Medical and Surgical Management of the Brain-Injured Pet

Chapter 35

Medical and Surgical Management of the Brain-Injured Pet

Severe brain injury in dogs and cats is an unfortunately frequent occurrence and is often associated with a guarded to poor prognosis, even with aggressive management. Much of the information regarding therapy for these patients is adapted from the human literature, although several veterinary-specific studies are available.15,20 In addition to the challenge of choosing and administering appropriate medical therapy for acute severe brain injury, the surgeon is often faced with the decision regarding whether or not surgical intervention is indicated for a particular patient. Although some differences in opinion have been expressed over what constitutes “appropriate” medical therapy for severe brain injury in veterinary and human patients, general agreement has been reached on most of the available treatments. Less agreement is seen among clinicians with respect to surgical intervention for severe brain injury, particularly in scenarios in which surgical therapy is being used as a decompressive maneuver in the absence of intracranial hemorrhage.13 This chapter will review the pathophysiology and treatment principles associated with severe brain injury in dogs and cats. Because of the lack of published information in the veterinary literature regarding surgical management of severe brain injury, the discussion on this aspect of management will be based on a combination of the human literature and the authors’ clinical experience.

Brain injury can be conceptually divided into primary and secondary injury. Primary brain injury occurs immediately following impact and initiates a number of biochemical processes, which result in secondary brain injury. Both primary and secondary brain injury contribute to increased intracranial pressure. A basic understanding of the mechanisms of brain tissue damage after injury and of intracranial pressure dynamics is essential for logical therapy of the severely head-traumatized patient.

Brain Injury

Primary brain injury refers to the physical disruption of intracranial structures that occurs immediately at the time of the traumatic event. Such injury includes direct damage to brain parenchyma, such as contusions, lacerations, and diffuse axonal injury. Damage to blood vessels may result in intracranial hemorrhage and vasogenic edema. Skull fractures can contribute to continued trauma to the brain parenchyma and blood vessels, especially if they are unstable (Figure 35-1). The extent of primary brain injury is a function of the force of impact. Acceleratory and deceleratory forces of both the impacting object(s) and the intracranial contents will affect overall tissue damage. Direct parenchymal damage associated with primary brain injury is generally beyond the control of the clinician. However, stabilization of skull fractures and evacuation of intracranial hemorrhage may decrease the morbidity associated with these primary injuries. In addition to continued hemorrhage and edema, the damage caused by the primary brain injury activates a number of interrelated biochemical pathways that act in concert to perpetuate further brain tissue damage and subsequent increases in intracranial pressure. These processes constitute secondary brain injury. Adenosine triphosphate (ATP) depletion disrupts the maintenance of cellular ionic homeostasis. Sudden, uncontrolled intracellular influx of sodium (Na+) and calcium (Ca2+) occurs. Cellular swelling (cytotoxic edema) and depolarization result. Uncontrolled depolarization leads to the release of large amounts of glutamate, an excitatory neurotransmitter, into the extracellular environment. Glutamate causes further increases in intracellular Ca2+ levels. Elevated Ca2+ levels activate a number of tissue-damaging pathways, including the arachidonic acid cascade (phospholipase A2 activation) and the xanthine oxidase (free radical producing) pathway. Iron (Fe2+) is a vital co-factor in the xanthine oxidase pathway, and free radical species generated via the Fenton reaction (e.g., hydroxyl and superoxide radicals) are preferentially damaging to cell membranes containing high levels of polyunsaturated fats and cholesterol. Brain tissue is rich in both Fe2+ and membranes with high levels of polyunsaturated fats and cholesterol. Intraparenchymal hemorrhage also increases the amount of Fe2+ available for perpetuation of oxidative damage. Free radical species are thus particularly damaging to neuronal membranes and probably play a major role in secondary brain injury. Their production is also induced by ischemia, arachidonic acid metabolites, catecholamine oxidation, and activated neutrophils. Other secondary autolytic processes induced after severe head trauma include the complement, kinin, and coagulation/fibrinolytic cascades. Elevated levels of nitric oxide and various cytokines (e.g., tumor necrosis factor, interleukins) also contribute to parenchymal injury in the damaged brain. Most of the mediators of tissue damage produced by these various reactions perpetuate their own continued production, as well as the production of other mediators. The maintenance of an ischemic environment perpetuates the previously mentioned processes and also leads to the accumulation of lactic acid (via anaerobic glycolysis). Lactic acid accumulation causes further damage to brain tissue. Hypotension and hypoxemia, extracranial conditions that are common in the traumatized patient, can worsen brain ischemia and thereby enhance the events responsible for secondary brain injury. The end result of these secondary processes is increased intracranial pressure. Unlike in primary brain injury, the clinician has some control over secondary brain injury.

