Postgraduate Medicine
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Glaucoma Jonathan E. Pederson MD To cite this article: Jonathan E. Pederson MD (1991) Glaucoma, Postgraduate Medicine, 90:7, 41-48, DOI: 10.1080/00325481.1991.11701121 To link to this article: http://dx.doi.org/10.1080/00325481.1991.11701121
Published online: 17 May 2016.
Submit your article to this journal
View related articles
Citing articles: 1 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ipgm20 Download by: [La Trobe University]
Date: 31 May 2016, At: 22:02
Symposium
Second of three articles on eye disorders
Downloaded by [La Trobe University] at 22:02 31 May 2016
Glaucoma A primer for primary care physicians
Preview What is the best indicator of the presence of glaucoma? What are the systemic side effects of the topical medications used to treat it? Which patients can safely undergo dilation for fundus examination? Dr Pederson answers these and other questions in this overview of the diagnosis and treatment of the major types of glaucoma.
Jonathan E. Pederson, MD
•!• The eye disease referred to as glaucoma is characterized by an elevated intraocular pressure that causes optic nerve damage and visual-field loss. Although elevated intraocular pressure increases the likelihood that optic nerve damage will develop, a substantial percentage of patients with moderately elevated pressure can tolerate it without such damage occurring; they are said to have ocular hypertension. On the other hand, some patients with normal intraocular pressure have glaucomatous cupping of the optic nerve; these patients are said to have low-tension glaucoma. Glaucoma is more common with advancing age or in patients with a family history of glaucoma.
Detecting glaucoma Glaucoma is usually diagnosed by measuring intraocular pressure, which is normally between 10 and 21 mm Hg. However, for screening purposes, the best indicator of the presence of glaucoma is optic nerve cupping (figure 1). Its detection requires no special equipment other than an ophthalmoscope. The surface of the normal optic nerve is generally flat or slightly elevated, with a small, depressed physiologic cup in the center-an empty space within the optic nerve head. Glaucoma results in vertical elongation of this cup. Thus a large, vertically oval cup is strongly suggestive of glaucoma. Such cupping occurs when the optic nerve tissue in the superior and inferior poles has been preferentially lost. Asymmetry of cupping
VOL 90/NO ?/NOVEMBER 15, 1991/POSTGRADUATE MEDICINE • GLAUCOMA
between the two eyes is another indicator of glaucoma. The cup-disk ratio compares the diameter of the cup to the diameter of the entire optic nerve head. The cup-disk ratio in the vertical meridian correlates best with visual-field loss in glaucoma. A cup-disk ratio of0.2 to 0.4 is considered normal; 0.5 to 0.6, borderline; and 0.7 or greater, abnormal. In a glaucomatous eye, the remaining disk-rim tissue is usually of normal pink color. A pale disk with shallow cupping is suggestive not of glaucoma, but of optic nerve atrophy from a neurologic disorder. A broad classification of glaucoma is based on the angle of the plane of the iris relative to the cornea. The great majority of patients with glaucoma have a deep anterior chamber with a large (open) angle, but some have a shallow anterior chamber with a small (narrow) angle. Gonioscopy using a special lens and slit lamp can differentiate between open-angle and narrow-angle glaucoma. Alternatively, illumination of the eye &om the side with a penlight can reveal narrow angles and potential angle closure (figure 2): A shadow is cast on the far side of the iris, because the central portion of the iris is farther forward than normal.
Open-angle glaucoma Open-angle glaucoma is the most common type of glaucoma and has no symptoms until late in the continued
41
Downloaded by [La Trobe University] at 22:02 31 May 2016
Filtering surgery is successful in more than 90% of patients with open-angle glaucoma, but it sometimes leads to later cataract formation.
Figure 1. Optic nerve cupping. a. Cup-disk ratio of 0.2 (physiologic). b. Cup-disk ratio of 0.6 (borderline glaucoma). c. Cup-disk ratio of 0.9 with vertically oval cup (advanced glaucoma).
Figure 2. Side illumination of narrowangled eye casts shadow on far side of iris.
disease. Typically, elevated intraocular pressure leads to optic nerve cupping, which results in visual field defects and, eventually, loss of central visual acuity. Visual-field loss begins in the nasal portion of the visual field, which overlaps with the visual Jonathan E. Pederson, MD Dr Pederson is senior physician, Hennepin County Medical Center, Minneapolis, and clinical professor of ophthalmology, University of Minnesota Medical SchoolMinneapolis. He has written numerous publications on the subject of glaucoma.
42
field of the other eye when both eyes are open. For this reason, the loss is not noticeable to the patient until the disease is quite advanced. Treatment of open-angle glaucoma consists of medical therapy, laser therapy, or surgery. In most patients, elevated intraocular pressure can be successfully controlled with medication. Glaucoma medications may be systemically absorbed, which can result in serious side effects (table 1). Many patients with glaucoma are taking multiple medications, and the drugs have additive effects. Laser therapy is used when medical treatment is not effective. The microscopic drainage pores of the trabecular meshwork in the angle are enlarged by thermally creating a burn that retracts and opens the adjacent pores. This is successful in 75% of cases, but the effect lasts for only 1 or 2 years. The treatment requires a specially modified slit lamp and is done with topical anesthetic. Patient recovery is rapid, often occurring within 1 day.
Filtering or fistulization surgery (also called trabeculectomy) is reserved for patients in whom visualfield loss is progressive despite full medical and laser treatment. A small (1 X 3 mm) opening is created in the deep sclera beneath a thin flap of overlying sclera to control the amount of fluid drainage. The overlying conjunctiva then balloons up like a vesicle, creating what is termed a filtering bleb (figure 3). This operation is successful in more than 90% of patients, but it sometimes leads to later cataract formation.
Acute angle-closure glaucoma The most dramatic form of glaucoma is acute angle-closure (narrowangle) glaucoma. In this condition, dilatation of the pupil causes the iris to cover the trabecular meshwork in the angle (much like a washcloth over a drain), and the intraocular pressure rises suddenly to alarming levels (50 to 80 mm Hg). This causes extreme pain, blurred vision, a cloudy cornea, and a mid-dilated continued
GLAUCOMA • VOL 90/NO ?/NOVEMBER 15, 1991/POSTGRADUATE MEDICINE
NAPROSYN. (NAPROXEN) 500mg tablets Briel Summary: Controlndlcatlons: Pat~ents who have had allergic reactiOns to NAPROSYN, ANAPROX or ANAPROX OS or 10 whom asp~rin or other NSAIOs ~nduce the syndrome ol asthma. rhinil1s. and nasal
Iridectomy should be performed within 1 week of an attack of angle-closure glaucoma.
