Head Injury in Adults

CASE
"A twenty four year old male involved in a road traffic accident was unconscious at the scene. Hewas intubated and ventilated prior to transfer to the emergency department where a cranial CTscan revealed an acute subdural hematoma. Secondary survey confirmed that there were noother significant injuries. The patient underwent craniotomy for evacuation of the hematoma andwas transferred to the neurosurgical ICU for postoperative monitoring and management. Over the next few days he developed intracranial hypertension and severe respiratory and cardiovascular instability. "


Objectives:

1. To Understand the important issues during resuscitation of a patient with a severe traumatic brain injury.

2. To Be aware of the monitoring techniques that may assist clinicians in managing patients with severe traumatic brain injury on the ICU.

3. Understand the causes of elevated intracranial pressure in a patient following evacuation of an intracranial hematoma and be aware of the treatment options.

4. Understand the relative merits of cerebral perfusion and intracranial pressure guided therapy and be aware of the potential disadvantages of each.

5. Be aware of the potential causes of systemic complications after severe traumatic brain injury and understand the potential management challenges.

Resuscitation:

Resuscitation after traumatic brain injury (TBI) should begin in the pre-hospital phase and is a key stage at which mortality and morbidity can be influenced. The primary goal of management is the prevention, recognition and treatment of conditions known to cause secondary brain injury, including identification and evacuation of surgically remedial compressive lesions and prevention of secondary systemic insults. The importance of cardiopulmonary stabilization cannot be overemphasized because the risk of secondary brain injury begins and continues from the moment of trauma. Consensus guidelines for the management of TBI have been issued.
Because of the well-established association between hypoxemia and worsened outcome after severe TBI, all patients should be intubated to allow controlled ventilation. During intubation the cervical spine must be protected with manual in-line immobilization because of the associated risk of cervical injury. Oral endotracheal intubation should be carried out following administration of an intravenous anaesthetic agent (thiopental, propofol or etomidate are appropriate choices), in a dose calculated to minimize the intracranial pressure (ICP) response to laryngoscopy whilst maintaining cardiovascular stability. A full stomach should be assumed and a rapid sequence induction is mandatory with placement of an oro-gastric tube post-intubation to decompress the stomach and prevent acute gastric dilatation. The use of succinylcholine in TBI remains controversial, although the benefits of rapid and full relaxation to facilitate expeditious airway control are likely to outweigh the potential disadvantages of a small and transient increase in ICP. Once the airway has been secured, mechanical ventilation should be commenced to maintain PaO2 > 13.5 kPa and PaCO2 between 4.0 - 4.5 kPa. Hypotension should be rapidly treated with volume replacement to maintain mean arterial blood pressure > 90mmHg.
Standard resuscitation fluids include iso-osmolar crystalloid and/or colloid solutions and blood products. The superiority of colloid or crystalloid for fluid replacement has not been resolved, although there is no advantage of one fluid over another in experimental models of head injury. However, glucose containing solutions should be avoided to minimize the risk of hyperglycemia. Volume resuscitation using hypertonic saline (HS) has been associated with lower ICP than resuscitation with crystalloid or colloid, but a clear benefit on outcome has not
yet been demonstrated in clinical studies . Following adequate volume resuscitation, the hypotensive effect of sedative agents may require additional support with modest doses of vasopressors or inotropes. In adults, hypotension is rarely caused by closed head injury alone and another injury site should be sought by a detailed secondary survey. Life-threatening extracranial injuries should be treated prior to definitive neurosurgical treatment but it is sufficient simply to stabilize non-life threatening injuries.
Intracranial hypertension is present in around 50% of comatose head-injured patients and, prior to placement of an ICP monitor, it must be assumed that ICP is elevated. This may be temporarily controlled in the acute phase using standardmethods such as moderate head-up position, sedation and controlled ventilation. Mannitol (0.5-1.0 g/kg) is also indicated if there are signs of herniation or other neurological deterioration.

