This procedure is fairly effective, but is rarely able to isolate anaerobic organisms that may be causing the inflammation, giving cause for further research and procedural development.Though they present with similar symptoms and often occur in tandem, meningitis and ventriculitis are two different diseases, so physicians must be able to distinguish between the two. Meningitis is the inflammation of the protective lining of the central nervous system, called meninges. Because of the similar pathologies and cause of the two types of inflammation, they are difficult to differentiate using chemical testing, but show very different visual effects in both the MRI and CT scans, hence their use as a validation that the patient does, in fact, have ventriculitis and not another, similar condition such as meningitis. Treatment
Treatment of ventriculitis is critical. If left untreated, it could lead to severe brain damage and even death in some cases. Currently, the only commonly employed treatments of ventriculitis involve an antibiotic regimen targeting the underlying infection causing the inflammation. Typically, the physician will order the patient be placed on broad-spectrum antibiotics in order to manage the symptoms and control the infection while the cerebrospinal fluid samples are analyzed. When a specific bacterial or viral cause is found, the doctor will change the treatment accordingly. There is some debate as to the most effective antibiotics and the best ways to introduce the drugs (e.g. intravenously, orally, etc. ), however it is agreed that drug effectiveness is limited by the difficulty of non-invasively allowing the drugs to enter the cerebrospinal fluid.
doxazosin)
SucralfatePotentially hazardous interactions with other drugs:

Analgesics: increased risk of kidney damage (nephrotoxicity) with nonsteroidal anti-inflammatory drugs; antagonism of diuretic effect with NSAIDs
Antiarrhythmics: a risk of cardiac toxicity exists with antiarrhythmics if hypokalemia occurs; the effects of lidocaine and mexiletine are antagonized. Antibacterials: increased risk of ototoxicity with aminoglycosides, polymyxins and vancomycin; avoid concomitant use with lymecycline
Antidepressants: increased risk of hypokalemia with reboxetine; enhanced hypotensive effect with MAOIs; increased risk of postural hypotension with tricyclic antidepressants
Antiepileptics: increased risk of hyponatremia with carbamazepine
Antifungals: increased risk of hypokalemia with amphotericin
Antihypertensives: enhanced hypotensive effect; increased risk of first dose hypotensive effect with alpha-blockers; increased risk of ventricular arrhythmias with sotalol if hypokalemia occurs
Antipsychotics: increased risk of ventricular arrhythmias with amisulpride, sertindole, or pimozide (avoid with pimozide) if hypokalemia occurs; enhanced hypotensive effect with phenothiazines
Atomoxetine: hypokalemia increases risk of ventricular arrhythmias
Cardiac glycosides: increased toxicity if hypokalemia occurs
Cyclosporine: variable reports of increased nephrotoxicity, ototoxicity and hepatotoxicity
Lithium: risk of toxicity. Mechanism of action
Furosemide, like other loop diuretics, acts by inhibiting the luminal Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle, by binding to the chloride transport channel, thus causing more sodium, chloride, and potassium to remain in the urine.The action on the distal tubules is independent of any inhibitory effect on carbonic anhydrase or aldosterone; it also abolishes the corticomedullary osmotic gradient and blocks negative, as well as positive, free water clearance.