Ординатура / Офтальмология / Английские материалы / Comprehensive Ophthalmology_Khurana_2007

Mechanism. The iron particle undergoes electrolytic dissociation by the current of rest and its ions are disseminated throughout the eye. These ions combine with the intracellular proteins and produce degenerative changes. In this process, the epithelial structures of the eye are most affected.

Clinical manifestations

1.The anterior epithelium and capsule of the lens are involved first of all. Here, the rusty deposits are arranged radially in a ring. Eventually, the lens becomes cataractous.

2.Iris. It is first stained greenish and later on turns reddish brown.

3.Retina develops pigmentary degeneration which resembles retinitis pigmentosa.

4.Secondary open angle type of glaucoma occurs due to degenerative changes in the trabecular meshwork.

Chalcosis

It refers to the specific changes produced by the alloy of copper in the eye.

Mechanism. Copper ions from the alloy are dissociated electrolytically and deposited under the membranous structures of the eye. Unlike iron ions these do not enter into a chemical combination with the proteins of the cells and thus produce no degenerative changes.

Clinical manifestations

1.Kayser-Fleischer ring. It is a golden brown ring which occurs due to deposition of copper under peripheral parts of the Descemet’s membrane of the cornea.

2.Sunflower cataract. It is produced by deposition of copper under the posterior capsule of the lens. It is brilliant golden green in colour and arranged like the petals of a sun flower.

3.Retina. It may show deposition of golden plaques at the posterior pole which reflect the light with a metallic sheen.

II Reaction of organic foreign bodies

The organic foreign bodies such as wood and other vegetative materials produce a proliferative reaction characterised by the formation of giant cells. Caterpillar hair produces ophthalmia nodosum, which is characterised by a severe granulomatous iridocyclitis with nodule formation.

Management of retained intraocular foreign bodies (IOFB)

Diagnosis

It is a matter of extreme importance particularly as the patient is often unaware that a particle has entered the eye. To come to a correct diagnosis following steps should be taken:

1.History. A careful history about the mode of injury may give a clue about the type of IOFB.

2.Ocular examination. A thorough ocular examination with slit-lamp including gonioscopy should be carried out. The signs which may give some indication about IOFB are: subconjunctival haemorrhage, corneal scar, holes in the iris, and opaque track through the lens. With clear media, sometimes IOFB may be seen on ophthalmoscopy in the vitreous or on the retina. IOFB lodged in the angle of anterior chamber may be visualised by gonioscopy.

3.Plain X-rays orbit. Antero-posterior and lateral views are indispensable for the location of IOFB, as most foreign bodies are radio opaque.

4.Localization of IOFB. Once IOFB is suspected clinically and later confirmed, on fundus examination and/or X-rays, its exact localization is mandatory to plan the proper removal. Following techniques may be used:

Radiographic iocialization. Before the advent of ultrasonography and CT scan, different specialized radiographic techniques were used to localize IOFBs; which are now obsolete. However, a simple limbal ring method which is still used is described below:

Limbal ring method. It is the most simple but now-a-days, sparingly employed technique. A metallic ring of the corneal diameter (Fig. 17.11) is stitched at the limbus and X-rays are taken. One exposure is taken in the anteroposterior view. In the lateral view three exposures are made one each while the patient is looking straight, upwards and downwards, respectively. The position of the foreign body is estimated from its relationship with the metallic ring in different positions (Fig. 17.12).

Ultrasonographic localization. It is being used increasingly these days. It can tell the position of even non-radioopaque foreign bodies.

Fig. 17.11. Limbal ring used for localization of an intraocular foreign body.

CT scan. With axial and coronal cuts, CT scan is presently the best method of IOFB localization. It provides cross-sectional images with a sensitivity and specificity that are superior to plain radiography and ultrasonography.

Treatment

IOFB should always be removed, except when it is inert and probably sterile or when little damage has been done to the vision and the process of removal may be risky and destroy sight (e.g., minute FB in the retina).

Removal of magnetic IOFB is easier than the removal of non-magnetic FB. Usually a hand-held electromagnet (Fig. 17.13) is used for the removal of magnetic foreign body. Method of removal depends upon the site (location) of the IOFB as follows:

1. Foreign body in the anterior chamber. It is removed through a corresponding corneal incision directed straight towards the foreign body. It should be 3 mm internal to the limbus and in the quadrant of the cornea lying over the foreign body (Fig. 17.14).

Magnetic foreign body is removed with a handheld magnet. It may come out with a gush of aqueous.

