Find information on thousands of medical conditions and prescription drugs.

Diamox

Acetazolamide, sold under the trade name Diamox®, is a carbonic anhydrase inhibitor that is used to treat glaucoma, epileptic seizures, benign intracranial hypertension and altitude sickness. For glaucoma sufferers, the drug decreases fluid formation around the eye resulting in lower internal pressure on the eye. Acetazolamide can only be obtained by prescription and is available as a generic drug. more...

Home
Diseases
Medicines
A
B
C
D
Dacarbazine
Dactinomycin
Dalmane
Danazol
Dantrolene
Dapoxetine
Dapsone
Daptomycin
Daraprim
Darvocet
Darvon
Daunorubicin
Daunorubicin
Daypro
DDAVP
Deca-Durabolin
Deferoxamine
Delsym
Demeclocycline
Demeclocycline
Demerol
Demulen
Denatonium
Depakene
Depakote
Depo-Provera
Desferal
Desflurane
Desipramine
Desmopressin
Desogen
Desogestrel
Desonide
Desoxyn
Desyrel
Detrol
Dexacort
Dexamethasone
Dexamfetamine
Dexedrine
Dexpanthenol
Dextran
Dextromethorphan
Dextromoramide
Dextropropoxyphene
Dextrorphan
Diabeta
Diacerein
Diacetolol
Dial
Diamox
Diazepam
Diazoxide
Dibenzepin
Diclofenac
Diclohexal
Didanosine
Dieldrin
Diethylcarbamazine
Diethylstilbestrol
Diethyltoluamide
Differin
Diflucan
Diflunisal
Digitoxin
Digoxin
Dihydrocodeine
Dihydroergotamine
Dihydrotachysterol
Dilantin
Dilaudid
Diltahexal
Diltiazem
Dimenhydrinate
Dimercaprol
Dimetapp
Dimethyl sulfoxide
Dimethyltryptamine
Dimetridazole
Diminazene
Diovan
Dioxybenzone
Diphenhydramine
Diphenoxylate
Dipipanone
Dipivefrine
Diprivan
Diprolene
Diproteverine
Dipyridamole
Disulfiram
Disulfiram
Dizocilpine
Dobutamine
Docetaxel
Docusate sodium
Dofetilide
Dolasetron
Dolobid
Dolophine
Domperidone
Donepezil
Dopamine
Dopram
Doral
Doramectin
Doriden
Dornase alfa
Doryx
Dostinex
Doxapram
Doxazosin
Doxepin
Doxil
Doxil
Doxorubicin
Doxy
Doxycycline
Doxyhexal
Doxylamine
Drisdol
Drixoral
Dronabinol
Droperidol
Drospirenone
Duloxetine
Durabolin
Duragesic
Duraphyl
Duraquin
Dutasteride
Dv
Dyclonine
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z

Uses

General

Acetazolamide is used in glaucoma and epilepsy. In epilepsy, its main use is in absence seizures, with some benefit in other seizure syndromes. It is also used to decrease generation of cerebrospinal fluid in benign intracranial hypertension.

Altitude sickness

Acetazolamide has been shown to relieve mild cases of altitude sickness in some people. The drug forces the kidneys to excrete bicarbonate, the base form of carbon dioxide thus counteracting the effects of hyperventilation that occurs at altitude. Some take acetazolamide prophylactically, anywhere between 125 milligrams (mg) to 500 mg per day. Others only take it when symptoms begin to appear so they can tell whether the drug really has any benefits for them. Acetazolamide can also be taken to treat sleep apnea that may develop at higher elevations as it stimulates the respiratory system to breathe more regularly. Note that acetazolamide is not an immediate quick fix – it speeds up acclimatization which in turn helps to relieve symptoms. This may take up to a day or two without any further rapid ascent.

Side-effects

Common side effects of using this drug include numbness and tingling in the fingers and toes, and taste alterations (especially for carbonated drinks); both are usually due to mild hypokalemia (low potassium levels). Some may also experience blurred vision but this usually disappears shortly after stopping the medication. Everyone will experience more frequent urination as a result of using acetazolamide. One should drink more fluids than usual to prevent dehydration and headaches.

Contraindications

Acetazolamide should not be taken by individuals if:

  • They are allergic to sulfa medications
  • They are allergic to any carbonic anhydrase inhibitor
  • They have liver or kidney disease
  • They have adrenal gland failure (i.e. Addison's disease)
  • They have diabetes

Myths

  • Acetazolamide covers up symptoms. Acetazolamide speeds up acclimatization which in turn helps to alleviate symptoms. However, if you still feel sick, you need to stop ascending immediately.
  • Acetazolamide prevents acute mountain sickness from getting worse. If your symptoms are not improving, continued ascent can lead to HAPE or HACE.
  • Stopping the drug causes symptoms to worsen. Your body will just return to its own acclimatization rate. If you are already acclimatized, the drug will not change that fact.

