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COLLEGE OF MEDICINE AND HEALTH SCIENCES

SCHOOL OF MEDCINE
DEPARTMENT OF ANESTHESIA &CRITICAL CARE
Anesthesia for Multiple
Trauma and Shocked Patients

Abraham T. (BSc, MSc)


abrahamtm2006@gmail.com
CMHS, Department of Anesthesia
University of Gondar

2
Overview Anatomy
of brain

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4
Brain

o The brain is composed of the cerebrum, cerebellum,


diencephalon and brainstem.

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Anatomy of brain

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Anatomy of brain …

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Anatomy of brain …

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Anatomy of brain …

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Anatomy of brain …

D. Diencephalon
 Thalamus
 Hypothalamus
 Pituitary gland

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Anatomy of brain …

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11 Neurophysiology relevant to
head injury
o When planning anesthesia for patients with TBI, an
understanding of CBF physiology is beneficial.

o Many anesthetic agents cause alterations in CBF and therefore


have the potential to cause further insult.

o Changes in CBF are a significant cause of cerebral injury after


head trauma.

o Prevention of ischemic damage by maintaining O2 delivery to


the brain contributes significantly to outcome.
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Cont …

o Hypoxia, hypotension, raised intracranial pressure (ICP) and


anemia all lead to a reduction in the delivery of oxygenated
blood to cerebral tissues.

o Hyperthermia and epilepsy both increase cerebral


metabolic rate, and therefore cerebral oxygen consumption.

o In addition, both hypoglycemia and hyperglycemia are


associated with a worse outcome.

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Cerebral blood flow (CBF)

o The brain withstand very short periods of lack of blood


supply (ischemia).

o If blood flow is not re-established rapidly, irreversible


cellular injury ensues in 3-8min.

o Therefore, adequate CBF must be maintained to ensure


delivery of nutrient and waste removal.

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CBF …
o CBF = 50ml/100g/min

o The adult brain weighs 1400g or 2% of the total body weight


with CBF 700ml/min or 15% of the resting COP

o This reflects the high oxygen consumption of the brain of


3.3ml/100g/min (50ml/min in total) which is 20% of the total
body consumption.

o This is often referred to as the cerebral metabolic rate for


oxygen or CMRO2.
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Cerebral Perfusion Pressure

o Perfusion of the brain is dependent on the pressure gradient


between the arteries and the veins and this is termed the
cerebral perfusion pressure (CPP).

o This is the difference between the mean arterial blood


pressure (MAP) and the mean cerebral venous pressure.

o CPP = MAP – (ICP + VP)

o CPP = MAP – ICP

o CPP is normally about 80mmHg (60mmHg – 160mmHg)


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CPP …

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CPP …

o In the immediate hours after severe head injury, cerebral


blood flow falls significantly, to approximately
25mls/100g/min.

o Irreversible neuronal damage occurs once cerebral blood flow


falls below 18 mls/100g/min (after severe head injury the
brain is extremely susceptible to further ischemic damage).

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CPP…

o CPP will be affected by anything that changes the MAP or

ICP.

 Blood loss causing hypotension will reduce MAP and CPP while an
intracerebral hematoma will increase ICP.

o In a normal brain, CBF remains constant over a wide range

of CPPs. This is achieved by a process called autoregulation.

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Intracranial volume

o Rigid box

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Cont ..

o Following head injury, a rise in intracranial pressure may


result from an increase:

 intracranial blood volume (e.g. extradural haematoma),

 cerebrospinal fluid volume (e.g. obstructive


hydrocephalus) or

 extracellular fluid volume (e.g. cerebral oedema).

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Cont …

o Since the skull is rigid, an increase in volume by any of its

contents without a concomitant reduction in the other

components results in an increase in pressure.

o The relationship between intracranial pressure and changes in

intracranial volume post-injury can be better understood by

reviewing the Monro-Kellie hypothesis.

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Monro-kellies’ Hypothesis

 Cranial compartment is rigid and has no room for expansion

 Cranium and its constituents (blood, brain tissue and CSF)


are at a state of volume equilibrium.

