: The hypoglossal nerve
VI: The abducens nerve
Literature Review
(Anatomy and Physiology of The Brain)
Meninges
Consist of 3 tissue layers: the pia, arachnoid, and the dura mater (inner to outside layer)

Figure. Meninges
Between the pia mater and the arachnoid mater is subarachnoid space, which contains cerebrospinal
fluid (CSF) patological condition: subarachnoid hemorrhage
Between the arachnoid mater and the dura mater is the subdural space patological
condition:subdural hematoma
Literature Review
(Anatomy and Physiology of The Brain)
Cerebrospinal fluid (CSF)
(Greeenstein et al., 2000).
Produced about 450
mL/day
The brain has 4
ventricles
CSF circulation
controlled by those
ventricles
Figure. CSF Circulation
Pathological condition:
hydrocephalus
Literature Review
(Anatomy and Physiology of The Brain)
Blood supply (Greeenstein et al., 2000)
Arteries: internal carotid artery and vertebral
artery
Internal carotid artery terminates into the
anterior cerebral artery, the middle cerebral
artery, and the posterior communicating
artery
Vertebral arteries join to form the basilar
artery, then gives rise to posterior cerebral
arteries and superior cerebellar arteries
Venous return to the heart through a
combination of deep cerebral veins and
superficial cortical veins Figure 7. Cerebral arterialcircle of Willis
 Literature Review
(Cerebral edema, Intracranial Hypertension, and Brain
Herniation)
Cerebral edema is a life-threatening condition as a result of an inflammatory
reaction (cerebral trauma, massive cerebral infarction, hemorrhages,
abscess, tumor, allergy, sepsis, hypoxia, and other toxic or metabolic factors)
Types of cerebral edema: vasogenic cerebral edema and cytotoxic cerebral
edema (Steiner et al., 2006).
Pathophysiology (Mokri, 2010) :

Cellular and Activation of

Inflammator Arachidonic Activated
blood vessel injury Edema
y response cascade mediator
damaged cascade
Literature Review
(Cerebral edema, Intracranial Hypertension, and Brain
Herniation)
Consequences of cerebral edema by Monro-Kelie hypothesis: total bulk of three
elements (inside the skull) i.e. brain - 1400 ml, cerebral spinal fluid (CSF) 150 ml and
blood 150 ml is at all times constant.

Figure 1. Monro-Kelie doctrine

Since skull is rigid - if the volume of one of these components increases, it will force the
reduction of volume of the other components.
Literature Review
(Cerebral edema, Intracranial Hypertension, and Brain
Herniation)
Greatly raised ICP eventually causes a reduction in cerebral blood flow
throughout the brain (Steiner, et al., 2006)

Figure 2. Cycle of raised ICP

Literature Review
(Cerebral edema, Intracranial Hypertension, and Brain
Herniation)
Herniation can be caused by a number of factors that cause amass effectand
increaseICP
Types of herniation:
Subfalcine herniation: the most common type of cerebral herniation
Transtentorial herniation: the innermost part of thetemporal lobe, theuncus, can be
squeezed so much that it moves towards thetentoriumand puts pressure on midbrain.
Posterior (parahippocampal) tentorial herniation: herniation of the medial temporal lobe
occurs more posteriorly. Causing Parinauds syndrome
Descending transtentorial herniation: consists of caudal descent of brain tissue through
the tentorial incisura, and occurs mainly in response to mass effect in the frontal,
parietal, and occipital lobes
Ascending transtentorial herniation: in association with a cerebellar mass or a
hydrocephalic ("trapped") fourth ventricle
Tonsillar (foramen magnum) herniation: inferior displacement of the cerebellar tonsils
through the foramen magnum into the cervical spinal canal
Literature Review
(Management of Raised Intracranial Pressure)

The goal for patients presenting with raised ICP is to identify and address
the underlying cause along with measures to reduce ICP
Avoidance of factors aggravating or precipitating raised ICP is important for
children with intracranial hypertension
ABC assessment and management is early management. Early endotracheal
intubation should be considered for those children with GCS <8.
Mild head elevation of 1530 has been shown to reduce ICP with no
significant detrimental effects on CPP or CBF by encouraged jugular venous
drainage (ensure that the child is euvolemic and not in shock)
Mannitol has been the cornerstone of osmotherapy in raised ICP with initial
bolus 0.251 g/kg (the higher dose for more urgent reduction of ICP)
followed by 0.250.5 g/kg boluses repeated every 2 6 h as per requirement
(maximal 48 to 72 hours). Attention to fluid balance (Steiner, et al., 2006)
Literature Review
(Management of Raised Intracranial Pressure)

