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Increased Intracranial Pressure




Our brain is a super cool organ. As it sits encased in the cranium, it is the machine of all machines when it comes to making our body function. Neurological emergencies are one of my favorite subjects (second to hypovolemic traumas) that really peaks my interest. The Monro-Kellie doctrine describes perfectly why neurological emergencies can occur. Our cranium is a ridged box that houses a constant sum of our brain, cerebral spinal fluid and blood vessels. Due to the cranium being a fixed size, these three things are so tightly auto-regulated that any insult to the noggin can have drastic effects. When one of these three increases in size, the functionality of the other two are compromised. We can have alterations causing increased cranial pressure due to cerebral edema, mass formation, intracranial bleeding, and or the inability to regulate, produce or remove cerebrospinal fluid. In this blog, we are going to discuss normal anatomical and physiological aspects of the brain, signs and symptoms of increased intracranial pressure and we will hit it home with interventions to help mitigate increased intracranial pressure in the prehospital setting. The Skull consists of eight cranial bones that are connected by immovable sutures. The Cranial floor houses many holes for the neurovasculature and cerebrospinal fluid to enter and exit the skull. Of importance is the Foramen Magnum, which is the largest opening at the base of the skull that allows the spinal cord to connect to the brain stem. Let’s take a look at what the cranium houses, because it’s not just “the brain”. Per the Monro-Kellie doctrine, the cranium is a fixed/ridged box whose volume tends to remain constant. In an attempt to simplify the reality of increased intracranial pressure, we have three main components that affect ICP: The Brain, Cerebrospinal Fluid and Blood.

1. THE BRAIN: Ok, I need to just prepare you guys. I’m about to throw some super cool shit down. The brain accounts for 2% of our body weight BUT it accounts for 15% of our total blood flow. Every 24 hours the brain requires: 1000L of blood flow, 71L of Oxygen and 100g of glucose. The brain utilized 80% of the cranial space. (10) That blows my mind 🤯🤓 (terrible pun intended). It’s a needy little thing… kinda like my kids… 2. CEREBROSPINAL FLUID: The Cerebral spinal fluid (CSF) is a clear colorless fluid that is housed in the ventricles and covers, or “bathes” the outside of the brain and spinal cord. Spinal fluid is produced at a rate of roughly 500mls each day by the blood vessels lining the floor of the ventricles. Much of the CSF is reabsorbed with the adult brain containing roughly 140mls of CSF at a time. 💦 This accounts for 10% of the cranial space. This CSF constantly flows through the central nervous system providing the glucose the brain needs as well as acting as a fluffy pillow for minor brain injuries. (10) 3. BLOOD: 🩸 The third component is blood flow. Blood is supplied to and from the brain via the carotid artery and jugular vein. Interruption of blood flow can cause irreversible brain damage if deprived of oxygen for longer than 4-5 minutes. The brain typically contains 750mls of blood, which accounts for 10% of the cranial space. (10)


Cerebral blood flow (CBF) allows a necessary, constant supply of oxygen and glucose to the brain. Cerebral autoregulation helps maintain the CBF over a wide range arterial pressure. When one of the three components increases, the other two are adjusted to compensate and maintain a sense of normalcy. Normal cerebral autoregulation adjusts mean arterial pressures to target and maintain a normal intracranial pressure (ICP) of 10-15 mm Hg. Cerebral blood flow is directly related to Cerebral perfusion pressure (CPP). A normal CPP is 60-80 mmHg. (2) Cerebral perfusion pressure is a product of mean arterial pressure (MAP) minus the ICP. Under normal circumstances without increased intracranial pressure, we aim for a MAP of >65 mmHg. This allows for adequate cerebral perfusion pressure to supply the brain with the necessary oxygen and glucose. If ICP were to become higher than the MAP, CBF would cease to exist. SOOOO… with increased intracranial pressure, we need to aim for a higher MAP to target a normal CPP. In the prehospital setting, we rarely have access to ICP monitoring capabilities. We are either transporting from a scene or transferring from a critical access hospital with minimal capabilities to a higher level of care. With critical thinking, if we are noting signs of increased intracranial pressure, our ICP is potentially >15-20 mmHg. It would be safe to gather that an adjustment to our MAP goal be >90 mmHg to maintain a targeted CPP >70mmHg in the presence of increased intracranial pressure. On the flip side, if you are transducing and the ICP is known, Adjust the MAP to target a CPP of at least 60mmHg.