~~~~P~- ~~;oar~ ~ta~~~~Y~~~~~~~~~~~~~~;t~~~a~Xti~~~~rtb~ ~~:~~~. 5
~:f;~/~t rftfngu~~;;~~~ ;,n~u~~P~~~~;~~~sgg~~~~~~s~~~ti~~:\~: anh 1
drug. Warnings: Serious Gl toxicity such as bleed~ng, ulceratiOn. and perforatiOn can occur at t1me, With. or Without warnmg
~re~tP\~~ 5Ui~~r~~~~n~sn~re~~ee~iggr~~ csaJ~h ~~~ie~~t ~vfn R~m:~~ 1
1 5
absence of previous Gl tract symptoms. In climcal trials. symptomatiC upper Gl ulcers, gross bleedmg or perforation appear to
~c~tio'~t a~?;~:~~a~~lfie~~~ a:r~:~~n~~:r~~~edy!~~. 31~~o~~n~~~·iea;1~ 001
0 5
~re p s ~~~a~g~,s ~~~~~~~;J~~:~~:s ~ave:~~~f ~~~~~~ii~~~~;;~u~~::
~~g;~~e~~~ naot~r~~;s~ 1~~~r~ve~~P~~~~g~~~~~ u~~~rnat~o~nadnd0~~:~d;~s~
factors known to be assoc1ated w1th pept1c ulcer disease. such as
~~e0nh~~~~~a~~o~~~~~·me~~eas~~ ~;~~- f~~~~r~~ ~~·8eb~~~te~e~!t~~~~~
seem to tolerate ulceration or bleedmg less well than others and most spontaneous reports of fatal Gl events are m thts population In cons1dering the use of relatively large doses (w1thm the recommended dosage range), sufficient benefit should be anticipated to
~~~et~~EP~~~t~6s;c~~asM;P~ko~ E~ ~~~~~b~~~~~t~~n~~~2 1
1
ANAPROX• (NAPROXEN SOOiuJl OR ANAPROX• DS (NAPROXEN SODIUM) SINCE THEY BOTH CIRCULATE IN PLASMA AS THE NAPROXEN ANION. Acute 1nterst1t1al nephritis with hematuria, protemuna. and nephrotiC syndrome has been reported. Patients w1th impaired renal function, heart failure. liver dysfunctiOn, pat1ents taking d1uret1cs. and the elderly are at greater risk of overt renal decompensation. If this occurs. discontinue the drug. Use w1th caution and monitor serum creatmine and/or creatmine clearance 1n pat1ents with Significantly 1mpa1red renal function. Use caut1on m pat1ents w1th baseline creatinine clearance less
~~a;a~1~nTsL~~t ~uct~io~~~ ~~;o ~~~s1,!~~e~~~veea~~s;r 6i:~~o~~~~r~~~~
Downloaded by [La Trobe University] at 22:02 31 May 2016
1
Table 1. Some systemic side effects of glaucoma medications Medications
Effects
Beta blockers Betaxolol HCI (Betoptic) Levobunolol HCI (Betagan) Timolol maleate (Timoptic)
Asthma, heart block, congestive heart failure, depression
Adrenergics Apraclonidine HCI (lopidine) Dipivefrin HCI (Propine) Epinephrine bitartrate (Epitrate) Epinephrine borate (Epinal, Eppy/N) Epinephrine HCI (Epifrin, Glaucon)
Hypertension. cardiac arrhythmias
Chol1nergics Carbachol (lsopto Carbachol) Pilocarpine HCI (Adsorbocarpine, lsopto Carpine, Pilopine HS) Pilocarpine nitrate (Pilagan)
Rare
Carbonic anhydrase inhibitors Acetazolamide (Diamox) D1chlorphenamide (Daranide) Methazolamide (Neptazane)
Renal calculi, hypokalemia, fatigue, paresthesias, confusion, aplastic anemia
Cholinesterase inhibitors Demecarium bromide (Humorsol) Echothiophate iodide (Phosphollne Iodide) Isoflurophate (Fioropryl) Physostigmine (lsopto Eserine, Eserine Salicylate)
Prolonged apnea and possible cardiovascular collapse if taken in conjunction with succinylcholine chloride (Anectine, Ouelicin, Sucostrin)
1
1
NSAIDs. borderline elevations of liver tests may occur m up to
~;;~si~~f~l~~t~.o~n~~e~~htr~~~~e~fev~~~~~n ofn~~atfe~r ~G8~ occurred m controlled clinical trials m less than 1% of patients
~=~:r~e~~p~~~r~:~c~~~~fY. 1~~~~~:n~s~~s~d~ce~~~~s f~~a1 f ~~~f~~\~
1
1
manifestations occur (e.g., eosmoph1ha or rash), discontinue ther-
~~YSI~:~~rao~~ ~g~:~:e ~;~~~;se~lg~e~~~~~~tg~e~~;~~ffe~t~~al~~~~g_ 1
mg adrenal msufficiency and exacerbation of arthnt1s symptoms Determme hemoglobin values periodically for patients with mitlal values of 10 grams or less who rece1ve long-term therapy. Penpheral edema has been reported. Therefore. use w1th caution 1n pat1ents with flUid retention. hypertens1on or heart fa1lure The
~~e~·sa~~t~l~~~e~~a~~~n.ari~~~~',':h~n~a~~~lr ~T~~v~~~f1c ~:ru;~~uoc;_ duct ophthalmic studies 1f any change or disturbance m VISion occurs. For patients w1th restricted sod1um mtake. note that the 0
8
1
0
~:f.~~~~ S~d~~~~~~t~sof NSA~b~~a~ casu s~ ~~Co~~~~~~~. ~ar~f;
0 1
there are more senous s1de effects. such as Gl bleedmg, wh1ch may result m hosp1ta11zation and even fatal outcomes. PhySICians may w1sh to d1scuss w1th patients the potential nsks and l1kely
~~~e~!~,g~sN~:~~~t~~ena~~~~~/t~~~~~~=~~Y w~~eo"u~~$A~~s u~~~ 'g;
an acceptable alternative. Pat1ents should use caution for actiVIties reqUiring alertness 1f they experience drowsmess. d1zz~ness. vertigo or depress1on dunng therapy. Laboratory Teals: Because senous Gl tract ulceratiOn and bleeding can occur Without warnIng symptoms. follow chromcally treated patients for signs and symptoms of these and Inform them of the importance of th1s
~~~~~~-~th ~~~~"1~~~~~!~oen~:n~~~a~au~~~~~.w:ehny8~~~gln~ ~~~~~~~
0
0
am1de or sulfonylurea: furosemide; llth1um: beta-blockers. ~robeneCid: or methotrexate. Drug/Laboratory Test Interactions:
t1~e d~~~n~r~~sdee~~~~~~l~~~~~~:! ~g~r1e~~~~ong=~~ ~~~~6~3s.b~ee~~g_ ranly stop therapy for 72 hours before domg adrenal function
~1~~g:::sf;:uj ~~~~~t~;:e~fu~~t~h~r~ne~Yngs;:,~~~~e ~f ~rc~~ci:
5 1
gen1c1ty. Pregnancy: Category B Do not use dunng pregnancy
Mn~1~;r~ :eX~~,ge~~:d;n A~~~~~~~e ~~{~~~s .a~e~~i~~nf{.,~~~~~~~~ ~o~t~ g~/ i;~ ~~/~n ~;~rdr~o~a~vde~i~~ ~~~;s ngt' :~;ee~.l~~r~~
1
1
Reactions: In a study, Gl reactions were more frequent and severe m rheumatoid arthnt1s pattents on 1.500 mglday than m those on 750 mg day In stud1es m children with Juvenile arthr1t1s, rash and prolonged bleedmg t1mes were more frequent, Gl and CNS reac-
~g~l~sa~~~~~!~~es~~~-te~n~h~~hf!/o ~e~~~~anb~el~sasu!~~~:~~\i~~~~i~~
Gl· The most frequent complamts related to the Gl tract: constipatiOn.· heartburn.· abdommal pam.· nausea.· dyspepsia. d1arrhea, stomat1t1s CNS headache.· diZZiness.· drowsiness.* light-headedness, vert1go Dermatologtc: 1tching (pruntus)," skm erupt1ons.· ecchymoses.· sweatmg. purpura. Special Senses: tinmtus; hearmg d1sturbances. v1sual disturbances. Cardiovascular. edema,* dyspnea,· palpitations General: th1rst. lnc1dence Less Than 1%. Probable Causal Relat1onsh1p: Gl: abnormal hver funct1on tests. coht1s. Gl bleedmg and/or perforation. hematemes1s. jaund1ce. melena, peptiC ulceratiOn w1th bleedmg and/Or perforation, vomltmg Renal· glomerular nephritis. hematuna. hyperkalemia, mterstltlat nephnt1s. nephrOtiC syndrome, renal disease, renal failure. renal pap1llary necros1s. HematoloQiC agranulocytosiS, eosmophllla. granulocytopenia. leukopenia. thrombocytopenia. CNS depress1on. dream abnormalities. mab1l1ty to concentrate. msom-
~:~·. ~~~;~;·e~~~~~J~a ~~~m~~~~~i~ ~:,anknr~ssshe~~rS~~~~~~?'Se~~~::heanng 1mpa1rment. CardiOvascular congest1ve heart failure. Respiratory eos1nophil1c pneumon1t1s General anaphylactoid react1ons. menstrual disorders. pyrex1a (ch1lls and fever) Causal Relat1onsh1p Unknown Hematolog1c· aplastic anem1a. hemolytiC anem1a CNS aseptiC men1ng1t1S, cogn1t1ve dysfunction. Dermatologlc ep1dermal necrolys1s. erythema multlforme, photosenSitiVIty react1ons resembling porphyna cutanea tarda and ep1dermolys1s bullosa. Stevens-Johnson syndrome. urticar1a Gl non-pept1c Gl ulceratiOn. ulcerative stomatitis. Cardiovascular vasculitiS General ang1oneurot1c edema, hyperglycemia. hypoglycemia Overdosage: May have drowsmess. heartburn. md1gest10n. nausea. vom1tmg A few pat1ents have had se1zures Empty 0
~~ a~~~~t=~~~:~c~!~~~ds~tfd ~~~vsem~~:~~r;~f nna~~~~ea~~ gi~~~~~~
0
:~~e,~a~e~~~o~f~~'Wi:s~~~C~~~s~~~o~~~~~~ •
1
pupil (figure 4). Angle-closure glaucoma may occur spontaneously (especially at night) or following dilatation with mydriatic drops. Pharmacologic treatment of acute angle-closure glaucoma consists of administering drops of a 4% solution of pilocarpine (Adsorbocarpine, Isopto Carpine, Pilagan, Pilopine
HS) to temporarily relieve the pressure. In addition, systemic osmotic agents (eg, a 50% solution of oral glycerin or a 20% solution of intravenous mannitol) should be given. Iridectomy (by laser or other means) is curative if it is performed within 1 week of the attack, before permanent iris adhesions (synechiae) develop.