Non-magnetic foreign body is picked up with toothless forceps.

2. Foreign body entangled in the iris tissue

(magnetic as well as non-magnetic) is removed by performing sector iridectomy of the part containing foreign body.

Fig. 17.12. Limbal ring method of radiographic localization of IOFB: Lateral view with eyeball in straight position; superimposed over lateral view with eyeball in down gaze.

Fig. 17.13. Hand-held magnet.

Fig. 17.14. Removal of a magnetic intraocular foreign body from the anterior chamber: A, the wrong incision;

B, correct incision.

3.Foreign body in the lens. Magnet extraction is usually difficult for intralenticular foreign bodies. Therefore, magnetic foreign body should also be treated as non-magnetic foreign body. An extracapsular cataract extraction (ECCE) with intraocular lens implantation should be performed. The foreign body may be evacuated itself along with the lens matter or may be removed with the help of forceps.

4.Foreign body in the vitreous and the retina is removed by the posterior route as follows:

i. Magnetic removal. This technique is used to remove a magnetic foreign body that can be well localized and removed safely with a powerful magnet without causing much damage to the intraocular structures.

An intravitreal foreign body is preferably

removed through a pars plana sclerotomy (5 mm from the limbus) (Fig 17.15A). At the site chosen for incision, conjunctiva is reflected and the incision is given in the sclera concentric to the limbus. A preplaced suture is passed and lips of the wound are retracted. A nick is given in the underlying pars plana part of the ciliary body. And the foreign body is removed with the help of a powerful hand-held electromagnet. Preplaced suture is tied to close the scleral wound. Conjunctiva is stitched with one or two interrupted sutures.

For an intraretinal foreign body, the site of incision should be as close to the foreign body as possible (Fig. 17.15 position ‘B’). A trapdoor scleral flap is created, the choroidal bed is treated with diathermy, choroid is incised and foreign body is removed with either forceps or external magnet.

ii. Forceps removal with pars plana vitrectomy. This technique is used to remove all non-magnetic foreign bodies and those magnetic foreign bodies that can not be safely removed with a magnet. In this technique, the foreign body is removed with vitreous forceps after performing three-pore pars plana vitrectomy under direct visualization using an operating microscope (Fig. 17.16).

Fig. 17.15. Removal of a magnetic intraocular foreign body from posterior segment.

Fig. 17.16. Removal of a non-magnetic foreign body through pars plana.

SYMPATHETIC OPHTHALMITIS

Sympathetic ophthalmitis is a serious bilateral granulomatous panuveitis which follows a penetrating ocular trauma. The injured eye is called exciting eye and the fellow eye which also develops uveitis is called sympathizing eye. Very rarely, sympathetic ophthalmitis can also occur following an intraocular surgery.

Incidence

Incidence of sympathetic ophthalmitis has tremendously decreased in the recent years due to meticulous repair of the injured eye utilizing microsurgical techniques and use of the potent steroids.

Etiology

Etiology of sympathetic ophthalmitis is still not known exactly. However, the facts related with its occurrence are as follows:

A. Predisposing factors

1.It almost always follows a penetrating wound.

2.Wounds in the ciliary region (the so-called dangerous zone) are more prone to it.

3.Wounds with incarceration of the iris, ciliary body or lens capsule are more vulnerable.

4.It is more common in children than in adults.

5.It does not occur when actual suppuration develops in the injured eye.

B. Pathogenesis. Various theories have been put forward. Most accepted one is allergic theory, which postulates that the uveal pigment acts as allergen and excites plastic uveitis in the sound eye.

Pathology

It is characteristic of granulomatous uveitis, i.e., there is nodular aggregation of lymphocytes, plasma cells, epitheloid cells and giant cells scattered throughout the uveal tract.

Dalen-Fuchs’ nodules are formed due to proliferation of the pigment epithelium (of the iris, ciliary body and choroid) associated with invasion by the lymphocytes and epitheloid cells. Retina shows perivascular cellular infiltration (sympathetic perivasculitis).

Clinical picture

I. Exciting (injured) eye. It shows clinical features of persistent low grade plastic uveitis, which include ciliary congestion, lacrimation and tenderness. Keratic precipitates may be present at the back of cornea (dangerous sign).