Monitoring on the ICU:

The aim of the intensive care management of head-injured patients is to anticipate, prevent and treat secondary physiological insults. Specialist neurocritical care, with ICP and cerebral perfusion pressure (CPP) guided therapy as part of a multi-faceted strategy of neuroprotection, is likely to improve outcome after TBI . The measurement of ICP is the cornerstone of modern neurocritical care and the indications for ICP monitoring after TBI are well established . ICP monitoring allows measurement of CPP and detection of abnormal ICP waveforms that occur due to phasic increases in ICP triggered by cerebral vasodilatation in response to a reduction in CPP. Transcranial Doppler ultrasonography (TCD) measures blood flow velocity in the middle cerebral artery and may be used to assesscerebral autoregulation and provide a non-invasive assessment of CPP. Because knowledge of actual CPP does not confirm its adequacy in a particular patient, the simultaneous measurement of cerebral oxygenation is valuable in the management of patients with severe TBI. Regional and global changes in cerebral hemodynamics and oxygenation occur
frequently after head injury and often go undetected by standard monitoring techniques . Positron emission tomography and magnetic resonance imaging/spectroscopy offer ‘gold standard’ measurement of both focal and global ischemic burdens but are not available routinely in many units. Furthermore, they are neither continuous nor bedside techniques. Jugular venous oxygen saturation (SjO2) monitoring is a bedside measure of the balance between cerebral oxygen supply and demand and may be used to guide therapy. Jugular venous desaturation is a useful indicator of inadequate CPP and SjO2 < style="font-weight: bold;">
Intracranial hypertension

Intracranial hypertension occurs in 50-70% of patients after evacuation of an intracranial hematoma . Surgically remedial causes of elevations in ICP should be excluded by prompt CT scanning and include post-operative hematoma, progressive focal contusions or hydrocephalus. Other causes of intracranial hypertension include diffuse brain swelling, seizures or systemic complications. Although there are no class 1 data, several clinical studies demonstrate that treatment of ICP > 20 mmHg reduces mortality and improves outcome. Sedation is an essential part of the management of severe TBI and propofol is widely used because its favorable pharmacological profile allows easy titration of sedation levels and rapid
wake-up. Propofol, in common with other iv anesthetic agents except ketamine, which should be avoided, causes a dose-dependant reduction in cerebral metabolic rate, CBF and ICP. Although the routine use of barbiturates in unselected patients does not reduce morbidity, they do have a place in the management of refractory intracranial hypertension so long as treatment-related hypotension is avoided . Neuromuscular blocking drugs have no direct effect on ICP but may prevent rises that are caused by coughing or straining on an endotracheal tube. Prolonged use is associated with an increased risk of pulmonary complications and increased length of ICU stay after TBI.
Hyperventilation was once the cornerstone of ICP control after TBI but empirical and excessive hyperventilation is associated with adverse neurological outcome . Moderate hyperventilation to PaCO2 < style="font-weight: bold;">
ICP vs CPP directed therapy

Over the last decade there has been a shift of emphasis from primary control of ICP to a multifaceted approach of maintenance of CPP and brain protection. Maintenance of an adequate CPP, either by a reduction ICP or an increase in mean arterial pressure, is the primary focus of treatment after TBI, although the CPP target remains the subject of debate . Aggressive fluid replacement and cardiovascular support with vasopressors and inotropes to augment mean arterial pressure and maintain CPP > 70 mmHg reduces mortality and improves outcome after severe TBI . Although this strategy is associated with a reduction in secondary cerebral ischemia, the mortality and morbidity is similar to other treatment options because of the high incidence of systemic (particularly respiratory) complications . There is now a substantial body of data to justify a CPP target of > 60 mmHg in most cases , but optimal CPP should be determined individually for each patient and situation . Both ICP and CPP-directed strategies have a role if applied appropriately and multi-modality monitoring guides tailored therapy.