prescriptiOn See pack-
~~~dr~n~;~~::td~r~~~~d~~~~t:~~s ~~~~gr:/o.
sT sYN-rEX-
u S patent nos 3.904.682. 3.998.966 and olhers. ' 1991 Syntex Puerto RICo. Inc Rev. 39 September 1990
44
GLAUCOMA • VOL 90/NO ?/NOVEMBER 15, 1991/POSTGRADUATE MEDICINE
Downloaded by [La Trobe University] at 22:02 31 May 2016
To identify patients at risk for angle-closure glaucoma, the penlight test should always be performed before the eyes are dilated.
Figure 3. Pale. diffuse bleb after successful filtering surgery.
The disease is bilateral, and prophylactic iridectomy is always recommended for the opposite eye. The question often arises as to who can safely undergo dilatation for fundus examination. Patients at risk for angle-closure glaucoma can be identified by the penlight test (figure 2). If a prominent shadow is cast on the far side of the iris with side illumination, the eye should not be dilated and slit-lamp examination should be done to determine whether the anterior chamber is shallow. Patients often ask about the warning label on certain over-the-counter decongestants stating that the medication should not be used by glaucoma patients. The warning is required because of the possible mydriatic effect of the medication; however, it applies neither to patients with open-angle glaucoma nor to those with acute angle-closure glaucoma who have had an iridectomy or are receiving pilocarpine therapy. The only group of patients at risk are those who have undetected narrow
Figure 4a. Acute angle-closure glaucoma. Note hazy cornea and mid-dilated pupil.
b. Opposite eye.
Figure 5. Enlarged eyes with hazy corneas in child with congenital glaucoma.
angles or who have refused treatment for angle-closure glaucoma (such refusal is rare). Thus for all practical purposes the warning is useless.
Congenital glaucoma Glaucoma may occur within the first few years oflife; symptoms of the congenital form of the disease include enlarged eyes, photophobia, tearing, and hazy corneas (figure 5). Visual loss can occur rapidly, and failure of early diagnosis may lead to
VOL 90/NO ?/NOVEMBER 15, 1991/POSTGRADUATE MEDICINE • GLAUCOMA
a lifetime of poor vision. In congenital glaucoma, the angle structures are maldeveloped and a simple incision into the angle (goniotomy) is curative. Congenital glaucoma sometimes occurs in conjunction with other congenital defects. Summary Glaucoma is best detected by examination of the optic disk, since intraocular pressure is not always continued on page 48 45
BuSpar(ruspironeHCO
Downloaded by [La Trobe University] at 22:02 31 May 2016
References: 1. Fe~ghner JP, Cohn JB Analysrs ol rndrvrdual symptoms rn generaliZed anxiety--a pooled mullisludy. double-blind evaluation ol busprrone Neuropsychobwlogy 1989.21124-130 2. Newton RE. Marunycz JD, Alderdrce MT Napolrello MJ. Revrew ollhe side-ellecl prairie of busprrone Am J Med 1986.80 (suppl38)17-21 1 Lader M Assessrng the polentral for busprrone dependence or abuse and effects of rls withdrawal Am J Med 1987,82 (suppi5A).20-26
Contralndicatlons: Hypersensitivity to buspirone hydrochloride. warnings: The administration ofBuSpar to a patient taking a monoamine 01idase Inhibitor (MAOI) may pose a hazard. Since blood pressure has become elevated when BuSpar was administered concomitantly with an MAOI. such concomitant use is not recommended. BuSpar should not be employed in lieu of appropriate antipsychotic treatment Precautions: General-Interference with cognitive and motor performance: Although buspirone is less sedating than other anxiolytics and does not produce significant functional impairment. its CNS effects in a given patient may not be predictable; therefore, patients should be cautioned about operating an automobile or using complex machinerr until they are reasonably certain that buspirone does not affect them adversely Although buspirone has no been shown to increase alcohol-induced impairment in motor and mental performance. it is Rrudent to avoid concomitant use with alcohol. Potential for wrthdrawal reactions in sedativelhypnoticlanxiotytic drug dependent patients: Because buspirone will not block the withdrawal syndrome often seen with cessat1on of therapy with benzodiazepines and other common sedative/hypnotic drugs, before starting buspirone withdraw patients gradually from their prior treatment. especially those who used a CNS depressant chronically. Rebound or withdrawal symptoms may occur over varying time periods, depending in part on the l)'pe of drug and its elimination hall-life The withdrawal syndrome can appear as any combination of irritability, anxiel)', agitation, insomnia, tremor, abdominal cramps, muscle cramps, vomiting, sweating, flu-like symptoms w1thout fever, and occasionally, even as seizures. Possible concerns related to buspirone's binding to dopamine receptors: Because buspirone can bind to central dopamine receptors. a question has been ra1sed about its potential to cause acute and chronic changes in dopamine mediated neurological function (eg, dystonia, pseudoparkinsonism, akathisia, and tardive dyskinesia) Clinical experience in controlled trials has failed to identify any significant neurolepticlike activity; however, asyndrome of restlessness. appearing shortly after initiation of treatment, has been reported; the syndrome may be due to increased central noradrenergic activity or may be attributable to dopaminerJliC effects lie, represent akathisial In/ormation lor Patients-Patients shou d be instructed to inform their physician about any medications, prescription or nonprescription, alcohol or drugs they are now taking or plan to take during treatment with buspirone. to inform their physician if they are pregnant, are P.lanning to become pregnant. or become pregnant while taking buspirone; to inform the1r physician ifthey are breasl feeding; and not to drive acar or operate potentially dangerous machinery until they experience how this medication affects them. Drua Interactions-Concomitant use with other CNS active drugs should be approached with caution (see Warnings) Concomitant use with trazodone may have caused 3- to 6-fold elevations on SGPT (All) in afew patients Concomitant admimstration of BuSpar and haloperidol resulted in increased serum haloperidol concentrations in normal volunteers. The climcal significance is not clear. Buspirone does not displace tightly bound drugs like phenytoin, propranolol, and warfarin from serum proteins, but may displace less firmly bound drugs like d1goxin However, there was one report of prolonged prothrombin time when busp_lrone was given to a gatient also treated with warfarin, phenytoin, phenobarbital, digoxin, and Synthroid Carclnoaenesis, /llutapenesis, Impairment of Fertility-No evidence of carcinogenic potential was observed in rats or m1ce; buspi:one did not induce point mutations, nor was DNA damage observed; chromosomal aberrations or abnormalities d1d not occur. Pregnancy: Teratoaenic Effects-Pregnancy Category B Should be used during pregnancy only if clearly needed Nursmg /lfolllers-Administration to nursing women should be avoided if clinically possible. Pediatric Use- The safety and effectiveness have not been determined in individuals below 18 years of age use in the Elderly-No unusual, adverse. age-related phenomena have been identified in elderly patients receiving a total, modal daily dose of 15 mg Use in Patients w/111 Impaired HepatiC or Renal Function-Since buspirone is metabolized by the liver and excreted by the kidneys, it is not recommended in severe hepatic or renal impairment Adverse Reactions (See also Precautions): Commonly Db11n11d-The more commonly observed untoward events, not seen at an equivalent mcidence in placebo-treated patients, include dizzmess. nausea. headache, nervousness. lightheadedness, and excitement Associated with Discontinuation o/Treatment-The more common events causing discontinuation included; central nervous system disturbances (3.4%), primarily dizziness. insomnia. nervousness, drowsiness. lightheaded feeling; gastrointestinal disturbances (1.2%), primarily nausea; miscellaneous disturbances (11%1, primarily headache and fatigue In addition. 