Introduction^{1, 17, 20, 22, 39, 56, 64, 67}

Pathophysiology of head trauma^{5, 6, 8, 17, 20, 22, 26, 27, 32, 34, 39, 49, 56, 64, 66, 67}

1. 
   

   Primary brain injury

   
   

   This type of 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 (Fig. 8.1) and vasogenic edema. Skull fractures can contribute to continued trauma to the brain parenchyma and blood vessels, especially if they are unstable (Fig. 8.2). 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.

   

   

   
   
2. 
   

   Secondary brain injury

   
   

   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 ICP (Box 8.1).

   
   

   Adenosine triphosphate (ATP) depletion disrupts the maintenance of cellular ionic homeostasis. Sudden, uncontrolled intracellular influx of sodium (Na⁺) and calcium (Ca⁺⁺) occurs. Cellular swelling (cytotoxic edema) and depolarization result. The uncontrolled depolarization leads to the release of large amounts of glutamate, an excitatory neurotransmitter, into the extracellular environment. Glutamate causes further increases in intracellular Ca⁺⁺ levels. Elevated Ca⁺⁺ 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 (Fe⁺⁺) is a vital cofactor 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 Fe⁺⁺ and membranes with high levels of PUFAs and cholesterol. Intraparenchymal hemorrhage also increases the amount of Fe⁺⁺ available for the 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 (NO) 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 above-mentioned processes and also leads to the accumulation of lactic acid (via anaerobic glycolysis). Lactic acid accumulation leads to 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 result of these secondary processes is increased ICP. Unlike primary brain injury, the clinician has some control over secondary brain injury.

   
   
3. 
   

   Intracranial pressure (ICP) dynamics

   
   

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

   
   
   
   
   
   
   

   The normal contents of the cranial cavity include brain parenchyma, blood, and cerebrospinal fluid (CSF). In the normal animal, these components exist in equilibrium with each other and ICP remains within normal limits. Between the MABP extremes of 50–150 mmHg, ICP remains constant. This phenomenon is called pressure autoregulation. Pressure autoregulation serves to link systemic blood pressure changes to brain vascular tone. If MABP rises, vasoconstriction occurs in the brain; if MABP falls, vasodilation occurs in the brain. In the normal animal, the former scenario prevents ICP from rising by decreasing CBF, and in the latter, prevents ICP from falling by increasing CBF. 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 MABP 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. Due to the inexpansible nature of the skull, one or more components of the cranial cavity must accommodate for the increased volume, or increased ICP will result. This accommodation or volume buffering is accomplished by fluid shifts in the brain vasculature and CSF 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 ICP increases. If intracranial volume increases beyond the abilities of compensatory mechanisms, progressively larger increases in ICP result per unit of volume increase (Fig. 8.3), CPP is compromised, and ischemic death of brain tissue occurs. In cases of severe head trauma, intracranial compliance often is quickly exhausted. If MABP decreases (hypotension), especially in combination with hypoxemia, the brain vasculature will vasodilate in an effort to preserve blood flow. The increase in blood volume increases ICP, but CPP 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 ICP.

   

Initial assessment and emergency treatment^{2, 9, 11, 17, 19, 20, 22, 24, 32, 36, 46, 50, 53, 57, 59, 62–64, 74, 78, 79} (Video 17)

1. Fluid therapy (Table 8.1)

   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   
   

   Fluid type	Recommended dose
   Isotonic crystalloid (0.9% NaCl preferred)	20–30 ml/kg dogs 10–20 ml/kg cats Administered over 15–20 min Reassess after
   Synthetic colloid (e.g. 6% hydroxyethyl starch)	5–10 ml/kg Administered over 15–20 min Reassess after
   7.5% sodium chloride	4 ml/kg Administered over 15–20 min Reassess after Always follow with crystalloid therapy
   3% sodium chloride	5.4 ml/kg Administered over 15–20 min Reassess after Always follow with crystalloid therapy
   1:2 ratio of 23.4% sodium chloride and 6% hydroxyethyl starch or other synthetic colloid	4 ml/kg Administered over 15–20 min Reassess after Always follow with crystalloid therapy
   Packed red blood cells	∼1 ml/kg Administer over less than 4 hrs/unit Target normalization of perfusion parameters and PCV = 25–30%
   Whole blood	∼2 ml/kg Administer over less than 4 hrs/unit Target normalization of perfusion parameters and PCV = 25–30%
   Fresh frozen plasma	10–15 ml/kg Administer over less than 4 hrs/unit Target normalization of coagulation times

   
   
2. 
   

