Increasing ICP has a devastating effect on the tissue perfusion of the brain. Because the brain is located in a vault of a fixed size there is little room for an increase in size. There are three components in the cranial vault, with the brain accounting for 80%, the blood and vessels accounting for 12%, and the cerebrospinal fluid accounting for 8%. Any increase in one of these components must be met by an equal decrease in another of the components in order to maintain a constant intracranial pressure. Should this fail to occur due for any reason it will cause a rise in intracranial pressure compressing important brain structures, the spinal column, restricting blood flow to the brain or causing herniation.
In order to understand the effects of an increasing ICP it is important to understand how the brain perfuses its tissues under normal circumstances. Inside the cranial vault there is a special pressure working against the mean arterial pressure (MAP) due to the fixed space. This pressure is known as intracranial pressure (ICP). ICP causes an interstitial hydrostatic pressure working against the intravascular hydrostatic pressure caused by the heart. Think of it as if you were trying to blow up a balloon, except that as you try to inflate it someone else has their hands around it trying to push the air back out, the harder they push the more difficult it becomes to inflate the balloon. Therefore, in order to find the actual cerebral perfusion pressure (CPP) the ICP must be subtracted from the MAP [CPP=MAP-ICP]. Put very simply, what this equation means is that an increase in MAP will result as an increase in CPP, while an increase in ICP will cause a decrease in CPP.
The body, generally, has a very efficient auto-regulatory system when MAP is between 60 mmHg and 160 mmHG and a CPP between 50 mmHg and 150 mmHg, with the ICP in a healthy adult approximately 0-15 mmHg. If CPP drops below an appropriate range, chemoreceptors sense this change and cause vasodilation allowing for increased cerebral blood flow (CBF) and increasing the cerebral blood volume (CBV), rapidly returning the CPP to an acceptable range.
As the ICP rises however, specifically above 35 mmHg (whether due to edema, intracranial bleed, tumour or other pathology) the body's auto-regulatory mechanisms begin to fail and can actually cause greater damage. As mentioned above, when the ICP increases, the CPP decreases. When the CPP decreases, vasodilation occurs in an attempt to increase CBF but also increases CBV in a space that already can't handle anymore volume, which increases ICP, further decreasing CPP and thus the cycle continues. As perfusion in the brain continues to decrease there is an activation of the sympathetic nervous system causing tachycardia and peripheral vascular constriction in an attempt to raise blood pressure and feed the brain as much as possible. This significant increase in blood pressure stimulates the baroreceptors in the aorta which causes an activation of the parasympathetic system which then slows the heart, causing bradycardia. As pressure continues to rise, pressure begins to impede the functions of portions of the brain including the brain stem which includes the respiratory centre. The increase in pressure on the respiratory centres cause irregular respirations. These actions taken by the body are observed as Cushing's Triad (widening pulse pressure, bradycardia, irregular respirations). As ICP continues to increase the brain is eventually pushed out of the skull by the pressure resulting in brain herniation which can quickly cause severe disability or death.
Proper identification and treatment of increased ICP is important to give the patient the best possible chance of a positive outcome, and one of the most widely discussed and fiercely debated treatments for ICP is hyperventilation. The reasoning behind hyperventilation is straightforward. Carbon dioxide (CO2) is a very potent vasodilator. Hyperventilation will decrease the amount of CO2 in the body causing vasoconstriction which should lower the CBV and thus lower ICP. It is also extremely fast acting requiring only seconds of before vasoconstriction begins. There are some serious issues with this simple solution however. Firstly, vasoconstriction can significantly reduce cerebral blood flow to the brain. Not only is the reduction in CBF an issue, but the low levels of CO2 increase the affinity of hemoglobin for oxygen (pushing the oxyhemoglobin dissociation curve to the left). This means that not only is there less blood flow, but the blood that does get through is less likely to supply an adequate amount of oxygen. Hyperventilation of a patient can also lead to an increase in intrathoracic pressure which will lead to a decrease in venous return which can also cause an increase in ICP.
All of that being said, hyperventilation therapy can be a lifesaving tool if used in the proper place, at the proper time and to the proper extent. As was discussed previously, CO2 is a very potent vasodilator, in fact, for every 1 mmHG drop in the PaCO2 there is a 3% decrease in the size of the arterioles. This can decrease the ICP but will also decrease cerebral blood flow, which can lead to ischemia and ultimately necrosis. Increasing ICP, however, can compress the blood vessels, compress vital regions of the brain as well as cause herniation. Under these dire circumstances, the lesser of two evils must be considered, and it may be better to cause ischemia in order to prevent herniation.
