Sonography of the Optic Nerve Sheath Diameter for Detection of Elevated Intracranial Pressure (ICP)

Elevated intracranial pressure (ICP) is seen in head trauma, hydrocephalus, intracranial tumors, hepatic encephalopathy, and cerebral edema. Intractable elevated ICP can lead to death or devastating neurological damage either by reducing cerebral perfusion pressure (CPP) and causing cerebral ischemia or by compressing and causing herniation of the brainstem or other vital structures. Prompt recognition is crucial in order to intervene appropriately.

Intractable high ICP is the most common "terminal event" leading to death in neurosurgical patients. The association between the severity of intracranial hypertension and poor outcome after severe head injury is well recognized. Outcomes tend to be good in patients with normal ICP, whereas those with elevated ICP are much more likely to have an unfavorable outcome. Elevated ICP carries a mortality rate of around 20%.

The rapid recognition of elevated ICP is therefore of obvious and paramount importance so that it can be monitored and so that therapies directed at lowering ICP can be initiated. A raised ICP is measurable both clinically and quantitatively. Continuous ICP monitoring is important both for assessing the efficacy of therapeutic measures and for evaluating the evolution of brain injury.

The goal of ICP monitoring is to ensure maintenance of optimal CPP. The ICP also forms a basis for medical or surgical intervention in cases of increased ICP with agents such as 3% sodium chloride (NaCl), mannitol, or diuretics (Loop diuretics), ventriculostomy, cerebrospinal fluid (CSF) diversion, and phentobarbital coma or surgical decompression in cases of intractable ICP elevation that do not respond to conservative management.

ICP monitoring may be discontinued when the ICP remains in the normal range within 48-72 hours of withdrawal of ICP therapy or if the patient's neurological condition improves to the point where he or she is following commands.

Since many investigators have questioned invasive ICP monitoring in improving patient outcomes, the invistigators tried to find noninvasive method of ICP monitoring.

The optic nerve sheath is contiguous with the dura mater, and its contents are contiguous with the subarachnoid space. Thus, raised intracranial pressure (ICP) leads to an increase in the optic nerve sheath diameter.

A-mode sonography was first used for visualization of the optic nerve sheath; however, it was not until 1994, when Hansen et al used B-mode sonography, when the approach to measurement was standardized. Sonographic studies of cadaveric optic nerves together with the work of Hansen et al established that the greatest degree of distension of the sheath occurred 3 mm behind the optic globe. This location has become the standard measurement point.

As a technique, ocular sonography is quickly learned; Tayal et al showed that with an experienced operator, 10 scans with 3 abnormal scans should be sufficient training, whereas in new ultrasound operators, 25 may be needed. In addition to these findings, measurement of both eyes can be performed in less than 4 minutes.

the invistigators chose CT as the reference gold standard for detection of raised ICP as simple noninvasive method in critically ill patients. Raised ICP is diagnosed with CT on a daily basis in clinical practice. Treatments are initiated, hemicraniectomies are performed, and intraventricular shunts are inserted, all on the basis of raised ICP as seen on imaging.

The findings of elevated ICP in cranial CT (CCT) include:

1. changes in ventricular sizes;
2. lessening in basilar cistern sizes;
3. narrowing or eliminating in sulci;
4. transfalcine herniation; and
5. changes in the rate of grey/white matter. So in this study the invistigators chose to measure optic nerve sheath diameter by sonography for diagnosis of elevated ICP in comparison to brain CT as the reference gold standard for detection of raised ICP