6.3 Anesthetic consideration for head and spinal cord injury 

Common injuries requiring immediate surgical intervention including epidural hematoma, subdural hematoma, and some penetrating brain injuries and depressed skull fractures shall be managed by specialist neurosurgeon and senior anesthetist/anesthesiologist in a resourceful hospital having an intensive care unit with mechanical ventilator. Therefore the patient will benefit, if he is transferred to hospitals who can manage head and spinal cord injury. Elevation of depressed skull fracture to alleviate elevated intracranial pressure and reduce brain ischemia might be done at the periphery until the patient has been transported to better hospital. The anesthetic assessment and management for head and spinal cord injury is a continuation of the general assessment and care, and the anesthetic considerations for emergency and trauma patient should be observed. The following should be included: 

6.3.1 Head injury anesthetic consideration 

• Patients suspected of sustaining head trauma should not receive any premedication that will alter their mental status (e.g., sedatives, analgesics) or neurological examination (eg, anticholinergic-induced pupillary dilation). 
• In-line stabilization should be used during airway manipulation to maintain the head in a neutral position. 
• Patients with obvious hypoventilation, an absent gag reflex, or a persistent total score below 8 on the GCS require tracheal intubation and hyperventilation. 
• All patients should be regarded as having a full stomach and should have cricoid pressure applied during ventilation and tracheal intubation. 
• Adequate preoxygenation and hyperventilation by mask. Mild hypothermia may prove beneficial in a patient with a head injury. 
• Administration of thiopental, 2–4 mg/kg, or propofol, 1.5–3.0 mg/kg, and rapid-onset relaxants. Suxamethonium should be avoided 48 hours following head and spinal cord injury or patient developed paraplegia. Available short acting non depolarizing muscle relaxant can be used. 
• Blind nasal intubation is contraindicated in the presence of a basilar skull fracture. Basilar skull fractures are often associated with bruising on the eyelids ("raccoon eyes") or over the mastoid process (Battle's sign), and cerebrospinal fluid (CSF) leaks from the ear or nose (CSF rhinorrhea). 
• Glucose-containing or hypotonic solutions should not be used. The hematocrit should be maintained above 30%. 
• Hypotension may occur after induction of anesthesia as a result of the combined effects of vasodilation and hypovolemia and should be treated with an -adrenergic agonist and volume infusion if necessary. 
• Subsequent hypertension is common with surgical stimulation but may also occur with acute elevations in ICP. Hypertension is often associated with bradycardia which can be treated with additional doses of the induction agent, or with antihypertensive. 
• The decision whether to extubate the trachea at the conclusion of the surgical procedure depends on the severity of the injury, the presence of concomitant abdominal or thoracic injuries, preexisting illnesses, and the preoperative level of consciousness. Young patients who were conscious preoperatively may be extubated following the removal of a localized lesion, whereas patients with diffuse brain injury should remain intubated. 
• In head injury a slight elevation (30oc) of the head will improve venous drainage and decrease intracranial pressure. 
• Burr hole is possible and good to be done under local anesthesia to avoid complications associated with intubation and to see the success of the procedure before patient leaves the theater in a cooperative patient. 

6.3.2 Spinal cord anesthetic consideration 

• The general principles of anesthetic management described for patients with traumatic brain injury also apply to the care of patients with spinal cord injury. Stabilizing the spine is critical to preventing additional injury to the spinal cord. 
• The degree of physiological derangement following spinal cord injury is proportional to the level of the lesion. Great care must be taken to prevent further injury during transportation and intubation. 
• Lesions of the cervical spine may involve the phrenic nerves (C3–C5) and cause apnea. Loss of intercostal function limits pulmonary reserve and the ability to cough. High thoracic injuries will eliminate sympathetic innervation of the heart (T1 –T4), leading to bradycardia. Acute high spinal cord injury can cause spinal shock, a condition characterized by loss of sympathetic tone in the capacitance and resistance vessels below the level of the lesion, resulting in hypotension, bradycardia, areflexia, and gastrointestinal atony. 
• Hypotension in these patients requires aggressive fluid therapy—tempered by the possibility of pulmonary edema after the acute phase has resolved. 
• Anesthetic management of patients with non acute transactions is complicated by the possibility of autonomic hyperreflexia. Autonomic hyperreflexia should be expected in patients with lesions above T6 and can be precipitated by surgical manipulations. Regional anesthesia and deep general anesthesia are effective in preventing hyperreflexia.