Heat loss can occur by convection, conduction, radiation and evaporation. Heat loss can be prevented by simple measures: increasing the OR temperature, warming IV fluids (particularly for large volumes), convection warming blankets, humidification of air provided by the ventilator, and heating lamps. It is much easier to prevent heat loss than to warm a patient. Hypothermia may lead to increased metabolic rate and changes in regional blood flow; which may lead to metabolic acidosis and then increased apnea in the neonate or ex-premie. Aseptic precautions must be used when placing intravenous lines and arterial lines, and giving intravenous medications. Communication is vitally important. The anesthesiologist should be aware of the flow of the operative procedure, the order of events and potential complications. Specific anesthetic concerns are summarized in Table 5. Good comminication between the surgeon and anesthesiologist is key to a successful conclusion to the patient's perioperative care.
Premature infants and neonates require intravenous fluids containing glucose because of their poor metabolic control and low glucose and glycogen stores. Concerns regarding hyperglycemia and worsening of cerebral injury in these patients are outweighed by the very real likelihood of hypoglycemia. Lactated Ringer's solution provides sufficient glucose and maintains a balanced salt solution.
1. Routine monitoring includes: pulse oximeter (preductal in a neonate), blood pressure (BP) cuff, EKG, end-tidal carbon dioxide (EtCO2) and temperature.
2. Consider an arterial line for a hemodynamically unstable patient, one with significant comorbid disease, in patients with frequent intraoperative BP or heart rate (HR) changes, or if frequent blood draws or hemat-ocrit checks will be necessary.
3. If venous air embolism (VAE) is a potential risk, a precordial doppler should be placed in the second intercostal space on the patient's right chest wall to detect the characteristic auditory pattern of air in the right atrium (see Table 6).
Table 5. Specific anesthetic concerns by surgical procedure
Airway exam Neurological exam Raised ICP
Associated congenital anomalies
Associated congenital defects Neurological exam Prematurity Latex precautions
Increased intracranial pressure Associated congenital defects
Secure airway and check frequently Blood loss & fluid management Adequate IV access: 2 large peripheral IVs Arterial line
Manage ICP with hyperventilation and diuretics
Prone position Temperature control Infection control Latex precautions
Lateral position complications Venous air embolism Rapid decompression Hypotension, arrythmias
Even minimal trauma or edema may require postoperative ventilation
Often kept intubated due to anticipated airway difficulties from edema secondary to fluid resuscitation and surgical trauma
Extubate when patient awake, following commands and moving extremities; regular respiratory pattern should be present
Modified from Conran AM, Kahana M. Anesthetic considerations in neonatal neurosurgical patients. In: Frim D, Madsen JR, eds. Neurosurgery of the Neonate. Neurosurgery Clinics of North America 1998; 9(1), with permission.
Table 6. Management of venous air embolism
"Mill wheel murmur" on precordial Inform surgeon who floods operative doppler field with saline, places bone wax on openings in the bone
Decrease in end-tidal CO2 Turn off N2O, which could expand VAE
Bubbles seen on transesophageal echo Change patient position to head down
Increase in nitrogen on airway Aspirate central line, if present gas monitor
Hemodynamic instability Resuscitate if unstable, consider arterial line
Safely positioning a patient is the responsibility of both the surgeon and anesthesiologist. Serious complications can occur if various common sites of compression are not checked with each procedure.Children with congential defects of any kind provide a challenge for safe positioning. Padding pressure points is especially important in infants with thin and delicate skin. Of particular importance is the unrepaired myelomeningocele lesion. Injury to the superficial and exposed position of the neural placode can occur if the lesion is not carefully protected by supporting the flanks when the infant is supine during induction. At times, with very large lesions, the infant may be intubed in the lateral position if necessary.
When a patient is moved from supine to prone or lateral positions, the head must be kept in a neutral position realtive to the body so that no rotation occurs along the axis of the cervical spine. Flexion and extension should, of course, be avoided. During surgery, the patient's head may be secured by pin fixation or by resting the head on a horseshoe headrest or on a foam support. Regardless of the means of immobilization, both the anesthesiologist and surgeon should confirm that venous return is not obstructed by extreme flexion or rotation. With horseshoe and foam head supports, great attention should be taken to ensure that no pressure whatsoever is transmitted to the eyes. Unrecognized pressure on the globes during a procedure can result in blindness. This should be rechecked throughout the surgery, since surgical manipulation may result in movement of the patient. The endotracheal tube should be checked for its position after a patient has been turned.
