Karen Kline, DVM
Neurologic emergencies are any structural or functional disturbance of the CNS which has an acute onset. Such emergencies can result in reversible neuronal impairment, but they must be treated aggressively to avoid irreversible changes or death.
Types of intracranial neurologic emergencies include for trauma, metabolic causes such as hypoglycemia or hepatic encephalopathy, neoplastic processes which induce inflammation and peritumoral edema, vascular disorders such as thromboembolism, and seizures. Spinal cord emergencies include acute intervertebral disk rupture, fibrocartilagenous embolism and trauma. Neuromuscular emergencies include myasthenia gravis and peripheral nerve injury.
The neurologic assessment of the patient with a neurologic emergency involves assessment of mentation (level and content of consciousness), cranial nerve reflexes and function, gait, (if possible), postural reactions, motor function and, finally, sensory function. The importance of the neurologic examination cannot be over emphasized. It allows the clinician and technician the ability to neurolocalize the lesion and prognosticate recovery. It is extremely important to conduct serial neurologic examinations to look for progression or regression.
Traumatic brain injury involves missile injuries, vehicular injuries, falls or cranial bite wounds. In each case, a progressive increase in intracranial pressure (ICP) is the most deadly sequelae. However, one must remember that the brain has remarkable compensatory powers and that patience is a virtue. Traumatic brain injury can be viewed as encompassing 2 parts: 1) primary injury in which parenchymal and/or vascular damage is accrued and 2) Secondary injury which entails ATP depletion, intracellular Na+ and Ca2+ accumulation, O2 free radial and/or cytokine production, nitric acid accumulation and lactic acidosis. The initial assessment of the patient is critical an involves the "ABC's" of trauma management (airway, breathing, cardiovascular status), quick assessment tests (PCV, T.P., blood glucose, lytes) and the immediate correction of hypoxemia and hypovolemia to avoid increased ICP. It is important to act calmly, but quickly. Limitation of fluid therapy is contraindicated and maintenance of blood pressure (MAP) not below 90 mmHg is recommended. Fluids of choice include hydroxyethylstarch (Hetastarch®): canine: 10-20 mg/kg, feline: 5 ml/kg over time) or hypertonic saline (4-5 ml/kg over 3-5 minutes) intravenously.
Assessment of oxygenation can be accomplished through pulse oximetry and blood gas analysis. Nasal oxygen, O2 cage or transtracheal O2 can be used to maintain it. Hyperventilation should be used judiciously since it can exacerbate cerebral edema if prolonged. Other therapies include head elevation of 15-30 degrees, physical therapy and nutritional support.
Drug therapies for intracranial trauma and neoplastic processes include mannitol, an osmotic diuretic that decreases ICP by reflex vasoconstriction. Its effects last for 2-5 hours and it is administered over 10-20 minutes at a dose of 0.5-1 mg/kg IV. No more than 3 doses should be given in 24 hours. Other therapeutics include furosemide (Lasix®) at 2-5 mg/kg IV, and glucocorticoids, whose use has been hotly debated. If used, the recommended route is IV with the "high-dose Methylprednisolone" (Solu-medrol®) protocol used at a dose of 30 mg/kg at time 0, then 15 mg/kg at 2 and 4 hours.
Other intracranial emergencies include status epilepticus, high ICP from brain neoplasia, hypoglycemia and hepatic encephalopathy. Primary control of status can be attained through the use of diazepam (Valium®) at a dose of 0.25-0.5 mg/kg IV slow or 0.5-1 mg/kg per rectally. If no response is attained after 2 doses, then other drugs such as pentobarbital (2-8 mg/kg IV to effect) or Propofol (used in humans) may be used. Concurrent Phenobarbital administration at 2 mg/kg TID may be instituted.
Brain neoplasms exert their effects by causing peritumoral edema (most likely vasogenic), which initially, may be quite steroid responsive. Prednisolone sodium succinate (Soludelta Cortef®) can be used (Dose: 20 mg/kg IV slowly over 5-10 minutes) as well as mannitol at a dose of 0.5-1 gm/kg IV slow over 10-20 minutes. Hypoglycemia and hepatic encephalopathy should be treated accordingly with medical management.
Spinal cord emergencies include spinal luxations/subluxations, Type 1 intervertebral disk disease, fibrocartilagenous embolism and meningitis. Neurolocalization of spinal cord lesions is important (C1-C5, C6-T2, T3-L3 and L4-S2) for prognostication and diagnostics. Prognostication is dependent upon the type of injury, the duration of clinical signs, the presence or absence of voluntary motor activity and the presence or absence of conscious pain perception. If conscious pain perception is lost for over 6 hours, the prognosis drops considerably. If present, (dependent on cause of injury) there is a > 75-80% chance of recovery. Conscious proprioception, voluntary motor, superficial and deep pain are progressively lost and return in the reserve order. Treatment of such injuries includes patient stabilization, neurologic assessment and the administration of Solu-medrol (Methylprednisolone sodium succinate) at an intravenous dose (preferably within 6 hours of the injury) of 30 mg/kg at time 0, then 15 mg/kg at 2 and 4 hours. Surgical intervention is indicated where appropriate and immediate referral is indicated when the patient has lost voluntary motor activity or is deteriorating neurologically. It is important to recognized the difference between the withdrawal reflex and conscious pain perception. An animal with a transected T3-L3 spinal cord may have a normal withdrawal reflex.
Neuromuscular emergencies can include fulminant acquired myasthenia gravis (MG) and traumatic peripheral nerve injury. The myasthenic crisis is managed with IV fluids, acetylcholinesterase inhibitor administration (injectable Pyridostigmine as a constant rate infusion (CRI) 0.01-0.03mg/kg/hr), injectable corticosteroids (Soludelta cortef®) and injectable antibiotics for aspiration pneumonia.
Evaluation of the neurologic patient is a must and should be done serially. One must look for trends (either good or bad) in consciousness, breathing patterns, pain perception and CNN function. Nothing should be taken for granted. Post-traumatic syndrome occurs secondary to brain injury and can include hemispheric damage, brainstem injury/compression, cerebrovestibular dysfunction, epilepsy, diabetes insipidus and the effect of hypovolemia and hypotension. The key points to remember in patients with neurologic emergencies are : acquisition of a thorough history, thorough physical and neurologic examinations, the ABC's of critical care, treating the animal and not its bloodwork, not to be too hasty on prognostication, look for trends, know when to refer, and that patience is a virtue.