Introduction
Intracranial pressure (ICP) may be raised whenever there is an increase in brain tissue volume, blood volume, CSF volume, and due to other metabolic factors. A raised ICP has the potential to cause serious damage to the body by compressing vital structures in the brain stem, and is associated with a high mortality and morbidity. This is because unlike other organs like the kidney or liver, the brain can withstand ischaemia only for a short time.
This essay is based on the case history of Adam, a 50-year-old male, who has suffered a subarachnoid bleed. The purpose of the essay is to explore the pathophysiology of raised intracranial pressure and outline the importance of assessment of vital signs in a patient with raised intracranial pressure.
A brief analysis of the intracranial anatomy, CSF, and subarachnoid hemorrhage is followed by analysis of the pathophysiology of raised intracranial pressure and assessment of vital signs.
Intracranial anatomy
The cranium of the normal adult brain is a nondistensible structure. The components making up the volume within the cranium includes: brain tissue-1400 ml, blood-150 ml, and cerebrospinal fluid (CSF)-150 ml (Samuels, 2004).
The brain and spinal cord are covered by three meninges; dura mater, arachnoid mater, and the pia mater. These are protective in nature (McCaffrey, 2008).
The dura mater is a two-layered membrane, which lines the skull and is the most superior of the three meningeal layers. The space above the dura mater is called epidural space. The epidural space is a potential space; if there is bleeding in the brain, it may collect here (McCaffrey 2008).
The space between the dura mater and the arachnoid mater is called subdural space. It is also a potential space, and blood may collect here (McCaffrey, 2008).
The arachnoid mater is the middle layer, which has projections (arachnoid granulation or arachnoid villi) into the sinuses of the dura mater. These projections transfer CSF from the ventricles into the bloodstream (McCaffrey, 2008).
The subarachnoid space is present between the arachnoid and pia mater, and contains the CSF (McCaffrey 2008). The pia mater is the innermost layer of the meninges, which is closely attached to the brain (McCaffrey, 2008).
The arachnoid and the pia mater are very thin and are called leptomeninges (Greenberg, 2000).
Cerebrospinal Fluid
The CSF is principally produced in the choroid plexus of each lateral ventricle. It exits the brain via the foramina of Luschka and Magendi, and flows over the cortex to be absorbed into the venous system along the superior sagittal sinus (Ropper, 1998). A small amount of CSF is produced by the ependymal surfaces of the ventricles, and a minimal amount by the brain through the small perivascular spaces surrounding the blood vessels entering the brain substance (Reichman & Simon, 2003).
CSF is produced at a rate of 0.34 mL/min (Samuels, 2004). Approximately 150 mL of CSF is present within the ventricles and surrounding the brain and spinal cord (Ropper, 1998), and approximately 500 mL of CSF is produced each day (Reichman & Simon, 2003).
CSF supplies oxygen and vital nutrients to portions of the brain without an independent blood supply. The CSF also cushions the brain against traumatic injury to the head (Ropper, 1998).
Subarachnoid hemorrhage
Subarachnoid hemorrhage (SAH) is the presence of blood within the subarachnoid space due to head trauma or nontraumatic causes. The nontraumatic causes include: rupture of a berry aneurysm or arteriovenous malformation (AVM) (Kazzi 2006). The mortality rate of SAH is 40% within the first week (Kazzi, 2006).
The symptoms of SAH include the acute onset of severe headache, and seizures (25%). Other signs and symptoms include: signs of meningeal irritation like neck stiffness, bilateral leg pain, and low back pain, nausea and/or vomiting, loss of consciousness, photophobia and visual changes (Kazzi, 2006).
Intracranial Pressure
The brain tissue, blood, and cerebral spinal fluid (CSF) all together, exert a pressure, which is known as the intracranial pressure (ICP) (Ropper, 1998). Normally, the ICP is maintained at a range of 2 to 12 mm Hg.
A volume change in any of the 3 intracranial components can cause abnormal variations in the intracranial volume with subsequent changes in the ICP. These volume changes include; increase in tissue volume (brain tumor, edema or bleeding), increased blood volume (vasodilatation of cerebral vessels or venous outflow obstruction), excess production, and decreased absorption or obstructed circulation of CSF (Porth, 2005).
