Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN
Small Animal Medicine & Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA, USA
Initial assessment should involve evaluation of the patient’s respiratory and cardiovascular system. An airway must be established, if necessary, through endotracheal intubation. Breathing patterns may be affected by thoracic trauma, but may also be secondary to brain injury. Auscultation of the thorax may detect pulmonary pathology or cardiac arrhythmias. Oxygen support should be given as necessary and mechanical or manual ventilation may be required with severe pulmonary injuries. Traumatic pneumothorax may require thoracocentesis or chest tube placement to allow proper ventilation. The cardiovascular system should be evaluated by monitoring heart rate, blood pressure, and electrocardiography. An electrocardiogram may demonstrate cardiac arrhythmias secondary to traumatic myocarditis, systemic shock, or brain injury. Arterial blood analysis and lactate concentrations may provide additional information regarding systemic perfusion and respiratory function.
Neurological assessment should be undertaken on any animal, which has experienced a trauma. Assessment of neurologic status in a patient after head trauma should initially be performed every 30 to 60 minutes. Frequent assessment allows for monitoring efficacy of treatment and early recognition of a deteriorating status. Primarily, neurological evaluation of the patient serves to determine whether there are neurological deficits suggesting structural neurological lesions, where the lesions are located (i.e., at least intracranial, spinal and peripheral nerve), and the severity of the lesion(s). Detection of a spinal and/or peripheral nerve (e.g., brachial plexus) lesion can impact on the prognosis of any patient with head trauma. Without any extracranial lesions, the prognosis associated with head trauma is dependent on the location and severity of the parenchymal lesions. The assessment should include evaluation of state of consciousness, motor function and reflexes, pupil size and responsiveness, position and movement of the eyes, and breathing pattern. The evaluation of pupil and eye function is the most accurate manner in which brainstem function can be assessed and this is the most important part of the examination prognostically. A scoring system has been developed in veterinary patients to provide an objective assessment and allow for rational diagnostic and treatment decisions.
Treatment strategies should be directed toward both systemic and neurologic stabilization in an effort to minimize secondary damage. Several aspects of treatment exist. Systemic stabilization involves correction of systemic shock and respiratory abnormalities with fluid therapy and oxygen therapy/management of ventilation, respectively. The second aspect of treatment involves measures to reduce elevations in intracranial pressure and cerebral metabolic rate. Finally, some animals require surgical intervention because of lack of improvement or a declining neurologic status.
The goal of fluid therapy of the head trauma patient is to restore a normovolemic state. It is deleterious to dehydrate an animal in an attempt to reduce cerebral oedema. Aggressive fluid therapy and systemic monitoring are required to ensure normovolemia to maintain adequate CPP. Crystalloid, hypertonic, and colloid fluids should be given concurrently to help restore and maintain blood volume following trauma. Crystalloids are usually given initially for the treatment of systemic shock. These balanced electrolyte solutions may be given at shock doses (90 ml/kg for dogs, 60 ml/kg for cats). Typically, it is recommended that the shock dose be given in fractions starting with one third to one fourth of the calculated volume, frequently reassessing the patient for normalisation of MABP, mentation and CVP if monitored, and giving additional fractions if needed. Unfortunately, crystalloid solutions will extravasate into the interstitium within one hour of administration requiring additional fluid resuscitation. Hypertonic and colloid fluid therapy can rapidly restore blood volume using low volume fluid resuscitation; additionally, colloids remain in the vasculature longer than crystalloid fluids. These fluids should be used with caution as without concurrent administration of crystalloid solutions, hypertonic and colloid solutions can lead to dehydration. Other benefits of hypertonic fluids include the ability to improve cardiac output, restore normovolemia, and reduce inflammation after trauma. Hypertonic saline may be preferred in hypovolemic, hypotensive patients with increased ICP.
Hypertonic saline improves cerebral perfusion pressure and blood flow by rapidly restoring intravascular blood volume. Additionally, the high sodium content of hypertonic saline draws fluid from the interstitial and intracellular spaces, subsequently reducing intracranial pressure. Contraindications to administration of hypertonic saline include systemic dehydration and hypernatremia. Hypertonic saline only remains within the vasculature for about one hour; therefore, it should be followed by colloids to maximize its effects. A dose of 5–6 ml/kg (dogs) and 2–4 ml/kg (cats) of 7.5% NaCl should be given over 5–10 minutes.
