Intracranial pressure ( ICP ) is the pressure inside the skull and thus in brain tissue and cerebrospinal fluid (CSF). ICP is measured in millimeters of mercury (mmHg) and, at rest, is usually 7-15 mmHg for a supine adult. The body has various mechanisms that make ICP stable, with CSF pressure varying about 1 mmHg in normal adults through a shift in the production and absorption of CSF. ICP changes are associated with volume changes in one or more of the constituents contained within the cranium. CSF pressure has been shown to be affected by sudden changes in intrathoracic pressure during cough (intra-abdominal pressure), valsalva maneuver, and communication with blood vessels (venous and arterial systems).
Intracranial hypertension , usually abbreviated IH , IICP or raised ICP , is an increase in pressure in the cranium. ICP is usually 7-15 mm Hg; at 20-25 mm Hg, upper limit of normal, treatment to reduce ICP may be required.
Video Intracranial pressure
Hipotesis Monro-Kellie
The pressure-volume relationship between ICP, CSF volume, blood, and brain tissue, and cerebral perfusion pressure (CPP) is known as the Monro-Kellie or Monro Hypothesis-Kellie doctrine.
The Monro-Kellie Hypothesis states that the skull compartment is incompressible and that the volume inside the skull remains. The cranium and its constituents (blood, CSF, and brain tissue) create a balance state of volume, so that any increase in the volume of one of the cranial constituents should be compensated by another volume decrease.
Main buffers for volume increase include CSF and, to a lesser extent, blood volume. This buffer responds to the increased volume of the remaining intracranial constituents. For example, increased volume of lesions (eg, epidural hematoma) will be compensated by decreased CSF and venous blood.
The Monro-Kellie Hypothesis was named after Edinburgh doctors Alexander Monro and George Kellie.
Maps Intracranial pressure
Improved ICP
One of the most damaging aspects of brain trauma and other conditions, which directly correlate with poor outcomes, is the high intracranial pressure. ICP is very likely to cause severe damage if it rises too high. Very high intracranial pressure is usually fatal if prolonged, but children can tolerate higher pressure for longer periods. Increased pressure, most often due to head injury leading to intracranial hematoma or cerebral edema, can destroy brain tissue, shift the brain structure, contribute to hydrocephalus, cause brain herniation, and limit the blood supply to the brain. This is the cause of reflex bradycardia.
Signs and symptoms
In general, symptoms and signs showing increased ICP include headache, vomiting without nausea, ocular palsy, altered consciousness, back pain and papilledema. If papilloedema is protracted, it can cause vision impairment, optic atrophy, and ultimately blindness. A classic headache is a morning headache that can wake them from sleep. The brain is relatively less supplied by oxygen due to mild hypoventilation during bedtime and also cerebral edema may worsen at night due to a lying position. The headache is worse on coughing, sneezing or bending and getting worse over time. There may also be a change of personality or behavior.
In addition to the above, if the mass effect is present by causing brain tissue transfer, additional signs may include pupil dilatation, palsi abducens, and Cushing triads. Triad Cushing involves increased systolic blood pressure, widened pulse pressure, bradycardia, and abnormal breathing patterns. In children, low heart rate mainly shows high ICP.
Irregular respirators occur when injuries to the part of the brain interfere with breathing. Biot Respiration, in which breathing progresses rapidly for a period and then is absent during the period, occurs due to injury to cerebral hemispheres or diencephalon. Hyperventilation can occur when the brainstem or tegmentum is damaged.
As a rule, patients with normal blood pressure maintain normal vigilance with ICP 25-40 mmHg (unless the tissue shifts at the same time). Only when ICP exceeds 40-50 mmHg, do CPP and cerebral perfusion to a level that causes loss of consciousness. Any further increase will cause brain infarction and brain death.
In infants and young children, the effects of ICP are different because their cranial sutures are not yet covered. In infants, crowns, or soft spots on the head where skull bones are not yet integrated, stands out when ICP becomes too high. ICP correlates with intraocular pressure (IOP) but appears to lack the accuracy necessary for near intracranial pressure management in the post-traumatic period.
