For symptoms that are not responsive to treatment within 10 days, a physician should evaluate for necrotizing external otitis. Acute otitis media (AOM) self-resolves within 24–48 hours in 80% of cases. If it does not self-resolve, AOM thought to be caused by bacteria is treated with systemic antibiotics. If symptoms do not respond to a week of treatment, a physician should evaluate for mastoiditis. Acute folliculitis. Auricular cellulitis. Suppurative otitis media. There is also a risk for tympanic membrane rupture. Perichondritis. An otorhinolaryngologist should also evaluate it and if a foreign body is present in the cartilage, this foreign body should be removed. If there is cartilage involvement, then more advance care with hospitalization is needed. Sinusitis can cause secondary ear pain. Treating the underlying sinusitis will treat the ear pain. (See sinusitis. )Some bacterial infections may require a more advanced treatment with evaluation by otorhinolaryngology, IV antibiotics, and hospital admission. Necrotizing external otitis is potentially fatal and should be evaluated by an otorhinolaryngologist with admission to the hospital and IV antibiotics. (See otitis externa.) Acute mastoiditis is treated with admission to the hospital, otorhinolaryngology consultation and empiric IV antibiotics. Cases with intracranial involvement are treated with a mastoidectomy with myringotomy. Chondritis. Procedures
Some causes of ear pain require procedural management alone, by a health professional, or in addition to antibiotic therapy. Keratosis obturans is treated with removal of impacted desquamated keratin debris in the ear canal. Chronic perichondritis and chondritis that continues to be symptomatic despite appropriate antibiotic management may require surgical debridement.
Found in the renal pelvis, ureter, and capillaries supplying the nephrons, capillary sclerosis is thought to lead to renal papillary necrosis and, in turn, chronic interstitial nephritis.How phenacetin and other analgesics lead to this damage is incompletely understood. It is currently thought that the kidney toxicities of NSAIDs and the antipyretics phenacetin and paracetamol may combine to give rise to analgesic nephropathy. A committee of investigators reported in 2000 that there was insufficient evidence to suggest that non-phenacetin analgesics by themselves are associated with analgesic nephropathy. Aspirin and NSAIDs
Proper kidney function depends upon adequate blood flow to the kidney. Kidney blood flow is a complex, tightly regulated process that relies on a number of hormones and other small molecules, such as prostaglandins. Under normal circumstances, prostaglandin E2 (PGE2) produced by the kidney is necessary to support adequate blood flow to the kidney. Like all prostaglandins, PGE2 synthesis depends upon the cyclooxygenases.Aspirin and other NSAIDs are inhibitors of the cyclooxygenases. In the kidney, this inhibition results in decreased PGE2 concentration causing a reduction in blood flow. Because blood flow to the kidney first reaches the renal cortex (outside) and then the renal medulla (inside), the deeper structures of the kidney are most sensitive to decreased blood flow. Thus the innermost structures of the kidney, known as the renal papillae, are especially dependent on prostaglandin synthesis to maintain adequate blood flow.