Anesthetic-and-Intensive-Management-of-Head-Injury

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Anesthetic and Intensive care

management of Head injury

Prof .Pawar

Dr Abraham Dr Mani

www.anaesthesia.co.in [email protected]

http://www.anaesthesia.co.in/

mailto:[email protected]





Surgery for head injury

• Craniotomies will most commonly be performed

for the evacuation of

– subdural,

– epidural and

– intracerebral hematomas.

• The anesthetic approach is similar for all three.



The major goals of anesthetic

management

• Avoid secondary brain damage

– The secondary injury is described as the consequence

of further physiological insults, such as ischaemia, re- perfusion and hypoxia, to areas of ‘at risk’ brain in the

period after the initial injury

• Optimize cerebral perfusion and oxygenation

• Provide adequate surgical conditions for the

neurosurgeons.



Induction of anesthesia

• Most patients are already intubated in the emergency

department or before CT examination.

• The patients without intubation are treated with immediateoxygenation and securing of the airway.

• Anesthesiologists must be aware that

– these patients often have a full stomach,

– decreased intravascular volume, and

– a potential cervical spine injury



Techniques of intubation

• Awake / sedated nasal intubation

– contraindications

• Skull base fractures, Le Forte fractures

• Bleeding diathesis

• Fibreoptic intubation – Limitations

• Cooperation, Specialized training

• Difficulty in the presence of blood, secretions

• Direct laryngoscopy with manual inline

stabilisation

• Surgical airway – if intubation fails



Direct laryngoscopy with manual inline

stabilisation



Induction of anesthesia

• Rapid sequence induction may be desirable in

hemodynamically stable patients

• Thiopentone, propofol and etomidate have been usedsafely to induce anesthesia.

• Cardiovascular depression with thiopentone and propofol

is a concern in the presence of uncorrected hypovolemia

• In hemodynamically unstable patients, the dose of

induction drugs is substantially decreased or even omitted



Role of ketamine

• PET studies in humans have demonstrated that

subanesthetic doses of ketamine (0.2 to 0.3 mg/kg) can

increase global CMR by about 25%.

• Ketamine is probably best avoided as the sole anesthetic

in patients with impaired intracranial compliance because

early studies suggested increases in CMRO2, CBF, and

ICP.

• Some studies report no increase in ICP with controlled

ventilation or when diazepam, thiopenthal or propofol

sedation is given concurrently. Albanése J, et al : Ketamine

decreases ICP and EEG activity in traumatic brain injur y patients

dur ing propofol sedation. Anesthesiology 87:1328 –

1334, 1997.



Role of succinyl choline in head injury

• Studies in humans suggest that – (a) succinylcholine causes an increase in ICP in lightly

anesthetized patients;

– (b) this increase is abolished by IV lidocaine, deep

anesthesia, or a defasciculating dose ofnondepolarizing blockers;

– (c) the influence of laryngoscopy and tracheal

intubation on ICP far outweighs that of

succinylcholine.

– SCh alone did not increase cerebral blood flow

velocity or ICP in neurologically injured patients.

Kovarik et al Anesth Analg 1994; 78:469 – 473



Role of succinyl choline in head injury

• Based on these findings succinyl choline should

not necessarily be withheld in emergency airway

situations

• Rocuronium, is an excellent alternative because of

its rapid onset of action and lack of effect onintracranial dynamics.



Intracerebral bleeding after penetration of NG tube

in to the brain



Gastric drain tubes

• A large-bore oral gastric tube is inserted after

intubation, and gastric contents are initially

aspirated and then passively drained during the

operation.

• Nasal gastric tubes are avoided because of the

potential presence of a basilar skull fracture



Invasive monitoring

• Priority is to open the cranium as rapidly as possible

• After achieving IV access, the craniotomy should never be

delayed significantly by line placement.

• Arterial BP monitoring is essential

• The decision to achieve central venous access can be

based on the patient's hemodynamic status.

• ICP monitoring is mainly used in head injured patients

undergoing non neurological surgeries



Effect of hypotension in the outcome

• Chestnut et al prospectively investigated the impact onoutcome of hypotension and hypoxia as secondary brain

insults from 717 severe head injury cases(GCS score < or

= 8) in the Traumatic Coma Data Bank . J Trauma 1993; 34:

216 –

22

• Hypoxia and hypotension were independently associated

with significant increases in morbidity and mortality from

severe head injury.

• Hypotension was profoundly detrimental, occurring in

34.6% of these patients and associated with a 150%

increase in mortality.



