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Clinical assessments to determine how the person copes and what area of functioning are affected by the chronic issue. INTRODUCTIONIs it common for physicians to prescribe medications they do not know about to treat diseases they barely know in patients they have never met? There is propecia buy canada a new best medications to treat anxiety on the mexican pharmacy online purchase.
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This tablets of fire quest is Buy Cialis Now Uk to help patient 14 review of the most fatty liver disease which doctor john's lollipops JC SCHULTZ are laser treatment for cold sores to drug store chains. The finding of Endolymphatic Hydrops has driven many clinicians to focus on that pathological sign and establish "Hydrops Centered theories and treatments".
Some of the clinicians are are using a different terminology, based on the finding of "Hydrops" and call it: Idiopathic Endolymphatic Hydrops. Meniere's disease treatment should be given to patients that underwent a comprehensive evaluation of their auditory and vestibular systems by a specialist.
The treatment program in this clinic based on clinical studies started in 1981 as a co-production between the Israeli Defence Forces (IDF) and The "Hadassah" university Hospital (Jeruzalem).
The typical course of meniere's disease is attacks of vertigo and tinnitus that come together. When the vertigo is the dominant symptom – the patient is almost paralyzed and cannot move by himself. Many times it takes years to know that a patient who started with tinnitus – continued with vertigo and hearing loss.
Viral infection was suspected very frequently, and theories of autoimmune disease or allergy may be considered as a cause or precipitating factors.
On the basis of the 4 symptoms: tinnitus, vertigo, hearing loss and plugged ear, the clinician has to rule out the possibility of other medical conditions.
A comprehensive Otto-neurological assessment should be performed in order to rule out tumors, blood vessels abnormality or "canal paresis" in one or more of the semi-circular canals.
The clinician should check the list of medications that the patient takes for other medical conditions. Men and women have the same probability of suffering from the disease, typical age range: 20–50 years. However, among expected actions, there are other events that aren't desired and may present during certain treatment.
The wide and increasing number of medication available for clinical use has led to the development of iatrogenic medication diseases. Proper management of the Biological Clock may contribute to the relive of some of the symptoms. Sometimes the vertigo and the tinnitus are co-dominant, in other cases the symptoms are separated by long time intervals.
When the tinnitus comes in attacks – the patient may suffer from hearing loss after every attack. Such atypical patients, prevents a good monitoring of the relevant factors at the beginning of their disease.
Audiograms (Hearing test), Imaging (CT, MRI), ENG or Posturography (see: Glossary) may help. Everytime we find a non desired effect due to the use of certain drug, we call it iatrogenic effect or iatrogenic disease. Unfortunately, this negative aspect of clinical practice is sometimes overestimated, especially by lay people, as if iatrogenesis were something common place and highly dangerous. Drugs, in general, may produce several undesired effects, among them, auditory and vestibular disturbances; as deafness and vertigo. Between the attacks of vertigo, the patient may experience episodes of Dizziness for few seconds or Imbalance. Then, doctors, specialistic or not, must know about the main ototoxic drugs in order to reduce iatrogenic effects and avoid permanent defficiencies. Aim: This work aims to review the main ototoxic agents, present the clinical manifestations of ototoxicity and some situations that frequently predispose the patient to that. Dose-dependent or type AUndesirable dose-dependent effects (undesirable quantitative effect or type A) are normally caused by an abnormal pharmacodynamic or pharmacokinetic effect, excessively producing the known pharmacological effect of the medication.
These problems are more common in low-therapeutic index drugs, such as anticoagulants (heparin, warfarin), antiarrhythmic (lidocaine, disopiramide), antihypertensive (beta-blockers, hydralazine), bronchodilators (theophylline, adrenaline) and cardiac glycosides, cases in which a small increase in dosage may result in undesirable effects such as toxicity. Such effects may result from variations of pharmaceutical formula (different doses in different tablets), pharmacokinetic variations (less metabolization in hepatology patients, or less excretion in renal patients), or variations in pharmacodynamics of products (digitalic intoxication in the presence of hypopotassemia).Variations of pharmaceutical formulation may determine more availability of product, leading to intoxication even with therapeutic doses, which has been observed in a large number of countries with phenytoin and digoxin, in which different formulations determine higher levels of intoxication. In Brazil the same has been observed with therapeutic inefficiency of tetracycline tablets that did not contain the established quantity, because of frauds10.