Without evidence of herniation, ventilation of a patient with increasing ICP should be maintained at a normal rate, approximately 12 breaths per minute. This will keep the partial pressure of CO2 (PaCO2) at approximately 40 mmHg, with 35-40 mmHg being the goal. In order to manage this, capnography should be used, the more accurate the better, seeing as falling out of this range can lead to poor patient outcomes. The patient should be monitored consistently for signs of cerebral herniation which include headache, one or both pupils dilated and unreactive to light, abnormal posturing (particularly decerebrate posturing), decreased LOC often with a GCS dropping 2 points or more (from a score of eight or less), vomiting, and irregular respirations. If the signs are present, acute hyperventilation may help to prevent severe disabilities or death. Monitor the PaCO2 to prevent it from dropping below 30 mmHg, as a patient who drops below a PaCO2 level of 30 mmHg is statistically more likely to have worse outcomes upon survival. It is also important to remember that hyperventilation is not the only treatment for an increased ICP and should be used as a last resort. Unfortunately, the most effective treatment for ICP is drainage of cerebrospinal fluid from the cavity but that option is not available in the prehospital setting. Fortunately, there are more options for those in the field.
Two of the most essential treatments are also the most simple. Sit the patient up to promote venous return and help prevent as much blood from getting trapped in the cranial vault and provide oxygen to keep the brain oxygenated. A look at the data suggests that there is a serious correlation between a drop in the PaO2 to below 60 mmHg in the arterioles of the brain and worse patient outcomes. A PaO2 of this level, even for a short time, was associated with a 50% mortality rate with approximately 50% of the survivors having severe disabilities. This is due to the fact that as oxygen saturation approaches 50 mmHg, the arterioles dilate increasing blood flow in an attempt to get more oxygen but also increasing ICP.
Intravenous fluids can also be a huge help to a patient suffering from increased ICP. Hypotension, below a systolic pressure of 90 mmHg, can cause significant issues for patients because of the fact that the CPP is decreasing at an exaggerated rate due to a decreasing MAP and increasing ICP. Fluid resuscitation is important, though the right type of fluid is still up for debate. Isotonic solutions are readily available are more than adequate to maintain a blood pressure. New studies, however, have shown that hypertonic solutions may be more beneficial due to their ability to shift fluid out of the tissues of the swelling brain and back to the vasculature (some studies suggest it is nearly as effective as mannitol). This also causes an increase in blood pressure with less solution as compared to an isotonic solution as fluid is pulled into the vasculature from the tissues. One of the issues with the hypertonic solution is the tendency to dilate the arteries. What the net difference is between a fluid shift out of brain tissue and a dilation of the arteries is yet to be determined.
Mannitol is a drug that can be given in the case of ICP. It works to create an osmotic gradient in the blood-brain barrier shifting fluid out of the tissues of the brain thereby lowering ICP. It lowers blood viscosity allowing blood to flow more easily and maintains cerebral blood flow. It has also been shown not to affect brain tissue oxygenation. It should be given as a bolus, as a continuous infusion has been shown to cause an uptake of mannitol into the brain tissue and shift the osmotic gradient in an undesired direction.
Sedatives have also been given to patients with ICP. These are only useful to patients with anxiety issues. Studies have only shown them to be effective at relaxing nervous patients to help prevent an increase in ICP. Giving patients without anxiety sedatives has been correlated with poorer patient outcomes and longer times spent in the intensive care unit. Another technique to controlling ICP involves putting the patient into a hypothermic state. Research has found that for every one degree Celsius that the body's temperature drops, there is a decrease in the cerebral metabolic rate of oxygen by 6%-7%. A lower metabolic rate means that less oxygen is used giving a slightly larger buffer before ischemia occurs. The induced hypothermia was generally maintained for between 24-48 hours in the analysis. Be conscious as to the duration, as some studies have shown that hypothermia in the field followed by rapid rewarming upon admission to the hospital may cause a rebound in ICP leading to problems. One analysis found that patients under 45 years old were 76% more likely to have better ICP control and lower chance of poor outcome if there were kept in a hypothermic state (just less than 35 degrees Celsius) for 48 hours as compared to patient warmed upon admission.
A patient with an increasing ICP is in a very serious predicament. The only definitive treatment is to get them to the hospital, though there are a few things to be done for them. Promote venous return by having the patient sit up if possible. Provide oxygen and prevent hypotension below 90 mmHg. If possible and within your scope, administer mannitol- a hypertonic fluid, or induce hypothermia. Hyperventilation should be used as a last resort against impending herniation of the brain. Understanding the signs and symptoms as well as understanding the benefits and limitations of the treatments is essential in delivering proper patient care.
References
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Obrist WD, Langfitt TW, Jaggi JL, Cruz J, Gennarelli TA: Cerebral blood flow and metabolism in comatose patients with acute head injury. Relationship to intracranial hypertension. J Neurosurg 61:241-253, 1984
Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, et al: Guidelines for the management of severe traumatic brain injury. XIV. Hyperventilation. J Neurotrauma 24 (1 Suppl):S87-S90, 2007
Di Bartolomeo S, Sanson G, Nardi G, Scian F, Michelutto V, Lattuada L: Effects of 2 patterns of prehospital care on the outcome of patients with severe head injury. Arch Surg 136:1293-1300, 2001
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