 Thus an increase in the volume of one constituent must be


accompanied by a decrease in the volume of the other two.

 Normal ICP can only be maintained via these compensatory


mechanism for volume less than 100-120mls

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Cont …

o The various clinical indicators of increased ICP include


headache, nausea and vomiting, blurred vision, somnolence,
and papilledema
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Cont …

Stage 1/2 = compensation phase.


 As one of the intracranial
constituents increases in volume, the
other two constituents decrease in
volume in order to keep the
intracranial pressure constant.

Stage 3/4 = decompensated phase.


 When compensatory mechanisms are
exhausted, small increases in the
volumes of intracranial constituents
cause large increases in ICP.
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Cont …

o Compensation is accomplished principally by the

 Translocation of cerebrospinal fluid (CSF) to the spinal


subarachnoid space and

 Venous blood to the extracranial veins

o Ultimately, when the compensatory potential is exhausted,


even tiny increments in volume of the intracranial contents
can result in substantial increases in ICP

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26 Intracranial Compartments and
Techniques for Manipulation of
Their Volume

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Cont …

 Engorgement of venous side of the circulation is a common


cause of increased ICP or poor conditions in the surgical field

 A head-up posture to ensure good venous drainage in


neurosurgical anesthesia and critical care

 Obstruction of cerebral venous drainage by extremes of


head position or circumferential pressure (e.g. collars, ETT
ties) should be avoided

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The pathophysiology of intracranial
hypertension

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Cont …

o Relationship between CBF and PaC02.

 At normotension, the relationship between PaCO2 & CBF is


almost linear.

 At a PaCO2 of 80mmHg CBF is approximately doubled. No


further increase in flow is possible at this point as the
arterioles are maximally dilated.

 Conversely at 20mmHg flow is almost ½ and again cannot fall


further as the arterioles are maximally vasoconstricted.
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Cont …

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Cont …

o Relationship between CBF and PaO2.

 CBF increases once PaO2 drops below 50mmHg (6.7kPa) so


that cerebral oxygen delivery remains constant.

 Hypoxia acts directly on cerebral tissue to promote the


release
of adenosine, and in some cases prostanoids that contribute
significantly to cerebral vasodilatation.

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Cont …

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Changes in CBF caused by independent
alterations in PaCO2, PaO2, and MAP

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Cont …

o Blood viscosity: as viscosity falls, CBF increases, though there


will also be a reduction in O2-carrying capacity of the blood.

 The optimal hematocrit is usually about 30%.

o Temperature: CMRO2 decreases by 7% for each 1°C fall in body


temperature.

 At 27°C, CBF is approximately 50% of normal.

 At 20°C, CBF is about 10% of normal.

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Cont …

o Drugs:

 Anesthetic drugs: volatile agents cause a reduction in the


tension of cerebral vascular smooth muscle  vasodilatation
and CBF.

 Concentration dependent response

 Vasodilatation can be countered by hyperventilation, without


serious risk of cerebral ischemia.

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Intracranial pressure (ICP)

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Summary

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Causes of raised ICP

1. Brain tissue

Cerebral edema 2o to trauma, infection, infarction, hyponatremia,

hypertensive encephalopathy, acute liver failure,

Cerebral abscess

Cerebral contusions

Tumors

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Causes of raised ICP …

2. Blood

o Intracerebral, SAH, subdural, extradural haematomas

o Arteriolar dilatation 2o to hypoxaemia, hypercarbia, anesthetic

drugs, hyperthermia, seizures, hypotension

o Venous dilatation 2o to venous obstruction from high PEEP,

coughing, straining, heart failure, venous sinus thrombosis, head-

down tilt, tight neck ties

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Causes of raised ICP …

3. CSF

o Hydrocephalus

o Meningeal diseases

o Choroid plexus tumors

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Effects of a Raised ICP

– As ICP rises, CPP falls eventually to a point when there is


no CBF, no cerebral perfusion and brain death.

