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Steve, a paramedic, and Dave, an EMT, are dispatched with an engine to a loading dock behind a local nightclub for an injury from an assault. Upon arrival, they note the presence of a small crowd, but police wave them in, indicating the scene is safe. The crew finds a 42-year-old male lying supine on the ground, unconscious, with snoring respirations.
While Steve calls for an ALS assist, Dave immediately places the patient’s cervical spine in a neutral inline position and opens the airway with a jaw thrust. Steve then inserts an oropharyngeal airway and connects a bag-valve mask to high-flow oxygen. Dave notes the patient’s airway is now clear, respirations are about 8/min. and irregular with shallow tidal volume, and there is a strong bradycardic carotid pulse. Dave assists the patient’s shallow ventilations, adding enough additional tidal volume to result in normal chest rise and fall, and adds a few ventilations per minute to bring the respiratory rate to 12.
As he exposes the patient and begins a rapid trauma assessment, Steve gets the story from the gathered crowd, who turn out to be the patient’s friends. They report that the patient, whose name is Mike, came out to this area to make a phone call. When he did not return after a few minutes, they looked for him, found him like this and called 9-1-1. The bystanders report Mike has a history of hypertension for which he takes an unknown medication. Steve’s rapid trauma exam reveals a contusion and crepitus to the left temporal region of the skull and a dilated and sluggish left pupil. An EMT from the engine obtains a set of vital signs and reports a heart rate of 48/min., respiratory rate of 12/min. with BVM assist, and a blood pressure of 210/140. With the help of the EMTs from the engine, the patient is fully immobilized and moved to the ambulance for transport to the trauma center. An EMT from the engine continues BVM ventilation while Steve repeats his rapid trauma assessment.
Increased intracranial pressure (ICP) is an increase of the normal pressure within the skull, and can occur as a result of both traumatic and medical etiologies (Table 1). An increase in ICP is a serious and life-threatening medical emergency. In addition to possibly being caused by injury, increased ICP will result in brain injury if allowed to progress unabated. Whether the result of direct injury or a medical cause, increased ICP can damage or alter the function of areas of the brain and restrict blood flow into it.
The clinical manifestations of increased ICP range from subtle in its early phases to profound when there is substantial rise in pressure. Recognition of the signs and symptoms associated with increased ICP is necessary to both initiate proper prehospital care and ensure rapid transport to an appropriate facility. Understanding the anatomy and physiology of the brain as well as the pathophysiology of increased ICP is useful in identifying and understanding the treatment of this condition. This article explores the pertinent anatomy and physiology of the brain and the pathophysiology of increased ICP to help improve its prehospital management.
Anatomy and Physiology
The human skull is made up of 22 bones. Fourteen are associated with the face, and eight with the cranium. The cranium consists of the paired temporal and parietal bones, as well as the frontal bone, sphenoid, ethmoid and occipital bone. Together, the fused cranial bones create the cranial cavity, which encloses and protects the brain. The bones of the cranium average between 2 and 6 mm in thickness in the adult, with the temporal bones usually being the thinnest. Exceptions to this include the newborn, whose fontanels are yet to close. The outsides of the cranial bones are smooth and articulate with the scalp via the pericranium, the deepest layer of the scalp.
The inside of the cranium is not as smooth. While the interiors of the superior and lateral sides of the cranial vault are relatively smooth (with the exception of grooves for cranial arteries), the cranial floor has numerous ridges and bony protrusions that can injure the brain if it moves violently within the cranial vault. Recall that contrecoup injuries occur opposite from the site of impact in head trauma as the moving brain strikes the opposite wall of the cranium; these injuries are exacerbated by the bony protrusions within the vault.
The average volume of the adult cranium is about 1,900 mL, about 80% of which is occupied by the brain.1 There are three major divisions of the brain: the cerebrum, cerebellum and brain stem. The cerebrum is divided into two lobes, and each is responsible for specific “higher functions,” such as consciousness and thought. The cerebellum is responsible for balance and fine-tuned movements. The brain stem is made up of the diencephalon, midbrain and medulla oblongata. The medulla oblongata connects the brain with the spinal cord and is responsible for control of cardiovascular and respiratory function.