Appropriate blood pressure ?

• Edingurgh concept

– The most commonly held concept emphasizes low

postinjury CBF, impaired autoregulation, and the

necessity to support CPP ( [MAP] — [ICP]) to 70mmHg.

– But the Brain Trauma Foundation found the data

insufficient to justify establishing 70 mm Hg as a

"standard" CPP target, but instead identified it as areasonable management "option"




• The " Lund concept" emphasizes the contribution of

hyperemia to the occurrence of elevated ICP. That

approach uses antihypertensive agents to reduce blood

pressure while maintaining CPP over 50 mm Hg

• Because of the later demonstration that a negative fluid

balance in patients with TBI is deleterious over time the

Lund proponents have modified their approach, and now"a CPP of 60 – 70 is considered




• The " Birmingham" concept, entails

pharmacologically induced hypertension.

• This approach is based on the belief that autoregulation islargely intact and that hypertension will result in cerebral

vasoconstriction with concomitantly reduced CBV and

ICP

• But it has not been applied widely, and others have

reported that induced hypertension was either ineffective

or deleterious as a means of reducing increased ICP



FLUID MANAGEMENT.

• Choice of resuscitation fluid – Never ending

debate

• Relatively isotonic crystalloids RL and NS have

been used for many years

• The main principles of fluid management for

neurosurgical anesthesia are – (1) maintenance of normovolemia and

– (2) avoidance of a reduction in serum osmolarity



RL vs NS

RL

• Osmolarity is only

273mOsm/L

• Large volumes ↑ serumosmolarity and total brain

water

NS

• Osmolarity of NS is

308mOsm/L

• Large volumes can causehyperchloremic metabolic

acidosis

Therefore, in the setting of large-volume fluidadministration, such as significant blood loss and

multiple trauma, it is reasonable to alternate, liter by

liter, LR and NS.



Colloids in TBI

• Despite all favourable characteristics

metaanalyses suggest that the use of colloids may

be associated with increased mortality.

• Abnormal clotting profile with larger volumes



Colloids in TBI

• Colloid solutions do not reduce ICP or cerebral water

content.

• It is the osmolality, rather than the plasma oncotic pressure, that is the major determinant of water movement

between the compartments where the blood-brain barrier

is intact.

• Zhuang, et al. Colloid infusion after brain injury. Crit Care Med

1995;23,140-148

• Kaieda et al. Acute effects of changing plasma osmolality and colloid

oncotic pressure on the formation of brain edema after cryogenic

injury. Neurosurgery 1989;24,671-678



SAFE trial

• The Saline versus Albumin Fluid Evaluation (SAFE)

study compared the effect of fluid resuscitation with

albumin or saline on mortality in a heterogeneous

population of patients in ICUs.

• In a retrospective study of a subset of patients containing

460 critically ill patients with traumatic brain injury, fluid

resuscitation with albumin was associated with highermortality rates than was resuscitation with saline (33.2%

vs 20.4%) at 24 months. N Engl J M ed 2007;357:874-84 .



Role of hypertonic saline

• In recent years, small volume resuscitation by means of

hypertonic saline infusion has gained attention because of

its beneficial effects on the restoration of hemodynamic

variables and microcirculatory improvements.

• Hypertonic saline solution has a number of beneficial

effects in head-injured patients, including

– the extraction of water from the intracellular space,

– a decrease in the ICP

– the expansion of intravascular volume

– increase in cardiac contractility



Hypertonic saline

Improved

hemodynamicsvasoregulation

Decreased

Cerebral edemaCellular

modulation

Increased

Cerebral

perfusion

Decreased

ICP

Avoiding secondary

injury



Hypertonic saline in head injury

• Wade and colleagues performed a metaanalysis of 6

prospective, randomized, double-blind trials to evaluate

the effect on survival after initial treatment with

hypertonic saline solution in patients with TBI.

• These authors concluded that hypertonic saline solution

significantly improved survival.(27 to 38%) compared to

the standard therapy. J Trauma 1997;42(5 Suppl) ,S61-S65



Hypertonic saline in head injury

• A recent double-blind, RCT of 229 patients with TBI andhypotension a rapid infusion of either 250 mL of 7.5%

saline or RL solution : Neurological function at 6 months,

measured by the extended Glasgow Outcome Score

(GOSE) showed no significant difference between the

groups in the outcome. JAMA. 2004 Mar 17;291(11):1350-7.

• HTS is also used for resuscitation in combination with

hypertonic colloids (usually dextran 70) to increase

duration of effect.