34% of patients had multiple complaints, none of which cou d be characterized as primary. . Incidence in Controlled Clinical Trials ~Adverse events reported by 1% or more of 477 pat1ents who received buspirone in four -week, controlled trrals. Cardrovascutar. Tachycardia/palpitations 1%. CNS: Dizziness 12%, drowsmess 10%, nervousness 5%, msomnra 3%, l1ghtheadedness 3%, decreased concentration 2%, excitement 2%, angerlhostilii)' 2%, confusion 2%, depression 2%. EENT Blurred vision 2%. Gastrornteslinal. Nausea 8%, dry mouth 3%, abdominal/gastric distress 2%, diarrhea2%, constipation 1%, vomiling 1%. Muscutosketetat- Musculoskeletal acheslpams 1%. Neurological: Numbness 2%, paresthesia 1%, incoordination 1%, tremor 1% Skin.· Skin rash 1% Miscellaneous: Headache 6%, fatigue 4%, weakness 2%, sweatinQ!clamminess 1%. Other Events 06sen1ed During the Entire Premartetinll Evaluation- The relative frequency of all other undesirable events reasonably associated with the use ol buspirone in approximately 3000 subjects who took multiple doses of the drug under well-controlled. open, and uncontrolled conditions is defined as follows: Frequent are those occurnng in at least 11100 patients, infrequent are those occurnng in 11100 to 111000 patients. and rare are those occurring in less than 111000 pahents. Cardiovascular -frequent: nonspecific chest pain; infrequent syncope, hypotension. hypertension; rare: cerebrovascular acc1dent. congestive heart failure. myocardial infarction, cardiomyopathy, bradycardia. Central Nervous Systemfrequent: dream disturbances, infrequent: depersonalization, dysphoria, noise intolerance. euphoria. akathisia, fearfulness, loss of interest, dissoc1at1ve reaction, hallucinations, suicidal ideation. seizures; rare: feelings of claustrophobia, cold intolerance, stupor, slurred speech, psychosis. EENT -frequent: tinnitus. sore throat, nasal congestion; infrequent: redness and itching of the eyes, altered taste, altered smell, conjunctivitis; rare inner ear abnormality, eye pain, photophobia, pressure on eyes. Endocrine-rare: galactorrhea. thyroid abnormality. Gastrointestinal-infrequent: flatulence, anorexia, increased appetite, salivation, irrilable colon, rectal bleeding; rare; burning of the tongue. Genitounnary-intrequent: urinary frequency, urinary hesitancy, menstrual Irregularity and spotting, dysuria; rare; amenorrhea, pelvic inflammatory disease. enuresis, nocturia. Muscutoskeletal-intrequent: muscle cramps, muscle spasms, rigid/stiff muscles. arthralgias. Neurotogrcat-intrequent: involuntary movements, slowed reaction time; rare: muscle weakness. Resprratory-intrequent: hyperventilation, shortness of breath, chest congestion; rare: epistaxis. Sexual Function-infrequent decreased or increased libido; rare: delayed eiaculation, impotence. Skininfrequent: edema, pruritus. flushing, easy bruising, hair loss. dry skm, facial edema, blisters; rare; acne, thinnmg of nails. Clinical Laboratory-infrequent: mcreases in hepatic aminotransferases (SGOT, SGPT); rare: eosinophil;a, leukopenia, thrombocytopenia. Mrscettaneous-infrequent: weight gain, fever, roaring sensation in the head, weight loss, malaise, rare: alcohol abuse, bleeding disturbance, ·loss of voice, hiecoughs. Posllntroduction Clinical Experience-Rare occurrences of allergic reactions, cogwheel rigidity, dystonic reactions. ecchymosis, emotional lability, tunnel vision, and urinary retention have been reported. Because of the uncontrolled nature of these spontaneous reports, acausal relationship to BuSpar has not been determined. Drug Abuse and Dependence: Controlled Substance Class-Not a controlled substance. Physical andPsycho/Oflica/ Oependence-Buspirone has shown no potential for abuse or diversion and there is no evidence that it causes tolerance, or either physical or pslchological dependence. However, since it is difficult to predict from experiments the ex1ent to which a CNS-active drug will be misused, diverted, and/or abused once marketed, physicians should carefully evaluate patients for a history of drug abuse and follow such patients closely, observing them for signs of buspirone misuse or abuse (eg, development of tolerance, incrementation of dose, drug-seeking behavior). Overdosage: Signs and Symptoms-At doses approaching 375 mg/day the following symptoms were observed: nausea, vomiting, dizziness, drowsiness, miosis, ana gastric distress. No deaths have been reflOrted in humans either wijh deliberate or accidental overdosage. Recommended Overdose Treatment-General symptomatic and supportive measures should be used along with immediate gastrrc lavage No specific antidote is known and dialyzability of buspirone has not been determined For comple/e details, see Prescnbing Information tji or consult your Mead Johnson Pharmaceutrcats !}!.J Representative. PHARMAcEuT•cAL s
Mead
U.S. Patent Nos. 3,717,634 and 4,182,763
MJL84270R2
·""7'·
iTi1BJJil
devated in patients with the condition. A large, vertically oval cup within the optic disk is strong evidence for glaucoma. Open-angle glaucoma, the most common fonn of the disorder, often is not detected until the disease is advanced. It can usually be treated successfully with topical medications, but systemic absorption of these can result in serious side effects. If medical treatment fails, laser therapy or filtering surgery may be hdpful. Acute angle-dosure glaucoma has a sudden onset marked by alanning devations in intraocular pressure. It is treated immediately with topical pilocarpine and systemic osmotic agents, and an iridectomy should be performed as soon as possible. Congenital glaucoma can be cured with goniotomy. IVt'l
-®
Earn credit on this article. See CME Quiz
Address for correspondence: Jonathan E. Pederson, MD, Department of Ophthalmology, Hennepin County Medical Center, 70 I Park AveS, Minneapolis, MN 55415.
Bibliography Epstein DL Chandler and Grant's glaucoma. 3d ed. Philadelphia: Lea & Febiger, 1986 Hoskins HD, Kass MA. Becker-Shaffer's diagnosis and therapy of the glaucomas. 6th ed. St Louis: Mosby-Year Book, 1989 Ritch R, Shields MB, Krupin T, eds. The glaucomas. StLouis: Mosby-Year Book, 1989 Shields MB. Textbook of glaucoma. 2d ed. Baltimore: Williams & Wilkins, 1987
ABn'>lol '-t.ro'iQultlbCu
~_;:r ~~till ~ ler>c'!·
os)-13
48
GLAUCOMA
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Glaucoma Jonathan E. Pederson MD To cite this article: Jonathan E. Pederson MD (1991) Glaucoma, Postgraduate Medicine, 90:7, 41-48, DOI: 10.1080/00325481.1991.11701121 To link to this article: http://dx.doi.org/10.1080/00325481.1991.11701121
Published online: 17 May 2016.