With a patient in the lateral position, a soft support must be placed under the chest wall near the axilla to prevent a compressive brachial plexus injury. The radial pulse in the dependent arm must be checked. In positioning the patient for optimal surgical exposure, the patient's head may be higher than the patient's heart. This relative positioning increases the risk of venous air embolism.
Managing Raised ICP
Prior to surgery, ICP can be inferred by a physical examination and preoperative imaging studies such as CT and magnetic resonance imaging (MRI) scans. Raised ICP secondary to a serious head injury and/or an intracranial mass lesion is often associated with increased cerebral blood flow, raised cerebral oxygen utilization, cellular injury and cytotoxic edema, or any combination of the above. Interventions that may reduce increased ICP or improve cerebral perfusion pressure (MAP-ICP) include modest hyperventilation, induced systemic hypertension, hyperosmolality, and, rarely, barbiturate coma.
Hyperventilation is straightforward in an anesthetized patient, with the target being a pCO2 between 30 and 35 mm. Mannitol (0.25-1 g/kg) is the osmotic diuretic of choice. Blood pressure is raised with judicious use of alpha agonists (e.g., phenylephrine) to maintain a CPP greater than 70 mm Hg. Phenylephrine may cause reflexive bradycardia in response to the increased blood pressure. If bradycar-dia persists in the pediatric patient, it can have its own hemodynamic consequences, namely hypotension in a patient dependent on increases in heart rate for increases in cardiac output.
With very high ICP, a surgical ventriculostomy can be performed both to monitor and treat intracranial hypertension. The monitor is transduced, as is any pressure line. CSF can be drained which is highly effective in reducing raised ICP. In rare circumstances of refractory intracranial hypertension, barbiturates are used to lower cerebral metabolic rate. However, the profound effect of barbiturates on cardiac performance and systemic vascular resistance limit their utility.
Anesthetic agents themselves will affect ICP (Table 7). Thiopental (4-7 mg/kg) may be used for its beneficial effect in decreasing ICP. However, any barbiturate
Table 7. Effects of anesthetics on cerebral blood flow (CBF)
Narcotics ^ or
Enflurane ft or
Nitrous Oxide ^
Adapted from Striker TW. Anesthesia for trauma in the pediatric patient. In: Gregory GA, ed. Pediatric Anesthesia. 2nd ed. New York: Churchill Livingstone, 1990, and Omoigui S. The Anesthesia Drug Handbook. 2nd ed. St. Louis: Mosby, 1995.
should be used cautiously in the hypovolemic patient since its vasodilation and myo-cardial depressant properties may result in pronounced hypotension, and, therefore, decreased cerebral perfusion pressure. Etomidate (0.2-0.3 mg/kg) also reduces ICP but without the reduction in mean arterial pressure seen with thiopental. Propofol is another option for induction, and it decreases cerebral blood flow, an advantageous feature in this patient population. Ketamine increases cerebral blood flow and hence
All inhalation agents increase cerebral blood flow, and therefore create a rise in ICP. Isoflurane's effect can be blunted with hyperventilation that is instituted prior to the administration of the halogenated agent, hence it is commonly used in the administration of a general anesthetic in the neurosurgical patient. Desflurane has a rapid emergence and therefore can be advantageous in providing the ability to rapidly assess the neurosurgical patient in the immediate postoperative period.
Succinylcholine has been reported to produce a rise in ICP secondary to increased afferent neural traffic from muscle spindle receptors beginnig minute after administration, and peaking at 3 minutes. This effect is most noticeable in patients with imaging evidence of decreased intracranial compliance. Hyperventilation, both voluntary and via mask ventilation, and premedication with nondepolarizing neu-romuscular relaxants will blunt the rise in ICP associated with succinylcholine. Nondepolarizing muscle relaxants have little effect on ICP.
Lidocaine (1.5 mg/kg) may also be used to blunt the ICP rise in response to laryngoscopy but needs to be given 3 to 4 minutes prior to intubation to be most effective.
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