   There is often concern that aggressive intravenous fluid therapy to counteract hypotension in the brain-injured patient may aggravate brain edema. There is both evidence to support and evidence to refute this concern. Because of this concern, there have been recommendations to volume-limit victims of severe head trauma. Such recommendations are not only unfounded, but strictly contraindicated. There is no debate over the disastrous consequences to the injured brain if hypotension is allowed to persist. Hypotension has been repeatedly shown to be a reliable predictor of sustained elevations of ICP 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 of less than 120 mmHg 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 (LRS, 0.9% NaCl). Hetastarch and hypertonic saline can improve MABP and thus CPP without exacerbating brain edema. If the patient is anemic, whole-blood or packed red blood cell (pRBC) 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:

   
   
   
   
   1. Synthetic colloids: 10–20 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 5–10 min in cats. Hetastarch is the author’s fluid of choice in restoring normal blood pressure in the euhydrated head-trauma victim. Dextran-70 is an acceptable alternative, but given as a sole fluid support it has not exhibited the beneficial effects demonstrated with hetastarch and hypertonic saline. Dehydrated trauma victims should receive isotonic crystalloid resuscitation.
      
   2. Hypertonic saline (7%): 4–5 ml/kg over 3–5 min for shock. 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 of 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 (BBB); 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, immunomodulatory effects, and reduces endothelial swelling. Although hypertonic saline has been shown to improve MABP and CPP and protect against increased ICP, 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 due to compromise of the BBB in these regions.
      
   3. Isotonic crystalloids (LRS, 0.9% saline): 20–30 ml/kg bolus over 15–20 min for shock. May be repeated as necessary after reassessment. Since overhydration with subsequent worsening of brain edema and increased ICP 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 above. If the entire volume is not necessary to restore euvolemia and normal MABP, fluid administration should be tapered when these physiologic goals are met. Since 0.9% saline has less free water than LRS, this crystalloid may be preferable for use in the brain-injured pet.
      
   4. Blood products: Administration of 1 ml/kg of pRBCs 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 10–15 ml/kg of pRBCs is a reasonable starting dose. Blood products are typically administered over 4 hrs, but may be given faster (to effect) if the patient is unstable. Boluses of blood products are acceptable in the severely anemic trauma patient. Goals of therapy with blood products are a PCV between 25 and 30%. Patients with demonstrated coagulopathy should also be treated with fresh frozen plasma (FFP) at a dose of 10–15 ml/kg 2–3 times per day until coagulopathy has resolved.
   
   
3. 
   

   Oxygenation and hyperventilation

   
   

   Hyperoxygenation is recommended for most acutely brain-injured animals. Oxygenation status of a head-trauma victim can be initially assessed based upon 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. It should be noted that, in the face of increased respiratory rate and effort, lung sounds may not consistently be decreased on auscultation in patients with pneumothorax. A rapid, shallow breathing pattern, pale oral mucous membranes, and evidence of respiratory distress should raise the clinician’s index of suspicion for the presence of pneumothorax. Thoracentesis should be done in any trauma patient in whom there is a suspicion of pneumothorax, and should be considered a diagnostic test as well as a therapeutic intervention. If negative pressure cannot be obtained via thoracentesis, a chest tube should be placed immediately. If arterial blood gas analysis is available, the partial pressure of oxygen in arterial blood (PaO₂) should be maintained at or above 90 mmHg for dogs, and 100 mmHg for cats. Pulse oximeters are extremely useful and relatively accurate estimators of oxygenation status. However, the reliability of pulse oximeters varies with model used, with the PaO₂ level (pulse oximeters may overestimate oxygenation status at lower PaO₂ levels), and with the patient’s hemodynamic status. In general, oxyhemoglobin saturation values (SpO₂

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