Hemodialysis also has the advantage of restoring electrolyte and acid-base abnormalities while removing salicylate.Salicylic acid has a small size (low molecular mass), has a low volume of distribution (is more water soluble), has low tissue binding and is largely free (and not protein bound) at toxic levels in the body; all of which make it easily removable from the body by hemodialysis.Indication for dialysis:

Salicylate level higher than 90 mg/dL
Severe acid base imbalance
Severe cardiac toxicity
Acute respiratory distress syndrome
Cerebral involvement/ neurological signs and symptoms
Rising serum salicylate level despite alkalinization/multidose activated charcoal, or people in which standard approaches to treatment ave failed
Unable to tolerate fluids with fluid overload

Epidemiology
Acute salicylate toxicity usually occurs after an intentional ingestion by younger adults, often with a history of psychiatric disease or previous overdose, whereas chronic toxicity usually occurs in older adults who experience inadvertent overdose while ingesting salicylates therapeutically over longer periods of time.During the latter part of the 20th century, the number of  poisonings from salicylates  declined, mainly because of the increased popularity of other over-the-counter analgesics such as paracetamol (acetaminophen). Fifty-two deaths involving single-ingredient aspirin were reported in the United States in 2000; however, in all but three of these cases, the reason for the ingestion of lethal doses was intentional—predominantly suicidal. History
Aspirin poisoning has controversially been cited as a possible cause of the high mortality rate during the 1918 flu pandemic, which killed 50 to 100 million people. See also
NSAID hypersensitivity reactions
Reye syndrome
Salicylate sensitivity

References
External links

Reingardiene, D; Lazauskas, R (2006). "[Acute salicylate poisoning]". Medicina (Kaunas, Lithuania). 42 (1): 79–83.
Blockage of a vein in the retina can cause engorgement of the other retinal veins causing them to leak fluid under or into the retina. The blockage may be caused, among other things, by atherosclerosis, high blood pressure and glaucoma. A number of drugs can cause changes in the retina that can lead to macular edema. The effect of each drug is variable and some drugs have a lesser role in causation. The principal medication known to affect the retina are:- latanoprost, epinephrine, rosiglitazone, timolol and thiazolidinediones among others. A few congenital diseases are known to be associated with macular edema for example retinitis pigmentosa and retinoschisis. Diagnosis
Classification
Cystoid macular edema (CME) involves fluid accumulation in the outer plexiform layer secondary to abnormal perifoveal retinal capillary permeability. The edema is termed "cystoid" as it appears cystic; however, lacking an epithelial coating, it is not truly cystic. The cause for CME can be remembered with the mnemonic "DEPRIVEN" (diabetes, epinepherine, pars planitis, retinitis pigmentosa, Irvine-Gass syndrome, venous occlusion, E2-prostaglandin analogues, nicotinic acid/niacin). Diabetic macular edema (DME) is similarly caused by leaking macular capillaries. DME is the most common cause of visual loss in both proliferative, and non-proliferative diabetic retinopathy. Treatment
Macular edema sometimes occurs for a few days or weeks after cataract surgery, but most such cases can be successfully treated with NSAID or cortisone eye drops. Prophylactic use of Nonsteroidal anti-inflammatory drugs has been reported to reduce the risk of macular edema to some extent.