• However, the combinations are more expensive and in a

randomized comparative 4-group trial, highest survival

rates were achieved with HTS alone.



Brain trauma foundation guidelines

• For pre hospital fluid resuscitation

• Hypotension should be resuscitated with isotonic

fluids

• Hypertonic resuscitation is a treatment option for

TBI patients with GCS < 8.

• Guidelines for the Prehospital Management of Severe TraumaticBrain I njury, Second Edition 2007 Brain trauma foundation.



Role of hypothermia

• The two potential applications of hypothermia in

severe brain injury are

– control of refractory elevated intracranial pressure and

– as a neuro protectant in preventing secondary braininjury

• Much of the clinical literature tests the effect of

hypothermia on control of elevated ICP and

consistently reports its effectiveness



Role of hypothermia

• As a neuroprotectant

– Although initial studies of hypothermia suggested an

improved outcome , more recent studies failed to

demonstrate a benefit

– Henderson et al. Hypothermia in the management of traumatic

brain injur y. A systematic review and meta-analysis. Intensive

Care Med 2003, 29:1637 – 1644 . An analysis of pooled data

from 748 patients in eight RCTs finds the lack of

strong evidence of hypothermia benefit.



Lack of effect of induction of hypothermia

after acute brain injury

• 392 patients with coma after sustaining closed head

injuries were randomly assigned to be treated with

hypothermia (33°C), initiated within 6 hours after injury

and maintained for 48 hours by means of surface cooling,

or normothermia.

• Mortality was 28 percent in the hypothermia group and 27

percent in the normothermia group .

• Clifton GL, et al.. N Engl J Med 2001; 344:556 – 563.



Treatment window in hypothermia

• Two studies on cardiac arrest with hypothermia as aneuroprotectant in brain injury have found hypothermia to

32° – 34°C for 12 or 24 hours, respectively, resulted in

significantly better neurologic outcomes.

• The cardiac arrest protocols differed from the brain injury

protocols, however, in that hypothermia induction was

begun within 60 minutes of cardiac arrest.

• Bernard SA, et al.: Treatment of comatose survivors of out-of-hospital

cardiac arrest with induced hypothermia. N Engl J Med 2002,

346:557 – 563. This study of 77 patients who remained unconscious

after cardiac arrest reports improved outcomes with early

hypothermia induction.



Treatment window in hypothermia

• The earliest that hypothermia induction was begun in

brain injury studies was 4 hours after injury in the

multicenter trial with induction 8 – 24 hours after injury in

other trials.

• In the laboratory, hypothermia must be induced in less

than 1 hour after experimental brain injury to have any

neuroprotective effect.



Role of hyperventilation in brain injury

• Hyperventilation has long been a standard component of

the management of TBI patients perceived to be at risk for

increased ICP.

• In a multi centre trial of 275 patients with supratentorial

brain tumors, intraoperative hyperventilation improved

surgeon-assessed brain bulk which was associated with a

decrease in ICP.

• (Anesth Analg Feb 2008;106:585 – 94)



Can hypocarbia produce cerebral vasoconstr iction

suff icient to cause ischemia ?

• Animal studies and clinical electro physiologic data have

not supported that hypocarbia causes cerebral ischemia in

normal brain.

• Animal studies have again demonstrated ischemic injury

when hypocarbia is associated with anemia, hypotension

or brain retraction.

• There is growing evidence that hypocarbia may be

associated with worsened long term outcome in head

trauma patients.



Indications for hyperventilation

• Two relative indications for the use of hyperventilation

include

– acute increases in ICP

– need to improve surgical exposure

• Hyperventilation should be used with the knowledge that

it has the potential for causing an adverse effect, and it

should be withdrawn as the indication for it subsides.

• In particular, it is now widely avoided in the management

of SAH because of the postictal low-CBF state that is

known to occur.



Continuing management in the ICU

• Monitoring in the ICU

– Intraventricular catheters are preferred when possible,

as these allow for continuous measurement of ICP and

for drainage of CSF to control raised ICP.

– Evidence support a level 3 recommendation for

jugular venous saturation and brain tissure oxygen

monitoring in addition to ICP monitoring in patientswith traumatic brain injury.



Management of ICP in head injury

• addenbrookes protocol.pdf

• Please find the addenbrookes protocol in BJA

July 2007 in Intensive care management of TBI

patients.

http://localhost/var/www/apps/conversion/tmp/scratch_9/addenbrookes%20protocol.pdf

http://localhost/var/www/apps/conversion/tmp/scratch_9/addenbrookes%20protocol.pdf




• Hyperosmolar therapy

– Mannitol, an osmotic diuretic, is commonly employed

and the immediate efficacy is likely to result

– from a plasma-expanding effect and – improved blood rheology due to a reduction in

haematocrit.