The Initial increases in ICP are countered by a translocation of CSF to the spinal subarachnoid space and increased reabsorption of CSF. The small amount of blood in the cerebral circulation, however, limits the compensatory ability of the blood compartment. As the volume-buffering capacity of this compartment becomes exhausted, venous pressure increases, and cerebral blood volume and ICP rise (Porth, 2005).
Intracranial compliance
Since the cranial vault is a rigid and fixed structure, any additional intracranial volume can lead to increased ICP. According to the Monroe-Kellie doctrine “When the volume of any of the three cranial components increases, the volume of one or both of the others must decrease or the ICP will rise” (Samuels 2004).
Subsequent to an increase in the volume, the intracranial contents get displaced. As a mass lesion expands in the intracranial vault, there is only a minimal increase in ICP initially because the CSF and blood are displaced (Samuels 2004). Once these mechanisms get overwhelmed, the intracranial compliance (change in volume divided by the change in pressure) and further small increments in intracranial volume leads to dramatic elevations of ICP (Samuels, 2004).
Cerebral perfusion and autoregulation
There needs to be a state of constant perfusion of the brain tissue so that important substrates like oxygen and glucose can be delivered to the brain. In order to preserve perfusion across a wide range of systemic blood pressures, the brain has the capacity for an adequate hemodynamic response (Samuels, 2004).
The cerebral perfusion pressure (CPP) is the difference between the ICP and blood pressure in the major cerebral arteries. When the CPP is below 20-30 mmHg, the raised ICP becomes detrimental (Ropper, 1998).
The brain maintains a constant cerebral blood flow by a process called autoregulation. By this process, the brain adjusts the intracranial vascular resistance by altering vessel diameter and tone. After any severe cerebral insult like a subarachnoid hemorrhage, this ability of the brain to autoregulate is lost. The CPP now becomes dependent on the mean arterial pressure. Therefore, in order to maintain CPP in the presence of a raised ICP, the systemic blood pressure needs to be raised (Kaye, 2005).
Brain herniation
Brain herniae may be of 3 types, depending on the cause of raised ICP, or the position of the intracranial mass. They include: transtentorial, foramen magnum, and subfalcine types.
In transtentorial herniation, there is displacement of the brain and herniation of the uncus of the temporal lobe through the tentorial hiatus. This leads to compression of the 3rd cranial nerve and the midbrain (Kaye, 2005).
Because the brainstem and the reticular activating system get compressed, there is a deterioration of the conscious state leading to coma, hypertension, and bradycardia (Cushing response). In addition, there is respiratory failure, which is initially manifest by Cheyne-Stokes periodic breathing (Kaye, 2005).
Respiratory failure occurs when the medulla gets compressed. With a progressive increase in the ICP, there is further downward herniation of the brain stem into the foramen magnum or ‘coning.’ With further herniation and destruction in the brainstem, the pupils change from dilated and fixed to midsize and unreactive. These are irreversible events leading to brainstem death (Kaye, 2005).
Assessment of vital signs
By regular monitoring of the vital signs like pupillary reaction, blood pressure, pulse rate, respiratory rate, and temperature, it is possible to identify rising ICP.
Pupillary responses-in addition to being a sign of increasing ICP, the assessment of pupillary responses helps in identifying the location of an expanding mass (Brooker & Nicol, 2003). It is necessary to record the size, shape, and reaction to light of both the pupils (Brooker & Nicol, 2003).
A pupil that is becoming oval, enlarging or losing the ability to react to light may be an indication of rising ICP (Brooker & Nicol 2003). This will happen before the pupil becomes fixed and dilated. The pupillary responses are controlled by two cranial nerves: optic (III) and the oculomotor (III) (Brooker & Nicol, 2003).
If there is an expanding lesion in the right cerebral hemisphere, which causes herniation of part of the temporal lobe through the tentorium, then the right oculomotor nerve will be compressed, leading to a fixed and dilated pupil (Brooker & Nicol 2003). If the pressure is unrelieved and continues to increase, the oculomotor nerve on the opposite side will also become compressed and the contralateral pupil to the side of the lesion will become fixed and dilated (Brooker & Nicol, 2003).
