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Anesthetic and Intensive care management of Head injury
Prof .Pawar
Dr Abraham
Dr Mani
www.anaesthesia.co.in [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 immediate oxygenation 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 used safely 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
Induction of anesthesia
• Role of etomidate
Unlike thiopental and propofol, etomidate reduces ICP without decreasing arterial blood pressure or cerebral perfusion pressure.
• Bergen JM, Smith DC. A review of etomidate for rapid sequence intubation in the emergency department. J Emerg Med 1997;15:221-30.
• Should etomidate be the induction agent of choice for rapid sequence intubation in the emergency department? Emerg
Med J. 2004 Nov;21(6):655-9.
• Adrenal suppression ?
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 injury patients during 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 of nondepolarizing 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 on intracranial 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
Maintenance of anesthesia
– Inhaled anesthetics - The order of vasodilating potency is approximately halothane enflurane > isoflurane > ≫desflurane > sevoflurane
– Although their administration will frequently be consistent with acceptable ICP levels when ICP is out of control or the surgical field is "tight," eliminating the inhaled anesthetics in favor of IV anesthetics is appropriate.
– For patients who are likely to remain tracheally intubated postoperatively, a narcotic - muscle relaxant usually serves well.
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 on outcome 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 70mm Hg.
– 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 a reasonable management "option"
Appropriate blood pressure ?
• 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
Appropriate blood pressure ?
• The "Birmingham" concept, entails pharmacologically induced hypertension.
• This approach is based on the belief that autoregulation is largely 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 ↑ serum osmolarity and total brain water
NS
• Osmolarity of NS is 308mOsm/L
• Large volumes can cause hyperchloremic metabolic acidosis
Therefore, in the setting of large-volume fluid administration, 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 higher mortality rates than was resuscitation with saline (33.2% vs 20.4%) at 24 months. N Engl J Med 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
Improvedhemodynamics
vasoregulationDecreased
Cerebral edemaCellular
modulation
Increased Cerebralperfusion
Decreased ICP
Avoiding secondaryinjury
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 and
hypotension 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.
Adverse effects of hypertonic saline
• The primary concerns with the use of HTS are the potential for
– Hypernatremia
– osmotic demyelination syndrome (ODS),
– Pulmonaryedema, CCF, acute renal insufficiency
– Rebound brain edema
– hematologic abnormalities including increased hemorrhage, coagulopathy, and red cell lysis.
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 Traumatic Brain Injury, 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 brain injury
• 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 injury. 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 hypothermiaafter 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 a neuroprotectant 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 vasoconstriction sufficient 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 – Protocols that incorporate ICP monitoring have shown
better outcome compared to earlier time periods without a protocol.
• Patel HC, Menon DK, Tebbs S et al. Specialist neurocritical care and outcome from head injury. Intensive Care Med 2002; 28: 547–53
– BTF recommends ICP monitoring in salvageable patients with traumatic brain injury with GCS of 3-8 and abnormal CT scan
• Guidelines for the Management of Severe Traumatic Brain Injury, third Edition 2007
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 patients with 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.
Management of ICP in head injury
• 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 vascular compartment.
Management of ICP in head injury
• 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.
Continuing management in the ICU
• 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.
Management of ICP in head injury
• Barbiturate coma– Many clinical studies have demonstrated that
barbiturate coma can effectively lower ICP
– The main disadvantages are two-fold.
• significant episodes of hypotension,
• the prolonged half-life makes clinical assessment difficult after barbiturates are stopped.
– Continuous EEG monitoring can be used to titrate barbiturate therapy and therefore minimize systemic complications.
– There is no good evidence for improved outcome.
Continuing management in the ICU
• 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
Continuing management in the ICU
• 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 short acting betablockers should be titrated against BP.
Continuing management in the ICUSedation 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 since
they 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
Continuing management in the ICU
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.
Continuing management in the ICU
• 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
Continuing management in the ICU
• 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.
Continuing management in the ICU
• 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.
Continuing management in the ICU
• 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.
Continuing management in the ICU
• 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.
Continuing management in the ICU
• 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.
