My question to the group –
At what level of ICP would you expect the appearance of Cushing reflex (Hypertension-Bradycardia-Irregular/shallow breathing). Is it always related to the occurrence of an herniation - Uncal or Tonsillar ? May it appear without any herniation - at what pressure and in how much time ?
I would appreciate your reply.
Normal ICP ranges from 0 to 15 mm Hg, depending on the total volume of brain tissue and the total volume of cerebrospinal fluid (CSF). Normal fluctuations in ICP are due to translocation of CSF into the subarachnoid space and to increased CSF absorption.
Possible triggers of a transient ICP increase in the clinical setting include prone positioning, suctioning, painful procedures, coughing, straining, REM sleep, and abnormal respiratory patterns. A sustained rise in ICP is seen when any added volume (mass, blood, abscess, cerebral edema) exceeds compensatory mechanisms. The magnitude of the increase depends on the amount and accumulation rate of the additional volume and the total volume of the intracranial cavity. The adverse effects of increased ICP are due to reduced cerebral blood flow, brain shift, and distortion. Signs and symptoms of increased ICP in addition to Cushing's triad include headache, vomiting, drowsiness, and lethargy. Studies have shown that common practices aimed at lowering ICP, such as intubation and hyperventilation, are often futile.
Cerebral edema is not uncommon after head injuries. The cause may be cytotoxic, vasogenic, or ischemic. Cytotoxic edema is associated with neuronal degeneration. Each neuron is equipped with a sodium pump to maintain fluid and electrolyte balance. Traumatic injury can cause dysfunction of this pump and consequent influx of sodium and water into the cells. Vasogenic edema is due to compromise of the blood-brain barrier by damaged capillaries that allow plasma leakage into brain tissue. Ischemic edema is due to a combination of cytotoxic and vasogenic processes.
Cerebral edema is the major cause of reduced blood flow to the brain. It is also a major contributor to increased ICP. Cerebral edema occurs between 1 and 18 hours after injury, peaking at day 3. Alcohol promotes cerebral edema by increasing the permeability of the blood-brain barrier. Common radiographic signs include small or absent sulci, low attenuation within adjacent white matter, compression of the ventricles, and poor gray-white differentiation.
The combination of increased ICP and cerebral edema with an expanding lesion is the cause of various herniation syndromes. The most common is tentorial herniation, in which the uncus of the temporal lobe is pushed over the edge of the tentorial notch. Typical findings include ipsilateral pupillary dilation, loss of light reflex, and ptosis due to compression of cranial nerve III. With compression of the midbrain as herniation progresses, patients will also have a decreased level of consciousness. Projectile vomiting is common. If the cerebral peduncles are also compressed, patients may display contralateral posturing. Patients have also been described as having Cheyne-Stokes respirations or central neurogenic hyperventilation.
A variant worth noting is cerebellar tonsil herniation syndrome, meaning that the cerebellar tonsils are being forced through the foramen magnum. This syndrome is usually associated with lesions in the posterior fossa. Respiratory arrest ensues as the respiratory centers are compressed in the medulla.
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