– Prior to this, brain structures begin to herniate.

– Physiological compensatory mechanisms occur to try and


maintain cerebral blood flow:-

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Reflexive Response to ICP

o Cushing’s reflex
 Protective response to preserve blood flow to the brain
 BP will increase
 SBP increasing as DBP stays same or increases
 Widening pulse pressure

 Heart rate will decrease


 Effort to lower elevating blood pressure

 Respirations may be irregular

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Measuring ICP

o If ICP is not measured directly, it is possible to estimate it and make


changes in MAP to maintain CPP.
 Patient drowsy & confused (GCS 9-13) ICP ∼ 20mmHg

 GCS ≤ 8 ICP ∼ 30mmHg

o Traditionally measured by use of a ventriculostomy, while now


measured by placing some form of measuring device within the brain
tissue or epidural space.

o Later one is unreliable at extremes of pressure.

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Sites

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How can ICP be influenced?

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CNS Trauma

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Head Trauma

o Common cause of trauma death (number one killer in trauma)


o 25% - 50% of all trauma deaths
o Hypoxia and hypotension double mortality
o The global incidence rate of TBI is estimated at 200 per
100,000 people/yr.
o High risk of C-spine injury

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Head Trauma …

o Use inspection/observational skills with MOI to


increase suspicion of head and neck injuries.

o A head injury may involve the scalp, skull, dura, blood


vessels, brain and spinal cord.

o Scalp and skull may not be of major consequence to


the brain, but serve as indicators.

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Manifestations of HI

o A head injury can be:

 Concussion

 Cerebral contusion

 Subarachnoid hemorrhage

 Diffuse axonal injury

 Epidural hematoma

 Subdural hematoma

 Intracerebral hematoma

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Concussion

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Cerebral Contusion

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SAH

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Diffuse Axonal Injury

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Diffuse Axonal Injury …

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Diffuse Axonal Injury …

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Acute Epidural Hematoma

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Acute Subdural Hematoma

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Intracerebral Hemorrhage

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Intracerebral Hemorrhage …

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Intracerebral Hemorrhage …

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Pathophysiology

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Pathophysiology …

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Pathophysiology …

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Pathophysiology …

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Management

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Types of Brain Injury

Primary brain injury

o occurs at time of accident

Secondary brain injury

o occurs after accident and might be preventable

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Primary injury's

o Primary TBI- is due to direct impact of trauma to the

brain. Which includes ;


 Concussion :- a temporary brief change in mental
functions without damage to the structure of the brain.
 Contusion :- bruises on the brain
 Lacerations :- when the tissue of the brain is

mechanically cut or torn.

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Secondary injuries

o These result as a consequence of the complications of

the primary injury.

o Secondary brain injury results from:

 Systemic hypotension

 Hypoxia, hypercarbia

 Biochemical changes

 Elevated Intracranial Pressure

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Causes of secondary brain injury

o Reduced brain blood flow


o Reduced brain oxygen supply
o Increased brain oxygen use
 fever, seizures
 low blood sugar
o Increased ICP
 low blood O2
 high blood CO2
 hematoma or brain swelling
 head down position
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Sign and symptoms of brain
injury

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Cont …

o CSF Ottorhea: o CSF Rhinorrhea

Seen in fracture base of skull


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Cont …

Battle sign --- a bruise that indicates Raccoon eyes------fracture base


a fracture at the bottom of skull of the skull.

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Bilateral Dilated Pupils

o Bilateral fixed, dilated, unresponsive

o Causes
 severe hypoxia
 hypothermia
 seizures

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Unilateral Dilated Pupil

o Unilateral fixed, dilated, unresponsive

o Causes

 expanding lesion on same side


 tentorial herniation

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Severity of Head Injury

o Severe GCS ≤8
o Moderate GCS 9-12
o Minor GCS 13-15

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Indication of CT scan

o GCS score still < 15 two hours after injury

o Neurologic deficit

o Open skull fracture

o Sign of basal skull fracture

o Extremes of age

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Management of a head injury

o History
 Amnesia

 Confusion and disorientation

 Difficulty remembering new information

 Headache

 Dizziness

 Blurry vision

 Nausea and vomiting

 Ringing in the ears

 Trouble speaking coherently

 Changes in emotions or sleep patterns

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Management of a head injury …

o ABCDE
o Hyperventilation
o Head elevation
o Paralysis and sedation
o Hypothermia
o Mannitol and hypertonic saline
o External CSF drainage
o Decompressive craniotomy
o Maintain normovolemia