Colloids (i.e., hetastarch, dextran 70) allow for low volume fluid resuscitation, especially if total protein concentrations are below 50 g/L or 5 g/dl. These fluids also draw fluid from the interstitial and intracellular spaces, but have the added benefit of staying within the intravascular space longer than crystalloids. Hetastarch is typically given at 5–6 ml/kg boluses in dogs and 2–4 ml/kg in cats over 5–10 min, with frequent patient reevaluation. A total dose of 20 ml/kg/day may be given. In addition to volume resuscitation, oxygen-carrying capacity should be considered, especially if the PCV<30%. The use of Oxyglobin and other haemoglobinbased oxygen carriers has not been well evaluated in head trauma, but initial studies suggest that they could play a valuable role.
Systemic blood pressure may require additional treatment to maintain adequate cerebral perfusion pressure. A mean arterial pressure of 80–100 mm Hg should be the target blood pressure. Hypotension should initially be treated with fluid resuscitation; however, persistent hypotension may require treatment with vasoactive agents (i.e., dopamine 2–10 mg/kg/min). Additionally, systemic hypertension may occur as a sequela to intracranial hypertension as a result of the Cushing reflex. Systemic hypertension secondary to ICP elevation should be treated by aggressively treating elevated ICP; the use of additional drugs to modulate the blood pressure should be avoided unless all attempts to lower ICP have been exhausted.
Oxygen Therapy and Management of Ventilation
Oxygen supplementation is recommended in all patients following head trauma. Control of PaO2 and PaCO2 is mandatory and will affect both cerebral haemodynamics and ICP. Permissive hypercapnea should be avoided because of its cerebral vasodilatory effect that increases ICP. Hypocapnea can produce cerebral vasoconstriction through serum and CSF alkalosis. Reduction in CBF and ICP is almost immediate although peak ICP reduction may take up to 30 minutes after PCO2 has been changed. The amount of oxygen within the blood can be assessed by measuring oxyhemoglobin saturation with a pulse oximeter (SpO2), measuring the PaO2 with blood gas analysis in conjunction with measurement of circulating haemoglobin concentration. Calculation of oxygen delivery to the tissues requires measurement of both arterial oxygen content and cardiac output. Measurement of mixed venous oxygen can provide an indirect measure of adequacy of oxygen supply to the tissues. The amount of carbon dioxide within the blood can also be assessed by arterial blood gas analysis as well as via capnography. Capnography provides breath by breath assessment of adequacy of ventilation assuming normal cardiovascular function. This technique measures CO2 in the expired patient gases (P'ETCO2), which approximates the CO2 tension in the alveoli. As alveolar gases should be in equilibrium with arterial blood, P'ETCO2 can be used to approximate PaCO2 unless severe pulmonary dysfunction is present.
The goal of oxygen therapy and management of ventilation is to maintain the partial pressure of oxygen in the arterial blood supply (PaO2) greater than or equal to 90 mm Hg and the PaCO2 below 35–40 mm Hg. If the patient is able to ventilate spontaneously and effectively, supplemental oxygen should be delivered via 'flow-by'; confinement within an oxygen cage prevents frequent monitoring. Face masks and nasal catheters should be avoided, if possible, as they can cause anxiety, which may contribute to elevations of intracranial pressure.
Intracranial pressure can be aggressively addressed with the administration of osmotic diuretics. Osmotic diuretics, such as mannitol, should not be given to any patient without being certain that the patient has been volume resuscitated. Mannitol improves cerebral blood flow and reduces intracranial pressure by decreasing edema. After administration, mannitol expands the plasma volume and reduces blood viscosity, which improves cerebral blood flow and delivery of oxygen to the brain. Additionally, mannitol assists in scavenging free radicals, which contribute to secondary injury processes. Vasoconstriction occurs as a sequela to the increased partial pressure of oxygen, leading to an immediate decrease in ICP. Additionally, the osmotic effect of mannitol reduces extracellular fluid volume within the brain. Mannitol (0.5–2.0 g/kg) should be given as a bolus over 15 minutes to optimize the plasma expanding effect. Continuous infusions of mannitol increase the permeability of the blood brain barrier exacerbating oedema. Lower doses of mannitol are as effective at decreasing ICP as higher doses, but may not last as long. Mannitol reduces brain oedema over about 15–30 minutes after administration and has an effect for approximately two to five hours.