II. Sympathizing (sound) eye. It is usually involved after 4-8 weeks of injury in the other eye. Earliest reported case is after 9 days of injury. Most of the cases occur within the first year. However, delayed and very late cases are also reported. Sympathetic ophthalmitis, almost always, manifests as acute plastic iridocyclitis. Rarely it may manifest as neuroretinitis or choroiditis. Clinical picture of the iridocyclitis in sympathizing eye can be divided into two stages:

1.Prodromal stage. Symptoms. sensitivity to light (photophobia) and transient indistinctness of near objects (due to weakening of accommodation) are the earliest symptoms.

Signs. In this stage the first sign may be presence of retrolental flare and cells or the presence of a few keratic precipitates (KPs) on back of cornea. Other signs includes mild ciliary congestion, slight tenderness of the globe, fine vitreous haze and disc oedema which is seen occasionally.

2.Fully-developed stage. It is clinically characterised by typical signs and symptoms consistent with acute plastic iridocyclitis (see page 141).

Treatment

A. Prophylaxis

I. Early excision of the injured eye. It is the best prophylaxis when there is no chance of saving useful vision.

II. When there is hope of saving useful vision, following steps should be taken:

1.A meticulous repair of the wound using microsurgical technique should be carried out, taking great care that uveal tissue is not incarcerated in the wound.

2.Immediate expectant treatment with topical as well as systemic steroids and antibiotics along with topical atropine should be started.

3.When the uveitis is not controlled after 2 weeks of expectant treatment, i.e., lacrimation, photophobia and ciliary congestion persist and if KPs appear, this eye should be excised immediately.

B. Treatment when sympathetic ophthalmitis has already supervened

I. If the case is seen shortly after the onset of inflammation (i.e., during prodromal stage) in the sympathizing eye, and the injured eye has no useful vision, this useless eye should be excised at once.

II. Conservative treatment of sympathetic ophthalmitis on the lines of iridocyclitis should be started immediately, as follows:

1.Corticosteroids should be administered by all routes, i.e., systemic, periocular injections and frequent instillation of topical drops.

2.In severe cases, immunosuppressant drugs should be started without delay.

3.Topical atropine should be instilled three times a day.

Note. The treatment should be continued for a long time.

Prognosis. If sympathetic ophthalmitis is diagnosed early (during prodromal stage) and immediate treatment with steroids is started, a useful vision may be obtained. However, in advanced cases, prognosis is very poor, even after the best treatment.

NON-MECHANICAL INJURIES

CHEMICAL INJURIES

Chemical injuries (Fig. 17.17) are by no means uncommon. These vary in severity from a trivial and transient irritation of little significance to complete and sudden loss of vision.

Fig. 17.17. A patient with chemical injury face including eyes.

Modes of injury

These usually occur due to external contact with chemicals under following circumstances:

1.Domestic accidents, e.g., with ammonia, solvents, detergents and cosmetics.

2.Agricultural accidents, e.g., due to fertilizers, insecticides, toxins of vegetable and animal origin.

3.Chemical laboratory accidents, with acids and alkalies.

4.Deliberate chemical attacks, especially with acids to disfigure the face.

5.Chemical warfare injuries.

6.Self-inflicted chemical injuries are seen in malingerers and psychopaths.

Types

In general, the serious chemical burns mainly comprise alkali and acid burns.

A. Alkali burns

Alkali burns are among the most severe chemical injuries known to the ophthalmologists. Common alkalies responsible for burns are: lime, caustic potash or caustic soda and liquid ammonia (most harmful).

Mechanisms of damage produced by alkalies includes:

1.Alkalies dissociate and saponify fatty acids of the cell membrane and, therefore, destroy the structure of cell membrane of the tissues.

2.Being hygroscopic, they extract water from the cells, a factor which contributes to the total necrosis.

3.They combine with lipids of cells to form soluble compounds, which produce a condition of

softening and gelatinisation.

The above effects result in an increased deep penetration of the alkalies into the tissues. Alkali burns, therefore, spread widely, their action continues for some days and their effects are difficult to circumscribe. Hence, prognosis in such cases must always be guarded.

Clinical picture. It can be divided into three stages:

1.Stage of acute ischaemic necrosis. In this stage;

i.Conjunctiva shows marked oedema, congestion, widespread necrosis and a copious purulent discharge.

ii.Cornea develops widespread sloughing of the epithelium, oedema and opalescence of the stroma.

iii.Iris becomes violently inflamed and in severe cases both iris and ciliary body are replaced by granulation tissue.

2.Stage of reparation. In this stage conjunctival and corneal epithelium regenerate, there occurs corneal vascularization and inflammation of the iris subsides.