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Hyperventilation

o Useful in initial resuscitation: effectively and rapidly

reduce ICP in acute rises until definitive therapy.

o Last resort for reducing ICP

o Generalized vasoconstriction   cerebral blood

volume   ICP

o Chronic hyperventilation should be avoided because 

CBF puts the brain at risk of ischemia

– Safety of duration is uncertain.

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Head elevation

o Head of bed at 20 to 30 degree optimizes cerebral


venous return

o Ensure neutral neck position

o Avoid Jugular vein occlusion

o Caution in hypovolemic patients to avoid reduction in


MAP and therefore CPP
 CPP = MAP – ICP

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Paralysis & Sedation

o To prevent excess motor activity (posturing,


coughing, straining against ventilator)

o Role of EEG

– Rule out ongoing seizure activity

– Titration of sedation with goal of achieving burst


suppression

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Hypothermia

o To  CMR and  CBF (must maintain MAP to improve CPP)

o Hypothermia, controversial

 Attenuates deleterious biochemical cascade

  CMR

  risk pneumonia,

 Wound infection

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Diuretics

 Diuretics are used widely in neurosurgery to reduce the volume

of the brain's intracellular and extracellular fluid compartment

 Osmotic diuretics, principally mannitol, are preferred clinically

because of their speed and efficacy

 Mannitol is effective only when some degree of blood-brain

barrier integrity is preserved in a significant portion of the

brain

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Mannitol

o Decreases ICP within 6 hrs – IV fluid shift


– 20% or 25% solution (0.25 – 1gm/kg IV)

– Dehydrates the brain but not the patient.

– Decrease blood viscosity & improved flow

– Decreases CSF production

o Furosemide 1mg/kg produces a reduction in ICP to the


same extent as mannitol at 1g/kg.

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Hypertonic saline

o Hypertonic saline, if refractory to Mannitol:

 BBB is impermeable to Na+ ions  Osmotic gradient

 Less electrolyte disturbances

 Lack of standard guideline (3-7.5% solution at 20-


40cc/h)

 Slow taper to avoid rebound hyponatremia

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External CSF drainage

o Therapeutic as well as diagnostic

 Technical issues

 Infectious issues

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Decompressive Craniectomy

o Surgical removal of cranial bone flap to relieve


intracranial pressure

o Useful in large ischemic CVA with profound edema

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Anticonvulsants

 The general principle is that any acute irritation of the


cortical surface has the potential to result in seizures;
this includes acute neurologic events such as head
injury and SAH

 Diphenylhydantoin should be administered at rates not


more rapid than 50 mg/min

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Intravenous Fluid Management

o The general principles of fluid management for


neurosurgical anesthesia are
 Maintain normovolemia, and
 Avoid reduction of serum osmolarity

o It is generally ideal to maintain a normal MAP in


patients undergoing most neurosurgical procedures and
neurosurgical critical care
o Normal saline and lactated Ringer's solution
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Maintain Euvolemia

o A single episode of hypotension (SBP< 90 mm Hg), is associated


with an increase in morbidity & doubled mortality after severe
TBI.

o Hypotension together with hypoxia is associated with a


threefold increase in mortality.

o Goal of MAP > 70 mm Hg MAP until ICP monitoring is instituted.

o Fluid resuscitation is the mainstay of therapy, followed by


vasoactive infusions as needed.
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Maintain euvolemia …

o Hence, BP needs to be augmented with drugs that produce


arterial vasoconstriction such as metaraminol or
noradrenaline.

o So by raising MAP, ICP can often be reduced.

o Correction of anemia from blood loss is the 1st priority,


with a goal hematocrit of greater than 30%.

o Avoid Hypotonic/glucose containing fluids.