Hypertonic saline has a clear advantage over mannitol in

children who are hypovolemic or hypotensive (bleeding,
rebound rise in ICP, hypokalemia, and hyperchloremic acidosis,
central pontine myelinolysis, acute volume overload, renal
failure, cardiac failure or pulmonary edema)
Administer hypertonic saline as a continuous infusion at 0.1 to
1.0 mL/kg/hr, to target a serum sodium level of 145155 meq/L
Monitoring of serum sodium and serum osmolality should be
done every 24 h till target level is reached and then followed
up with 12 hourly estimations (Steiner, et al., 2006)
Literature Review
(Decompressive Craniectomy)
Decompressive craniectomy (DC) refers to the removal of an area of skull
in order to enhance the potential volume of the intracranial
compartment.
At present, however, it is commonly accepted as a means of rapidly
relieving intracranial hypertension associated with a number of clinical
conditions (Aarabi, et al., 2006)
DC: removal of an area of skull bone to convert the closed intracranial
compartment into an open one (Schneider et al., 2002)
Adverse effects of intracranial hypertension due to compression is
impairment of cerebral blood flow. DC reduces this pressure and
enhances blood flow (Skoglund et al., 2006).
A craniectomy of at least 12 cm is recommended (Cooper et al., 2011)
Literature Review
(Decompressive Craniectomy)
A study said that large DC is superior to routine DC
improving the outcome of severe TBI, reducing the
chances of reoperation, higher incidence of delayed
complications (Cooper et al., 2011)
Clinical data also indicate that DC reduces mortality,
improves functional recovery, reduces duration of stay
in intensive care unit and improves the Barthel Index
Score, especially when it is performed early (Servadei
et al., 2011)
Literature Review
(Decompressive Craniectomy)
Indication (Servadei et al., 2011)
there are no clearly defined indications for, or
optimal timing of the procedure.
Several studies used a indications for late
decompression (i.e. more than 24 hours) an
intractable intracranial hypertension with ICP of
above 35 mm Hg, absence of pupillary reflexes and
CT abnormalities.
Literature Review
(Decompressive Craniectomy)
Surgical procedure
Preparation and define the sugical site
Patient is placed in a suitable position
Incision and drill a burrhole: scalp incisions should be made
in such a way that they can easily be converted into a
questionmark- type flap
Opening the dura: it is better to complete the standard six
burrholes to exclude an extradural hematoma before
opening the dura in search of an acute subdural hematoma
(Sahuquillo and Arikan, 2006)
Literature Review
(Anesthetic Management for Decompressive
Craniotomy)
The perioperative management of patients undergoing craniotomy depends
on recognizing the potential anaesthetic risks, the ability to manipulate
intracranial physiology, and early intervention for postoperative
complications.
Aims:
Preoperative assessment and optimization of associated medical conditions
Haemodynamic stability
Maintain cerebral perfusion and prevent increases in intracranial pressure
Facilitate surgery by providing a slack brain
Provide cerebral protection if required
Rapid recovery to enable neurological assessment in the immediate
postoperative period
Literature Review
(Anesthetic Management for Decompressive
Craniotomy)

