P. 410

An Urban Experience
volume. Additionally, the high sodium content of hypertonic saline draws  uid 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 2-4ml/kg (cats) of 7.5% NaCl should be given over 5-10 minutes.
Colloids (i.e., Hetastarch, Dextran-70) allow for low volume  uid resuscitation especially if total protein concentrations are below 50g/L or 5g/dl. These  uids also draw  uid from the interstitial and intracellular spaces, but have the added bene t 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 mins, with frequent patient re- evaluation. A total dose of 20ml/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 haemoglobin- based oxygen carriers has not been well evaluated in head trauma but initial studies suggest that they could play a valuable role.
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 mmHg and the PaCO2 below 35-40mmHg. If the patient is able to ventilate spontaneously and effectively, supplemental oxygen should be delivered via ‘ ow-by’; con nement 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  ow and reduces intracranial pressure by decreasing edema. After administration, mannitol expands the plasma volume and reduces blood viscosity, which improves cerebral blood  ow 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  uid volume within the brain. Mannitol (0.5 g/kg-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  ve hours.
Systemic blood pressure may require additional treatment to maintain adequate cerebral perfusion pressure. A mean arterial pressure of 80-100 mmHg should be the target blood pressure. Hypotension should initially be treated with  uid resuscitation; however, persistent hypotension may require treatment with vaso-active 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 re ex. 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

   408   409   410   411   412