3.Stage of complications. This is characterised by development of symblepharon, recurrent corneal ulceration and development of complicated cataract and secondary glaucoma.

B. Acid burns

Acid burns are less serious than alkali burns. Common acids responsible for burns are: sulphuric acid, hydrochloric acid and nitric acid.

Chemical effects. The strong acids cause instant coagulation of all the proteins which then act as a barrier and prevent deeper penetration of the acids into the tissues. Thus, the lesions become sharply demarcated.

Ocular lesions

1.Conjunctiva. There occurs immediate necrosis followed by sloughing. Later on symblepharon is formed due to fibrosis.

2.Cornea. It is also necrosed and sloughed out. The extent of damage depends upon the concentration of acid and the duration of contact. In severe cases, the whole cornea may slough out followed by staphyloma formation.

Grading of chemical burns

Depending upon the severity of damage caused to the conjunctiva and cornea, the extent of chemical burns may be graded as follows (Table 17.1):

Treatment of chemical burns

1.Immediate and thorough wash with the available clean water or saline.

2.Chemical neutralization. It should be carried out when the nature of offending chemical is known. For example, acid burns should be neutralized with weak alkaline solutions (such as sodium bicarbonate) and alkali burns with weak acidic solutions (such as boric acid or mix) Ethylenediamine tetra acetic acid (EDTA) 1% solution can also be used as neutralizing agent.

3.Mechanical removal of contaminant. If any particles are left behind, particularly in the case

Table 17.1: Grades of chemical burns

of lime, these should be removed carefully with a swab stick.

4.Removal of contaminated and necrotic tissue.

Necrosed conjunctiva should be excised. Contaminated and necrosed corneal epithelium should be removed with a cotton swab stick.

5.Maintenance of favourable conditions for rapid and uncomplicated healing by frequent application of topical atropine, corticosteroids and antibiotics.

6.Prevention of symblepharon can be done by using a glass shell or sweeping a glass rod in the fornices twice daily.

7.Treatment of complications

i.Secondary glaucoma should be treated by topical 0.5 percent timolol instilled twice a day along with oral acetazolamide 250 mg 3-4 times a day.

ii.Corneal opacity may be treated by keratoplasty.

iii.Treatment of symblepharon (see page 354).

THERMAL INJURIES

Thermal injuries are usually caused by fire, or hot fluids. The main brunt of such injuires lies on the lids. Conjunctiva and cornea may be affected in severe cases.

Treatment for burns of lids is on general lines. When cornea is affected, it should be treated with atropine, steroids and antibiotics.

ELECTRICAL INJURIES

The passage of strong electric current from the area of eyes may cause following lesions:

1.Conjunctiva becomes congested.

2.Cornea develops punctate or diffuse interstitial opacities.

3.Iris and ciliary body are inflamed.

4.Lens may develop ‘electric cataract’ after 2-4 months of accident.

5.Retina may show multiple haemorrhages.

6.Optic nerve may develop neuritis.

RADIATIONAL INJURIES

1.Ultraviolet radiations. These may cause (i) photo-ophthalmia (see page 111) and (ii) may be responsible for senile cataract.

2.Infrared radiations. These may cause solar macular burns (see page 271).

3.Ionizing radiational injuries. These are caused followingradiotherapytothetumoursinthevicinity of the eyes. The common ocular lesions include (i) radiation keratoconjunctivitis; (ii) radiation dermatitisof lids;and(iii)radiationcataract.

OCULAR THERAPEUTICS

Modes of administration

Antibacterial agents

Antiviral drugs

Ocular antifungal agents

Mydriatics and cycloplegics

Antiglaucoma drugs

Corticosteroids

Nonsteroidal anti-inflammatory drugs

Viscoelastic substances

LASERS

Production of laser beam

Mechanisms of laser effects and their therapeutic applications

CRYOTHERAPY IN OPHTHALMOLOGY

Principle

Mode of action

Uses

OCULAR THERAPEUTICS

MODES OF ADMINISTRATION

Ocular pharmacotherapeutics can be delivered by four methods: topical instillation into the conjunctival sac, periocular injections, intraocular injections and systemic administration.

1. Topical instillation into the conjunctival sac

This is the most commonly employed mode of administration for ocular therapeutics. The drugs can be administered topically in the form of eyedrops, ointments, gels, ocuserts and with the help of soft contact lenses.