Submit your article to this journal
View related articles
Citing articles: 1 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ipgm20 Download by: [La Trobe University]
Date: 31 May 2016, At: 22:02
Symposium
Second of three articles on eye disorders
Downloaded by [La Trobe University] at 22:02 31 May 2016
Glaucoma A primer for primary care physicians
Preview What is the best indicator of the presence of glaucoma? What are the systemic side effects of the topical medications used to treat it? Which patients can safely undergo dilation for fundus examination? Dr Pederson answers these and other questions in this overview of the diagnosis and treatment of the major types of glaucoma.
Jonathan E. Pederson, MD
•!• The eye disease referred to as glaucoma is characterized by an elevated intraocular pressure that causes optic nerve damage and visual-field loss. Although elevated intraocular pressure increases the likelihood that optic nerve damage will develop, a substantial percentage of patients with moderately elevated pressure can tolerate it without such damage occurring; they are said to have ocular hypertension. On the other hand, some patients with normal intraocular pressure have glaucomatous cupping of the optic nerve; these patients are said to have low-tension glaucoma. Glaucoma is more common with advancing age or in patients with a family history of glaucoma.
Detecting glaucoma Glaucoma is usually diagnosed by measuring intraocular pressure, which is normally between 10 and 21 mm Hg. However, for screening purposes, the best indicator of the presence of glaucoma is optic nerve cupping (figure 1). Its detection requires no special equipment other than an ophthalmoscope. The surface of the normal optic nerve is generally flat or slightly elevated, with a small, depressed physiologic cup in the center-an empty space within the optic nerve head. Glaucoma results in vertical elongation of this cup. Thus a large, vertically oval cup is strongly suggestive of glaucoma. Such cupping occurs when the optic nerve tissue in the superior and inferior poles has been preferentially lost. Asymmetry of cupping
VOL 90/NO ?/NOVEMBER 15, 1991/POSTGRADUATE MEDICINE • GLAUCOMA
between the two eyes is another indicator of glaucoma. The cup-disk ratio compares the diameter of the cup to the diameter of the entire optic nerve head. The cup-disk ratio in the vertical meridian correlates best with visual-field loss in glaucoma. A cup-disk ratio of0.2 to 0.4 is considered normal; 0.5 to 0.6, borderline; and 0.7 or greater, abnormal. In a glaucomatous eye, the remaining disk-rim tissue is usually of normal pink color. A pale disk with shallow cupping is suggestive not of glaucoma, but of optic nerve atrophy from a neurologic disorder. A broad classification of glaucoma is based on the angle of the plane of the iris relative to the cornea. The great majority of patients with glaucoma have a deep anterior chamber with a large (open) angle, but some have a shallow anterior chamber with a small (narrow) angle. Gonioscopy using a special lens and slit lamp can differentiate between open-angle and narrow-angle glaucoma. Alternatively, illumination of the eye &om the side with a penlight can reveal narrow angles and potential angle closure (figure 2): A shadow is cast on the far side of the iris, because the central portion of the iris is farther forward than normal.
Open-angle glaucoma Open-angle glaucoma is the most common type of glaucoma and has no symptoms until late in the continued
41
Downloaded by [La Trobe University] at 22:02 31 May 2016
Filtering surgery is successful in more than 90% of patients with open-angle glaucoma, but it sometimes leads to later cataract formation.
Figure 1. Optic nerve cupping. a. Cup-disk ratio of 0.2 (physiologic). b. Cup-disk ratio of 0.6 (borderline glaucoma). c. Cup-disk ratio of 0.9 with vertically oval cup (advanced glaucoma).
Figure 2. Side illumination of narrowangled eye casts shadow on far side of iris.
disease. Typically, elevated intraocular pressure leads to optic nerve cupping, which results in visual field defects and, eventually, loss of central visual acuity. Visual-field loss begins in the nasal portion of the visual field, which overlaps with the visual Jonathan E. Pederson, MD Dr Pederson is senior physician, Hennepin County Medical Center, Minneapolis, and clinical professor of ophthalmology, University of Minnesota Medical SchoolMinneapolis. He has written numerous publications on the subject of glaucoma.
42
field of the other eye when both eyes are open. For this reason, the loss is not noticeable to the patient until the disease is quite advanced. Treatment of open-angle glaucoma consists of medical therapy, laser therapy, or surgery. In most patients, elevated intraocular pressure can be successfully controlled with medication. Glaucoma medications may be systemically absorbed, which can result in serious side effects (table 1). Many patients with glaucoma are taking multiple medications, and the drugs have additive effects. Laser therapy is used when medical treatment is not effective. The microscopic drainage pores of the trabecular meshwork in the angle are enlarged by thermally creating a burn that retracts and opens the adjacent pores. This is successful in 75% of cases, but the effect lasts for only 1 or 2 years. The treatment requires a specially modified slit lamp and is done with topical anesthetic. Patient recovery is rapid, often occurring within 1 day.
Filtering or fistulization surgery (also called trabeculectomy) is reserved for patients in whom visualfield loss is progressive despite full medical and laser treatment. A small (1 X 3 mm) opening is created in the deep sclera beneath a thin flap of overlying sclera to control the amount of fluid drainage. The overlying conjunctiva then balloons up like a vesicle, creating what is termed a filtering bleb (figure 3). This operation is successful in more than 90% of patients, but it sometimes leads to later cataract formation.
Acute angle-closure glaucoma The most dramatic form of glaucoma is acute angle-closure (narrowangle) glaucoma. In this condition, dilatation of the pupil causes the iris to cover the trabecular meshwork in the angle (much like a washcloth over a drain), and the intraocular pressure rises suddenly to alarming levels (50 to 80 mm Hg). This causes extreme pain, blurred vision, a cloudy cornea, and a mid-dilated continued
GLAUCOMA • VOL 90/NO ?/NOVEMBER 15, 1991/POSTGRADUATE MEDICINE
NAPROSYN. (NAPROXEN) 500mg tablets Briel Summary: Controlndlcatlons: Pat~ents who have had allergic reactiOns to NAPROSYN, ANAPROX or ANAPROX OS or 10 whom asp~rin or other NSAIOs ~nduce the syndrome ol asthma. rhinil1s. and nasal
Iridectomy should be performed within 1 week of an attack of angle-closure glaucoma.
