Surgery of the Brain

Chapter 39


Surgery of the Brain



General Principles and Techniques



Definitions


Creating a defect in the skull to access the brain is a craniotomy. Standard craniotomies typically performed in dogs and cats include lateral or rostrotentorial craniotomy, transfrontal craniotomy, and suboccipital craniotomy. Intracranial pressure (ICP) is the pressure exerted by tissues and fluid within the cranial vault and is normally in the range of 5 to 12 mmHg in dogs and cats. Cerebral perfusion pressure (CPP) represents the forward (i.e., arterial to venous) driving pressure that is the main determinant of brain blood flow and hence brain oxygenation and nutrient support. Autoregulation refers to the intrinsic ability of the brain to maintain a constant ICP within the mean arterial blood pressure MAP extremes of 50 to 150 mmHg. However, significant variability has been noted between individuals, and these numbers serve only as a guideline. Pressure autoregulation links brain vascular tone with systemic blood pressure (when MAP increases, vasoconstriction in brain blood vessels prevents an ICP increase and vice versa), whereas chemical autoregulation refers to the direct responsiveness of brain vasculature to the partial pressure of carbon dioxide (PaCO2) in arterial blood (hypercapnia leads to brain vascular dilation and vice versa). Compliance is a change in volume per unit change in pressure within the intracranial compartment and reflects the ability of that compartment to accommodate excess volume (e.g., mass, hematoma) by shifting fluids within the compartment.



General Considerations


The three main types of craniotomy are sometimes combined to provide increased exposure to parts of the brain for various conditions; they may be modified when necessary. For example, bilateral rostrotentorial craniotomies may be required at times; this may also involve removing the top of the skull. Increased ventral exposure may be needed in some cases during a rostrotentorial craniotomy; this may require resection of part of the zygomatic arch and/or the coronoid process of the mandible. When working in the caudal fossa region, it may be necessary to extend a suboccipital craniotomy laterally by sacrificing one of the transverse sinuses. Sometimes more room is needed caudally in this approach, which is achieved by partial or complete removal of the dorsal arch of the atlas (C1). Ventral approaches to the brain are seldom performed in dogs and cats and therefore will not be discussed in this chapter. The relationship between ICP and CPP and MAP is as follows: CPP = MAP − ICP. Compliance decreases as intracranial volume increases, as is shown in Figure 39-1. Once an intracranial volume is reached that is close to the limit of the compliance ability of the intracranial compartment, even small increases in intracranial volume (e.g., brain edema, brain vasodilation from anesthesia) will lead to large increases in ICP.




Preoperative Management


The specifics of preoperative management for the brain surgery patient depend to a large degree on the underlying disease process. With increased availability of magnetic resonance imaging (MRI) in dogs and cats, the repertoire of surgical brain disorders in these species has expanded (see also Chapter 15). Patients with disorders typified by slow-growing mass lesions (e.g., brain tumors, intracranial arachnoid cysts) will likely benefit from low doses of oral prednisone (e.g., 0.5 mg/kg every 12 hours) in the time period before surgery is scheduled and for some time afterward. This dose of prednisone alleviates edema surrounding the lesion and typically improves the patient’s neurologic status dramatically within 24 to 48 hours. Glucocorticoids should not be given as an emergency treatment for acute brain injury (particularly the “high-dose methylprednisolone” protocol) because they have repeatedly failed to demonstrate any statistically significant benefit in terms of central nervous system trauma, and they have the potential for serious adverse effects.


