Neuroanesthesia for South American Camelids
Anesthesia for neurosurgery, particularly brain surgery, is a specialization that requires appropriately trained staff, some specialized anesthetic equipment, and the means for postoperative intensive care. Neurologic disease in South American camelids (SACs) is relatively common, and as increasing numbers are being farmed, a veterinary surgeon dealing with this species may have to plan and carry out anesthesia for neurologic cases. This chapter details the physiologic principles behind the management of neurologic anesthesia and is separated into two sections: (1) neurologic anesthesia for brain surgery and (2) neurologic anesthesia for spinal surgery.
SACs may suffer from a variety of neurologic diseases, including congenital defects such as hydrocephalus, in which the neonatal nature of the animal also has to be taken into consideration.1 Infectious and parasitic diseases such as listeriosis, equine herpes virus, West Nile Virus, rabies, meningeal worm, and brain abscesses and meningoencephalitis from a multitude of pathogens may all cause neurological signs in the SAC.2–9 Careful handling and disinfection of anesthesia equipment are needed in these cases to prevent transmission of pathogens to other patients or staff. Neoplasia has also been reported as a cause of space-occupying lesions causing neurologic signs in llamas and alpacas.10,11
Anesthesia may be required for investigations such as cerebrospinal fluid (CSF) sampling and imaging and for modalities such as magnetic resonance imaging (MRI). Both CSF sample acquisition and MRI require additional considerations for anesthesia. Anesthesia may also be required for the surgical treatment of certain conditions.
If the volume of one component increases, it has to be balanced by a decrease in another. However, the volume of brain parenchyma cannot be altered easily, although intracranial blood volume and intracranial CSF volume may be altered by a small amount. So, for example, if brain parenchyma volume increases (e.g., through a space-occupying lesion such as an abscess), then to compensate, some of the CSF may move into the subarachnoid space around the spinal cord. However, at a certain point the compensatory mechanisms are exhausted, and intracranial pressure rises, often producing clinical signs (Figure 51-1 and Box 51-1).
Normal intracranial pressure (ICP) should be between 5 and 15 mm Hg in most mammals. ICP may be increased by several pathologies affecting one or more of the three skull contents (i.e., blood, CSF, or brain parenchyma). In addition, extraparenchymal swelling (e.g., abscesses or subdural hemorrhage) will also increase ICP.
Brain parenchyma may increase in volume because of edema, hemorrhage, inflammation, or space-occupying lesions. CSF volume may increase from an increased production (e.g., choroid plexus tumor) or decreased drainage (e.g., caused by space-occupying lesions). The volume of blood in the intracranial contents may be increased for a variety of reasons. Increased central venous pressure (CVP) may be caused by the head lying lower than the heart, occluding the jugular veins, Valsalva maneuvers (forced expiration against a closed glottis), and intermittent positive pressure ventilation (IPPV) with high inspiratory pressures. Intracranial blood volume is also affected by the degree of vasodilation or vasoconstriction, that is, vasomotor tone. Cerebral vasomotor tone is normally “responsive” to a number of stimuli (Figure 51-2 and Table 51-1). As seen in Table 51-1, within the “normal” range for arterial blood pressure, ICP should not be altered by small changes in blood pressure. This is because the cerebral circulation is usually governed by “autoregulation”; that is, cerebral blood flow (CBF) is maintained over a wide range of blood pressures. It must be remembered, however, that in a “diseased brain” autoregulation may not function “normally.”
|With increasing partial pressures, up to 80 mm Hg
|With decreasing partial pressures, down to 20 mm Hg
|<50 mm Hg
|>300 mm Hg
|Mean arterial blood pressure
|>160 mm Hg
|<60 mm Hg
In general, SACs with brain disease should be stabilized as much as possible before anesthesia, following aims similar to those required for the anesthetic management of other animals with brain disease. ICP, if elevated, should be reduced to normal, or at least further elevations should be avoided. Cerebral autoregulation should be promoted, whenever possible, by maintaining blood pressure and partial pressures of arterial oxygen and carbon dioxide (PaO2 and PaCO2) within normal limits. Seizure activity should be controlled in the perianesthetic period; commonly used antiepileptics include diazepam and phenobarbital. It must be remembered that general anesthesia, per se, will stop seizure activity. Neuroprotection should also be afforded, whenever possible. Prevention of hyperthermia (common with seizures) and tight regulation of blood glucose are also effective strategies for protection of the brain.
To reduce the volume of blood in the intracranial space, the head may be raised to an angle of 30 degrees from the horizontal position to aid venous drainage. It should be noted that a steeper angle than this may compromise the airway and may worsen venous drainage by “kinking” the neck. While the skin of SACs overlying the jugular vein is thick, occlusion of the jugular veins, which may occur inadvertently during restraint or inappropriate positioning during surgery, should be avoided. Any Valsalva-like maneuver (e.g., coughing, retching, or gagging) increases jugular venous pressure and, thus, ICP and so should be avoided. While IV fluid therapy is suggested to maintain blood pressure, overperfusion of the circulatory system may also increase CVP with a secondary increase in ICP.
The use of diuretics is often advocated to reduce the volume of brain parenchyma, blood, and CSF. The patient’s hydration status must, however, be taken into account when using these drugs. Oncodiuretic therapy (i.e., the combination of colloids and diuretics) may be used to create normovolemic dehydration, but the animal must be monitored very carefully if this is attempted.
Mannitol is an osmotic diuretic, usually used at a dose rate of 1 gram per kilogram (g/kg). It is infused intravenously, slowly over 30 minutes, after it has been warmed thoroughly to dissolve crystals that tend to form at cooler room temperatures. Additional benefits of mannitol administration include free radical scavenging (which may prove helpful in the face of reperfusion injury) and a reduction in blood viscosity, which will improve oxygen delivery to tissues at a cellular level. However, mannitol is not an innocuous substance. It may elevate ICP initially because of a drawing of water into the intravascular compartment before diuresis occurs, and if mannitol moves into cells (which is possible after repeat administrations), cellular volumes and ICP will increase.
Furosemide (1–2 mg/kg) is also a potent diuretic and is often used in conjunction with mannitol. If given before mannitol, furosemide may protect against transient increase in ICP, as mentioned above. Besides acting as a diuretic, furosemide also reduces the production of CSF. The use of glucocorticoids is controversial, and even if advocated, the doses, individual compounds, and dosing regimens are as yet not agreed upon. Potential beneficial effects (at least in non-trauma cases) include diuresis, membrane stabilization, and reduction of inflammation edema.
Two additional techniques that could be employed in an emergency require more invasive measures and, thus, general anesthesia. Aspiration of CSF from the ventricles may be undertaken to “buy time” before surgical intervention. Craniotomy and durotomy may also be undertaken to relieve ICP.