~~~~P~- ~~;oar~ ~ta~~~~Y~~~~~~~~~~~~~~;t~~~a~Xti~~~~rtb~ ~~:~~~. 5
~:f;~/~t rftfngu~~;;~~~ ;,n~u~~P~~~~;~~~sgg~~~~~~s~~~ti~~:\~: anh 1
drug. Warnings: Serious Gl toxicity such as bleed~ng, ulceratiOn. and perforatiOn can occur at t1me, With. or Without warnmg
~re~tP\~~ 5Ui~~r~~~~n~sn~re~~ee~iggr~~ csaJ~h ~~~ie~~t ~vfn R~m:~~ 1
1 5
absence of previous Gl tract symptoms. In climcal trials. symptomatiC upper Gl ulcers, gross bleedmg or perforation appear to
~c~tio'~t a~?;~:~~a~~lfie~~~ a:r~:~~n~~:r~~~edy!~~. 31~~o~~n~~~·iea;1~ 001
0 5
~re p s ~~~a~g~,s ~~~~~~~;J~~:~~:s ~ave:~~~f ~~~~~~ii~~~~;;~u~~::
~~g;~~e~~~ naot~r~~;s~ 1~~~r~ve~~P~~~~g~~~~~ u~~~rnat~o~nadnd0~~:~d;~s~
factors known to be assoc1ated w1th pept1c ulcer disease. such as
~~e0nh~~~~~a~~o~~~~~·me~~eas~~ ~;~~- f~~~~r~~ ~~·8eb~~~te~e~!t~~~~~
seem to tolerate ulceration or bleedmg less well than others and most spontaneous reports of fatal Gl events are m thts population In cons1dering the use of relatively large doses (w1thm the recommended dosage range), sufficient benefit should be anticipated to
~~~et~~EP~~~t~6s;c~~asM;P~ko~ E~ ~~~~~b~~~~~t~~n~~~2 1
1
ANAPROX• (NAPROXEN SOOiuJl OR ANAPROX• DS (NAPROXEN SODIUM) SINCE THEY BOTH CIRCULATE IN PLASMA AS THE NAPROXEN ANION. Acute 1nterst1t1al nephritis with hematuria, protemuna. and nephrotiC syndrome has been reported. Patients w1th impaired renal function, heart failure. liver dysfunctiOn, pat1ents taking d1uret1cs. and the elderly are at greater risk of overt renal decompensation. If this occurs. discontinue the drug. Use w1th caution and monitor serum creatmine and/or creatmine clearance 1n pat1ents with Significantly 1mpa1red renal function. Use caut1on m pat1ents w1th baseline creatinine clearance less
~~a;a~1~nTsL~~t ~uct~io~~~ ~~;o ~~~s1,!~~e~~~veea~~s;r 6i:~~o~~~~r~~~~
Downloaded by [La Trobe University] at 22:02 31 May 2016
1
Table 1. Some systemic side effects of glaucoma medications Medications
Effects
Beta blockers Betaxolol HCI (Betoptic) Levobunolol HCI (Betagan) Timolol maleate (Timoptic)
Asthma, heart block, congestive heart failure, depression
Adrenergics Apraclonidine HCI (lopidine) Dipivefrin HCI (Propine) Epinephrine bitartrate (Epitrate) Epinephrine borate (Epinal, Eppy/N) Epinephrine HCI (Epifrin, Glaucon)
Hypertension. cardiac arrhythmias
Chol1nergics Carbachol (lsopto Carbachol) Pilocarpine HCI (Adsorbocarpine, lsopto Carpine, Pilopine HS) Pilocarpine nitrate (Pilagan)
Rare
Carbonic anhydrase inhibitors Acetazolamide (Diamox) D1chlorphenamide (Daranide) Methazolamide (Neptazane)
Renal calculi, hypokalemia, fatigue, paresthesias, confusion, aplastic anemia
Cholinesterase inhibitors Demecarium bromide (Humorsol) Echothiophate iodide (Phosphollne Iodide) Isoflurophate (Fioropryl) Physostigmine (lsopto Eserine, Eserine Salicylate)
Prolonged apnea and possible cardiovascular collapse if taken in conjunction with succinylcholine chloride (Anectine, Ouelicin, Sucostrin)
1
1
NSAIDs. borderline elevations of liver tests may occur m up to
~;;~si~~f~l~~t~.o~n~~e~~htr~~~~e~fev~~~~~n ofn~~atfe~r ~G8~ occurred m controlled clinical trials m less than 1% of patients
~=~:r~e~~p~~~r~:~c~~~~fY. 1~~~~~:n~s~~s~d~ce~~~~s f~~a1 f ~~~f~~\~
1
1
manifestations occur (e.g., eosmoph1ha or rash), discontinue ther-
~~YSI~:~~rao~~ ~g~:~:e ~;~~~;se~lg~e~~~~~~tg~e~~;~~ffe~t~~al~~~~g_ 1
mg adrenal msufficiency and exacerbation of arthnt1s symptoms Determme hemoglobin values periodically for patients with mitlal values of 10 grams or less who rece1ve long-term therapy. Penpheral edema has been reported. Therefore. use w1th caution 1n pat1ents with flUid retention. hypertens1on or heart fa1lure The
~~e~·sa~~t~l~~~e~~a~~~n.ari~~~~',':h~n~a~~~lr ~T~~v~~~f1c ~:ru;~~uoc;_ duct ophthalmic studies 1f any change or disturbance m VISion occurs. For patients w1th restricted sod1um mtake. note that the 0
8
1
0
~:f.~~~~ S~d~~~~~~t~sof NSA~b~~a~ casu s~ ~~Co~~~~~~~. ~ar~f;
0 1
there are more senous s1de effects. such as Gl bleedmg, wh1ch may result m hosp1ta11zation and even fatal outcomes. PhySICians may w1sh to d1scuss w1th patients the potential nsks and l1kely
~~~e~!~,g~sN~:~~~t~~ena~~~~~/t~~~~~~=~~Y w~~eo"u~~$A~~s u~~~ 'g;
an acceptable alternative. Pat1ents should use caution for actiVIties reqUiring alertness 1f they experience drowsmess. d1zz~ness. vertigo or depress1on dunng therapy. Laboratory Teals: Because senous Gl tract ulceratiOn and bleeding can occur Without warnIng symptoms. follow chromcally treated patients for signs and symptoms of these and Inform them of the importance of th1s
~~~~~~-~th ~~~~"1~~~~~!~oen~:n~~~a~au~~~~~.w:ehny8~~~gln~ ~~~~~~~
0
0
am1de or sulfonylurea: furosemide; llth1um: beta-blockers. ~robeneCid: or methotrexate. Drug/Laboratory Test Interactions:
t1~e d~~~n~r~~sdee~~~~~~l~~~~~~:! ~g~r1e~~~~ong=~~ ~~~~6~3s.b~ee~~g_ ranly stop therapy for 72 hours before domg adrenal function
~1~~g:::sf;:uj ~~~~~t~;:e~fu~~t~h~r~ne~Yngs;:,~~~~e ~f ~rc~~ci:
5 1
gen1c1ty. Pregnancy: Category B Do not use dunng pregnancy
Mn~1~;r~ :eX~~,ge~~:d;n A~~~~~~~e ~~{~~~s .a~e~~i~~nf{.,~~~~~~~~ ~o~t~ g~/ i;~ ~~/~n ~;~rdr~o~a~vde~i~~ ~~~;s ngt' :~;ee~.l~~r~~
1
1
Reactions: In a study, Gl reactions were more frequent and severe m rheumatoid arthnt1s pattents on 1.500 mglday than m those on 750 mg day In stud1es m children with Juvenile arthr1t1s, rash and prolonged bleedmg t1mes were more frequent, Gl and CNS reac-
~g~l~sa~~~~~!~~es~~~-te~n~h~~hf!/o ~e~~~~anb~el~sasu!~~~:~~\i~~~~i~~
Gl· The most frequent complamts related to the Gl tract: constipatiOn.· heartburn.· abdommal pam.· nausea.· dyspepsia. d1arrhea, stomat1t1s CNS headache.· diZZiness.· drowsiness.* light-headedness, vert1go Dermatologtc: 1tching (pruntus)," skm erupt1ons.· ecchymoses.· sweatmg. purpura. Special Senses: tinmtus; hearmg d1sturbances. v1sual disturbances. Cardiovascular. edema,* dyspnea,· palpitations General: th1rst. lnc1dence Less Than 1%. Probable Causal Relat1onsh1p: Gl: abnormal hver funct1on tests. coht1s. Gl bleedmg and/or perforation. hematemes1s. jaund1ce. melena, peptiC ulceratiOn w1th bleedmg and/Or perforation, vomltmg Renal· glomerular nephritis. hematuna. hyperkalemia, mterstltlat nephnt1s. nephrOtiC syndrome, renal disease, renal failure. renal pap1llary necros1s. HematoloQiC agranulocytosiS, eosmophllla. granulocytopenia. leukopenia. thrombocytopenia. CNS depress1on. dream abnormalities. mab1l1ty to concentrate. msom-
~:~·. ~~~;~;·e~~~~~J~a ~~~m~~~~~i~ ~:,anknr~ssshe~~rS~~~~~~?'Se~~~::heanng 1mpa1rment. CardiOvascular congest1ve heart failure. Respiratory eos1nophil1c pneumon1t1s General anaphylactoid react1ons. menstrual disorders. pyrex1a (ch1lls and fever) Causal Relat1onsh1p Unknown Hematolog1c· aplastic anem1a. hemolytiC anem1a CNS aseptiC men1ng1t1S, cogn1t1ve dysfunction. Dermatologlc ep1dermal necrolys1s. erythema multlforme, photosenSitiVIty react1ons resembling porphyna cutanea tarda and ep1dermolys1s bullosa. Stevens-Johnson syndrome. urticar1a Gl non-pept1c Gl ulceratiOn. ulcerative stomatitis. Cardiovascular vasculitiS General ang1oneurot1c edema, hyperglycemia. hypoglycemia Overdosage: May have drowsmess. heartburn. md1gest10n. nausea. vom1tmg A few pat1ents have had se1zures Empty 0
~~ a~~~~t=~~~:~c~!~~~ds~tfd ~~~vsem~~:~~r;~f nna~~~~ea~~ gi~~~~~~
0
:~~e,~a~e~~~o~f~~'Wi:s~~~C~~~s~~~o~~~~~~ •
1
pupil (figure 4). Angle-closure glaucoma may occur spontaneously (especially at night) or following dilatation with mydriatic drops. Pharmacologic treatment of acute angle-closure glaucoma consists of administering drops of a 4% solution of pilocarpine (Adsorbocarpine, Isopto Carpine, Pilagan, Pilopine
HS) to temporarily relieve the pressure. In addition, systemic osmotic agents (eg, a 50% solution of oral glycerin or a 20% solution of intravenous mannitol) should be given. Iridectomy (by laser or other means) is curative if it is performed within 1 week of the attack, before permanent iris adhesions (synechiae) develop.