Adequate fluid support must be provided before anesthesia is given. Concern has arisen that overzealous intravenous fluid administration may exacerbate brain edema, especially in trauma patients; however, fluid restriction is strictly contraindicated. The response of the vasculature to hypotension is vasodilation. In a closed vault such as the cranium, the result is an increase in space taken up by the vasculature. The patient with brain pathology may have additional elevations in ICP caused by this vasodilatory response to hypotension. Conversely, marked hypertension causes an increase in cerebral blood volume and promotes cerebral edema. Therefore, the goal is to keep blood pressure within the normal range, avoiding hypotension and marked hypertension. Patients that present with an increase in ICP often have systemic hypertension—an indication that efforts to reduce ICP are necessary. Normal saline is the fluid of choice for brain surgery. Because of the blood-brain barrier, osmotic pressure, not oncotic pressure, is the driving force for movement of water out of the vasculature and into the interstitial and intracellular fluid compartments of the brain. In other words, sodium is of vital importance. To minimize brain edema, serum tonicity should be maintained. This is best done by using normal saline and rechecking serum sodium levels when diuretics such as mannitol are used. In acute brain injury patients, hypertonic saline and/or colloid solutions (e.g., hetastarch) are usually advised in combination with normal saline to support normal blood pressure while minimizing the likelihood of further brain edema (see Table 4-5 on p. 34).


Depending on the specific disease process, it may be necessary to provide supplemental oxygen to the brain surgery patient before and after surgery. This is often required for victims of severe brain injury. Patients who are conscious and are not obviously deteriorating neurologically should be administered supplemental oxygen via face mask, nasal oxygen catheter, or transtracheal oxygen catheter (see p. 31). Face masks tend to stress dogs and cats and should be used only temporarily, until another form of oxygen (O2) delivery can be instituted (e.g., nasal O2). Use of an O2 cage is generally an ineffective method of administering supplemental O2 to severely brain-injured patients because most of these patients require frequent or constant monitoring. Oxygen cages do not allow for concomitant close patient observation (requires opening the cage door) and maintenance of a high-oxygen environment. With nasal and transtracheal O2 catheters, an inspired oxygen concentration of 40% is provided with flow rates of 100 ml/kg/min and 50 ml/kg/min, respectively. In cases of traumatic brain injury, care must be taken to avoid placing nasal O2 catheters farther than the level of the medial canthus (to avoid entering the cranial vault through a fracture site). Inadvertent jugular vein compression, which can cause increased ICP, should be avoided while transtracheal O2 catheters are placed. High flow rates with nasal O2 catheters may induce sneezing, which has the potential to raise ICP. Patients who are losing or have lost consciousness should be intubated and ventilated. In the patient with oscillating levels of consciousness or airway obstruction secondary to trauma, a tracheostomy tube may be indicated for assisted ventilation.


Intravenous mannitol (0.5 to 1.0 g/kg over 10 to 20 minutes) is the drug of choice for decreasing ICP in brain surgery patients. The most clinically important and immediate (within a few minutes) beneficial effect of mannitol is a decrease in ICP due to decreased blood viscosity and reflex vasoconstriction of brain arterioles. If mannitol is given rapidly, it causes vasodilation with subsequent increases in cerebral blood volume and ICP and a corresponding decrease in systemic blood pressure. To avoid these blood pressure changes, it is recommended that mannitol be given over 10 to 20 minutes. Over the next 15 to 30 minutes after mannitol administration, fluid is osmotically drawn from extracellular spaces throughout the body, including the brain. Other effects of mannitol include scavenging free radical species and reducing cerebrospinal fluid (CSF) production. Beneficial effects of mannitol last between 2 and 5 hours. Concerns regarding the potential of mannitol to exacerbate preexisting hemorrhage or to cause a reverse osmotic shift are unfounded.


Antiseizure drugs should be administered to dogs and cats with brain disorders characterized by recurrent seizure activity. A number of alternatives to phenobarbital and potassium bromide are available for managing seizures in dogs and cats (Table 39-1). Most of these drugs are generic and inexpensive. Zonisamide is particularly advantageous to use in dogs with brain tumors. Phenobarbital (PB) has the tendency to cause profound sedation in dogs with brain tumors, even at low doses; this effect is sufficiently severe that PB is not recommended in these dogs. Zonisamide does not typically cause sedation and is both effective and inexpensive. Other potentially useful antiseizure drugs for dogs include gabapentin, levetiracetam, felbamate, and pregabalin. Pregabalin, the “next generation” of gabapentin, has a longer half-life of elimination than its predecessor and is considered to be more effective. Both pregabalin and gabapentin can cause sedation, although this effect is typically mild. Levetiracetam (LEV) is an extremely useful drug in dogs and cats with brain tumors, particularly when the intravenous form of the drug is used for short-term management. Levetiracetam typically has no side effects, even at high doses. A single bolus injection (20 mg/kg over several minutes) of LEV results in therapeutic plasma levels of the drug for 8 to 12 hours. Levetiracetam has no known drug-drug interactions and does not undergo hepatic metabolism. Oral levetiracetam is a useful oral drug in both dogs and cats, although a “honeymoon effect” is often seen in dogs with this drug, in which it becomes apparently less effective over time. Felbamate is an effective and safe antiseizure drug for dogs that does not cause sedation; however, it is expensive and therefore is used infrequently. For cats, PB, levetiracetam, zonisamide, gabapentin, and pregabalin are useful antiseizure drugs. Phenobarbital is very effective in cats and usually does not cause side effects commonly encountered in dogs. Oral diazepam and bromide are contraindicated in cats.