The partial pressure of carbon dioxide (PaCO2) and oxygen (PaO2) contribute to our ability to auto-regulate our CBF. I would like to further explain this as it’s something we can use to our benefit with intervention to help decrease intracranial pressures. Vasodilation occurs with hypercapnia and hypoxia, increasing CBF. This means that a decrease in co2 is linked to vasoconstriction which decreases the CBF, thus playing a part in decreasing volume in a fixed space. A really great read “Evaluation and management of elevated intracranial pressure in adults”, notes that for every 1 mmHg change in PaCO2, it is associated with a 3% change in CBF. (1)

Signs and symptoms Injured tissues are subjected to swelling and bleeding, the brain is no different. If the we cannot autoregulate and adjust blood flow and or cerebral spinal fluid flow to accommodate for the increased volume, we increase our intracranial pressure and the signs and symptoms are a direct result of said increased ICP. Obtaining a thorough initial neurological assessment can help when reassessing and trending neurological assessments. Signs and symptoms are relative to volume change and duration of that change and can correlate with compression of CSF, nerves, blood flow and brain tissue. The increase in intracranial pressure occurring from a large volume shift in a short duration produces a more definitive case presentation than one with a minimal change in volume over a longer duration. With that, when performing our assessment, it is very critical to get a detailed history to help correlate signs and symptoms.


📌 Severe Headache 📌 Blurred vision 📌 Fatigue 📌 Weakness

📌 Uncoordinated movements 📌 Vomiting 📌 Nausea 📌 Unilateral deficits

📌 Loss of consciousness 📌 Altered mental status 📌 Pupillary changes 📌 Seizure 📌 Decerebrate posturing 📌 Cushing’s Triad





The last thing we want for our patients is for them to herniate. This is a very loose term as there are many types of brain herniations that can occur. Essentially, cerebral herniation is a shift or displacement of cerebral tissue from its normal location to an adjacent location in the cranium. When we speak in terms of brain herniation, I would bet that many of us think of the “tonsillar herniation” which is a downward shift of the brainstem or the cerebellum being displaced thought the Foramen Magnum (the big hole in the bottom of the cranium). Another herniation we might confuse the for a Tonsillar hernia is one of the most common cerebral hernia, Descending Translatorial Hernia (DTH). This DTH causes paralysis of the 3rd cranial nerve resulting in non reactive pupils. However, other herniations can happen in the brain that include midline shifts, outward shifts, or upward shift…. All the shifts. I digress. 🧠 Many of these herniations present with classic herniation symptoms including, unresponsiveness or decreasing level of consciousness, unilateral pupils or a blown pupil (Cranial nerve 3 compression), seizure like activity, decerebrate posturing and Cushing’s Triad.



Picture retrieved from: “Types of Cerebral Herniation and Their Imaging” (6)