Systemic complications

Acute lung injury (ALI) is common after TBI and occurs secondary to direct pulmonary injury, aspiration injury, neurogenic pulmonary edema and as a complication of treatment . Pneumonia occurs in over 40% of patients and usually presents some days after injury. Significant cardiovascular complications may also occur and include cardiac arrhythmias, neurogenic hypertension and myocardial ischemia. Supraventricular tachycardia, sinus bradycardia, heart block and repolarization abnormalities, such as T-wave inversion and alterations in the S-T segment, are common features. Myocardial ischemia occurs in about 50%
of patients after severe TBI and is likely to be related to hyperstimulation of the sympathetic nervous system . This acute, usually reversible, cardiac injury ranges from hypokinesis with normal cardiac index to low output cardiac failure. Endocrine disturbances, related to both anterior and posterior pituitary insufficiency, may contribute to cardiovascular instability in some patients. Management of systemic complications presents a significant challenge because established ventilatory strategies for the management of ALI may be inappropriate in some brain-injuredpatients. The prone position(?) and permissive hypercapnea are both contraindicated in the presence of intracranial hypertension and fluid restriction to reduce alveolar edema is in conflict with the requirement to maintain cerebral perfusion. The classic teaching of no or low level positive end expiratory pressure (PEEP) to prevent rises in ICP is no longer appropriate because ventilation without PEEP often fails to correct hypoxemia. With adequate volume resuscitation PEEP <10cmH20 does not increase ICP and may in fact result in a decrease because of improved cerebral oxygenation . Hemodynamic instability is a common feature after severe TBI and the initial hyperdynamic phase is often followed by hypotension refractory to fluid resuscitation and catecholamine vasopressors. Such patients may respond to low-dose vasopressin infusion. Good neurologic outcome depends upon the prevention of hypoxemia and hypotension at all stages of management and invasive monitoring, full investigation and appropriate intervention are required early to optimize cardiorespiratory function and minimize the risk of secondary
ischemic injury after TBI.

BRONCOSCOPY : SIMULATOR

Trans Cranial Doppler (TCD)

APPLICATIONS OF
TRANSCRANIAL DOPPLER ULTRASOUND
IN NEUROANESTHESIA

CONTENTS

1. Doppler ultrasound in medicine
2. Cerebral hemodynamics: physical principles and physiological factors
3. Techniques examining cerebral hemodynamics
4. Anesthetics and cerebral hemodynamics
5. TCD: Transcranial Doppler ultrasonography
6. History
7. Physical principles of Doppler and spectral analysis
.1. The Doppler effect
.2. The Doppler equation
8. Examination techniques
8.1. Window search
.2. Artery identification
.3. Normal values
.4. Doppler parameters
.5. Cerebral arterial blood flow velocity and cerebral blood flow
9. Transcranial Doppler in Neuroanesthesia
10. Refereneces

Craniosynostosis

3-Month-Old Boy With Sagittal Craniosynostosis : Learning Points


1. Preoperative workup of an infant undergoing craniofacial surgery.
2. Relative risks for performing the repair at an early age.
3. Different surgical approaches and respective anesthetic management of
sagittal craniosynostosis 4. Anesthetic management of the infant 5. Rationale for administering fluids and blood products in infants.
6. Management of venous air embolism in infants.


Case: 3-month-old boy with sagittal craniosynostosis is scheduled for a surgical
repair of his defect.

Preoperative Evaluation:

1. What significant preexisting issues in a 3 month old boy presenting for
craniofacial surgery?
2. What are the inherent risks of early versus late correction of sagittal
craniosynostosis?
3. What are the different types of sagittal craniosynostosis? What are the significant
issues affecting the conduct of anesthesia?

The surgeon decides to perform an anterior pi procedure.
Anesthetic management issues:

1. How would you induce anesthesia on this infant?
2. What monitors are essential for the pi procedure? Would you apply the same
monitors if an open or endoscopic-assisted strip craniectomy were performed?
3. What are your end-points for fluid administration?


After induction of anesthesia and placement of monitors, the infant’s vital sign are, BP 68/30, HR 120, esophageal temperature of 36.4°C. During the craniotomy the surgeon notes increased blood loss. At the same time the blood pressure falls to 42/20.


1. What is your differential diagnosis for this sudden change? How would you
confirm your diagnosis?
2. What would be your therapeutic maneuvers?
3. Your arterial catheter fails to provide an arterial trace and you are unable to draw
a blood sample for measuring the hematocrit. What will be your triggers for fluid
and blood administration?


The infant is now hemodynamically stable, however his hematocrit is now 24%.
After the closure of the scalp incision, the surgeon would like to perform a
neurological examination at the conclusion of the surgery.