In any patient with suspected increased ICP, care should be taken not to compress the jugular veins. Additionally, when these patients are recumbent or are being prepared for surgery, the head should be slightly elevated (about 30 degrees) to encourage venous drainage from the head and limit venous congestion.


In animals undergoing brain surgery, IV antibiotics (e.g., cefazolin 22 mg/kg) should be administered perioperatively (30 minutes before surgery is begun and every 90 to 120 minutes thereafter during surgery) and should be discontinued after surgery or within 24 hours. Some neurosurgeons (including the author) prefer to continue them orally (e.g., cefadroxil 22 mg/kg every 8 hours) for 10 to 14 days postoperatively.



Anesthetic Considerations


Premedication in patients with increased ICP should be avoided. Decreased respirations and hypercapnia may increase ICP and may be lethal. Those patients that do not have an increase in ICP can be given midazolam or diazepam. Corticosteroids and anticonvulsant therapy should be continued until the time of surgery.


The induction period needs to be highly controlled in these patients. Barbiturates and propofol are the induction agents of choice (Table 39-2). A smooth induction and intubation should be performed, with every effort made to avoid blood pressure extremes and prolonged apnea. Hypertension and tachycardia with intubation may have to be treated by administering esmolol or by deepening the anesthetic with additional boluses of propofol or thiopental.




Hypotension should be quickly treated with vasopressors such as ephedrine and phenylephrine, but not with fluid boluses (see Table 39-2). The airway needs to be secured very carefully because access to the head will be restricted during surgery. Positioning of the animal with its head elevated is beneficial for patients with increased ICP.


Anesthetic agents influence cerebral blood flow (CBF), cerebral metabolism, CO2 reactivity, and cerebral blood pressure autoregulation. Barbiturates, propofol, isoflurane, and sevoflurane all have been shown to decrease cerebral metabolism. Although these anesthetic agents decrease cerebral blood flow, it is the concomitant decrease in cerebral metabolic rate that provides neuroprotection. Barbiturates have been extensively studied in neuroanesthesia and have been used primarily because of their hypnotic effect, decrease in cerebral metabolic rate, and anticonvulsant activity. Even though they cause dose-dependent decreases in cerebral blood flow, barbiturates cause a corresponding decrease in cerebral metabolic rate and cerebral oxygen requirements uniformly throughout the brain. Combined with their apparent ability to increase CSF absorption, barbiturates generally cause a decrease in ICP. Propofol acts very similarly, with decreases to CBF, cerebral metabolic rate, and ICP. It also has significant anticonvulsant properties. However, systemic vasodilation and subsequent hypotension with propofol administration should be anticipated and treated. Although etomidate decreases ICP, it is avoided in neurosurgery patients because it causes increased seizure activity and thus an increased cerebral metabolic rate. Inhalant anesthetics cause a dose-dependent decrease in cerebral metabolic rate, as well as an increase in cerebral perfusion. This is especially desirable during periods of hypotension. Isoflurane is the inhalant anesthetic agent of choice because of its ability to increase CSF absorption and to minimally increase ICP (see Table 39-2). Halothane and desflurane should be avoided because of their greater increases in ICP.