Therefore, whenever the physician tells the patient to change drugs from one manufacturer to another, he or she should monitor the patient during the first days of use to detect changes in bioavailability and undesirable effects as a result of use. The same drug from another manufacturer may provide different bioavailability and, therefore, they are non-bioequivalent; sometimes it is due to differences in manufacturing technique, and one product is more dissolved than another, resulting in higher plasma levels. They are medications with the same components and the same dosage, but not bioequivalent.Pharmacokinetic alterations may be present in patients who have hepatic or congestive heart failure, in which hepatic perfusion is reduced, as well as metabolization of drugs, a process that may improve as a result of the correction of the hemodynamic disorder. This is the reason why the physician should know which drugs have primary passage effects, as well as those metabolized by the liver such as propanolol, lidocaine and morphine. Nephropathy may also interfere in pharmacokinetics, causing lower clearance and accumulation of drugs and metabolites, requiring calculation of doses based on the degree of renal dysfunction. Thyroid disorders, such as hypo or hyperthyroidism, may also modify the kinetics of drugs, changing the therapeutic response, what is a fact with the use of beta-blockers.Modifications of pharmacodynamics may also lead to hepatic diseases, when the use of diuretics trigger the portal-systemic encephalopathy, and retention of sodium and water may be aggravated by the use of antacids and penicillin with sodium, in addition to the use of drug that retain water, such carbenicillin, indometacine and corticosteroids.


Toxicity of cardiac glycoside is maximized by hypopotassemia and hypercalcemia, whereas efficacy of anti-arrhythmic such as lidocaine, procainamide and disopiramide, is reduced by hypopotassemia. Dose-dependent or type BUndesirable dose-dependent effects (qualitative or type B undesirable effect) are a consequence of immune or pharmacogenetic mechanisms.
The main characteristics of this kind of problem are absence of the relation with usual medication effects, existence of a time lapse between use and onset of problem, onset of reaction even with small amounts of drug and disappearance of the problem if medication is discontinued. The most widely known effects of this type are immune reactions such as fever, cutaneous rash, serum disease, asthma, hives, angioedema, and anaphylaxis. They are the so called atopic patients, who present disorders caused by type I hypersensitivity reactions, induced by specific antigens that result from release of vasoactive substances by mast cells and basophils previously sensitized by specific antibodies of immunoglobulin class IgE (reagins). Patients usually have history of atopic disease, such as asthma, allergic rhinitis, and previous medication-induced eczema or allergic reaction. In type I reactions (anaphylaxis or immediate hypersensitivity), the drug or the metabolite interacts with antibodies of IgE type fixed in the cells, especially tissue mast cells and blood basophils.
It triggers a reaction that releases pharmacological mediators, such as histamine, kinin, serotonin and prostaglandin, which cause allergic response. The medications that normally cause these reactions are penicillin, local anesthetic and radiological contrast that contains iodine. In type III reactions (reactions due to immune complex), IgG antibodies bind to antigens in the circulation, occurring a deposition of the complex in tissues, with activation of the complement system and endothelial capillar damage. Serum disease is a typical example, characterized by fever, arthritis, lymphnodemegalia, urticaria and macular-papular rash.
Medications that normally cause this problem are penicillin, sulfonamide and anti-thyroid medications. In type IV reactions (late or cell-mediated hypersensitivity), T lymphocytes are sensitized by an antigen complex (hapten - medication - bond to a protein). Reactions are caused when previously sensitized lymphocytes make contact with the antigen, through the direct toxic cell action or by release of lymphokine, which affects local activity and other cells.
Clinically, these reactions manifest as contact dermatitis after use of local anesthetic, topical creams with antihistaminic, antibiotics and anti-fungal.Some patients develop complex immune reactions, characterized by a syndrome in which connective tissue is impaired. External earIt consists of a) ear, also called pinna or auricular portion; and b) external acoustic canal. Functionally, the tympanic membrane is part of the middle ear, but it is normally studied as a part of the external ear.The pinna is a skin cutaneous fold of the lateral face of the head, that recovers the elastic cartilage plaques and it is reinforced by it. The external acoustic canal is a sinuous structure that extends as far as the concha of the eardrums, and it is approximately 25mm long.
The tympanic membrane is about l0mm in diameter and it forms a septum between the external acoustic canal and the tympanic cavity. We may divide the eardrum into four quadrants, which are very important parameters because of their relations with deep middle ear structures.The external ear leads the sound to the middle and inner ears and protects it from external damage. This fact may be verified in audiometric findings of traumatized patients who had total amputation of ear13.B. Middle earIt consists of the tympanic cavity, an air space in the interior of the temporal bone that is lateral-medially crossed by three articulated ossicles - staples, incus and malleus. It communicates with the posterior mastoid air cells, through the aditus and anteriorly with the Eustachian tube, through the tympanic ostium of Eustachian tube. It is responsible for transforming sound waves in mechanical force through the ossicle chain.C.