Through childhood and the prime years of adulthood, the brain takes up most of the space within the cranium. As people age, however, the brain begins to atrophy and shrink. While there is no set timeframe for brain atrophy, it is exacerbated by dementia and Alzheimer’s and theorized to also be exacerbated by nonuse (sedentary lifestyles). The consequence of this atrophy is that upon brain injury, the brain has an increased space in which to bleed and/or swell, potentially delaying the onset of the symptoms of increasing ICP. That can delay recognition as well. Conversely, this extra space can afford the patient more time for treatment access and in some ways be helpful.
The brain and spinal cord are covered by a protective layer of tissue called the meninges. There are three layers: the pia mater, the arachnoid membrane and the dura mater. The pia mater is a thin membrane bound tightly against the brain’s surface. The arachnoid membrane lies above the pia mater, and between the two is the subarachnoid space, which is filled with cerebrospinal fluid (CSF). Outside the arachnoid membrane is the dura mater, the outermost layer of the meninges. There are two tough, fibrous layers that make up the dura matter. The outer layer is fused to the periosteum of the inside of the cranium, and the inner layer lies over the top of the arachnoid membrane, with a space between them. This inner layer of the dura mater extends deep into the cranial cavities in several areas to form dural folds. These act as restraints for the brain, holding it in position within the cranium. Examples of these dural folds include the falx cerebri and the tentorium cerebelli (Figure 1). The falx cerebri separates the two hemispheres of the brain from one another, and the tentorium cerebelli separates the cerebellum and brain stem from the cerebrum.
The brain is suspended in cerebrospinal fluid, which is produced in the choroid plexus located in the ventricles of the brain. CSF passes from the ventricles into the subarachnoid space of the meninges that covers the brain and spinal cord. In addition to cushioning the brain and protecting it from trauma, CSF also serves as a transport system for waste products, nutrients, chemical messengers and gases such as carbon dioxide and oxygen.
The brain requires a constant and significant supply of oxygen and glucose to function properly. Accordingly, it has a rich vascular supply and receives about 15% of total cardiac output. Additionally, the brain is responsible for 20% of the body’s total oxygen demand.2 The paired carotid and vertebral arteries (which fuse to form the basilar artery) ensure a constant flow of blood to the brain, or cerebral blood flow (CBF). Cerebral blood flow is controlled by a process termed autoregulation, in which the volume of the cerebral vasculature is tightly controlled to allow just enough blood to ensure adequate cerebral perfusion. This is important because too little blood flow fails to meet the brain’s oxygen and glucose demands, while too much can actually cause a rise in ICP. To support autoregulation, the cerebral vasculature is extremely sensitive to the concentration of carbon dioxide in the blood (partial pressure, or pCO2). Increased pCO2 (hypercapnia) results in vasodilation and increased CBF, and decreased pCO2 (hypocapnia) results in vasoconstriction of the cerebral vasculature and decreased CBF. The normal pCO2 is 35–45 mmHg. The vascular response to changes in pCO2 is nearly linear between values of 20–60 mmHg, and results in a change in the diameter of cerebral blood vessels by 2%–3%.2,3
Adequate CBF also depends on the cerebral perfusion pressure (CPP), the pressure of the blood flowing into the brain. CPP is unique because it is not related to blood pressure alone. Rather, it depends on the relationship between the mean arterial pressure (MAP) and intracranial pressure (Table 2). Normal MAP is between 70–110 mmHg. Normal ICP is between 7–15 mmHg, or about 10 mmHg. This means there is always some intracranial pressure. An adequate CPP is at least 70 mmHg. When cerebral perfusion pressure drops below 70 mmHg for sustained periods, cerebral hypoxia and ischemia occur. Under normal physiologic conditions, autoregulation ensures CPP is kept between 70–90 mmHg, which is enough to ensure adequate cerebral blood flow. Autoregulation occurs primarily via control of the cerebral vasculature.