Particular attention should be paid to PaCO2 in anesthetized brain surgery patients because hypercapnia can lead to severe increases in ICP and decreased CPP. Most anesthetic drugs used clinically have the potential to cause hypoventilation and resultant hypercapnia. Arterial blood gas measurement is the best way to monitor PaCO2 levels. End-tidal CO2 (EtCO2) measurement is a useful monitoring tool but tends to underestimate true PaCO2 levels. In patients that have normal pulmonary function, EtCO2 is approximately 5 mmHg greater than PaCO2. In younger animals, the number is lower, and in animals younger than a year, EtCO2 may be equal to PaCO2. These gradients cannot be unilaterally assumed with all patients because of alterations in pulmonary function, especially in anesthetized patients, in which atelectasis and ventilation/perfusion mismatching occur. Nevertheless, EtCO2 can serve as a guideline and, when used with arterial blood gases during neurosurgery, is an important part of monitoring. Venous CO2 levels (PvCO2) are also helpful and are usually less than 5 mmHg greater than PaCO2. However, in patients with perfusion deficits, peripheral PvCO2 levels can be significantly higher than arterial values and should be interpreted cautiously. Historically it has been recommended to keep PaCO2 levels in the range of 25 to 35 mmHg to prevent excessive brain vasodilation. Recent evidence suggests that PaCO2 less than 30 mmHg may lead to excessive vasoconstriction with subsequent impairment of CPP. Excessive hyperventilation may be deleterious to patients whose ICP elevation is not caused by hypercarbia-induced dilation of brain vasculature. Mild hyperventilation to keep PaCO2 between 30 and 35 mmHg is currently used in human neurosurgical patients. Indiscriminate use of hyperventilation to decrease ICP should be avoided, especially in trauma patients. However, it may be warranted for short periods in emergent cases in which the brainstem is herniating, until more definitive therapy can be initiated.


In general, anesthetic agents considered preferable for use in brain surgery patients include benzodiazepines (e.g., diazepam, midazolam), barbiturates (e.g., pentobarbital), propofol, opioids, isoflurane, and sevoflurane (see Table 39-2). Opioids have little to no effect on ICP, and pentobarbital, propofol, and benzodiazepines decrease ICP with some neuroprotective properties. The potential adverse effects of opioids on ICP are minimal to nonexistent if appropriate doses are used. The concern is for depression and inadequate respirations causing elevations in PaCO2. Therefore it is recommended that opioids not be used in the preoperative period, but rather that they be used during surgery, when ventilation is controlled, and during the postoperative period. Poorly controlled pain is much more likely to increase ICP than is judicious use of opioids postoperatively. Additionally, continuous rate infusions (CRIs) of opiates (e.g., fentanyl, morphine) begun during surgery and continued into the postoperative period are less likely to lead to respiratory depression with a subsequent ICP increase due to hypercapnia (see p. 138).


Because of known negative effects on brain autoregulatory mechanisms and tendencies to increase ICP, anesthetic drugs to be avoided include ketamine, halothane, and desflurane. Ketamine is a controversial drug that was initially considered contraindicated in patients with increased ICP. Traditionally it was thought to always increase cerebral blood flow; however, it has been shown NOT to increase cerebral blood flow or ICP in mechanically ventilated animals. In fact, in mechanically ventilated traumatic brain injury human patients it has been shown to decrease ICP. Ketamine may also have a neuroprotective effect because of the antagonism of N-methyl-d-aspartate (NMDA) receptors, but this is unproven. Nevertheless, giving ketamine to already intubated and ventilated patients is not the same as inducing with ketamine. There are better choices that do not carry the risk of marked hypertension at induction, and ketamine is not recommended.


The α2-agonists dexmedetomidine, medetomidine, and xylazine have some neuroprotective qualities. Both dexmedetomidine and medetomidine cause a decrease in ICP in patients already anesthetized with an inhalant anesthetic. Unfortunately, their variable effects on blood pressure make them less appropriate as induction drugs. However, if used in low doses in a balanced anesthesia protocol, they may reduce the hypertension followed by hypotension seen in these patients (see Table 39-2).


