Description, Causes and Risk Factors:
Papilledema specifically refers to optic nerve head swelling secondary to increased intracranial pressure (IICP). The anatomy of the optic nerve makes it a sensitive marker for problems inside the brain. This nerve is a thick cord that connects the back of each eyeball and its retina to the brain. In its short span between the brain and the eye, the optic nerve's whole surface is bathed in cerebral spinal fluid. This fluid protects the nerve from sudden movement. However, even slight increases in the pressure of this fluid, from swelling of the brain, can compress the optic nerve around its whole circumference in a "choking" manner. When this nerve is exposed to high pressure, or when it develops inflammation on its own, it can bulge into the back wall of the eyeball, causing papilledema.
Some important causes of increased pressure from cerebral spinal fluid and papilledema are brain tumors and brain infections, such as a brain abscess, meningitis or encephalitis. A significant proportion of people who are diagnosed with brain tumors have some evidence of papilledema. A pressure increase resulting from bleeding or from very high blood pressure also can cause papilledema.
One condition can cause increased pressure in the cerebral spinal fluid without associated swelling of the brain or ventricles. This condition, called pseudotumor cerebri or benign intracranial hypertension, is caused when the body makes too much spinal fluid. It is more common in women who are obese and of childbearing age. The condition seems to be triggered at times that the body is adjusting to hormone changes, such as pregnancy, the start of birth control pills, the first menstrual period, or menopause.
The pathophysiology behind this association between anemia and papilledema has not been clearly explained. Many hypotheses have been put forward. It has been thought a loss of iron dependent enzymes due to anemia may result in lowering oxygen carrying capacity with resultant papilledema and cerebral edema causing raised intracranial pressure.
Most cases of papilledema are bilateral, although the optic nerve appearance can be asymmetric. Any reported unilateral papilledema should be viewed skeptically and is more likely optic disc edema. Papilledema is relatively uncommon in infants due to the lack of fusion of skull bones.
Patients with papilledema often complain of headaches, worse upon awakening,nausea, and vomiting. In early stages of papilledema patients may have no visualcomplaints or only be aware of enlargement of the physiologic blind spot. Aspapilledema worsens, patients may experience transient obscurations of vision believedto be secondary to fluctuating ICP, nerve compression and/or or nerve ischemia.Patients with papilledema secondary to an intracranial mass may also have homonymousvisual field defects from lesions in the intracranial visual pathway.
Differential diagnosis of papilledema includes pseudopapilledema (anomalous elevated optic disc) and optic nerve edema caused by direct nervecompression, inflammation, vascular, or infiltrative diseases.
Diagnosis of papilledema is made by direct or indirect ophthalmoscopic examination of the optic nerves. Hyperemia of the nerve head, blurring of the optic disc margins, peripapillary flame-shaped hemorrhages, dilation of the capillaries on the surface of the nerve, and absence of spontaneous venous pulsation are all clinical signs of papilledema. It must be remembered that not all individuals have spontaneous venous pulsations so that their absence alone does not indicate IICP. Nerve fiber layer hemorrhages are the most common finding and often indicate an acute process. In severe IICP, circumferential retinal folds known as Paton's lines may develop.
Treatment of papilledema is directed at the underlying disorder causing IICP. Papilledema generally resolves 6-8 weeks after ICP is normalized. Surgical intervention is employed when patients present with vision threatening compressive optic neuropathy or when primary treatment failed to lower the IICP. Cerebrospinal fluid diversion by ventriculoperitoneal shunt is the most common method for reducing ICP and optic nerve compression. Optic nerve sheath decompression has been effectively used to acutely reduce the CSF pressure in the subarachnoid space of the optic nerve; a surgical window of the nerve sheath allows the CSF to flow into the orbital soft tissues. The technique is usually employed in severely elevated ICP such as pseudotumor cerebri. Papilledema may improve in less than a week following optic nerve sheath decompression surgery. However, the long term effectiveness of this procedure in reducing IICP is poor.
NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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