1. Would you administer blood to this infant? If the hematocrit is 22% at the end of
the surgery would you administer blood before leaving the operating room?
2. What are you criteria for extubating the infant’s trachea?
3. Does this infant need to be admitted to the intensive care unit?Sagittal Craniosynostosis


Craniosynostosis results from premature fusion of one of or a combination of cranial sutures in an infant. Although majority of craniosynostosis are solitary deformities with an incidence of 1 in 2100 children, craniofacial syndromes include some form of premature fusion of cranial sutures. Sagittal craniosynostosis is the most common form and represents 40-60% of nonsyndromic craniosynostosis. Since brain growth occurs rapidly in the in utero to the third year of life, the restrictive nature of this defect can lead to; impaired brain growth1, increased intracranial pressure, and psychologically devastating craniofacial deformities.2,3 Since all three progressively worsens with age, repairs of craniosynostosis are likely to have the best result if done early in life.1
However, these procedures are associated with loss of a significant percentage of an
infant’s blood volume, with great losses occurring when more sutures are involved.4
However, the physiologic nadir of the infant’s hematocrit is around 3 month, thus
decreasing the reserve for blood loss and increasing the necessity for blood transfusions.
Furthermore, there appears to be increased morbidity and mortality associated with
younger infants undergoing surgery due to undiagnosed congenital anomalies and
inadvertent anesthetic overdoses.5 Several surgical approaches for repair of sagittal craniosynostosis have been advocated. The most common is a sagittal strip craniectomy where the fused sagittal suture is resected. Jimenez and Barone have recently modified this approach by applying endoscopic surgical techniques, thus minimizing blood loss and extensive surgical dissection and exposure.6,7 Jane and colleagues advocate a more extensive complex vault remodeling (CVR) by proposing a pi procedure, which entails a pi shape craniectomy with extensive remodeling of the adjacent cranial plates.
Perioperative Blood Loss
Several investigators have reported the effect of the surgical procedure on blood
loss. Kearney and colleagues reported that sagittal craniectomies were associated with a mean blood loss of 24% of the estimated blood volume (EBV) or 20 ml/kg. Meyer and colleagues estimated a mean blood loss of 60±24.5% of EBV in strip craniectomies and 170.6±10.3% of EBV in CVR.8 They also reported postoperative blood loss of
35.9±38.4% and 44.5±97.6% of EBV for strip craniotomies and CVR respectively.
Faberowski and Black confirmed that simple strip craniectomies have substantially less blood loss than more extensive strip craniectomies with osteotomies and remodeling of the adjacent cranial plates.9 Furthermore, they reported that 96.3% of their patients received a blood transfusion. Rapid blood transfusion in an infant can result in hyperkalemia and cardiac arrest, primary due to high concentration of potassium in stored blood.10,11 Furthermore, coagulopathy is associated with blood loss approaching 1.5 times EBV.12 Given the inherent risks of blood transfusion, several investigators have advocated the use of autologous blood transfusion and induced hypotension.13-16 However, induced hypotension may not be suitable in infants because of the potential for venous air embolism and sudden hemorrhage.
Venous Air Embolism
Venous air embolism (VAE) detected by echocardiography and precordial
Doppler occurred in 66% to 83% of open craniectomies in infants.4,17 A precordialDoppler ultrasound can detect minute VAE and should be routinely used in conjunction with an end-tidal carbon dioxide analyzer and arterial catheter in all craniotomies to detect VAE. The Doppler probe is best positioned on the anterior chest, usually just to the right of the sternum at the fourth intercostal space. An alternate site on the posterior thorax can be used in infants weighting approximately 6 kg or less.18 Other monitors for VAE include, sudden drops in end-tidal CO2 and dysrrhythmias and/or ischemic changes in the electrocardiogram. Fortunately, direct morbidity and mortality rarely occur and the issue of Doppler monitoring has been challenged by Meyer.19 Recently, Tobias reported an 8% incidence of VAE during endoscopic-assisted strip craniectomies.20 Standard neurosurgical techniques may elevate the head of the table to improve cerebral venous drainage, which can increase the risk for air entrainment into the venous system through open venous channels in bone and sinuses.21 Patients with cardiac defects and potential for left to right shunt, such as patent foramen ovale or ductus arteriosus are at risk for paradoxical air emboli through these defects. Venous air emboli can be minimized by early detection with continuous precordial Doppler ultrasound and maintaining euvolumia. Therefore, induced hypotension should be avoided. When hemodynamic instability does occur, the operating table can be placed in the Trendelenburg position, flooding the surgical field with warm saline and sealing the sites of egress with bone wax and direct pressure. These maneuvers will augment the patient’s blood pressure and prevent further entrainment of intravascular air. Routine insertion of central venous
catheters for withdrawal of air is limited by the diminutive size of the infant and catheter because the ability of rapidly aspirate air decreases with the size of the catheter.
Hemodynamic Monitoring
Infants undergoing major craniectomies and CVR are at risk of sudden
hemodynamic instability due to VAE and hemorrhage. The slope of the autoregulatory in
an infant and rises significantly at the lower and upper limits of the curve, respectively. This narrow range, with sudden hypotension and hypertension at either end of the autoregulatory curve, places the infant at risk for cerebral ischemia and intraventricular hemorrhage respectively. Another developmental difference between adults and infants is the larger percentage of cardiac output that is directed to the brain, since the head of the infant and child accounts for a large percentage of the body surface area and blood volume. These factors place the infant at risk for significant hemodynamic instability during neurosurgical procedures and emphasize the importance of continuous blood pressure monitoring. An arterial catheter will also provide access for sampling serial blood gases, electrolytes and hematocrit. The utility of central venous catheterization remains controversial. Cannulation of the jugular or subclavian veins with multi-orificed catheters in adults is preferred, particularly to treat VAE. However, these catheters are too large for infants and most children. Furthermore, monitoring of the central venous pressure may not accurately reflect intravascular volume in small children, particularly in
the prone position. Therefore the risks may outweigh the benefits of a central venous
catheter. In infants, central venous catheter used for aspirating venous air was only
successful 33% of the time, presumably because of the high resistance of the small gauge catheters used in these patients.22
Postoperative Issues
The decision to extubate the infant’s trachea and admission to the intensive care
unit depends on the severity of blood loss and duration of the surgery. Since most of the surgical procedure is localized to the cranium, the airway rarely becomes edematous. Certainly the ability to maintain spontaneous respirations and demonstrate purposeful movement dictates the removal of the endotracheal tube. Postoperative pain can be initially managed with intravenous morphine in monitored settings and rapidly changed to acetaminophen. The major issue in the postoperative period is ongoing blood loss through the drains and incision.8,9 Serial hematocrits should be measured in order to guide additional blood transfusions.