The Monro-Kellie doctrine illustrates the relationship between intracranial pressure, the volume of cerebral spinal fluid, blood, brain tissue and cerebral perfusion pressure.4,5 As discussed earlier, the cranial vault is a closed, rigid, nonflexible container with a fixed volume. Located in it are the brain, CSF and blood (within the cerebrovascular system). ICP represents a balance of the pressures exerted by these cranial constituents. These components create a state of pressure-volume equilibrium, and an increase in the volume of any one of them will result in an increase in pressure. If the volume of any one of these constituents increases, there must be a decrease in the volume of one or more of the others, or ICP will increase. Increased ICP is defined as CSF pressure greater than 15 mmHg.6
There is a buffer system in place to compensate for any increase in one of the constituents. CSF can be shifted from the intracranial space into the spinal column, and to a lesser degree blood volume can be shifted out of the cerebral vasculature. So for an increase in, say, the volume of an expanding hematoma from an epidural bleed, CSF is shifted into the spinal column, and venous blood out of the cranium. These compensatory mechanisms maintain a normal ICP for any change in volume less than approximately 100–120 mL.6
Let’s put this into more practical terms. Inside your cranium are your brain, blood and CSF. Together, these things fill up the volume of your cranium and exert a certain amount of pressure, the ICP. As long as you are able to maintain an adequate MAP, CPP will be adequate, and your body will be able to force arterial blood into the cranium and perfuse your brain.
But say something happens to change this equilibrium. Maybe you hit your head, suffer an epidural hematoma and start bleeding into your brain. Maybe it’s an aneurysm. Maybe you have lung cancer, and it metastasizes to your brain and starts to grow. In all of these scenarios, we are introducing into the cranium a new constituent that is taking up space (because it has volume). Initially, an increase in ICP is prevented by CSF shifting out of the cranium and into the spinal cord. In addition, venous blood is shifted retrograde out of the cranium as well. When these compensatory mechanisms are depleted, ICP will start to rise as this new cranial constituent continues to take up space.
As ICP Rises
As ICP increases above 15 mmHg, numerous events occur that contribute to additional progressive, life-threatening increases.
Cerebral hypoxia, both local and global, can cause injury and eventual death to brain cells, resulting in cerebral edema. Cerebral edema compresses cerebral arteries, further decreasing cerebral perfusion. As cerebral perfusion is compromised, CO2 accumulation results in vasodilation, increasing ICP. When ICP reaches a point where CPP is compromised, autoregulation is lost, and further vasodilation of the cerebral vasculature occurs, further increasing ICP.
Even though the signs and symptoms of increasing intracranial pressure may seem overwhelmingly complicated, they tend to develop in a predictable pattern. The best indicator of rising ICP is a changing mental status. Early symptoms begin with disorientation (confusion), which progresses into irritability and then combativeness. When patients decline to verbal or pain or are unresponsive on the AVPU scale, they are typically in the later stages of increasing ICP.
Other reliable early indicators of increasing ICP include severe headache and persistent vomiting. A severe headache will commonly occur in the setting of a subarachnoid hemorrhage, typically following the rupture of an aneurysm. Free blood will irritate the meninges, causing the classic “thunderclap” or “worst headache of my life.” Vomiting, which can be projectile, occurs as the area of the brain that controls emesis is compressed and irritated.
Besides a declining level of consciousness, other late symptoms include seizures, a blown pupil, posturing and Cushing reflex. Seizures can occur for a variety of reasons, including metabolic abnormalities or toxic injections; however, in these cases it is typically the result of either direct cortex compression by an expanding hematoma or mass, or irritation of brain tissue by free blood increasing edema. The “blown” pupil, or mydriasis, is the result of compression of the third cranial nerve that controls papillary constriction, eyelid elevation and most of the extraocular muscles. The parasympathetic fibers that control constriction run along the outside of the nerve and so are the first to be compressed with increasing ICP. Interruption of the parasympathetic flow allows for unopposed sympathetic stimulation to the pupil and resulting dilation. Posturing occurs as the corticospinal tracts of the spinal cord, within which motor fibers lie, are compressed during herniation, along with the pontine and midbrain structures that influence them.