Preoperative management: patient history, drug

history, acute neurological condition, examination
of radiological images, and an evaluation of
concurrent disease
Literature Review
(Anesthetic Management for Decompressive
Craniotomy)
Intraoperative management positioning (Ledwith et al., 2010):
Supine position: access to the anterior cranial fossa through a frontal
craniotomy with or without extension through the temporal bone
A neutral position of head with a reversed Trendelenburg tilt (15 head up):
venous drainage from the cranium and helps to reduce ICP
Prone position: good access to midline structures in the posterior fossa but
bleeding can obscure the surgical field
Head-up tilt: reduce haemorrhage, but increases the risk of air embolism
Lateral position: for approaches to lesions not in the midline, particularly
the cerebellopontine angle
Sitting position: surgical access to midline structures in the posterior fossa,
improves surgical orientation and good drainage of blood and CSF
Literature Review
(Anesthetic Management for Decompressive
Craniotomy)
Intraoperative management management of anaesthesia:
The anaesthetic technique depends on the ability to control ICP,
maintain haemodynamic stability, and provide rapid emergence
Total intravenous anaesthesia, with propofol infusion has been
used successfully in several studies. Intravenous induction agents
reduce the cerebral metabolic requirement of oxygen (CMRO2 ),
thereby reducing CBF and cerebral blood volume (CBV)
Addition of opioid: haemodynamic stability, reduces anaesthetic
agents requirments
Fluorinated volatile inhalational agents: increase CBF and CBV by
a direct intrinsic effect causing vasodilatation
Literature Review
(Anesthetic Management for Decompressive
Craniotomy)
Intraoperative management management of anaesthesia:
During craniotomy, intraoperative fluids and electrolytes
balance is affected by diuretics administered to decrease ICP
and to facilitate intracranial dissection. The adjunct of
potassium sparing diuretics to mannitol therapy can contribute
to increase its safety and to reduce related complication.
Perioperative blood loss can be associated with intraoperative
coagulopathy and anemization that are especially dangerous in
neuroanesthesia. Artificial colloids and mannitol, because of
dilutional effect, decrease whole blood clot strength and
increase the risk of bleeding (Butterworth, 2013; Pasternak
and Lanier, 2013)
Literature Review
(Anesthetic Management for Decompressive
Craniotomy)
Postoperative care
The neurological state is assessed as soon as possible in the recovery room
and any gross abnormality should be brought to the notice of the surgical
team
Simple analgesics such as paracetamol or mild opioids (e.g. codeine
phosphate) may be adequate. However, many patients require more potent
analgesia to control postoperative pain
Patients undergoing craniotomy, there is a tight relationship between
anesthesia and the quality of postoperative recovery and complications rate
Latest evidence highlights that the use of shorter acting opioid anesthetics
(remifentanil) is not associated with earlier recovery of physiological
variables and that appropriate management of postoperative pain is
effectively associated with pain control (Pasternak and Lanier, 2013)
Conclusion

Goal for raised ICP: identify and address the underlying

cause along with measures to reduce intracranial pressure
DC is commonly performed to protect the brain from the
damaging effects of propagating oedema and intracranial
hypertension
Improving patient selection and optimising timing of the
procedure may be expected to further improve outcome in
severely brain-injured patients
Anesthesia for craniotomy should address multiple patient-
based and disease-based needs, in the elective and
emergency setting
References

Aarabi, B; Hesdorffer DC; Ahn ES; Aresco C; Scalea TM; Eisenberg HM. 2006. Outcome following
decompressive craniectomy for malignant swelling due to severe head
injury.JournalofNeurosurgery.104(4):69479.
Butterworth JF, Mackey DC, Wasnick JD. 2013. Morgan and Mikhails Clinical Anesthesiology. Fifth
Edition. Depertement of Anesthesiology, Lubbock, Texas: Lange.
Cooper, DJ; et al. 2011. Decompressive craniectomy in diffuse traumatic brain
injury.NewEnglandJMedicine.364(16):1493502
Geenstein, B, et al. 2000. Color atlas of Neuroscience: Neuroanatomy and neurophysiology. Thieme
Stuttgart: New York.
Ledwith MB, Bloom S, Maloney-Wilensky E, et al. 2010. Effect of body position on cerebral oxygenation
and physiologic parameters in patients with acute neurological conditions. J Neurosci Nurs; 42:280287.
Mokri B. 2001. The Monro-Kellie hypothesis: applications in CSF volume depletion.Neurology.56(12):
17468.
Moore KL, Agur AMR, Dalley AF. 2010. Essential Clinical Anatomy. Fifth Ed. Philadelphia Wolters
Kluwer
References

Pasternak JJ, Lanier WL. 2013. Neuroanesthesiology update. J Neurosurg Anesthesio;

25:98134.
Sahuquillo J, Arikan F. 2006. Sahuquillo, Juan, ed. Decompressive craniectomy for the
treatment of refractory high intracranial pressure in traumatic brain injury.Cochrane
Database of Systematic Reviews(1): CD003983.
Schneider, GH; Bardt T; Lanksch WR; Unterberg A. 2002. Decompressive craniectomy
following traumatic brain injury: ICP, CPP and neurological outcome.Acta
Neurochirurica.81: 7779
Servadei, F (2011). Decompressive craniectomy in diffuse traumatic brain injury.New
England J Medicine.364(16): 1493502
Skoglund, TS; Eriksson-Ritzen C; Jensen C; Rydenhag B. 2006. Aspects on decompressive
craniectomy in patients with traumatic head injuries.Journal of Neurotrauma.23(10):
15021059.
Steiner LA, Andrews PJ. 2006.Monitoring the injured brain: ICP and CBF.British Journal
of Anaesthesia.97(1): 2638.
Thank You