Intracranial pressure

Causes of increased intracranial pressure can be classified by the mechanism in which ICP is increased:

• Mass effect such as brain tumor, infarction with edema, contusions, subdural or epidural hematoma, or abscesses all tend to deform the adjacent brain.
• Generalized brain swelling can occur in ischemic-anoxia states, acute liver failure,[7] hypertensive encephalopathy, hypercarbia (hypercapnia), and Reye hepatocerebral syndrome. These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts.
• Increase in venous pressure can be due to venous sinus thrombosis, heart failure, or obstruction of superior mediastinal or jugular veins.
• Obstruction to CSF flow and/or absorption can occur in hydrocephalus (blockage in ventricles or subarachnoid space at base of brain, e.g., by Arnold–Chiari malformation), extensive meningeal disease (e.g., infection, carcinoma, granuloma, or hemorrhage), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption).
• Increased CSF production can occur in meningitis, subarachnoid hemorrhage, or choroid plexus tumor.
• Idiopathic or unknown cause (idiopathic intracranial hypertension, a common cause in otherwise well people especially younger women)
• Craniosynostosis

One of the most damaging aspects of brain trauma and other conditions, directly correlated with poor outcome, is an elevated intracranial pressure.[8] ICP is very likely to cause severe harm if it rises too high.[9] Very high intracranial pressures are usually fatal if prolonged, but children can tolerate higher pressures for longer periods.[10] An increase in pressure, most commonly due to head injury leading to intracranial hematoma or cerebral edema, can crush brain tissue, shift brain structures, contribute to hydrocephalus, cause brain herniation, and restrict blood supply to the brain.[11] It is a cause of reflex bradycardia.[12]

Spontaneous intracranial hypotension may occur as a result of an occult leak of CSF into another body cavity. More commonly, decreased ICP is the result of lumbar puncture or other medical procedures involving the brain or spinal cord. Various medical imaging technologies exist to assist in identifying the cause of decreased ICP. Often, the syndrome is self-limiting, especially if it is the result of a medical procedure.

If persistent intracranial hypotension is the result of a lumbar puncture, a "blood patch" may be applied to seal the site of CSF leakage. Various medical treatments have been proposed; only the intravenous administration of caffeine and theophylline has shown to be particularly useful.[13]

The pressure–volume relationship between ICP, volume of CSF, blood, and brain tissue, and cerebral perfusion pressure (CPP) is known as the Monro–Kellie doctrine or hypothesis.[16][17][18]

The Monro–Kellie hypothesis states that the cranial compartment is inelastic and that the volume inside the cranium is fixed. The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another.[18] *This concept only applies to adults, as the presence of fontanelles and open suture lines in infants that have not yet fused means there is potential for a change in size and intracranial volume.

The principal buffers for increased volumes include CSF and, to a lesser extent, blood volume. These buffers respond to increases in volume of the remaining intracranial constituents. For example, an increase in lesion volume (e.g., epidural hematoma) will be compensated by the downward displacement of CSF and venous blood.[18]

The Monro–Kellie hypothesis is named after Edinburgh doctors Alexander Monro and George Kellie.[19]

In people who have high ICP due to an acute injury, it is particularly important to ensure adequate airway, breathing, and oxygenation. Inadequate blood oxygen levels (hypoxia) or excessively high carbon dioxide levels (hypercapnia) cause cerebral blood vessels to dilate, increasing the flow of blood to the brain and causing the ICP to rise.[23] Inadequate oxygenation also forces brain cells to produce energy using anaerobic metabolism, which produces lactic acid and lowers pH, also dilating blood vessels and exacerbating the problem.[8] Conversely, blood vessels constrict when carbon dioxide levels are below normal, so hyperventilating a person with a ventilator or bag valve mask can temporarily reduce ICP. Hyperventilation was formerly a part of the standard treatment of traumatic brain injuries, but the induced constriction of blood vessels limits blood flow to the brain at a time when the brain may already be ischemic—hence it is no longer widely used.[24] Furthermore, the brain adjusts to the new level of carbon dioxide after 48 to 72 hours of hyperventilation, which could cause the vessels to rapidly dilate if carbon-dioxide levels were returned to normal too quickly.[24] Hyperventilation is still used if ICP is resistant to other methods of control, or there are signs of brain herniation, because the damage herniation can cause is so severe that it may be worthwhile to constrict blood vessels even if doing so reduces blood flow. ICP can also be lowered by raising the head of the bed, improving venous drainage. A side effect of this is that it could lower pressure of blood to the head, resulting in a reduced and possibly inadequate blood supply to the brain. Venous drainage may also be impeded by external factors such as hard collars to immobilize the neck in trauma patients, and this may also increase the ICP. Sandbags may be used to further limit neck movement.

In the hospital, the blood pressure can be increased in order to increase CPP, increase perfusion, oxygenate tissues, remove wastes, and thereby lessen swelling.[24] Since hypertension is the body's way of forcing blood into the brain, medical professionals do not normally interfere with it when it is found in a person with a head injury.[4] When it is necessary to decrease cerebral blood flow, MAP can be lowered using common antihypertensive agents such as calcium channel blockers.[8]

If there is an intact blood–brain barrier, osmotherapy (mannitol or hypertonic saline) may be used to decrease ICP.[25]

It is unclear whether mannitol or hypertonic saline is superior, or if they improve outcomes.[26][27]

Struggling, restlessness, and seizures can increase metabolic demands and oxygen consumption, as well as increasing blood pressure.[23][28] Analgesia and sedation are used to reduce agitation and metabolic needs of the brain, but these medications may cause low blood pressure and other side effects.[8] Thus if full sedation alone is ineffective, people may be paralyzed with drugs such as atracurium. Paralysis allows the cerebral veins to drain more easily, but can mask signs of seizures, and the drugs can have other harmful effects.[23] Paralysing drugs are only introduced if patients are fully sedated (this is essentially the same as a general anaesthetic)

Craniotomies are holes drilled in the skull with the help of cranial drills to remove intracranial hematomas or relieve pressure from parts of the brain.[8] As raised ICP's may be caused by the presence of a mass, removal of this via craniotomy will decrease raised ICP's.

A drastic treatment for increased ICP is decompressive craniectomy,[29] in which a part of the skull is removed and the dura mater is expanded to allow the brain to swell without crushing it or causing herniation.[24] The section of bone removed, known as a bone flap, can be stored in the patient's abdomen and resited back to complete the skull once the acute cause of raised ICP's has resolved. Alternatively a synthetic material may be used to replace the removed bone section (see cranioplasty)