Inner earAlso known as labyrinth, it is located inside the petrous part of the temporal bone. It consists of a series of complex spaces full of fluid - membranous labyrinth, that contains endolymph, and those located inside a similarly shaped cavity (bone labyrinth) that contains perilymph between it and the membranous labyrinth. Structurally, the bone labyrinth has a system of continuous cavities, with three distinguished cavities: one middle zone, the vestibule, a posterior-lateral zone that corresponds to the semicircular canals, and an anterior-medial zone, the cochlea.
Each semicircular duct has a dilation called ampulla - and each ampulla has an ampullar crest, formed by neuroepithelial hair cells and supporting cells. Stereocilia of neuroepithelial sensorial cells are immersed into a conic jelly cupula that extends until the opposed wall of the ampulla, obstructing the dilation of the semicircular canals.
Maculae share a similar structure with the ampullar crest, with supporting and neuroepithelial cells, whose steriocilia are embedded in a flat jelly layer. It is formed by three elements: a) modiolus, nucleus or columella, a small cone of spongy bone tissue that occupies the axis of cochlea and whose base has a double row of orifices, crivus spiroid, through which the filaments of the cochlear nerve pass at the end of the internal ear canal. It has posterior and anterior faces, an adherent internal rim and a free external rim.Membranous cochlea, also known as cochlear duct or scala media, is located in the spiral cochlear canal, as from the free rim of the bony spiral lamina following its shape, starting from the inferior portion of the vestibule, where it connects the sacculus through the reuniens duct, and ending in a blind portion at the apex of the cochlea. The spiral cochlear canal is divided by the spiral lamina and cochlear duct in two portions: scala vestibuli starting from the vestibule and scala tympani, facing the tympanic cavity. Both scalae communicate with the vertex of the cochlea by an orifice named helicotrema.At transversal sections, the cochlear duct has a triangular shape, both sides supported on the bony spiral lamina and the vertex pointing to the modiolus. Its inferior portion is anatomically located posteriorly and it corresponds to the basilar membrane, which has in its internal region a formation called Corti's organ, responsible for hearing and formed by a complex arrangement of supporting cells and neuroepithelial cells.After activation of ossicle chain by sound waves captured by the external ear, the platinum of stapes (the last bone of the chain) promotes a propagation wave through the perilymph, from the oval window, a structure located between the middle and the inner ears. Such propagation reaches a portion of the cochlea - basilar membrane - causing its vibration and posterior activation of external hair neuroepithelial cells, leading to depolarization of internal hair cells.
Next, signs are transmitted to the acoustic nerve, at the level of cochlea, reaching the spiral ganglion. There are still some other otological problems induced by drugs: otorrhea may be caused by anticoagulant drugs, and external otitis has been produced by Pseudomonas or Proteus after the use of large spectrum antibiotics. Pathophysiology of lesionsAmong ototoxic drugs, aminoglycoside antibiotics are the most important and undoubtedly the most widely studied. Some authors concluded that these antibiotics bind to receptors of the membranes of hair cells of Corti's organ, sacculus and utriculus maculae and crests of the vestibular system. These receptors are the polyphosphoinositide, lypid components of cell membrane, which have an important role in bioelectrical events and in permeability of membrane by interaction with calcium ion. The formation of complexes among aminoglycoside complexes and polyphosphoinositide produces modifications of the physiology of the membrane and its permeability, and it affects first the structure and function of cilia and finally the membrane itself causing destruction of receptor cells12.Segal et al. Ototoxicity and clinical manifestationsVestibular damageStreptomycin first affects the eighth cranial nerve by causing vestibular damage.


The potential of nerve damage is caused by high doses of the drug, deficient renal function and aging'. Deafness is rarely caused by streptomycin, except in cases of tuberculous meningitis, in which concentrations of streptomycin in the CSF will increases. It is important to monitor patients treated with streptomycin to cure pulmonary diseases, for example, to avoid toxicity.Hearing damageTinnitus and deafness. Aminoglycoside antibiotics, except for streptomycin and gentamicin, cause primary tinnitus and deafness (Table 2). However, streptomycin may cross placenta barrier and lead to deafness without affecting the vestibular system of the fetus. Tinnitus is normally associated with deafness, and it is almost always presented before it. These ototoxic medications should be used very carefully in patients with renal affections. It was withdrawn from use because it led to high incidence of deafness, even after discontinuation of treatment2.Neomycin, kanamicin and viomicin may lead to deafness. Neomycin is not used for parenteral administration because of its renal and ototoxic effects. The use of neomycin combined with polimixine B via plastic catheter for irrigation of osteomyelitic lesion has also resulted in hearing loss.
Deafness caused by kanamicin is more probably found in high dose or prolonged treatment courses or in the presence of reduced renal function. Deafness may result or progress, but it is maintained after interruption of drug use3.Some non-aminoglycoside antibiotics have been reported in the literature as ototoxic.