Papilledema, or swelling of the optical disc, can be a reliable sign that ICP is increasing. Unlike other conditions that can cause swelling of the optical disc, this is in the case of papilledema that may not be affected by vision.
Cause
The causes of increased intracranial pressure can be classified by the mechanism by which ICP increases:
- mass effects such as brain tumors, infarction with edema, bruising, subdural or epidural hematoma, or abscess all tend to damage adjacent brains.
- total brain swelling may occur in ischemic anoxia, acute liver failure, hypertensive encephalopathy, hypercarbia (hypercapnia), and Reye hepatoserebral syndrome. This condition tends to lower the pressure of cerebral perfusion but with minimal tissue shift.
- increased venous pressure may be due to venous sinus thrombosis, heart failure, or superior or superior jawular venous or javular obstruction.
- CSF flow obstruction and/or sequestration may occur in hydrocephalus (ventricular or subarachnoid substrate at the base of the brain, for example, by Arnold-Chiari malformation), extensive meningeal disease (eg, infection, carcinoma, granuloma, or hemorrhage), or obstruction in cerebral convexity and superior sagittal sinus (decreased absorption).
- increased production of CSF may occur in meningitis, subarachnoid hemorrhage, or choroid plexus tumors.
- Causes of idiopathic or unknown (idiopathic intracranial hypertension)
- craniosynostosis
or child abuse
Pathophysiology
Cerebral perfusion pressure (CPP), blood pressure flowing to the brain, is usually fairly constant due to autoregulation, but for abnormal abnormal average abnormal (MAP) or ICP pressure, cerebral perfusion pressure is calculated by reducing intracranial pressure from mean arterial pressure : Ã, CPPÃ, = Ã, MAPÃ, -Ã, ICPÃ,. One of the major dangers of increased ICT is that it can cause ischemia by lowering CPP. After ICP approaches the average systemic stress level, cerebral perfusion falls. The body's response to CPP decline is to increase systemic blood pressure and dilate the blood vessels of the brain. This results in an increase in cerebral blood volume, which increases ICT, lowers the CPP further and causes a vicious circle. This results in a wide reduction in brain flow and perfusion, eventually leading to ischemia and cerebral infarction. An increase in blood pressure may also make bleeding more rapidly bleeding intracranial, as well as improving ICT.
A severe ICP arise, if caused by unilateral occupational lesions (eg hematomas) can cause a shift in the midline, a dangerous sequel in which the brain moves to one side as a result of massive swelling in the cerebral hemispheres. Midline shifts may compress the ventricle and cause hydrocephalus.
Treatment
Treatment for IH depends on the cause. In addition to the underlying cause management, the main consideration in the acute treatment of ICP elevation is related to brain stroke and trauma management.
A very common treatment for long-term cranial hypertension, especially idiopathic, is a drug with special diuretics, especially those prescribed by neurologists.
In patients with high ICP due to acute injury, it is important to ensure adequate airway, breathing and oxygenation. Inadequate blood oxygen levels (hypoxia) or too high levels of carbon dioxide (hypercapnia) cause cerebral blood vessels to dilate, increase blood flow to the brain and cause increased ICP. Inadequate oxygenation also forces brain cells to produce energy using anaerobic metabolism, which produces lactic acid and lowers pH, also dilates blood vessels and exacerbates problems. Conversely, blood vessels constrict when the carbon dioxide levels are below normal, so hyperventilation of patients with ventilators or pouch bag masks may reduce ICP temporarily. Hyperventilation was previously part of standard care of traumatic brain injury, but the narrowing of blood vessels induced limits blood flow to the brain when the brain may be ischemic - hence it is no longer widely used. Furthermore, the brain adjusts to a new level of carbon dioxide after 48 to 72 hours of hyperventilation, which can cause the vessels to dilate rapidly if carbon dioxide levels return to normal state too quickly. Hyperventilation is still used if ICP is resistant to other control methods, or there are signs of brain herniation, because herniation damage can cause very severe that it may be beneficial to constrict blood vessels even though it reduces blood flow. ICP can also be lowered by raising the head of the bed, improving venous drainage. The side effect of this is that it can lower blood pressure to the head, so the blood supply is reduced and may be inadequate to the brain. Venous drainage may also be inhibited by external factors such as hard collar to paralyze the neck in traumatized patients, and this may also increase ICT. Sandbags can be used to restrict the movement of the neck further.