A particularly late finding is the Cushing reflex, which indicates a significantly increased ICP. It is characterized by increased systolic blood pressure, bradycardia and inadequate respirations. Hypertension develops as autoregulatory mechanisms attempt to generate an adequate MAP to maintain CPP and perfuse the brain. Specifically, sympathetic nervous system stimulation results in alpha-1 adrenergic receptor stimulation and subsequent arterial vasoconstriction, increased systemic vascular resistance, and increased blood pressure. This resultant increase in blood pressure is detected by baroreceptors in the aortic and carotid sinuses, which in turn activate a parasympathetic response via the vagus nerve. Increased vagal tone results in bradycardia, an attempt to correct the developing hypertension. Inadequate respirations occur as a result of herniation of the brain stem causing compression of the respiratory control centers in the medulla oblongata.7
Cerebral herniation occurs when increased ICP displaces the brain within the cranial vault, pressing it up against structures such as the tentorium cerebelli or through the cranial foramen. There are numerous specific mechanisms by which cerebral herniation can occur (Figure 2).8,9 Cingulate herniation, the most common type, occurs when the middle lobe of the brain herniates under the falx cerebelli. Uncal (transtentorial) herniation occurs when the uncus of the brain is pressed up against the tentorium cerebelli as the brain is forced through the tentorial hiatus. Central transtentorial herniation occurs when pressure is exerted on the brain from above, herniating the brain across the tentorium cerebelli. Cerebellotonsillar herniation occurs when the cerebellum herniates through the foramen magnum, resulting in compression of the brain stem. Upward transtentorial herniation occurs when the cerebellum herniates upward through the tentorial opening. Transcalvarial herniation occurs when increased ICP forces brain tissue out through a fracture or surgical site in the cranium.
Signs and Symptoms of Increased ICP
Early in the development of increased ICP, the associated signs and symptoms are related to the effects on the cerebral cortex and upper brain stem. Systolic blood pressure and pulse pressure will increase as the brain attempts to maintain a MAP sufficient to produce an adequate CPP. The heart rate will decrease, and bradycardia may develop. Alteration in the respiratory pattern, such as Cheyne-Stokes respirations, may occur. An altered mental status and decreased level of consciousness will develop. The patient may exhibit decorticate, or flexor, posturing.
As ICP continues to increase and the middle brain stem is generally affected, central neurogenic hypoventilation can develop, along with a wide pulse pressure and bradycardia. The pupils may be sluggish to light or nonreactive, and the patient may exhibit decerebrate, or extensor, posturing.
As the lower brain stem and medulla are affected, further deterioration of respiratory status may result in ataxic respirations. The heart rate may fluctuate widely, as may the blood pressure. The pupil may appear fixed and dilated once the nerve tracts feeding it are completely compressed. Brain stem reflexes such as blinking to stimulation, coughing and gagging will be absent. Such findings typically suggest a level of ICP that is typically not survivable.
Management of ICP
Ultimately, increased ICP kills via decreased cerebral perfusion. The prehospital management of increased ICP centers around the symptoms, which means protecting airway, breathing and circulation in an attempt to control ICP and maintain adequate cerebral perfusion.
Open the airway, administer oxygen and assure adequate ventilation. If the patient is not ventilating effectively, initiate BVM ventilation with 100% oxygen. For patients showing signs of herniation (posturing, fixed and dilated pupil, erratic respirations), hyperventilation can be considered as a short-term bridging treatment until ICP can be relieved.
The basis for hyperventilation in the treatment of increased ICP is the normal physiologic response of the cerebral vasculature to pCO2. As pCO2 decreases with hyperventilation, cerebral vasoconstriction occurs, and the volume of blood within the cranial vault deceases. This small decrease in blood volume may serve as a temporary buffer against uncontrolled increasing ICP. Hyperventilation is not without risks, however. The vasoconstriction produced by extreme changes in pCO2 can be severe enough that cerebral hypoxia and ischemia can develop, both locally and globally.2 It is therefore important that hyperventilation be controlled and monitored, with a goal of maintaining the pCO2 between 30 and 35 mmHg, and reserved for patients who are showing signs of herniation.10,11 This target can easily be achieved with the use of end-tidal CO2 monitoring. When CO2 monitoring is not available, EMTs and paramedics are often told to ventilate at a rate of 20 per minute. This can be dangerous, as the provider will not know the degree to which they are causing vasoconstriction, and hypocapnea can develop, resulting in severe cerebral vasoconstriction and cerebral hypoxia.
As discussed earlier, patients with increased ICP need to maintain MAP to produce an adequate CPP to perfuse their brain. As such, these patients cannot tolerate hypotension. If hypotension develops, administer isotonic fluids with the goal of maintaining a systolic blood pressure of at least 90 mmHg. A landmark 1993 study showed that patients with head injury and episodes of hypotension and hypoxia had double the mortality compared to those who did not experience episodes of hypotension and hypoxia.13
The administration of osmotic diuretics, specifically mannitol, has been debated and used in prehospital care and emergency departments for the emergent treatment of critically high intracranial pressures for decades. Osmotic diuretics increase the osmolarity of the blood, causing more fluid to be pulled from tissues (specifically the brain) into the intravascular space. Once it’s there, the body can then eliminate the excess fluid. For increased intracranial pressure, the theory is that this pulls excess fluids out of the brain and back into the blood. By decreasing the fluid in the brain, the total volume within the cranium is decreased as well. This theory works well when the buildup of edema is the cause of increased intracranial pressure; there is little benefit when bleeding is the cause of an ICP rise. Unfortunately it is difficult to distinguish between bleeding and edema etiologies of increased ICP, making the prehospital application of osmotic diuretics difficult at best.