References

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37: 182-8
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Neurosurg. 1998; 88: 209-14
3. Renier D, Lajeunie E, Arnaud E, et al. Management of craniosynostoses. Childs
Nerv.Syst. 2000; 16: 645-58
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craniectomy for craniosynostosis repair. Anesthesiology 2000; 92: 20-3
5. Morray JP, Geiduschek JM, Ramamoorthy C, et al. Anesthesia-related cardiac
arrest in children: initial findings of the Pediatric Perioperative Cardiac Arrest
(POCA) Registry. Anesthesiology 2000; 93: 6-14
6. Jimenez DF, Barone CM: Endoscopic craniectomy for early surgical correction of
sagittal craniosynostosis. J.Neurosurg. 1998; 88: 77-81
7. Jimenez DF, Barone CM, Cartwright CC, et al. Early management of
craniosynostosis using endoscopic-assisted strip craniectomies and cranial
orthotic molding therapy. Pediatrics 2002; 110: 97-104
8. Meyer P, Renier D, Arnaud E, et al. Blood loss during repair of craniosynostosis.
Br.J.Anaesth. 1993; 71: 854-7
9. Faberowski LW, Black S, Mickle JP: Blood loss and transfusion practice in the
perioperative management of craniosynostosis repair. J Neurosurg Anesthesiol.
1999; 11: 167-72
10. Brown KA, Bissonnette B, MacDonald M, et al. Hyperkalaemia during massive
blood transfusion in paediatric craniofacial surgery. Can.J.Anaesth. 1990; 37:
401-8