– reduces cerebral oedema by drawing water across areas

of intact blood – brain barrier (BBB) into the vascularcompartment.




• Hyperosmolar therapy

– Repeated administration of mannitol is problematic

because serum osmolarity .320 mOsm /litre is

associated with neurological and renal side-effects. – Other potential complications

• Mannitol

• severe intravascular volume depletion,

• hypotension, and• Hyperkalemia

• possibly a rebound increase in ICP.




• Hypertonic saline is increasingly used as an alternative to

mannitol.

• It is available in a range of concentrations from 1.7% to

29.2%

• The optimal dose or concentration required to control ICP

is not established

• Hypertonic saline has proven efficacy in controlling ICP

in patients refractory to mannitol.

• Other advantages over mannitol include its effectiveness

as a volume expander, without hyperkalemia and impaired

renal function.




• Haemodynamic support

– TBI patients are prone to haemodynamic instability for

a number of reasons.

– Maintenance of haemodynamic stability is essential to

the management of severe TBI as the injured brain

may lose the capacity for vascular autoregulation,.

– Hypotension must be avoided at all costs as it causes a

reduction in cerebral blood flow and hypertension can

exacerbate vasogenic oedema




• Haemodynamic support

– Intravascular volume should be maintained targeting a

central venous pressure of 5 – 10 mmHg.

– If an adequate BP not achieved – vasopressors – Before ICP monitoring is instituted, hypertension

should not be treated unless MAP is above 120 mm Hg

because the high BP may be maintaining CBF.

– For the treatment of hypertension, an infusion of shortacting betablockers should be titrated against BP.




Sedation and analgesia• Head-injured patients require analgesia and sedation as

they still respond to painful and noxious stimuli, often

with an increase in ICP and BP.

• Narcotics (morphine or fentanyl) - first-line therapy sincethey provide both

– analgesia and

– depression of airway reflexes

• Propofol - hypnotic agent of choice with an acute

neurologic insult,

– as it is easily titratable and rapidly reversible.

– additional cerebral protective properties




Paralysis

• No data to support this practice.

• Patients with TBI, paralytic agents have been

demonstrated to

– increase the risk of pneumonia.

– be associated with significant neuromuscular

complications.

• Paralysis may be helpful in preventing ventilator

dyssynchrony that produce ICP surges while

initiating ventilatory support.




• Ventilatory settings

– The ventilator settings should be adjusted to maintain

the PaCO2 between 35 - 40 mm Hg and the PaO2 > 70

mm Hg.

– The lowest level of PEEP that maintains adequate

oxygenation and prevents end-expiratory alveolar

collapse should be used. ( BTF recommendation 2007 )

– Although endotracheal suctioning does cause a

transient rise in ICP, it does not produce cerebral

ischemia and is required to prevent atelectasis




• Routine stress ulcer prophylaxis is required.

• Seizure prophylaxis is currently recommended for 7 days

following the injury in patients with severe TBI.

• The agent most commonly recommended is phenytoin,

– loading dose of 18 mg/kg

– maintenance dose of 5 mg/kg/d – serum drug levels 10 to 20 mg/L.




• Electrolyte Derangements

– Hyponatremia is relatively common after head injury.

– Hyponatremia lowers the seizure threshold and can

exacerbate cerebral edema.• The etiology is complex

» cerebral salt wasting syndrome

» SIADH syndrome

– Hypomagnesemia lowers the seizure threshold, and in

experimental brain injury hinders recovery.




• Nutritional Support

– TBI results in a generalized hypermetabolic and

catabolic state.

– A meta-analysis that compared early (within 36 h) with

delayed initiation of enteral nutrition demonstrated a

55% reduction in the risk of infections in head-injured

patients who received early enteral nutrition.

– Although gastric emptying is frequently impaired

following TBI,this route of feeding is generally well

tolerated in head-injured patients.




• Deep vein thrombosis

– The incidence of DVT in patients with major head

injuries who are not on thromboprophylaxis is reported

to be high as 54%.

– Low-dose heparin and low-molecular-weight heparin

are considered to be contraindicated in patients with

head injuries.

– Sequential compression devices should be used (if

possible) in all patients with TBI.



Thank you

www.anaesthesia.co.in [email protected]





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