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Cervical Spine

 Approximately 2% of blunt trauma victims who survive to


reach a hospital and 8% to 10% of TBI victims with GCS
less than 8 have a fracture of the cervical spine

 The incidence of intubation-related neurologic injury is


underreported

 When a hypnotic muscle-relaxant sequence is used, the


standard approach includes the use of cricoid pressure and
in-line axial stabilization
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Cervical Spine …

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Summary

 Assessment and management of ABC’s


 Early intubation if; GCS <8
 Mild head elevation of 15–30° (Ensure euvolemia)
 Hyperventilation: Target PaCO2: 30–35 mm Hg (suited for
acute, sharp increases in ICP or signs of hernia)
 Mannitol: Initial bolus: 0.25–1 g/kg, then 0.25–0.5 g/kg,
q 2–6 h as per requirement, up to 48 h
 Hypertonic Saline: Preferable in presence of Hypotension,
Hypovolemia, Serum osmolality >320 mOsm/kg, Renal failure

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Summary measures …

 Adequate sedation and analgesia


 Prevention & treatment of seizures: use BDZ followed by
phenytoin as initial choice.
 Avoid noxious stimuli: use lignocaine prior to ET
suctioning (nebulized or intravenous)
 Control fever: antipyretics, cooling measures
 Maintenance IV Fluids: Only isotonic or hypertonic, No
Hypotonic fluids
 Maintain blood sugar: 80–120 mg/dL

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Anesthesia
management

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Initial assessment and management
of the head injured patient

o Patients may present with head injuries in isolation or in


conjunction with other injuries.

o Up to 50% of patients with severe traumatic brain injury


have major extra-cranial injuries.

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Assessment

o Airway patency should be assessed and the cervical spine


immobilized.

o The airway should be secured, by tracheal intubation, in


patients who do not have a patent airway or who are
significantly obtunded (GCS ≤ 8).

o The chest should be examined and any life-threatening


injuries (e.g. tension pneumothorax) promptly treated.

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Assessment …

o The circulatory state should be assessed using clinical


parameters such as blood pressure and heart rate.

o Any sites of external hemorrhage should be directly


compressed.

o Patients with suspected or confirmed on-going


hemorrhage will require operative intervention.

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Assessment …

o The patient should be completely exposed to assess for other


injuries, whilst taking care to prevent hypothermia.

o All aspects of the primary survey should be completed and


identified life-threatening conditions treated, before commencing
the secondary survey.

o In the situation where life-threatening airway, thoracic or


circulatory problems present together with life-threatening
neurological injuries, priority is given to the definitive treatment of
the former
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Assessment …

o Pupillary size and response to light should be assessed and


recorded.

o Ipsilateral pupillary dilatation, unreactive to light, may indicate


life-threatening intracranial pressure.
 In this situation, pupillary dilatation results from compression of the
oculomotor nerve against the tentorium.

 Alternative causes include ocular trauma and the administration of certain


drugs.

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103 Specific Neurological Assessment and
Investigation

o The Glasgow Coma Score is used to formally assess the


conscious level of the patient.

 composed of 3 components: eye-opening, verbal and motor


response.

 The best response in each component is used to calculate


the final score, which ranges from 3, at worst, to 15, at
best.

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Specific Neurological Assessment
and Investigation …

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105 Specific Neurological Assessment and
Investigation …

o Following head injury, the diagnostic investigation of


choice is a CT scan of the head.

o Indications for patients requiring an urgent CT scan:

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Initial Management: Airway

o If the cervical spine has not been cleared manual in-line


stabilization is required for intubation.

o The dose and type of induction agent(s) chosen should be


selected with the aims of rapidly securing the airway with
minimal hemodynamic disturbance and minimal rise in ICP.