Let’s discuss Cushing’s Triad. I love my history facts. Cushing’s triad was first described by Dr. Harvey Cushing in 1901 (3). Once intracranial pressure reaches a threshold, a Cushing’s reflex is triggered which results in symptoms of the Cushing’s Triad: hypertension, or widening pulse pressure to be more specific, bradycardia and irregular respirations. Cushing’s reflex is stimulated by significantly increased intracranial pressure. This activates the sympathetic nervous system that causes vasoconstriction and increased cardiac output. This increases arterial blood pressure attempts to restore cerebral perfusion, resolve hypoxia and prevent infarction. The Bradycardia is thought to be the result of one or two things. The increased arterial blood pressure stimulates the baroreceptors of the carotid bodies which causes bradycardia and or, bradycardia results from intracranial vagal nerve compression. Lastly, we have irregular respirations. This irregular breathing is characterized by irregular shallow breaths and periods of apnea. This occurs due to compression of the brain stem which is the control center for our breathing. (7) Patients do not need to present with all three signs to indicate herniation. Recognizing the signs and symptoms of increased ICP early allows us to intervene as early as possible. Time is Tissue. ⏰ (The brain isn’t a muscle)



Interventions


In the prehospital setting interventions are aimed at decreasing intracranial pressure to prevent secondary brain injuries related to hypotension and hypoxia. It is well documented that even one episode of hypoxia or hypotension increases mortality. When signs of increased intracranial pressure are present, we can start by improving our patient outcome with small but important interventions and escalating to more aggressive interventions reserved for signs and symptoms of herniation.


Let’s start with simple interventions. When the head of the bed is elevated, we are allowing gravity to help blood flow down and out of the cranial cavity. Maintaining the head midline, or in anatomical position, helps by decreasing blood flow restriction. A c-collar placed on a trauma patient can be both beneficial and detrimental. The c-collar helps maintain the head midline however if placed too tight can cause blood flow restriction. Consider applying the c-collar as loose as possible, placing a soft Aspen collar as soon as possible, or finding another way to maintain c-spine such as towel rolls or head blocks. Additionally, a blood sugar should be taken on every patient that presents with signs and symptoms of increased intracranial pressure. Glucose is vital for brain function. 🎂🍰🧁


If we need to manage an airway, there are several ways to help positively impact a patient with a head injury. During our set up of RSI, our laryngoscope can be a “bad guy” in this situation. According to, The Walls Manual of Emergency Airway Management, if we are not gentle with our blade during insertion and manipulation of the larynx we could stimulate what is known as the Reflex Sympathetic Response to Laryngoscopy (RSRL). This stimulation is caused by aggressive use of the laryngoscope blade during intubation that causes a stimulation of the sympathetic nervous system leading to a catecholamine surge. Of course, we all know that a SNS response leads to increased heart rate and BP which correlates with increased cerebral blood flow. The issue that arises is the increased CBF, increasing volume leading to increasing ICP. It is recommended to use video laryngoscope and the most experienced provider to intubate. (5)


I’m about to swallow my pride on this next one, and talk highly of Succinylcholine. Before I do, I would like to preface that it is provider preference and knowledge-based/evidence-based reasons why roccuronium is a fan favorite of mine. This is however a relatively opinion-based blog, right? (See my slurry of sources at the bottom.) However, with Succinylcholine and Neurological patients, there is a benefit to the short duration that this depolarizing paralytic offers. Not only can we gather a good patient Neuro assessment prior to intubation, we can also do trending Neuro assessments post intubation as well. Another benefit is that the receiving hospitals are able to gather a relatively good assessment, granite the patient will most likely have sedation and pain on board but none the less this allows rapid assessment for more timely surgical interventions if necessary. I will say that after Intubation, the 45-60 minutes it takes for Roccuronium to wear off would most likely have occurred by the time the patient arrives at the receiving hospital and has a CT/Imaging done…. So, there’s that…. Moving on.