(a)Eyedrops (gutta). This is the simplest and most convenient method of topical application, especially for daytime use. Eyedrops may be in the form of aqueous solutions (drug totally dissolved) or aqueous suspensions (drug is present as small particles kept suspended in the aqueous medium) or oily solutions. Application in the form of eyedrops makes the drug available for immediate action but it is quickly diluted by tears within about a minute.

(b)Eye ointment (oculenta or ung). Topical application in the form of an eye ointment increases

the bioavailability of the drug by increasing tissue contact time and by preventing dilution and quick absorption. However, the drug is not available for immediate use and ointments blur the vision. These are best for bedtime application or when ocular bandage is to be applied.

(c)Gels. These have prolonged contact time like ointments and do not cause much blurring of vision. However, they are costly and difficult to prepare.

(d)Ocuserts. These form a system of drug delivery through a membrane. These can be placed in the upper or lower fornix up to a week and allow a drug to be released at a relatively constant rate. Pilocarpine ocuserts have been found very useful in patients with primary open-angle glaucoma; by efficiently controlling intraocular pressure with comparatively fewer side-effects.

(e)Soft contact lenses. These are very good for delivering higher concentrations of drugs in emergency treatment. A pre-soaked soft contact lens in 1 percent pilocarpine has been found as effective as 4 percent pilocarpine eyedrops in patients with acute angle closure glaucoma. Soft contact lenses are also used to deliver antibiotics and antiviral drugs in patients with corneal ulcers.

Intraocular penetration of topically instilled drugs

Topically instilled medications largely penetrate intraocularly through the cornea. The main barrier through cornea is its epithelium, which is lipophilic, and crossed readily by non-polar drugs. Stroma being hydrophilic allows rapid passage of the drug through endothelium into the anterior chamber. So following features will allow better penetration of drugs through the cornea:

Drugs which are soluble both in water and fats.

Pro-drug forms are lipophilic and after absorption through epithelium are converted into proper drugs which can easily pass through stroma.

Agents that reduce surface tension increase corneal wetting and therefore present more drug for absorption. Benzalkonium chloride used as preservative also acts as a wetting agent and thus increases the drug absorption.

2. Periocular injections

These are not infrequently employed to deliver drugs. These include subconjunctival, sub-Tenon, retrobulbar and peribulbar injections.

(a)Subconjunctival injections. These are commonly used to achieve higher concentration of drugs. Further, the drugs which cannot penetrate the cornea owing to large-sized molecules can easily pass through the sclera.

(b)Sub-Tenon injections. These are preferred over subconjunctival injection. Anterior sub-Tenon injections are used mainly to administer steroids in the treatment of severe or resistant anterior uveitis. Posterior sub-Tenon injections are indicated in patients with intermediate and posterior uveitis.

(c)Retrobulbar injections. These are used to deliver drugs for optic neuritis, papillitis, posterior uveitis and also for administering retrobulbar block anaesthesia.

(d)Peribulbar injections. These are now frequently used for injecting anaesthetic agents. Peribulbar anaesthesia has almost replaced retrobulbar and facial block anaesthesia.

3. Intraocular injections

Such injections are made in desperate cases (e.g., endophthalmitis) to deliver the drugs in maximum concentration at the target tissue. These include: intracameral injection (into the anterior chamber), and intravitreal injection (into the vitreous cavity).

4. Systemic administration

The systemic routes include oral intake and intramuscular and intravenous injections. The intraocular penetration of systemically administered drugs mainly depends upon the blood-aqueous barrier. The passage through blood-aqueous barrier in turn is influenced by the molecular weight and the lipid solubility of the drug.

Only low molecular weight drugs can cross this blood-aqueous barrier. No passage is allowed to largesized molecules, such as penicillin. Out of the borderline molecular weight drugs, those with high lipid solubility can pass easily e.g., sulphonamides have the same molecular weight as sucrose but are 16 times more permeable due to their lipid solubility. Similarly, chloramphenicol being lipid soluble also enters the eye easily.

COMMON OCULAR THERAPEUTICS

The agents commonly used in ophthalmology include: antibacterial, antiviral, antifungal, antiglaucoma, corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs) and viscoelastic substances.

ANTIBACTERIAL AGENTS

Antimicrobial drugs are the greatest contribution of the present century to therapeutics. As there are a wide range of microorganisms, there are also specific antibiotics for almost each organism. Depending on the type of action, these can be either bacteriostatic or bactericidal. A few common antimicrobials described here are grouped on the basis of their chemical structure.

