In today’s VETgirl online veterinary continuing education blog, Dr. Garret Pachtinger, DACVECC reviews specific treatment for head trauma in the dog and cat. Last week, he discussed the underlying pathophysiology of brain/spinal injury, neurologic evaluation, and Modified Glascow Coma scoring, so make sure to check out that head trauma: Part 1 blog HERE.
Initial diagnostic tests should include a minimally invasive, global patient assessment. This includes a complete blood count (CBC), serum chemistry panel, and venous blood gas. Jugular veins should be avoided as holding off the vein and phlebotomy may increase ICP. Blood pressure and pulse oximetry are also recommended. In the context of trauma, ultrasonographic evaluation of the chest and abdomen (AFAST/TFAST) are also helpful. Due to the need for sedation or restraint, radiographs are rarely performed on initial patient assessment.
The use of computed tomography (CT) and magnetic resonance imaging (MRI) are more sensitive at detecting intracranial lesions. An MRI is considered to be the best imaging modality for detection of fibrocartilagenous emboli (FCE).
Emergency Treatment of Head and Spinal Trauma
Initial assessment for any trauma patient should address any life-threatening abnormalities. Patients presenting with head or spinal trauma should be assessed for other life threatening abnormalities including shock. Rushing to assess the neurological status without addressing life threatening shock may result in further morbidity and mortality as well as an incorrect neurological diagnosis as patients in shock often exhibit depressed mentation due to the hypotensive state without any true brain injury.
Stabilization of the head and spine are important priorities with brain and spinal cord injury. WITH head trauma, the patient is placed on a board where their body is supported ultimately resulting in an elevation of the head 15–30 degrees. The goal of this positioning is to encourage cerebral venous drainage, ultimately to decrease intracranial pressure. During this procedure it is important to avoid pressure on the jugular veins or bending of the neck which can decrease venous drainage and increase ICP.
If spinal cord injury is suspected, the patient should be immobilized on a firm, flat surface such as a backboard.
Decreased oxygen delivery is an important contributor to secondary neurological injury. For this reason, oxygen delivery is a priority in treatment of CNS trauma. During initial patient assessment, oxygen can be administered, via ‘flow-by’ or mask. This delivery method allows continued patient assessment and treatment as opposed to an enclosed oxygen cage which will prevent further patient assessment.
Along with oxygen therapy to address hypoxemia, hypovolemia and shock need to be addressed. Volume resuscitation should be addressed with a goal of a mean arterial blood pressure of 80–100 mm Hg. Fluid therapy options include isotonic crystalloid therapy (LRS, 0.9% NaCl, P-Lyte), hypertonic crystalloid therapy (7.2% NaCl), synthetic colloid therapy (Hetasarch, Vetstarch), or a combination of therapies. Unless there is concurrent complicating disease such as cardiac disease, fluid therapy is important in head trauma patients as hypovolemia compromises cerebral perfusion pressure (CPP). Careful administration of intravenous crystalloid fluids at ¼ – 1/3 of the calculated shock volume of fluids (90 ml/kg in dogs and 60 ml/kg in cats) should be administered with frequent patient reassessment to assess response to therapy. Alternatively, 2-5 ml/kg of a synthetic colloid such as Hetastarch or vetStarch can be administered as an IV bolus.
If the patient presents obtunded, stuporous, or comatose, hyperosmotic solutions such as mannitol are commonly considered. Mannitol has a rapid onset of action with effects lasting as long as 6 hours. The benefits of mannitol include an immediate plasma expanding effect, reduction in blood viscosity, increased CBF, and increased cerebral oxygen delivery. Treatment should be followed with crystalloids or colloids to maintain intravascular volume. The dose of mannitol 20% is 0.5–1.5 g/kg in dogs and cats. Mannitol is most commonly administered in boluses over 15-20 minutes rather than a CRI to prevent rebound hypotension.
Hypertonic Saline is an alternative hyperosmotic agent and preferred in hypovolemic patients. Hypertonic saline creates an osmotic effect, pulling water out of the CNS and decreasing ICP. The recommended dose for volume expansion is 5-10 ml/kg of 7.5% sodium chloride. The volume expanding effects are immediate but redistribution is rapid, within 15–75 minutes. To create a solution with longer effects, a 1:2 ratio combining 23.4% hypertonic saline with 6% hetastarch can be used, termed “turbostarch.”
Corticosteroid use is not currently recommended in the treatment of traumatic brain injury. Although corticosteroids have anti-inflammatory effects, they are associated with several negative issues including hyperglycemia, immunosuppression, delayed wound healing, and gastric ulceration. Hyperglycemia has been shown to be a negative prognostic indicator in humans and dogs with severe head injury.
Regarding spinal trauma, the use of methylprednisolone sodium succinate (MPSS) is currently considered the gold standard of care in spinal trauma (30 mg/kg IV once, then 15 mg/kg IV 2 and 4–6 hours later). The time frame for reported benefits in human patients is administering the MPSS within 8 hours of the traumatic event. After this time frame, there has been no documented benefit of steroid use in helping improve prognosis for return to function.
Traumatic brain injury and spinal trauma are common presentations to the small animal clinician. Initial assessment must be a global patient assessment, with careful evaluation of the ABCDs of triage medicine. Rapid and direct patient assessment are best made to reduce morbidity and mortality in the polytrauma patient.
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