prescriptiOn See pack-
~~~dr~n~;~~::td~r~~~~d~~~~t:~~s ~~~~gr:/o.
sT sYN-rEX-
u S patent nos 3.904.682. 3.998.966 and olhers. ' 1991 Syntex Puerto RICo. Inc Rev. 39 September 1990
44
GLAUCOMA • VOL 90/NO ?/NOVEMBER 15, 1991/POSTGRADUATE MEDICINE
Downloaded by [La Trobe University] at 22:02 31 May 2016
To identify patients at risk for angle-closure glaucoma, the penlight test should always be performed before the eyes are dilated.
Figure 3. Pale. diffuse bleb after successful filtering surgery.
The disease is bilateral, and prophylactic iridectomy is always recommended for the opposite eye. The question often arises as to who can safely undergo dilatation for fundus examination. Patients at risk for angle-closure glaucoma can be identified by the penlight test (figure 2). If a prominent shadow is cast on the far side of the iris with side illumination, the eye should not be dilated and slit-lamp examination should be done to determine whether the anterior chamber is shallow. Patients often ask about the warning label on certain over-the-counter decongestants stating that the medication should not be used by glaucoma patients. The warning is required because of the possible mydriatic effect of the medication; however, it applies neither to patients with open-angle glaucoma nor to those with acute angle-closure glaucoma who have had an iridectomy or are receiving pilocarpine therapy. The only group of patients at risk are those who have undetected narrow
Figure 4a. Acute angle-closure glaucoma. Note hazy cornea and mid-dilated pupil.
b. Opposite eye.
Figure 5. Enlarged eyes with hazy corneas in child with congenital glaucoma.
angles or who have refused treatment for angle-closure glaucoma (such refusal is rare). Thus for all practical purposes the warning is useless.
Congenital glaucoma Glaucoma may occur within the first few years oflife; symptoms of the congenital form of the disease include enlarged eyes, photophobia, tearing, and hazy corneas (figure 5). Visual loss can occur rapidly, and failure of early diagnosis may lead to
VOL 90/NO ?/NOVEMBER 15, 1991/POSTGRADUATE MEDICINE • GLAUCOMA
a lifetime of poor vision. In congenital glaucoma, the angle structures are maldeveloped and a simple incision into the angle (goniotomy) is curative. Congenital glaucoma sometimes occurs in conjunction with other congenital defects. Summary Glaucoma is best detected by examination of the optic disk, since intraocular pressure is not always continued on page 48 45
BuSpar(ruspironeHCO
Downloaded by [La Trobe University] at 22:02 31 May 2016
References: 1. Fe~ghner JP, Cohn JB Analysrs ol rndrvrdual symptoms rn generaliZed anxiety--a pooled mullisludy. double-blind evaluation ol busprrone Neuropsychobwlogy 1989.21124-130 2. Newton RE. Marunycz JD, Alderdrce MT Napolrello MJ. Revrew ollhe side-ellecl prairie of busprrone Am J Med 1986.80 (suppl38)17-21 1 Lader M Assessrng the polentral for busprrone dependence or abuse and effects of rls withdrawal Am J Med 1987,82 (suppi5A).20-26
Contralndicatlons: Hypersensitivity to buspirone hydrochloride. warnings: The administration ofBuSpar to a patient taking a monoamine 01idase Inhibitor (MAOI) may pose a hazard. Since blood pressure has become elevated when BuSpar was administered concomitantly with an MAOI. such concomitant use is not recommended. BuSpar should not be employed in lieu of appropriate antipsychotic treatment Precautions: General-Interference with cognitive and motor performance: Although buspirone is less sedating than other anxiolytics and does not produce significant functional impairment. its CNS effects in a given patient may not be predictable; therefore, patients should be cautioned about operating an automobile or using complex machinerr until they are reasonably certain that buspirone does not affect them adversely Although buspirone has no been shown to increase alcohol-induced impairment in motor and mental performance. it is Rrudent to avoid concomitant use with alcohol. Potential for wrthdrawal reactions in sedativelhypnoticlanxiotytic drug dependent patients: Because buspirone will not block the withdrawal syndrome often seen with cessat1on of therapy with benzodiazepines and other common sedative/hypnotic drugs, before starting buspirone withdraw patients gradually from their prior treatment. especially those who used a CNS depressant chronically. Rebound or withdrawal symptoms may occur over varying time periods, depending in part on the l)'pe of drug and its elimination hall-life The withdrawal syndrome can appear as any combination of irritability, anxiel)', agitation, insomnia, tremor, abdominal cramps, muscle cramps, vomiting, sweating, flu-like symptoms w1thout fever, and occasionally, even as seizures. Possible concerns related to buspirone's binding to dopamine receptors: Because buspirone can bind to central dopamine receptors. a question has been ra1sed about its potential to cause acute and chronic changes in dopamine mediated neurological function (eg, dystonia, pseudoparkinsonism, akathisia, and tardive dyskinesia) Clinical experience in controlled trials has failed to identify any significant neurolepticlike activity; however, asyndrome of restlessness. appearing shortly after initiation of treatment, has been reported; the syndrome may be due to increased central noradrenergic activity or may be attributable to dopaminerJliC effects lie, represent akathisial In/ormation lor Patients-Patients shou d be instructed to inform their physician about any medications, prescription or nonprescription, alcohol or drugs they are now taking or plan to take during treatment with buspirone. to inform their physician if they are pregnant, are P.lanning to become pregnant. or become pregnant while taking buspirone; to inform the1r physician ifthey are breasl feeding; and not to drive acar or operate potentially dangerous machinery until they experience how this medication affects them. Drua Interactions-Concomitant use with other CNS active drugs should be approached with caution (see Warnings) Concomitant use with trazodone may have caused 3- to 6-fold elevations on SGPT (All) in afew patients Concomitant admimstration of BuSpar and haloperidol resulted in increased serum haloperidol concentrations in normal volunteers. The climcal significance is not clear. Buspirone does not displace tightly bound drugs like phenytoin, propranolol, and warfarin from serum proteins, but may displace less firmly bound drugs like d1goxin However, there was one report of prolonged prothrombin time when busp_lrone was given to a gatient also treated with warfarin, phenytoin, phenobarbital, digoxin, and Synthroid Carclnoaenesis, /llutapenesis, Impairment of Fertility-No evidence of carcinogenic potential was observed in rats or m1ce; buspi:one did not induce point mutations, nor was DNA damage observed; chromosomal aberrations or abnormalities d1d not occur. Pregnancy: Teratoaenic Effects-Pregnancy Category B Should be used during pregnancy only if clearly needed Nursmg /lfolllers-Administration to nursing women should be avoided if clinically possible. Pediatric Use- The safety and effectiveness have not been determined in individuals below 18 years of age use in the Elderly-No unusual, adverse. age-related phenomena have been identified in elderly patients receiving a total, modal daily dose of 15 mg Use in Patients w/111 Impaired HepatiC or Renal Function-Since buspirone is metabolized by the liver and excreted by the kidneys, it is not recommended in severe hepatic or renal impairment Adverse Reactions (See also Precautions): Commonly Db11n11d-The more commonly observed untoward events, not seen at an equivalent mcidence in placebo-treated patients, include dizzmess. nausea. headache, nervousness. lightheadedness, and excitement Associated with Discontinuation o/Treatment-The more common events causing discontinuation included; central nervous system disturbances (3.4%), primarily dizziness. insomnia. nervousness, drowsiness. lightheaded feeling; gastrointestinal disturbances (1.2%), primarily nausea; miscellaneous disturbances (11%1, primarily headache and fatigue In addition. 