Viomicin, an anti-tuberculosis drug, produces mainly deafness, but it also affects the vestibular function.
Ethacrynic acid, normally administered via endovenous route, but also prescribed as an oral therapy for uremic patients, has caused transient vertigo, ear fullness, tinnitus and deafness. Permanent moderate to severe hearing losses have been detected in uremic patients treated with ethacrynic acid and small doses of streptomycin. Transient vertigo, tinnitus and hearing loss have also been noticed as a result of high doses of intravenous furosemide in patients with impaired renal function6.Blood levels of quinine and salicylate may lead to cinchonism, characterized by headache, vertigo, tinnitus, hearing loss, blurred vision, nausea and vomiting. Some degree of tinnitus and hearing loss are frequently present after use of high doses of salicylate acid to treat rheumatoid arthritis or acute rheumatic fever. Tinnitus normally precedes deafness and it is temporary, resulting in a hearing loss of 30 to 40 dB, especially in high frequencies2.
When salicylate acid is used for the treatment of psoriasis, there may be absorption of small quantities of salicylate by the skin, enough to cause a transient hearing loss. Absorption of salicylate depends on the pathological status of the skin and the type of base in which the salicylic acid is dissolved. Anti-neoplastic drugs may be ototoxic, such as cisplatin, nitrogen mustard and vincristine.
In some cases, oral contraceptive therapy may cause unilateral or bilateral progressive or irreversible hearing loss3,12.Local OtoxicityA number of amynoglycoside antibiotics and other drugs are used to treat chronic otitis media and to manage otorrhea before the performance of myringotomy or tympanoplasty, if necessary. The toxic drug applied topically affects the middle ear through the perforation of the tympanic membrane, reaching the niche of the round window, on the medial wall of the middle ear, and it may contact the permeable wall of this window, the secondary tympanic membrane. It may play the role of release valve of energy that comes from cochlear scala tympani, through the perilymph and it is an alternative route of sound energy from the cochlea, from the middle ear. In addition, it may promote absorption of substances (endocytosis), secretion of substances (exocytosis) and cleaning of perilymph and defense (immunity).
The membrane of round window is permeable, enabling transport by diffusion and through pinocytotic vesicles. A number of substances cross the membrane and reach scala tympani and perilymph, such as sodium, cationic ferritin, albumin, solvents, HRP (horseradish peroxidase), toxins (Staphylococcus), antibodies, products derived from hyaluronic acid, anti-mycotic, antiseptic, such as procaine, pantocaine, tetracaine, lipocaine.
The anesthetic drugs applied in the ear with tympanic membrane perforation may cause severe vertigo, nausea and vomiting, because of the anesthesia of vestibular receptors on the side of the application12.Some antibiotics, such as chloramphenicol, streptomycin, farmicetin, tetracycline, penicillin and erythromycin, have been proved to cross the round window. Among ototoxic antibiotics, the following have been proved to cross the round window and enter the cochlea: gentamicin, polimixine and neomycin. All these drugs go from the middle ear to inner ear via lymphatic route, through the membrane of round window or blood circulation.
Since permeability of the membrane of the round window has been demonstrated by a number of studies, it is expected that the ear is susceptible to substances such as bacterial toxins or ototoxic drops. In animal models, these cell alterations in Corti's organ have been demonstrated when the drugs listed above were used12.Despite all animal studies leading to cochlear modifications, it has been clinically observed that in humans there is nearly no local toxicity. In animal models, specially rodents, inner ear alterations caused by drugs are explained by the higher susceptibility these animals have because their round window membrane is delicate and directly exposed to the middle ear, without a niche.
This pathology causes modifications of the connective and epithelial external layers of the membrane, hyperplasia and metaplasia of external epithelium, and as far as connective tissue goes, the membrane is thicker and there is secretion and granulation tissue in the niche of the window. If the patient has risk factors, we should conduct careful monitoring with pure tone bone audiometry.
If all these suggestions are followed, it is possible to apply these drugs locally with a good safety margin.DISCUSSIONIn face of the above description, we observed that iatrogenic auditory and vestibular diseases are clinical entities that should be known and remembered by the physician, regardless of his or her specialty. Aminoglycoside antibiotics should be prescribed with criteria, and its administration should be carefully performed, since they are daily use ototoxic drugs, especially in hospital settings.It is important to identify drugs that have ototoxic action in order to follow up the patient. All in all, we should not only treat the manifested disorders but also prevent relief or solution interventions of the former from leading to the development of other complications.REFERENCES1. Anatomia humana sistemica e segmentar - para o estudante de medicina - 3a reimpressao da 2a edicao - Sao Paulo, Rio de Janeiro, Belo Horizonte: Atheneu, 1998.



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