Intracranial pressure (ICP) is the pressure exerted by tissues and fluids within the cranial vault. Normal intracranial pressure values for dogs and cats range between 5 and 12 mm Hg. Cerebral perfusion pressure is a primary determinant of cerebral blood flow and hence brain oxygenation and nutritional support. Cerebral perfusion pressure (CPP) is defined by the following equation:


where MABP = mean arterial blood pressure

The normal contents of the cranial cavity include brain parenchyma, blood, and cerebrospinal fluid. In the normal animal, these components exist in equilibrium with each other, and intracranial pressure remains within normal limits. Between the mean arterial blood pressure extremes of 50 and 150 mm Hg, intracranial pressure remains constant. This phenomenon is called pressure autoregulation. Pressure autoregulation serves to link systemic blood pressure changes to brain vasculature tone. If mean arterial blood pressure rises, vasoconstriction occurs in the brain; if mean arterial blood pressure falls, vasodilation occurs in the brain (see Figure 29-2). In the normal animal, the former scenario prevents intracranial pressure from rising by decreasing cerebral blood flow, and in the latter, intracranial pressure is prevented from falling by increasing cerebral blood flow. Chemical autoregulation refers to the direct responsiveness of brain vasculature to the partial pressure of carbon dioxide in arterial blood (PaCO2); elevated PaCO2 levels cause cerebral vasodilation, whereas decreased PaCO2 levels cause cerebral vasoconstriction. Both forms of autoregulation often remain intact in people with severe head injury, but pressure autoregulation may be compromised in approximately 30% of patients. In some of these individuals, the lower mean arterial blood pressure extreme may become “reset” to a higher value, resulting in significantly decreased blood flow to the brain with even mild systemic hypotension. With severe head trauma, both intracranial hemorrhage and edema can add to the volume of the intracranial compartment. Because of the inexpansile nature of the skull, one or more components of the cranial cavity must accommodate for the increased volume, or increased intracranial pressure will result. This accommodation or volume buffering is accomplished by fluid shifts in the brain vasculature and cerebrospinal fluid pathways and is referred to as intracranial compliance. Compliance is expressed as the change in volume per unit change in pressure. Intracranial compliance has limitations and decreases as intracranial pressure increases. If intracranial volume increases beyond the abilities of compensatory mechanisms, progressively larger increases in intracranial pressure result per unit of volume increase (see Figure 29-3), cerebral perfusion pressure is compromised, and ischemic death of brain tissue occurs. In cases of severe head trauma, intracranial compliance often is quickly exhausted. If mean arterial blood pressure decreases (hypotension), especially in combination with hypoxemia, the brain vasculature will vasodilate in an effort to preserve blood flow (see Figure 29-2). The increase in blood volume increases intracranial pressure, but cerebral perfusion pressure remains inadequate. In addition, the secondary autolytic processes occurring in the injured brain are enhanced by hypotension and hypoxemia, and further brain injury and edema occur with a resultant rise in intracranial pressure.

Physical Examination

Initial physical assessment of the severely brain-injured patient focuses on imminently life-threatening abnormalities. Many patients suffering severe head trauma present to the clinician in a state of hypovolemic shock. A patient’s neurologic status may improve dramatically once the shock state is corrected. Remember that traumatized, hypovolemic patients with no appreciable brain injury often exhibit depressed mentation, due primarily to the hypotensive state. The clinician must first focus on the ABCs of trauma management (airway, breathing, cardiovascular status). In doing so, the brain will benefit, as will the rest of the patient. Quick assessment tests (QATs), including packed cell volume (PCV), total solids (Azostix), and blood glucose, are part of the initial patient assessment. In human beings with head trauma, the deleterious effects of elevated intracranial pressure are accentuated in patients that are hypovolemic and hypoxemic. Because of the strong correlation between increased intracranial pressure, hypovolemia, hypoxemia, and increased mortality, hypovolemia and hypoxemia need to be addressed immediately.

Fluid Therapy

Concern is often expressed that aggressive intravenous fluid therapy to counteract hypotension in the brain-injured patient may aggravate brain edema. Evidence is available to support and to refute this concern. Because of this concern, recommendations have been made to volume-limit victims of severe head trauma. Such recommendations not only are unfounded, they are strictly contraindicated. No debate discusses the disastrous consequences to the injured brain if hypotension is allowed to persist. Hypotension has been shown repeatedly to be a reliable predictor of sustained elevations of intracranial pressure and increased mortality in human head-trauma victims. Blood pressure must be restored to normal levels as soon as possible. A patient with a systolic blood pressure less than 90 mm Hg is considered hypotensive. Some volume replacement fluids (hetastarch, hypertonic saline) afford some protection to the edematous brain, even if used with large volumes of crystalloids (lactated Ringer’s solution, 0.9% NaCl). Hetastarch and hypertonic saline can improve mean arterial blood pressure and thus cerebral perfusion pressure without exacerbating brain edema. If the patient is anemic, whole-blood or packed red blood cell transfusion may assist in maintaining normovolemia, as well as adequate tissue oxygenation, by improving blood oxygen content, the major determinant of which is hemoglobin concentration. Fluid support may include one or more of the following choices:

• Hypertonic saline (7%): 4 to 5 mL/kg over 5 to 10 minutes for hypovolemic shock in dogs, 2 mL/kg in cats. Hypertonic saline is also available as 23.4% solution, which cannot be administered undiluted, but may be mixed 1 : 3 with hetastarch or dextran-70 (e.g., 20 mL 23.4% hypertonic saline +40 mL hetastarch or dextran-70 in a 60 mL syringe) to produce a solution of synthetic colloid suspended in a 7% hypertonic saline solution. Sodium does not freely cross the blood-brain barrier; therefore, hypertonic saline can reduce cerebral edema via an osmotic pull of fluid out of the brain parenchyma and into the intravascular space. It also has positive inotropic effects and immunomodulatory effects, and reduces endothelial swelling. Although hypertonic saline has been shown to improve mean arterial blood pressure and cerebral perfusion pressure and to protect against increased intracranial pressure, sodium has recently been implicated as the major osmotic agent contributing to brain edema. Hypertonic saline may have a global protective effect on the brain, but theoretically may lead to increased compromise to focal areas of damaged parenchyma caused by compromise of the blood-brain barrier in these regions. Because it provides rapid volume expansion and treats cerebral edema, hypertonic saline is the authors’ resuscitation fluid of choice in the euhydrated, hypovolemic head-trauma patient. Dehydrated trauma victims should receive isotonic crystalloid resuscitation.

• Synthetic colloids: 10 to 20 mL/kg to effect (up to 40 mL/kg/hr) for shock. This can be given as a rapid bolus in dogs; give it in 5 mL/kg increments over 5 to 10 min in cats. Dextran-70 is an acceptable alternative but, when given as sole fluid support, has not exhibited the beneficial effects demonstrated with hetastarch and hypertonic saline. Because the volume expansion effects of synthetic colloids are limited in dehydrated patients, isotonic crystalloid fluids should be used in these cases.

• Isotonic crystalloids (lactated Ringer’s solution, 0.9% saline): 20 to 30 mL/kg bolus over 15 to 20 minutes for shock. May be repeated as necessary after reassessment. Because overhydration with subsequent worsening of brain edema and increased intracranial pressure is a concern with crystalloid administration, the “shock dose” (90 mL/kg in the dog, 60 mL/kg in the cat) of crystalloids should be given incrementally to effect, as described previously. If the entire volume is not necessary to restore euvolemia and normal mean arterial blood pressure, fluid administration should be tapered when these physiologic goals are met.

• Blood products: Administration of 1 mL/kg of packed red blood cells (RBCs) or 2 mL/kg of whole blood will increase the PCV by 1%. The severity of anemia will dictate the total dose to be administered, but 10 to 15 mL/kg of packed (RBCs) is a reasonable starting dose. Blood products are typically administered over 4 hours, but may be given faster (to effect) if the patient is unstable. Boluses of blood products are acceptable in the severely anemic trauma patient. The goal of therapy with blood products is to correct the anemic state to a PCV between 25% and 30%. Patients with demonstrated coagulopathy should also be treated with fresh frozen plasma at a dose of 10 to 15 mL/kg 2 to 3 times per day until coagulopathy has resolved.

Oxygen Therapy

Hyperoxygenation is recommended for most acutely brain-injured animals. Oxygenation status of a head-trauma victim can be assessed initially on the basis of breathing rate and pattern, mucous membrane and tongue color, and thoracic auscultation. Pneumothorax and pulmonary contusions are common sequelae of trauma and need to be addressed, if present.

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. 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). The use of an O2 cage is generally an ineffective method of administering supplemental O2 to the severely brain-injured patient, as 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. Oxygen concentrations as high as 95% can be delivered at proportionately higher flow rates. Nasal O2 catheters must not be placed in the nasal cavity caudal to the level of the medial canthus (to avoid entering the cranial vault through a possible fracture site). Inadvertent jugular vein compression, which can cause increased intracranial pressure, should be avoided while placing a transtracheal O2 catheter. High flow rates with nasal O2 catheters may induce sneezing, which has the potential to raise intracranial pressure. 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. Arterial blood gas measurement is the best way to monitor PaCO2 levels. End-tidal CO2 measurement is a useful monitoring tool, but tends to underestimate true PaCO2 levels. Venous CO2 levels (PvCO2) are also helpful, and are usually less than 5 mm Hg greater than PaCO2. However, in patients with perfusion deficits, peripheral PvCO2 levels can be significantly higher than arterial values and should be interpreted cautiously. Ventilatory rates of 10 to 20 breaths per minute should keep PaCO2 levels between 25 and 35 mm Hg in the absence of significant pulmonary parenchymal disease. Although this has been the recommended range of PaCO2 levels to prevent excessive brain vasodilation, recent evidence suggests that PaCO2 <30 mm Hg may lead to excessive vasoconstriction with subsequent impairment of cerebral perfusion pressure. Hyperventilation may be deleterious to patients whose intracranial pressure elevation is not due to hypercarbia-induced dilation of brain vasculature. Indiscriminate use of hyperventilation to decrease intracranial pressure should be avoided, as excessive vasoconstriction of brain vasculature can decrease cerebral perfusion pressure.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Medical and Surgical Management of the Brain-Injured Pet
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