34% of patients had multiple complaints, none of which cou d be characterized as primary. . Incidence in Controlled Clinical Trials ~Adverse events reported by 1% or more of 477 pat1ents who received buspirone in four -week, controlled trrals. Cardrovascutar. Tachycardia/palpitations 1%. CNS: Dizziness 12%, drowsmess 10%, nervousness 5%, msomnra 3%, l1ghtheadedness 3%, decreased concentration 2%, excitement 2%, angerlhostilii)' 2%, confusion 2%, depression 2%. EENT Blurred vision 2%. Gastrornteslinal. Nausea 8%, dry mouth 3%, abdominal/gastric distress 2%, diarrhea2%, constipation 1%, vomiling 1%. Muscutosketetat- Musculoskeletal acheslpams 1%. Neurological: Numbness 2%, paresthesia 1%, incoordination 1%, tremor 1% Skin.· Skin rash 1% Miscellaneous: Headache 6%, fatigue 4%, weakness 2%, sweatinQ!clamminess 1%. Other Events 06sen1ed During the Entire Premartetinll Evaluation- The relative frequency of all other undesirable events reasonably associated with the use ol buspirone in approximately 3000 subjects who took multiple doses of the drug under well-controlled. open, and uncontrolled conditions is defined as follows: Frequent are those occurnng in at least 11100 patients, infrequent are those occurnng in 11100 to 111000 patients. and rare are those occurring in less than 111000 pahents. Cardiovascular -frequent: nonspecific chest pain; infrequent syncope, hypotension. hypertension; rare: cerebrovascular acc1dent. congestive heart failure. myocardial infarction, cardiomyopathy, bradycardia. Central Nervous Systemfrequent: dream disturbances, infrequent: depersonalization, dysphoria, noise intolerance. euphoria. akathisia, fearfulness, loss of interest, dissoc1at1ve reaction, hallucinations, suicidal ideation. seizures; rare: feelings of claustrophobia, cold intolerance, stupor, slurred speech, psychosis. EENT -frequent: tinnitus. sore throat, nasal congestion; infrequent: redness and itching of the eyes, altered taste, altered smell, conjunctivitis; rare inner ear abnormality, eye pain, photophobia, pressure on eyes. Endocrine-rare: galactorrhea. thyroid abnormality. Gastrointestinal-infrequent: flatulence, anorexia, increased appetite, salivation, irrilable colon, rectal bleeding; rare; burning of the tongue. Genitounnary-intrequent: urinary frequency, urinary hesitancy, menstrual Irregularity and spotting, dysuria; rare; amenorrhea, pelvic inflammatory disease. enuresis, nocturia. Muscutoskeletal-intrequent: muscle cramps, muscle spasms, rigid/stiff muscles. arthralgias. Neurotogrcat-intrequent: involuntary movements, slowed reaction time; rare: muscle weakness. Resprratory-intrequent: hyperventilation, shortness of breath, chest congestion; rare: epistaxis. Sexual Function-infrequent decreased or increased libido; rare: delayed eiaculation, impotence. Skininfrequent: edema, pruritus. flushing, easy bruising, hair loss. dry skm, facial edema, blisters; rare; acne, thinnmg of nails. Clinical Laboratory-infrequent: mcreases in hepatic aminotransferases (SGOT, SGPT); rare: eosinophil;a, leukopenia, thrombocytopenia. Mrscettaneous-infrequent: weight gain, fever, roaring sensation in the head, weight loss, malaise, rare: alcohol abuse, bleeding disturbance, ·loss of voice, hiecoughs. Posllntroduction Clinical Experience-Rare occurrences of allergic reactions, cogwheel rigidity, dystonic reactions. ecchymosis, emotional lability, tunnel vision, and urinary retention have been reported. Because of the uncontrolled nature of these spontaneous reports, acausal relationship to BuSpar has not been determined. Drug Abuse and Dependence: Controlled Substance Class-Not a controlled substance. Physical andPsycho/Oflica/ Oependence-Buspirone has shown no potential for abuse or diversion and there is no evidence that it causes tolerance, or either physical or pslchological dependence. However, since it is difficult to predict from experiments the ex1ent to which a CNS-active drug will be misused, diverted, and/or abused once marketed, physicians should carefully evaluate patients for a history of drug abuse and follow such patients closely, observing them for signs of buspirone misuse or abuse (eg, development of tolerance, incrementation of dose, drug-seeking behavior). Overdosage: Signs and Symptoms-At doses approaching 375 mg/day the following symptoms were observed: nausea, vomiting, dizziness, drowsiness, miosis, ana gastric distress. No deaths have been reflOrted in humans either wijh deliberate or accidental overdosage. Recommended Overdose Treatment-General symptomatic and supportive measures should be used along with immediate gastrrc lavage No specific antidote is known and dialyzability of buspirone has not been determined For comple/e details, see Prescnbing Information tji or consult your Mead Johnson Pharmaceutrcats !}!.J Representative. PHARMAcEuT•cAL s
Mead
U.S. Patent Nos. 3,717,634 and 4,182,763
MJL84270R2
·""7'·
iTi1BJJil
devated in patients with the condition. A large, vertically oval cup within the optic disk is strong evidence for glaucoma. Open-angle glaucoma, the most common fonn of the disorder, often is not detected until the disease is advanced. It can usually be treated successfully with topical medications, but systemic absorption of these can result in serious side effects. If medical treatment fails, laser therapy or filtering surgery may be hdpful. Acute angle-dosure glaucoma has a sudden onset marked by alanning devations in intraocular pressure. It is treated immediately with topical pilocarpine and systemic osmotic agents, and an iridectomy should be performed as soon as possible. Congenital glaucoma can be cured with goniotomy. IVt'l
-®
Earn credit on this article. See CME Quiz
Address for correspondence: Jonathan E. Pederson, MD, Department of Ophthalmology, Hennepin County Medical Center, 70 I Park AveS, Minneapolis, MN 55415.
Bibliography Epstein DL Chandler and Grant's glaucoma. 3d ed. Philadelphia: Lea & Febiger, 1986 Hoskins HD, Kass MA. Becker-Shaffer's diagnosis and therapy of the glaucomas. 6th ed. St Louis: Mosby-Year Book, 1989 Ritch R, Shields MB, Krupin T, eds. The glaucomas. StLouis: Mosby-Year Book, 1989 Shields MB. Textbook of glaucoma. 2d ed. Baltimore: Williams & Wilkins, 1987
ABn'>lol '-t.ro'iQultlbCu
~_;:r ~~till ~ ler>c'!·
os)-13
48
GLAUCOMA