Traditionally, acepromazine has been thought to potentiate seizure activity in patients predisposed to seizures. Recent clinical evidence contradicts this historical dogma. Very low doses of acepromazine (0.01 to 0.02 mg/kg IV) are often helpful in relieving what appears to be postoperative dementia in some brain tumors and brain trauma patients. As with other drugs, acepromazine at higher doses can cause hypotension, which can have deleterious effects on ICP and CPP. Furthermore, patients with intracranial masses are often older patients, and acepromazine may have long-lasting effects.



Standard Surgical Approaches to the Brain


Important vascular structures to avoid during brain surgery are the dorsal sagittal sinus and the transverse sinuses (Fig. 39-2). Laceration of these structures can cause life-threatening hemorrhage. Ligation or obstruction of the dorsal sagittal sinus (particularly the caudal two-thirds of the sinus), the confluens sinuum (the midline juncture of the paired transverse sinuses), or both transverse sinuses will likely lead to fatal brain swelling. During the suboccipital approach, it is common to experience hemorrhage from occipital emissary veins at the ventrolateral limits of the supraoccipital bone during periosteal muscle elevation; this hemorrhage is controlled by pushing bone wax into the mastoid foramen, through which this vessel traverses.



For all standard approaches, the author prefers a midline incision. Unless brain exposure is very large (e.g., removal of the top portion of the calvarium) or the craniotomy procedure is likely to lead to an obviously abnormal cosmetic appearance postoperatively (e.g., removal of the zygomatic process of the frontal bone), the craniotomy defect is not repaired. If repair of the skull defect is considered necessary, titanium mesh and polymethylmethacrylate (PMMA) can be used (Fig. 39-3). The PMMA is placed on either side of the mesh; the mesh keeps the PMMA from sagging into the craniotomy site during hardening. Titanium rather than steel is used so that repeat MRI is possible if necessary. Postoperative CSF leakage is a clinical problem encountered in human brain surgery; however, this phenomenon does not occur in dogs and cats following craniotomy. Replacing resected dura/arachnoid with autologous or synthetic dural substitute generally is not indicated in dogs and cats. A layer of Gelfoam can be placed over the exposed brain before the time of closure.



Once the dura/arachnoid is opened and the brain is exposed, it is important for the surgeon to be efficient in his or her use of time. Although surgery is “not a race,” prolonged brain tissue exposure appears to be associated with increased postoperative morbidity, even when appropriate measures are taken to keep the brain moist during surgery (e.g., moistened lint-free cottonoid sponges placed on the brain surface).



Rostrotentorial (Lateral) Craniotomy


Shave the skin and aseptically prepare the area from the level of the medial canthi rostrally to the cranial aspect of the second cervical vertebra caudally; the lateral limits of the prepared region are the zygomatic arches. Shave and aseptically prepare any aspect of the ears that may be in the surgical area. Make a midline incision from approximately the level of the lateral canthi to several centimeters past the external occipital protuberance. Sharply incise the cutaneous coli muscles and transect the cervicoscutilaris muscle near midline, leaving about a centimeter for reattachment during closing. Sharply incise the temporalis fascia with a No. 11 blade, leaving at least several millimeters attached to the skull for reattachment purposes. Reflect the temporalis musculature ventrally by elevating it off the side of the skull with Freer periosteal elevators (cats and small dogs) or Army-Navy osteotomes (large dogs). Create an oval outline of the intended defect with a high-speed air drill. Deepen the edges of this outline until a thin layer of periosteum is left. The ventral aspect of the defect does not have to be drilled full thickness. Once the dorsal and lateral aspects of the craniotomy defect outline are completely drilled, use a periosteal elevator to lever the bone flap off the skull after positioning the elevator in the dorsal aspect of the defect (Fig. 39-4). Once the bone flap is removed, further enlarge the craniotomy defect using rongeurs. After removal of the bone flap, use bipolar cautery to stop hemorrhage from bleeding meningeal vessels.




