Furthermore, mannitol acts in a dose-dependent manner and will not lower ICP if it is not elevated. However, the common limitation of the use of mannitol is its tendency to cause low blood pressure hypotension. Compared to hypertonic saline, mannitol may be more effective at increasing cerebral perfusion pressures and may be preferable in those with hypoperfusion. Loop diuretics, commonly furosemide, act within kidney to increase excretion of water and solutes. Combination with mannitol produces a profound diuresis and increases the risk of systemic dehydration and hypotension. Their use remains controversial. Acetazolamide, a carbonic anhydrase inhibitor, acts as a weak diuretic and modulates CSF production but has not role in the management of cerebral edema from acute brain injuries. It can be used in the outpatient management of cerebral edema caused by idiopathic intracranial hypertension (pseudotumor cerebri). Glucocorticoids
Glucocorticoids, such as dexamethasone, have been shown to decrease tight-junction permeability and stabilize the blood-brain barrier. Their main use has been in the management of vasogenic cerebral edema associated with brain tumors, brain irradiation, and surgical manipulation. Glucocorticoids have not been shown to have any benefit in ischemic stroke and have been found to be harmful in traumatic brain injury. Due to the negative side effects (such as peptic ulcers, hyperglycemia, and impairment of wound healing), steroid use should be restricted to cases where they are absolutely indicated. Hyperventilation
As mentioned previously, hypoxia and hypercapnia are potent vasodilators in the cerebral vasculature, leading to increased cerebral blood flow (CBF) and worsening of cerebral edema.
The location of the ulcer depends somewhat on the cause. Central ulcers are typically caused by trauma, dry eye, or exposure from facial nerve paralysis or exophthalmos. Ulcers in the inferior nasal cornea may be caused by foreign material trapped under the third eyelid. Entropion or distichiae may cause ulceration of the peripheral cornea. Immune-mediated eye disease can cause ulcers at the border of the cornea and sclera. Symptoms
Corneal ulcers are painful due to nerve exposure, and can cause tearing, squinting, and pawing at the eye. There may also be signs of anterior uveitis, such as miosis (small pupil), aqueous flare (protein in the aqueous humour), and redness of the eye. An axon reflex may be responsible for uveitis formation — stimulation of pain receptors in the cornea results in release inflammatory mediators such as prostaglandins, histamine, and acetylcholine. Diagnosis
Diagnosis is through direct observation of the ulcer with the use of fluorescein stain, which is taken up by exposed corneal stroma and appears green (see photos above and below). With descemetoceles, Descemets membrane will bulge forward and after staining will appear as a dark circle with a green boundary, because it does not absorb the stain. Other tests that may be necessary include a Schirmers test for keratoconjunctivitis sicca and an analysis of facial nerve function for facial nerve paralysis. Treatment
Treatment of corneal ulcers includes topical antibiotic therapy to prevent infection, and pain medications, including topical atropine to stop spasms of the ciliary muscle. Atropine may decrease tear production and interfere with corneal healing.