Steroid use, while often discussed, is contraindicated in patients with traumatic brain injury (TBI). A large 2004 study seeking to answer the debate was halted early after steroid use in TBI clearly showed an increase in mortality.14 However, steroids for isolated spinal cord trauma patients are still commonly used despite contradictory evidence. This should always be done in accordance with local protocols, and only in cases where no TBI is thought to exist.
Patients who are combative should be sedated to prevent transient increases in ICP that can occur with such behavior. Barbiturates are particularly effective in such circumstances, as they not only provide sedation but also have the benefit of reducing the metabolic demands of injured brain tissue.6 Another option for combative patients, though admittedly one that is not readily available for many paramedics, is rapid sequence intubation (RSI).15,16 The administration of paralytics will prevent patient movement and muscular contractions and subsequent increases in ICP that accompany these events. The administration of lidocaine during RSI has been thought to limit increases in ICP during the procedure, though significant debate still exists on its efficacy.17,18
Convinced the patient has an isolated head injury (most likely from an epidural hematoma) and increased ICP, Steve ensures Dave is responding to the local Level 1 trauma center. Noting that the EMT ventilating the patient is able to do so without difficulty and the trauma center is only a short distance away, he elects to not perform endotracheal intubation. Steve does, however, instruct the EMT to hyperventilate the patient, as the presence of Cushing reflex and the sluggish pupil suggests he is herniating. A capnograph is placed between the mask and bag-valve device, and the patient is ventilated at a rate of 14 breaths per minute, which produces an EtCO2 between 30–35 mmHg. The patient is also placed on the cardiac monitor, and an intravenous line is established with a 16-gauge catheter. He is transported to the trauma center without incident or further changes, and a full report is given to the ED staff upon arrival.
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2. Zwienenberg M, Muizelaar J. Vascular Aspects of Severe Head Injury. In Miller L, Hayes R, eds., Head Trauma: Basic, Preclinical and Clinical Directions. New York: Wiley-Liss, 2001.
3. Laffey JG, Kavanagh BP. Hypocapnia. N Engl J Med 347: 43, 2002.
4. Kellie G. An account of the appearances observed in the dissection of two of the three individuals presumed to have perished in the storm of the 3rd, and whose bodies were discovered in the vicinity of Leith on the morning of the 4th November 1821 with some reflections on the pathology of the brain. The Transactions of the Medico-Chirurgical Society of Edinburgh, 1824 1: 84–169, 1824.
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6. Biros MH, Heegaard WG. Head Injury. In Marx, Rosen’s Emergency Medicine, 7th ed. Philadelphia: Mosby/Elsevier, 2010.
7. Greenberg M. Handbook of Neurosurgery, 7th ed. New York: Thieme, 2010.
8. Dawodu ST. Traumatic Brain Injury. Medscape, http://emedicine.medscape.com/article/326510-overview.
12. Roberts I, et al. Effect of intravenous corticosteroids on death within 14 days in 10,008 adults with clinically significant head injury (MRC CRASH trial): Randomised placebo-controlled trial. Lancet 364(9,442): 1,321–8, Oct 2004.
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14. Op. cit., Roberts.
15. Bernard SA, et al. Prehospital rapid sequence intubation improves functional outcome for patients with severe traumatic brain injury: a randomized controlled trial. Ann Surg 252(6): 959–65, Dec 2010.
16. Davis DP, et al. Prehospital airway and ventilation management: A trauma score and injury severity score-based analysis. J Trauma 69(2): 294–301, Aug 2010.
17. Salhi B, Stettner E. In defense of the use of lidocaine in rapid sequence intubation. Ann Emerg Med 49(1): 84–86, Jan 2007.
18. Vaillancourt C, Kapur AK. In opposition of the use of lidocaine in rapid sequence intubation. Ann Emerg Med 49(1): 86–87, Jan 2007.