Head Trauma management:
In the case of head trauma, particularly blunt head trauma, we are primarily concerned with elevated ICP. The human skull cavity is a fixed volume space. It houses the brain, blood vessels, nerves, and spinal fluid. The sum of all these parts is 100% utilization of the volume of the skull cavity. This is important because, if any one of these variables increases (blood volume, CSF volume, cerebral swelling, etc) it comes at the expense of the space available to the other contents of the skull. This applies to ICP (intracranial pressure), in that: any rise in ICP will result in displacement of the brain downward, toward the only exit point from the cranial cavity (the foramen magnum); in a process known as cerebral herniation. Cerebral herniation presents a major problem for the first responder because, the bottom of the brain, AKA the brainstem, is home to the pons and medulla. These areas contain the centres for vital functions including respiration. In the event of herniation, the brainstem is squeezed downward and does not function properly. To further complicate this issue; elevated ICP causes impaired cerebral circulation, and cerebral hypoxia. As we know, the brain needs an uninterupted supply of oxygen and glucose to function; any impairment is a major problem. The human brain needs to maintain a CPP (cerebral perfusion pressure) of 60 to 80 mmHg in order to sustain vital functions. The formula for CPP is MAP – ICP = CPP. This means that our mean arterial pressure to the brain drops by the amount ICP increases. The higher the ICP, the lower the CPP.
In blunt head trauma, where swelling and intracranial bleeding may occur, ICP can climb rapidly.
So how can we, the first responders address this problem? We arent neurosurgeons after all.
Well, the short answer is: we can’t fix the problem. BUT, we can slow down the process until definitive care is reached. We do this by addressing the H Bombs of head trauma:
- Hypotension
- Hypoxia
- Hyperventilation
We know that the main problem we have is a perfusion one. Our MAP is not sufficient to overcome the ICP and maintain CPP. To address this, we want to target a MAP of at least 90 mmHg (or 110 mmHg systolic BP). This allows us to ensure that, despite elevated ICP, we are still perfusing the brain.
Next we want to ensure adequate ventilation and oxygenation. Patients with elevated ICP often display a triad of Hypertension, Bradycardia, and irregular respirations (Cushing’s Triad). Because the Pons is under pressure, the respiratory group is not functioning properly. The patient cannot exchange CO2 effectively. CO2 is a vasodilator, which means that it causes leakage of fluid in the cerebral vessels and contributes to cerebral swelling. Our goal is to ventilate these patients and target an ETCO2 of 30-35 mmHg. We want to blow off the extra CO2 and hyperoxygenate the patient. Oxygen, unlike CO2, is a vasoconstrictor. If we target an SPO2 of 94 to 98% we can reduce cerebral swelling and minimize ICP elevation.
Even doing these things doesn’t get us out of the woods completely. We still have to assess regularly for evidence of worsening ICP and herniation. We want to watch for:
- Irregular or unresponsive pupils
-Hemiparalysis
- Decorticate or decereberate posturing
Seizures are also a possibility, so have benzodiazepines on standby.
Comments