Blood pressure-unrelieved raised ICP causes brain hypoxia and compromises cerebral perfusion. The vasomotor center responds to this by attempting to increase cerebral blood flow by raising the mean arterial blood pressure (Brooker & Nicol, 2003).
Serial blood pressure monitoring will show an upward rise in both diastolic and systolic blood pressure, and because the mean arterial blood pressure is rising, there will be a widening gap between the diastolic and systolic pressures. It is more important to observe this widening gap than just a general blood pressure measurement (Brooker & Nicol, 2003).
Pulse rate-this usually falls with rising ICP. This is because the baroreceptors detect an abnormally rising blood pressure and attempts to reduce it by slowing the heart rate and therefore reducing the cardiac output (Brooker & Nicol, 2003).
Temperature-this usually increases in the end stages of unrelieved raised ICP. This is because of loss of temperature control due to compression of the hypothalamus (Brooker & Nicol, 2003).
Respiratory rate-this begins to decrease as the ICP rises, because there is cerebral hypoxia and compression of the respiratory center within the brain stem. In the end stages, the respiration will become shallow, slow, and irregular (Brooker & Nicol, 2003).
Conclusion
The cranium of the normal adult brain is a nondistensible structure inside which the brain tissue, blood, and cerebral spinal fluid all together, exert a pressure, which is known as the intracranial pressure. A volume change in any of the 3 intracranial components can cause abnormal variations in the intracranial volume with subsequent changes in the ICP.
Initially, as a mass lesion expands in the intracranial vault, there is only a minimal increase in ICP because the CSF and blood are displaced; later, these mechanisms get overwhelmed, and the intracranial compliance and further small increments in intracranial volume leads to higher rises in the ICP.
The cerebral perfusion pressure (CPP) is the difference between the ICP and blood pressure in the major cerebral arteries. A CPP below 20-30 mmHg, makes the raised ICP very dangerous. After a subarachnoid hemorrhage, the autoregulating ability of the brain is also lost.
Rising ICP leads to brain herniation, which is of three types: transtentorial, foramen magnum, and subfalcine types. When the herniating brain compresses
the brainstem and the reticular activating system, it leads to coma, hypertension, and bradycardia (Cushing response). In addition, respiratory failure also occurs.
In the given scenario, Adam has suffered a subarachnoid bleed. As a result of rising ICP, his heart rate dropped because the baroreceptors detected an abnormally rising blood pressure and attempted to reduce it by slowing the heart rate. His vasomotor center responded to the brain hypoxia by attempting to increase cerebral blood flow by raising the mean arterial blood pressure.
Initially, his right pupil dilated and did not react to light because herniation of part of the temporal lobe through the tentorium compressed the right oculomotor nerve. In a short while, the left pupil also became fixed and dilated due to compression of the oculomotor nerve on the opposite side.
With a progressive increase in the ICP, there was further downward herniation of the brain stem into the foramen magnum or ‘coning.’ Further herniation and destruction in the brainstem lead to brain stem death.
References
- Brooker, C, & Nicol, M 2003, Nursing Adults: The Practice of Caring. Elsevier Health Sciences.
- Greenberg, MS 2000, Handbook of Neurosurgery, 5th edn, Thieme Medical Publishers, New York.
- Kaye, AH 2005, Essential Neurosurgery. Blackwell Publishing.
- Kazzi, AA 2006. Subarachnoid Hemorrhage. Web.
- McCaffrey, P 2008. The Meninges and Cerebrospinal Fluid.
- Porth, CM 2005, Pathophysiology: Concepts of Altered Health States. Lippincott Williams & Wilkins.
- Ropper, AH, 1998, Harrison’s Principles of Internal Medicine. McGraw-Hill.
- Reichman, E & Simon, RR 2003, Emergency Medicine Procedures. McGraw-Hill Professional.
- Samuels, MA 2004, Manual of Neurologic Therapeutics. Lippincott Williams & Wilkins.