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Initial Management: Airway …

o With the exception of ketamine, most of IV induction agents


cause a reduction in CBF, cerebral metabolism and
intracranial pressure.

o In the uncomplicated airway a modified RSI induction using a


pre-determined dose of thiopentone or propofol together
with an opioid and sux can be used.

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Initial Management: Airway …

o With the availability of sugammadex, rocuronium can be


used as an alternative to suxamethonim.

o Following intubation and confirmation of endotracheal


placement, the tube should be well secured in a fashion
that ensures venous return is not obstructed.

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109 Indications for Intubation Post-Head Injury

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110
Initial Management: Breathing

o Both hypoxia and hypo- and hypercapnia should be avoided in


patients with head injuries as these worsen outcome.

o Hypercapnia, through increasing cerebral blood flow, causes a rise in


ICP.

o To achieve adequate cerebral perfusion, without significantly


increasing ICP, a PaCO2 of 4.5 – 5.0kPa (34-38mmHg) is targeted.

o In the patient with clinical or radiological evidence of intracranial


hypertension hyperventilation can be instituted, but maintaining
PaCO2 above 4kPa (30mmHg).
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Initial Management: Circulation

o Hypotension increases morbidity and mortality in severe traumatic

brain injury.

o A cerebral perfusion pressure of 50 – 70 mmHg should be targeted.

o In cases where the ICP is not measured but suspected to be raised,

maintenance of a MAP of over 80mmHg should ensure an adequate


cerebral perfusion pressure in most severe cases of raised ICP.

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Initial Management: Circulation …

o Once normovolemia has been achieved a vasopressor, such


as metaraminol or noradrenaline, may be required to
maintain MAP at this level and offset the hypotensive
effect of any anesthetic agents used.

o The aim is to achieve a balance between maintaining


normovolemia and end-organ perfusion without worsening
cerebral edema through excessive fluid administration.

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Initial Management: Disability

o Both hypoglycemia and hyperglycemia can worsen brain


injury.
o A blood glucose of 4 – 8 mmol/l is targeted.
o Seizures increase cerebral oxygen consumption and can
produce cerebral ischaemia.
 Seizures should be treated promptly with appropriate anti-
epileptics (e.g. phenytoin, 18mg/kg).
o Hyperthermia, a temperature of greater than 37ºC,
should be avoided.

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Summary of Therapeutic Targets in
Managing Severe Head Injury

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Selection of Anesthesia Agent

o To be addressed in detail in other course.

o In selection of agents for TBI patients, specific properties


of the agent that must be considered include:

 The effects on cardiovascular and ventilatory function,

 Effects on intracranial hemodynamics, and

 Potential neuroprotective properties.

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Selection cont’d…

o Minimizing CVS and respiratory compromise with


maintaining CPP remains a top priority when selecting an
anesthetic protocol.

o Selection of anesthetic protocol for use in head trauma


patients (Fig)

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Selection cont’d…

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Selection cont’d…

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Anesthetic Agents

INHALATIONAL INTRAVENOUS

 Increase CBF  Decrease CBF

 Increase ICP  Decrease ICP

Decrease CMRO2  Decrease CMRO2

 EEG burst suppression  EEG burst suppression


120
Increased ICP Mx during anesthesia

o Methods to rapidly reduce ICP include hyperventilation &


administration of hypermolar agents.
 Hyperventilation - Most rapid & effective method to ↓ICP.
 Regarded as an emergency therapy only.
 Maintain a PaCO2 of 30mmHg for up to 30 minutes
 Hyperosmolar agents: such as Mannitol can be used to
decrease ICP. Mannitol acts as an osmotic diuretic to
↓cerebral edema.
 Ensure intact BBB before mannitol.
 Hypertonic saline is an option

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Increased ICP Mx during anesthesia …

o Smooth anesthetic technique

 Reduce coughing & straining

 Postoperative analgesia and sedation

o Other management strategies

 Prevention of hyperthermia,

 Moderate hypothermia (31–34oC) (experiment)

 Head elevation, & avoiding occlusion of jugular veins

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122

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