Transfrontal Craniotomy


The most common reason for performing a transfrontal craniotomy is the need for removal of canine meningiomas in the olfactory bulb region of the brain. Several variations of this approach provide excellent access to the olfactory bulb area and the rostral frontal lobe (prefrontal area) of the cerebrum—areas that are difficult or impossible to access via a standard rostrotentorial craniotomy. As with other approaches, this transfrontal craniotomy approach can be expanded caudally, on either side of the skull, should increased exposure or further brain decompression be required.


Shave the skin and aseptically prepare it from the level of the infraorbital foramina rostrally to the level of the caudal aspect of the zygomatic arches dorsally. Extend the lateral limits of the prepared skin area to the level of the zygomatic arches and include the skin around the eye. Make a midline incision rostrally from the level of the medial canthi to the level of the bregma. Using a combination of sharp dissection and Freer elevators, separate the underlying subcutaneous tissues and frontalis musculature from the underlying bone. Remove the outer bone plate of the frontal sinus to expose the frontal sinus, the ethmoturbinates, and the internal table of the frontal bone.


This bone can be removed in a variety of sizes and shapes with the use of a high-speed air drill or an oscillating saw blade. A triangular shape is often chosen for a unilateral approach, a diamond pattern for a bilateral approach (Fig. 39-5). Because of the limited exposure (most olfactory meningiomas occupy the majority of the olfactory bulb region bilaterally) provided by the unilateral approach, the bilateral approach is typically performed. If the bone plate is to be replaced, use the saw blade or a small drill bit when removing the bone.




Suboccipital Craniotomy (Foramen Magnum Decompression [FMD])


The most common indication for a suboccipital craniotomy in dogs is to relieve compression at the craniocervical junction in cases of Chiari-like malformation (CLM); in this scenario, the craniotomy is combined with a dorsal laminectomy of the atlas (C1) and is referred to as a foramen magnum decompression (FMD). For other purposes (e.g., brain tumor removal), the suboccipital craniotomy is typically performed without including the C1 dorsal laminectomy. For either version of this procedure, place the dog in sternal recumbency with the neck ventroflexed. Shave and aseptically prepare the dorsal aspect of the head and neck from the level of the bregma to the level of the third or fourth cervical vertebra, with a width approximately equal to the width of the atlas. Make a dorsal midline incision extending from approximately 1 cm rostral to the external occipital protuberance cranially to the middle of the second cervical vertebra caudally. Separate the superficial dorsal cervical musculature (Fig. 39-6, A) at the median raphe, exposing the underlying biventer cervicis muscles. Separate the paired biventer cervicis muscles on midline, exposing the rectus capitis dorsalis muscles (Fig. 39-6, B). Remove the caudal aspects of the rectus capitis dorsalis muscles from the cranial half of C2 using sharp dissection and periosteal elevation, and split these muscles on the midline. Sharply incise the cranial aspects of the rectus capitis dorsalis muscles from the nuchal crest, exposing the caudal portion of the occiput and the arch of the atlas. Control hemorrhage with bipolar electrocautery. Use a high-speed air drill with a 3- to 4-mm diameter round drill bit and Lempert rongeurs to remove a portion of the occiput and the dorsal aspect of the first cervical vertebra (Fig. 39-6, C, D). Approximately 75% of the length of the dorsal arch of C1 is routinely removed. In cases in which there appears to be dorsal constriction at C1/C2 (see Chapter 40), remove the entire arch of C1 as well as part of the dorsal lamina of C2.





Suture Materials and Special Instruments


Several essential instruments are required for performing brain surgery, including a high-speed air drill, rongeurs of several styles (e.g., Lempert, Kerrison, Ruskin), microsurgical instrumentation (e.g., several sizes of probes, strabismus and tenotomy scissors, nontoothed Bishop-Harmon forceps, lens loops), and several sizes of Frazier suction tips. Small needle holders (e.g., Castroviejo) and 5-0 to 6-0 suture material (polypropylene or polydioxanone) are also required when meningeal suturing is necessary. Monopolar cautery is needed for hemorrhage during the surgical approach. Bipolar cautery is required for dealing with meningeal, tumor, and brain parenchymal hemorrhage. Gelfoam and Surgicel are also helpful in controlling meningeal and parenchymal hemorrhage. Bone wax is used to control hemorrhage from cancellous bone and transverse sinuses (if transected). Lint-free cottonoid sponges are used to keep the brain moist while it is exposed. Magnification is often useful and typically is provided by optical telescopes. An additional light source (e.g., headlamp) may be needed for some procedures. A Cavitron ultrasonic aspirator (CUSA) is very useful for resecting infiltrative masses or working near blood vessels; the high cost of this equipment may limit its use, however. Intraoperative ultrasound is useful both in locating intra-axial lesions and in judging the completeness of their removal before the time of closure.