Sulphonamides

These are bacteriostatic agents that act by competing with PABA (para-aminobenzoic acid) which is essential for the bacterial cell nutrition. Thus, they prevent susceptible microorganisms from synthesizing folic acid.

In ophthalmology, these are used topically and systemically in the treatment of chlamydial infections, viz., trachoma and inclusion conjunctivitis. They are also helpful as an adjunct to pyrimethamine in the treatment of toxoplasmosis.

Beta-lactam antibiotics

These antibiotics have a beta-lactam ring. The two important groups are penicillins, and cephalosporins. All beta-lactam antibiotics act by interfering with the synthesis of bacterial cell wall.

A.Penicillins. These are produced by growing one of the penicillium moulds in deep tanks. These may be categorised as: natural penicillins and semisynthetic penicillins.

In deep-seated inflammations of the orbit or lids, penicillin is given parenterally. In superficial inflammations of the conjunctiva and cornea it is administered locally as drops or ointments. In intraocular infections it is given as subconjunctival injections. Commonly used preparations are as follows:

1. Benzyl penicillin. A dose of 500,000 units twice daily is sufficient for sensitive infections and produces high levels in all tissues except CNS and eye.

2. Procaine penicillin. This is an intramuscular depot preparation which provides tissue levels up to 24 hours.

3. Methicillin, cloxacillin and flucloxacillin. These penicillins are not affected by penicillinase and are, therefore, used for staphylococcal infections which are resistant to other penicillins.

4. Carbenicillin. It is resistant to the penicillinase produced by some strains of Proteus, Pseudomonas and coliform organisms. It is ineffective by mouth.

5. Ampicillin. It is a broad-spectrum penicillinasesensitive penicillin. It is acid resistant and usually administered orally.

Its dosage is 0.25-2 g oral/i.m./i.v. depending upon the severity of infection every 6 hours. Paediatric dose is 25-50 mg/kg/day.

6. Amoxycillin. Its spectrum is similar to ampicillin except that it is less effective against Shigella and H. influenzae. Its oral absorption is better than ampicillin and thus higher and more sustained blood levels are produced. Incidence of diarrhoea is less with it than with ampicillin and is thus better tolerated orally.

B.Cephalosporins. These drugs have a similar structure and mode of action as penicillin. All the cephalosporins have a bactericidal action against a wide range of organisms. By convention these have been categorised into three generations of broadly similar antibacterial and pharmacokinetic properties: 1. First-generation (narrow spectrum) cephal-

osporins. These are very active against gram-

positive cocci and thus have useful antistaphylococcal activity. These include cefazolin, cephradine, cephalexin and cephadroxyl.

2.Second-generation (intermediate spectrum) cephalosporins. These have antistaphylococcal activity and are also effective against certain gram-negative organisms. They comprise cefuroxime, cefamandole and cefoxitin.

3.Third-generation (wide spectrum) cephalosporins. These are mainly effective against gramnegative organisms but not against staphylococci. These include: cefotaxime, cefixime and cefotetan.

Side-effects. Cephalosporins have a low frequency of adverse effects in comparison to antimicrobials in general. The most usual are allergic reactions of the penicillin type. If these are continued for more than 2 weeks, thrombocytopenia, neutropenia, interstitial nephritis or abnormal liver function tests may occur. These resolve on stopping the drug.

Aminoglycosides

These are bactericidal and act primarily against gramnegative bacilli. These are not absorbed orally, distributed mainly extracellularly and are excreted unchanged in the urine. These are ototoxic and nephrotoxic. Certain aminoglycosides are too toxic for systemic use and hence used only topically. Commonly used preparations are as follows:

1.Streptomycin. It is used mainly in tuberculosis.

2.Gentamicin. It has become the most commonly used aminoglycoside for acute infections. It has a broader spectrum of action and is effective against Pseudomonas aeruginosa. It is nephrotoxic, therefore, its dose must be precisely calculated according to body weight and renal function. For an average adult with normal renal function, the dose is 1-1.5 mg/kg intramuscularly 8 hourly. Topically, it is used as 0.3% eyedrops.

3.Tobramycin. It is 2-4 times more active against

Pseudomonas aeruginosa and Proteus as compared to gentamicin. Topically, it is used as 1% eyedrops.

4.Amikacin. It is recommended as a reserve drug for hospital acquired gram-negative bacillary infections where gentamicin resistance is increasing.

5.Neomycin. It is a widespectrum aminoglycoside, active against most gram-negative bacilli and