Once we have successfully intubated our patient, we can aid in decreasing our intracranial pressure with our ventilator settings. According to The Walls Manual of Emergency Airway Management, mechanical ventilation of patients presenting with increased ICP should focus on oxygenation, normocapnia and avoidance of High PEEP and PIPs (to decrease venous congestion). (5) As described earlier, low PaCO2 causes vasoconstriction, lowering cerebral blood flow which aids in lowering increased ICP. We do NOT want to hyperventilate our patients so much that we cause so much vasoconstriction that results in tissue ischemia from the lack of blood flow -- this is legit a balance act. We can aid in decreasing ICP while still maintaining CBF by keeping our ETCO2 on the low side of normal; 35-40 cmH2O. (5) (10)


Blood Pressure is of great importance in patients with head injuries. Every effort in managing these patients must include thought for the cerebral blood flow. More importantly, the mean arterial pressure for reasons described earlier in this blog. In the presence of increased ICP, aim for a MAP > 90 mmHg or a Systolic BP >100-110 mmHg. (10) I know this is a very vague paragraph regarding blood pressure and increased ICP but this is such a big topic that it could be its own blog. If thats something you are all interested in, let me know!


Osmotic medications are used for patient presenting with moderate to severe signs of elevated ICP. Osmotic medications have been shown to decrease ICP in the acute setting, it has not been shown to improve long term outcomes. (8) The two most common medications are Hypertonic saline and Mannitol.


Hypertonic saline is a very commonly used medication for treatment of increased herniation presenting with signs and symptoms of herniation. Typically, this fluid comes in many concentrations with 3% hypertonic saline being the most common. The mechanism of action for Hypertonic saline involves shifting fluids from the interstitial space to the intravascular space. This occurs because Hypertonic saline has a higher concentration of solute (more sodium) than that of plasma and interstitial fluid. This difference in gradient helps drive fluid from the interstitial space (the brain tissue) and into the intravascular space.


Mannitol is a diuretic osmotic agent. Mannitol inhibits the reabsorption of water and electrolytes and increase urinary output. In relation to ICP, mannitol aids in reduction of cerebral blood flow and withdrawing water from the brain tissue. Reduction of ICP occurs within 15-30 minutes after administration. (9)


Surgical Interventions are typically the definitive treatment for patients with increased intracranial pressure. For this reason, as prehospital providers, move with a purpose. Surgical treatments that could be considered are Burr holes, bone flap removals, hematoma excavations and VP shunts just to name a few.


Let’s not forget the crazy story of the EZ-IO. This was performed by a Doctor, NOT a prehospital provider! Lol. Don’t get any crazy ideas. While this was a one-off procedure attempt that was successful, it remains just that, a one off. I commend the provider for performing this procedure as it was a last-ditch effort when faced with a critically deteriorating patient and a delayed transport to a pediatric level 1 trauma center. While this may not be the main stay in evacuating hematomas, maybe it will one day. (For doctors only, lol)






Management of neurological emergencies related to increased intracranial pressure should have a primary focus on decreasing intracranial pressures and decreasing secondary injuries from hypotension and hypoxia. As prehospital providers we must remember that an adequate history correlating with patient presenting signs and symptoms can help guide us in our prehospital cares. Thank you for taking the time to read this and making it this far. I hope you all enjoyed the read!




Brittany Grandfield, Flight Nurse. ✌️🚁


Award winning expert safety napper of 2022. 😴 🥇 🛏 🏆






Citation






5. Walls Manual of Emergency Airway Management. WOLTERS KLUWER MEDICAL, 2022.


6. Gilardi, Berta Riveros, et al. “Types of Cerebral Herniation and Their Imaging Features.” RadioGraphics, 7 Oct. 2019, https://pubs.rsna.org/doi/10.1148/rg.2019190018.


7. “NCBI Bookshelf.” Cushing's Reflex, Mar. 2022, https://www.ncbi.nlm.nih.gov/books/NBK549801/.




10. Rajajee. “Management of Acute Moderate and Severe Brain Injury.” UpToDate, 22 Aug. 2022, https://www.uptodate.com/contents/management-of-acute-moderate-and-severe-traumatic-brain-injury?search=mannitol+cerebral+edema§ionRank=1&usage_type=default&anchor=H17&source=machineLearning&selectedTitle=1~150&display_rank=1#H14.


11. McEvoy, Mike, et al. Critical Care Transport. 3rd ed., Jones & Bartlett Learning, 2023.




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