Contusiones Cerebrales. Trucos.

Maintaining cerebral perfusion pressure (CPP), cerebral hemodynamic and metabolism are of paramount importance. End goal directed therapy EGDT is the cornerstone to ensure microcirculatory perfusion and early detection of treatment failure.

The approach to the patient with encephalic trauma should be systemized and follow the ABC emergency protocols giving priority to the airway control, breathing and ventilation and correction of circulatory disturbances. A throughout emergency anamnesis, primary stabilization and finally the complete neurological examination should be performed.

This sequence essentially protects the brain from hypoxia, hypoventilation and hypotension which are determinants of poor prognosis.

Evidence-based strategies for the treatment of the encephalic trauma patient include the following:

 Maintain mean arterial pressure MAP >65 mm Hg (systolic pressure >100 mm Hg) to prevent secondary neurologic injury. Fluid therapy is based on EGDT key goals in patients with TEC. Hypotension is a proven factor responsible for the reduction in CPP and increase in mortality in human patients with encephalic trauma.

 Mannitol intravenously infuse 0.5–1 g/kg of the 20% solution in 10 to 20 minute infusion (after securing the minimum hemodynamic parameters). It reduces blood viscosity, brain edema, and intracranial pressure ICP thus increasing blood flow and CPP. Do not administer more than three boluses within 24 hours to prevent side effects and osmolarity >320 mOs/L.

 Maintain adequate oxygenation and ventilation (SaO >95%; PaO >80 mm Hg; EtCO and PaCO₂ 30–35 mm Hg). Hyperventilation has been associated with worsening of ischemic lesions and its therapeutic benefit is controversial. Hyperventilation should only be applied in those cases of ICP refractory to mannitol and sedation. It is better to increase respiratory rate and not tidal volume to avoid prejudicing the venous return. The goal is to keep PaCO₂ at 30 mm Hg, reserving levels of 25 mm Hg for severe and refractory cases.

 Raise the patient body as whole 45 degree in the prone position; this facilitates venous drainage and reduces the ICP. Avoid compressing the jugulars and exaggerated inclination that could increase intra-abdominal pressure IAP. Monitor IAP with the aim to early detect any interference on blood pressure and cerebrospinal fluid (CSF) drain.

 Use sedation protocols, only when agitation compromise the maintenance of compartment pressures. However, heavy sedation increases mortality.

 Early endotracheal intubation, if needed to keep oxygenation and ventilation.

 Controlled hypothermia (1.5–2.5°C below normal) it has neuroprotective effects by reducing excitatory amino acids, lipid peroxidation and endogenous consumption of antioxidants.

 Do not administer furosemide. Furosemide does not reduce brain edema and it does increase hypovolemia.

 Administer hypertonic saline NaCl 7.5%, it improves systemic arterial pressure, has anti-inflammatory and anti-free radicals properties, increases osmolarity maintaining intravascular volume, generates an osmotic gradient through the intact blood-brain barrier, reduces edema, promotes diuresis and significantly rapidly decreases the ICP.

 Do not administer high-dose corticosteroids. Despite its excellent anti-inflammatory action on the CNS, several prospective studies in humans showed no significant advantages of their use in encephalic trauma. The final results from the randomized CRASH Trial presented by the end of 2006, concluded that the percentage of death and long term neurological dysfunction in adults with severe encephalic trauma and altered consciousness at presentation in which corticosteroids at high doses were used, was higher than the control group.

 Glycemic control. Hyperglycemia is directly associated with increased mortality in people with severe encephalic trauma. Excessive glucose offer to the ischemic brain results in severe cerebral lactic acidosis and increased brain damage.

 Surgical approach. Early decompressive craniotomy and craniectomy for immediate reduction of the ICP. Craniectomy involves removing an area of the skull to allow adequate expansion brain; this area should be big enough to allow brain expansion without damaging the brain tissue.

 Monitor and control IAP. There are some reports of nonsurgical and surgical abdominal decompression treatment for refractory increased ICP in encephalic trauma patients.

Monitoring

The evaluation of the ICP is still not routinely used in veterinary medicine, but if possible it should be performed whenever the patient has an adapted Glasgow coma score GCS of less than 8 points and abnormalities on the CT scan or MRI and in cases were systolic pressure is less than 100 mm Hg in association with signs of decerebration.

References

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