At the hospital, blood pressure can be increased artificially to increase CPP, increase perfusion, oxygen tissue, dispose of waste, and thereby reduce swelling. Because hypertension is the body's way of forcing blood into the brain, medical professionals usually do not intervene when found in patients with head injury. When necessary to reduce cerebral blood flow, MAP can be derived using a common antihypertensive agent such as a calcium channel blocker. If there is a complete blood brain barrier, osmotherapy may be performed by IV administration of mannitol to create a hypertonic solution in the blood to draw water out of the neuron. It helps reduce fluid inside the intracranial space; However, prolonged administration may lead to an increase in ICT.
Fighting, anxiety, and seizures can increase metabolic and oxygen consumption requirements, and increase blood pressure. Analgesia and sedation (especially in pre-hospital, ER, and intensive care settings) are used to reduce the need for agitation and brain metabolism, but these drugs can cause low blood pressure and other side effects. So if full sedation alone is not effective, the patient may be paralyzed with drugs such as atracurium. Paralysis allows the cerebral vein to flow more easily, but it can mask seizures, and drugs can have other harmful effects. A crippling drug is only introduced if the patient is completely sedated (this is basically the same as general anesthesia)
Intracranial pressure can be measured continuously with an intracranial transducer. The catheter can be inserted into one of the lateral ventricles of the brain and can be used to drain CSF (cerebrospinal fluid) to decrease ICP. This type of channel is known as the EVD (extraventricular channel). In rare situations where only a small amount of CSF should be dried to reduce ICP, CSF drainage through lumbar puncture may be used as a treatment. There are many clinical studies on non-invasive intracranial pressure measurement methods currently proposed, aiming to find a reliable and accurate way to measure non-invasive ICP. Such methods can improve the diagnostic of traumatic brain injury and many other conditions associated with intracranial hypertension.
The craniotomy is a hole drilled in the skull to remove the intracranial hematoma or reduce the pressure from the part of the brain. When lifting ICP may be due to mass, this removal through craniotomy will decrease ICP increase.
The drastic treatment for improving ICT is a decompression craniectomy, in which the skull part is lifted and the dura mater is expanded to allow the brain to swell without destroying it or causing herniation. The part of the released bone, known as the bone flap, can be stored in the patient's abdomen and recovered to complete the skull after the acute cause of ICP increase has been resolved. Or synthetic materials can be used to replace the removed bone (see cranioplasty)
Low ICP
Spontaneous intracranial hypotension can occur as a result of CSF occult leakage into other body cavities. More generally, decreased ICP is a result of lumbar puncture or other medical procedures involving the brain or spinal cord. Various medical imaging technologies exist to help identify the causes of ICP decline. Often, this syndrome limits itself, especially if it is the result of a medical procedure.
If persistent intracranial hypotension is the result of lumbar puncture, a "blood patch" can be applied to close the CSF leak site. Various medical treatments have been proposed; only intravenous administration of caffeine and theophylline has proven to be very useful.
See also
- Brain Trauma Foundation
- Neurocritical treatment
- Cushing triad
- Traumatic brain injury
- external ventricular duct
- Non-invasive intracranial pressure measurement method
- The pressure reactivity index (PRx)
References
External links
- Gruen P. 2002. "Monro-Kellie Model" Infonet Nerve Surgery. USC Neurosurgery. Retrieved 4 January 2007.
- Clearing the National Guidelines. 2005. Guidelines for management of severe traumatic brain injury. Firstgov. Retrieved 4 January 2007.
- Intracranial pressure at the US National Library of Medicine's Medical Subject Headings (MeSH)
Source of the article : Wikipedia
0 Comments