start of surgery then every q 24 hours for a maximum of 3 days Cats: 1 mg/kg PO once daily for a maximum of 3 days
CRI, constant rate infusion; ICP, intracranial pressure; IM, intramuscularly; IOP, intraocular pressure; IV, intravenously; NMDA, N‐methyl‐d‐aspartate; PO, per os (orally); SIADH, syndrome of inappropriate anti‐diuretic hormone.
Fluid therapy in the burned veterinary patient requires special consideration, especially with respect to percentage of total body surface area affected. For information on fluid therapy for the burned patient, see Chapter 53.
Regardless of fluid type and rate used to treat shock and or dehydration, frequent patient reassessment is critical. General recommendations for patient re‐evaluation are listed in Table 1.2.
Neurologic Assessment
Initial neurologic assessment often occurs concurrently with respiratory and cardiovascular triage. Patients with normal consciousness are alert and aware of their environment. Obtunded patients have decreased responsiveness that can vary in severity. Stuporous patients are only responsive to noxious or excessive stimuli, whereas comatose patients do not respond to any stimuli. Decreased cerebral perfusion and oxygenation from hypovolemic, hypoxemic, distributive, and cardiogenic shock can have profound effects on mentation, so the patient's initial neurologic assessment must be made with patient's global perfusion status in mind. In both veterinary and human patients with traumatic brain injury, most have also sustained concurrent injuries to other major body systems that can have secondary neurologic consequences [76, 77]. Hypoglycemia (metabolic shock) can also lead to decreased mentation and must be treated before an accurate neurologic examination can be performed. As with other body systems, frequent neurologic reassessment is imperative.
While performing the neurologic evaluation, until adequate oxygenation is confirmed, supplemental oxygen should be provided by mask, flow by, or placement of the patient in an oxygen cage. In patients with head trauma, nasal prongs or nasal oxygen catheter are avoided to decrease the risk of sneezing, which can increase their intracranial pressure (ICP). Heart rate and blood pressure values can also provide important insight about the presence of increased ICP. The Cushing's reflex, which is hypertension and reflex bradycardia, is commonly seen in patients with cerebral edema, hemorrhage, skull fractures, and intracranial masses. To maintain cerebral perfusion pressure (CPP) in the face of intracranial hypertension, arterial blood pressure (MAP) is increased, since CPP equals MAP minus ICP. Pressure receptors in the aortic arch and carotid bodies trigger a decreased heart rate in response to the increase systemic blood pressure. Treatment of intracranial hypertension is imperative and is accomplished with a combination of patient positioning and pharmacologic intervention with mannitol or hypertonic saline. If there is any evidence of or concern for head trauma or ICP, the patient's head should be elevated 15–30 degrees using a flat board or other rigid surface. Pillows should not be used to elevate the patient's head, as this can cause compression of the jugular vein(s), which impairs cerebral venous outflow. Jugular venipuncture should also be avoided. Mannitol (0.25–1 g/kg IV over 15–20 minutes) is an effective osmotic diuretic to decrease intravascular volume and facilitate fluid movement from the central nervous tissue, as with cerebral edema. The resultant diuresis will lead to dehydration if mannitol administration is not followed by intravenous fluid therapy in patients that cannot or will not drink. Hypertonic saline (7.5%, 3–5 ml/kg IV over 15–20 minutes in dogs, 2–3 ml/kg IV over 15–20 minutes in cats) is also effective for treating intracranial hypertension secondary to cerebral edema and works via free water osmotic shifting out of the tissue and into the hypertonic intravascular space created by the increased sodium load [78]. Concentrated (21%) sodium chloride can be combined with 0.9% saline to create a 7.5% solution by mixing 17 ml of 21% saline with 43 ml of crystalloid. The use of corticosteroids is contraindicated in patients with head trauma, as they can contribute to gastrointestinal ulceration, especially after an episode of hypoperfusion, and precipitate hyperglycemia, which has been associated with a worsened neurologic injury in veterinary patients [79].
Veterinary patients with any history of or concern for cervical or spinal trauma should be secured to a backboard until a complete assessment of injuries is performed. In trauma patients, assessment of cranial nerves, visual examination for external signs of head trauma, and any abnormalities of body position, spinal reflexes, and the presence or absence of pain sensation should be determined before administration of drugs that may impact interpretation of findings, including analgesics and atropine. However, assessment for the presence of a head tilt, physiologic nystagmus, and postural reflexes should only be performed if it is safe to move the patient's neck and limbs. Body position changes that can be seen in patients with trauma, spinal cord lesions, or intracranial disease include Schiff–Sherrington (forelimb extensor rigidity and hindlimb flaccidity associated with a T2‐L4 spinal cord lesion), decerebrate rigidity (neck extension, hyperextension of all four limbs, and decreased consciousness), and decerebellate rigidity (thoracic limb hyperextension, variable changes in the pelvic limbs, and appropriate consciousness).
A veterinary modified Glasgow Coma Scale score (mGCS) has been developed and evaluated retrospectively for assessing the severity of neurologic injury [80]. Scores are determined after assessment of level of consciousness, cranial nerve function, and motor function with higher scores (15–18) being associated with a better prognosis than lower scores (3–8 for grave prognosis and 9–14 for poor to guarded). Scoring and exact prognostication should be performed with caution however, since the mGCS has not been prospectively evaluated and patient scores may improve with therapeutic intervention and time. In a study of injured dogs and cats for whom the mGCS was used as part of trauma scoring for a veterinary trauma database, mGCS scoring system corresponded with outcome in dogs and cats with known head trauma [81, 82].
For patients with deficits in conscious proprioception, motor function, and pain sensation, spinal reflexes should be used for neurolocalization of spinal cord dysfunction to segments C1–C5, C6–T2, T3–L3, L4–S1, and S1–S3. Common causes of spinal cord disease in veterinary patients include intervertebral disc disease (IVDD), trauma, neoplasia, vascular events, and infectious/inflammatory processes. Surgical intervention could be indicated for traumatic, neoplastic, and IVDD, especially those conditions resulting in neurologic dysfunction. Patients with rapidly progressive neurologic changes and loss of deep pain may require emergency diagnostic imaging and surgical intervention, especially if IVDD is the cause. Patients with cervical lesions (C1–C5) are at risk of ventilatory failure due to phrenic and intercostal nerve involvement, particularly after surgical decompression, as there will be the added impact of secondary surgical swelling and hemorrhage. Respiratory pattern, effort, and objective measures of ventilation (PvCO2 or PaCO2) should be monitored very closely. Changes in oxygenation (PaO2 and SpO2) as a result of ventilatory failure may be late findings and should not be the sole determinant of effective ventilation and respiration. Mechanical ventilation may be necessary in patients with cervical lesions and should be anticipated in all postoperative patients with cervical neurolocalization.
Urinary Assessment
Many injuries and abnormalities of the urinary tract are not readily apparent on initial triage and physical examination. Historical information from the pet owner regarding changes in water consumption, urine production, stranguria, pigmenturia, and recent trauma can raise suspicion for urinary tract dysfunction, however, some patients have vague and non‐specific historical signs. For example, many male cats with urethral obstruction present for lethargy and/or constipation, as many owners are unable to differentiate stranguria from tenesmus.
After respiratory, cardiovascular, and neurologic
