Presentation on theme: "Anesthetic and Intensive care management of Head injury"— Presentation transcript:
1Anesthetic and Intensive care management of Head injury Prof .PawarDr AbrahamDr Mani
2Surgery for head injury Craniotomies will most commonly be performed for the evacuation ofsubdural,epidural andintracerebral hematomas.The anesthetic approach is similar for all three.
3The major goals of anesthetic management Avoid secondary brain damageThe 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 injuryOptimize cerebral perfusion and oxygenationProvide adequate surgical conditions for the neurosurgeons.
4Induction 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 thatthese patients often have a full stomach,decreased intravascular volume, anda potential cervical spine injury
5Techniques of intubation Awake / sedated nasal intubationcontraindicationsSkull base fractures, Le Forte fracturesBleeding diathesisFibreoptic intubationLimitationsCooperation, Specialized trainingDifficulty in the presence of blood, secretionsDirect laryngoscopy with manual inline stabilisationSurgical airway – if intubation fails
6Direct laryngoscopy with manual inline stabilisation
7Induction of anesthesia Rapid sequence induction may be desirable in hemodynamically stable patientsThiopentone, propofol and etomidate have been used safely to induce anesthesia.Cardiovascular depression with thiopentone and propofol is a concern in the presence of uncorrected hypovolemiaIn hemodynamically unstable patients, the dose of induction drugs is substantially decreased or even omitted
8Induction of anesthesia Role of etomidateUnlike 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:Should etomidate be the induction agent of choice for rapid sequence intubation in the emergency department? Emerg Med J Nov;21(6):655-9.Adrenal suppression ?
9Role of ketaminePET 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.
10Role 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
11Role of succinyl choline in head injury Based on these findings succinyl choline should not necessarily be withheld in emergency airway situationsRocuronium, is an excellent alternative because of its rapid onset of action and lack of effect on intracranial dynamics.
12Intracerebral bleeding after penetration of NG tube in to the brain
13Gastric drain tubesA 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
14Maintenance of anesthesia Inhaled anesthetics - The order of vasodilating potency is approximately halothane ≫ enflurane > isoflurane > desflurane > sevofluraneAlthough 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.
15Invasive monitoringPriority is to open the cranium as rapidly as possibleAfter achieving IV access, the craniotomy should never be delayed significantly by line placement.Arterial BP monitoring is essentialThe 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
16Effect 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: 216–22Hypoxia 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.
17Appropriate blood pressure ? Edingurgh conceptThe 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"
18Appropriate 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 HgBecause 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
19Appropriate 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 ICPBut 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
20FLUID MANAGEMENT. Choice of resuscitation fluid – Never ending debate Relatively isotonic crystalloids RL and NS have been used for many yearsThe main principles of fluid management for neurosurgical anesthesia are(1) maintenance of normovolemia and(2) avoidance of a reduction in serum osmolarity
21RL vs NS RL Osmolarity is only 273mOsm/L Large volumes ↑ serum osmolarity and total brain waterNSOsmolarity of NS is 308mOsm/LLarge volumes can cause hyperchloremic metabolic acidosisTherefore, 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.
23Colloids in TBIDespite all favourable characteristics metaanalyses suggest that the use of colloids may be associated with increased mortality.Abnormal clotting profile with larger volumes
24Colloids in TBIColloid 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,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,
25SAFE trialThe 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:
26Role 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, includingthe extraction of water from the intracellular space,a decrease in the ICPthe expansion of intravascular volumeincrease in cardiac contractility
28Hypertonic 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
29Hypertonic 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 Mar 17;291(11):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.
30Adverse effects of hypertonic saline The primary concerns with the use of HTS are the potential forHypernatremiaosmotic demyelination syndrome (ODS),Pulmonaryedema, CCF, acute renal insufficiencyRebound brain edemahematologic abnormalities including increased hemorrhage, coagulopathy, and red cell lysis.
31Brain trauma foundation guidelines For pre hospital fluid resuscitationHypotension should be resuscitated with isotonic fluidsHypertonic 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.
32Role of hypothermiaThe two potential applications of hypothermia in severe brain injury arecontrol of refractory elevated intracranial pressure andas a neuro protectant in preventing secondary brain injuryMuch of the clinical literature tests the effect of hypothermia on control of elevated ICP and consistently reports its effectiveness
33Role of hypothermia As a neuroprotectant Although initial studies of hypothermia suggested an improved outcome , more recent studies failed to demonstrate a benefitHenderson 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.
34Lack 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.
35Treatment 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.
36Treatment 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.
37Role 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)
38Can 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.
39Indications for hyperventilation Two relative indications for the use of hyperventilation includeacute increases in ICPneed to improve surgical exposureHyperventilation 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.
40Continuing management in the ICU Monitoring in the ICUProtocols 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: 547–53BTF recommends ICP monitoring in salvageable patients with traumatic brain injury with GCS of 3-8 and abnormal CT scanGuidelines for the Management of Severe Traumatic Brain Injury, third Edition 2007
41Continuing management in the ICU Monitoring in the ICUIntraventricular 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.
42Management of ICP in head injury addenbrookes protocol.pdfPlease find the addenbrookes protocol in BJA July 2007 in Intensive care management of TBI patients.
43Management of ICP in head injury Hyperosmolar therapyMannitol, an osmotic diuretic, is commonly employed and the immediate efficacy is likely to resultfrom a plasma-expanding effect andimproved 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.
44Management of ICP in head injury Hyperosmolar therapyRepeated administration of mannitol is problematic because serum osmolarity .320 mOsm /litre is associated with neurological and renal side-effects.Other potential complicationsMannitolsevere intravascular volume depletion,hypotension, andHyperkalemiapossibly a rebound increase in ICP.
45Continuing 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 establishedHypertonic 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.
46Management of ICP in head injury Barbiturate comaMany clinical studies have demonstrated that barbiturate coma can effectively lower ICPThe 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.
47Continuing management in the ICU Haemodynamic supportTBI 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
48Continuing management in the ICU Haemodynamic supportIntravascular volume should be maintained targeting a central venous pressure of 5–10 mmHg.If an adequate BP not achieved – vasopressorsBefore 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.
49Continuing management in the ICU 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 since they provide bothanalgesia anddepression of airway reflexesPropofol - hypnotic agent of choice with an acute neurologic insult,as it is easily titratable and rapidly reversible.additional cerebral protective properties
50Continuing management in the ICU ParalysisNo data to support this practice.Patients with TBI, paralytic agents have been demonstrated toincrease 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.
51Continuing management in the ICU Ventilatory settingsThe ventilator settings should be adjusted to maintain the PaCO2 between 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
52Continuing 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/kgmaintenance dose of 5 mg/kg/dserum drug levels 10 to 20 mg/L.
53Continuing management in the ICU Electrolyte DerangementsHyponatremia is relatively common after head injury.Hyponatremia lowers the seizure threshold and can exacerbate cerebral edema.The etiology is complexcerebral salt wasting syndromeSIADH syndromeHypomagnesemia lowers the seizure threshold, and in experimental brain injury hinders recovery.
54Continuing management in the ICU Electrolyte DerangementsHyponatremia is relatively common after head injury.Hyponatremia lowers the seizure threshold and can exacerbate cerebral edema.The etiology is complexcerebral salt wasting syndromeSIADH syndromeHypomagnesemia lowers the seizure threshold, and in experimental brain injury hinders recovery.
55Continuing management in the ICU Nutritional SupportTBI 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.
56Continuing management in the ICU Deep vein thrombosisThe 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.