Increased Intracranial Pressure: The Basics
Introduction
Everyone has some level of intracranial pressure, and a variety of things can increase or decrease it throughout the day. For instance, intracranial pressure spikes with coughing, sneezing, and intense muscle movements like a deadlift. ICP is measured in mmHg just like blood pressure, and can be specifically measured using an indwelling/placed catheter into the cranium. In the prehospital world, we can unfortunately only make our best educated guesses on intracranial pressure based off our assessment findings.
Pathophysiology of Increased ICP
The Monroe-Kelli Doctrine
The Monroe-Kelli doctrine is a simple principle used to explain the end effects of intracranial pressure. The doctrine spells out that the cranial vault is composed of 3 things: brain (80 percent), blood (10 percent), and cerebrospinal fluid (10 percent). The cranial vault has limited room beyond the above stated substances. If any one of the above substances has an increase in their volume, then the rest of the contents of the cranial vault are displaced. There is no buffer zone for changes in pressure. This increase in volume without a reciprocal decrease in another substance’s volume ends up forcing the brain against the edges of the cranium and eventually down into the foramen magnum at the base of the skull. This end-stage process is called herniation.
Visual representation of the Monro-Kellie Doctrine
As the image above shows, the brain is able to moderately compensate for small changes in volume by diverting out fluid, venous, and arterial volumes. However, most patients that are experiencing ICP issues post-injury in the EMS world are beyond that point.
Brain Perfusion
The brain is an extremely delicate organ that requires extensive nutrition and perfusion to maintain normal function. The brain itself uses an astronomic amount of blood flow in comparison to other major organs in the body.
During times of extreme intracranial pressure that affects the body’s ability to perfuse the brain, the body actually compensates by soaring hypertension. This hypertension is a way for the body to work against the excess pressures of the increased ICP/cerebral edema and continue to perfuse. Imagine a blockage in a pipe - as fluid stacks up and tries to clear the obstruction to make it the rest of the way through, the pressure that the fluid runs increases (Pinto, 2022). As a result of this excess pressure, the baroreceptors of the aortic arch and carotid arteries signal an activation of the parasympathetic nervous system, which in turn lowers the heart rate to bradycardic levels. These are two parts of Cushing’s triad. Irregular respirations, the third part of Cushing’s triad, occurs because of the excess pressure on the respiratory centers of the brain. Bradycardia and hypertension are the compensatory mechanism, with irregular respirations being a symptom of the greater problem (Pinto, 2022).
Cerebral perfusion pressure is the pressure at which the brain is perfusing blood and thus oxygen into the brain. However, if ICP is in excess of the cerebral perfusion pressure, the CPP fails to work against the ICP and fails to perfuse the brain as a result. The body cannot physically drive blood and thus vital nutrients into the brain if ICP is higher than the CPP. CPP is calculated by subtracting ICP values (mmHg) from mean arterial pressure (MAP).
Hypertension in a patient with increased ICP is not something we want to try to control or drop prehospitally - or even really at all. Hypertension is the means by which the body is attempting to compensate for and continue to perfuse the brain. This is why modern protocols typically have an exception or clinical pearl regarding blood pressure goals for those with suspected TBIs versus general trauma patients.
What actually raises ICP?
We most commonly see ICP raises in EMS as a result of a traumatic brain injury. Traumatic brain injuries can prompt cerebral edema as a response to the injury which in turn works against the other volumes in the cranial vault as per the Monro-Kellie doctrine described above. As inflammatory mediators and additional fluid flows to heal the newly inflamed cells, the cells of the brain swell.
Other afflictions that can raise ICP include brain tumors, hydrocephalus (an increase in the fluid volume in the brain without another primary cause), or a brain abscess.
Herniation
As pressures rise in the cranial vault, the brain and other contents are forced to the path of least resistance. The brain will begin to herniate, or shift, out of place and towards other areas of the cranial vault. We will discuss the most common presentations below.
Uncal Herniation
The uncus is a small brain structure found just superior to the brainstem itself. It is part of the temporal lobe of the brain. It is responsible for the processing of memory, the sense of smell, and processing emotions (Uncus | Anatomy, n.d.). The uncus is situated just anterior to the brainstem’s connection into the brain and just posterior to the midbrain as shown below.
When intracranial pressure spikes and is maintained at high levels, it can prompt the uncus to shift posterior into the midbrain and brainstem. In doing so, it compresses the oculomotor nerve (CN III), arousal pathways of the brain, and the corticospinal tract (Decker, 2022). The posterior cerebral artery can also be occluded and destroyed in the process.
Contrary to popular belief, the pupils do not “blow” during increased ICP due to hemorrhage behind the eye itself. In actuality, uncal herniation compresses CN III and thus cuts off innervation for the eyes. CN III is responsible for the movement of the eye up, down, medially, and the actual motion of the pupil. It is responsible for the constriction or dilation of the pupil in response to stimuli.
With innervation to the oculomotor nerve lost, the pupil is no longer able to maintain its normal levels of constriction appropriate to the environment. As a result, the pupil fully dilates. This compression can be one sided, resulting in the ipsilateral blown eye appearance portrayed above. The patient may be fully alert and conscious during this time. With time, the trochlear and abducens cranial nerves may become dominant, pulling the eye downwards and laterally without the oculumotor function opposing them (Decker, 2022).
As uncal herniation continues, the patient will begin to experience further damage to arousal pathways and eventually lose consciousness. Thus, ipsilateral eye issues can be an early indicator of an uncal herniation in a TBI patient.
Tonsillar Herniation
Tonsillar herniation is the movement of the cerebellar tonsils down into the foramen magnum as a result of superior pressure shifting the brain downwards. With time, this will compress the brainstem, cutting off essential life functions (Knight, 2023).
It is important to remember that the brainstem is responsible for the most basic of life functions, and includes parts such as the midbrain, pons, and medulla oblongata. The pons in particular is responsible for the rate of respirations, while the medulla oblongata is primarily responsible for regulating blood pressure, heart rate, and the depth of respirations. The midbrain serves as a nexus for crossing sensory information into the brain and sending efferent signals back down the spinal cord.
With compression and herniation of these vital areas of the brain, the patient will experience rapid loss of consciousness, abnormal respiratory patterns and rate, bradycardia, sensory deficits, and eventual death if left untreated.
Clinical Signs & Symptoms of Increased ICP
What is done for increased ICP?
EMS
EMS interventions for increased ICP are unfortunately limited to prompt recognition, triage to the appropriate comprehensive trauma center, and supportive measures.
Current standard protocol endorses basic ICP measures such as elevating the head of the stretcher 30 degrees, slight hyperventilation to target ETCO2 within 30-35 mmHg, and maintaining blood pressure over 110mmHg in head trauma patients specifically.
Hospital
Definitive treatment for acute ICP issues/TBI include craniotomy, drainage, and use of hypertonic solutions such as Mannitol in order to pull fluid out of sites of cerebral edema.
Works Cited
Decker, R. (2022, August 8). Uncal Herniation. StatPearls - NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK537108/
Knight, J. (2023, February 12). Tonsillar Herniation. StatPearls - NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK562170/ Pinto, V. L. (2022, August 1). Increased Intracranial Pressure. StatPearls - NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK482119/ Uncus | anatomy. (n.d.). Encyclopedia Britannica. https://www.britannica.com/science/uncus