Postoperative Care and Assessment


All postoperative craniotomy patients should be recovered in an intensive care unit and monitored for 3 to 5 days postoperatively. The cage should be padded (e.g., bubble-wrap) to avoid injury to the surgical site. Because postoperative brain surgery patients may have subtle pharyngeal dysfunction, nothing is given per os for the first 24 hours. After this time, small “meatballs” of canned food are offered several times a day, in addition to water. For patients on oral prednisone therapy, this therapy is gradually tapered over 5 to 7 days. Antibiotics are continued according to the specifics of the disease process and clinician preference. Anticonvulsant drugs are administered as needed. Analgesic drugs are also administered (see Table 39-2). Especially in cats, serial PCV measurements should be made for the initial 24 hours post surgery and blood transfusion performed if necessary. Oxygenation and ventilation status should be assessed via blood gas analysis, depending on the specific case. Supplemental oxygen is provided, if necessary. For patients that are unable or unwilling to voluntarily ambulate, frequent turning (e.g., every 4 hours) is essential to avoid pulmonary atelectasis and subsequent pneumonia. The patient’s neurologic status should be assessed several times per day, and any deterioration should be addressed medically (e.g., mannitol) and/or surgically (reimaging and reoperation). Suspected pneumonia (typically older, large dogs following brain tumor removal) should be treated aggressively (e.g., nebulization/coupage, broad-spectrum IV antibiotics) and in a timely manner. Following hospital discharge, recheck examinations focus on the rate of neurologic recovery and on wound healing.





Specific Diseases



Congenital Hydrocephalus




General Considerations and Clinically Relevant Pathophysiology


The pathophysiology of central nervous system (CNS) damage associated with hydrocephalus is complex and involves destruction of the ependymal lining of the ventricles, white matter damage by interstitial fluid accumulation, and eventual neuronal injury in the cerebral cortex.


Conventional theories regarding the pathophysiology of hydrocephalus contend that ventriculomegaly results from obstruction of CSF flow within the ventricular system (e.g., mesencephalic aqueduct stenosis) and/or insufficient absorption of CSF into the venous system at the arachnoid villi level. These theories are based on the “bulk flow” concept of CSF, in which most CSF is presumed to be absorbed by the arachnoid villi. A more recently proposed theory, called the hydrodynamic theory, maintains that hydrocephalus develops as the result of abnormal (reduced) intracranial compliance and the resultant effect of this compliance defect on brain capillaries. In the normal animal, individual brain capillaries remain open during the entire cardiac cycle (systole and diastole). This is important because much of CSF absorption actually occurs at the capillary level, rather than at the arachnoid villi. Hydrocephalic patients are believed to have poor intracranial compliance as an underlying disorder that leads to hydrocephalus. The increased capillary pulse pressure caused by decreased compliance leads to a pulsatile transmantle pressure gradient directed from the cerebral tissue toward the lateral ventricles. These abnormal capillary pulsations occur within normal mean intracranial pressure limits. Rebound pressure from the recurring gradient, as well as hyperdynamic CSF flow in the mesencephalic aqueduct, leads to ventricular enlargement over time. The end result is that hydrocephalus develops within the confines of normal intracranial pressure (i.e., normal pressure hydrocephalus). Hydrocephalus, especially if progressive, can cause neurologic dysfunction from compression and stretching of brain parenchyma, as well as from brain ischemia and interstitial edema.



Diagnosis



Clinical Presentation


Sep 11, 2016 | Posted by in SMALL ANIMAL | Comments Off on Surgery of the Brain
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