Read more at Wikipedia.org


[List your site here Free!]


When the Pressure is On
From Optometric Management, 2/1/04 by Williams, Scott

Dealing with mixed mechanism angle closure.

Angle closure, with its subsequent potential for TOP elevation and glaucomatous optic neuropathy, may occur through a variety of mechanisms. Most common among these is the well-established pupillary block, followed by iris bombe, typically managed with laser periphery iridotomy. Occasionally, despite a patent iridotomy, the degree of angle improvement may be limited and appositional closure remains. This situation, where additional factors, including plateau iris, phacomorphic or malignant glaucoma, may act to maintain angle closure, is referred to as mixed-mechanism angle-closure glaucoma.

About the patient

G.N., a 60-year-old Asian male, presented to our clinic with a six-month history of a dull left brow ache. G.N. described photosensitivity and blurry vision in his left eye, which he admitted had occurred intermittently in the past. He had no complaint regarding his right eye. G.N. denied taking any medications and reported an unremarkable ocular and medical history.

Taking a clinical look

His best corrected visual acuity (BCVA) was 20/20 OD with a manifest refraction of +2.50 -0.50 x 106 and 20/60-1 OS through +1.75DS. Confrontation fields were full to finger count OD; however, peripheral field constriction was apparent in all quadrants OS, with significant fixation difficulty. The field loss OS was confirmed with Humphrey 30-2 field analysis, which showed a nearly complete peripheral field defect. Pupil testing revealed a mid-dilated pupil OS with a limited, sluggish response to light. The pupil OD was round and reacted well to light. Extraocular muscles were unrestricted in all gazes. Goldmann tonometry measured 11 mmHg OD and 42 mmHg OS. Slit lamp biomicroscopy evaluation revealed clear ocular adnexa, a quiet bulbar and palpebral conjunctiva OU, except for some mild injection OS. The cornea was intact and clear OD. Mild corneal edema was apparent OS. Anterior chambers appeared quiet yet shallow OU. The crystalline lenses had moderate nuclear sclerosis and the anterior vitreous was quiet OU. No angle structures were visible 360 degrees OU via gonioscopy. Undilated fundus examination by slit lamp with 90D lens showed cup-to-disc ratios of .47.4 OD and .91.9 OS. The optic nerve head margins were distinct with healthy appearing rim tissue OD and slightly pale rim tissue OS. Retinal vessels appeared normal with an arterial-venous ratio of 2/3 noted OU. Both eyes had normal appearing maculae.

Immediately after I diagnosed G.N. with angle-closure glaucoma, I gave him two 250 mg tablets of acetazolamide (Diamox), two drops of brimonidine tartrate ophthalmic solution 0.2% (Alphagan) OS and one drop of pilocarpine HCl 1% (Pilocar) to reduce the IOP. After discussing the risks and benefits of sequential argon and Nd:YAG laser peripheral iridotomy, I (Dr. Williams) performed this at 10:00 and 1:00 o'clock OS. The IOP OS was 29 mmHg one hour after the laser treatment and 22 mmHg at two hours. I prescribed brimonidine t.i.d. OS, prednisolone acetate 1 % (Pred Forte) q.i.d. OS, and acetazolamide 500 mg p.o. b.i.d to control inflammation and pressure. I scheduled G.N. for a follow-up appointment the following day.

FOLLOW-UP #1 The next day, G.N. returned with a BCVA of 20/70 OS. His IOPs were 10 mmHg and 30 mmHg OD and OS, respectively. The anterior chamber OS appeared quiet but still shallow. At this point, Dr. Henry repeated the laser iridotomies to ensure patency. I administered oral acetazolamide (two 250-mg tablets), two drops brimonidine and one drop of pilocarpine 1%.

Gonioscopy at one hour post laser retreatment revealed a grade 2 angle inferiorly, grade 1 temporally and closed angles superionasally. Because G.N.'s IOP OS was down to 20 mmHg, I didn't make any changes to the prescribed medications and advised G.N. to return in two days.

FOLLOW-UP #2 As instructed, G.N. presented two days later with an TOP OS of 14 mmHg and slightly improved visual acuity of 20/60+2 OS. I discontinued all medications and made a followup appointment for one month later with a plan to perform a prophylactic iridotomy OD.

FOLLOW-UP #3 One month later, G.N. reported that his vision OS was still blurry. The BCVA in that eye was stable at 20/60. However, the TOP was 43 mmHg OS. Gonioscopy showed nearly complete closure in all quadrants OU. Despite patent iridotomies in the left eye, the anterior chamber was shallow, leading to a diagnosis of mixed-mechanism glaucoma. I again prescribed hyperosmotics and aqueous suppressants and scheduled cataract extraction for the left eye in two days. I postponed the iridotomy scheduled for this day.

Extracting the cataract

A surgeon performed a routine cataract extraction via a small, clear cornea incision using a foldable intraocular lens implant. G.N. came in the next day for a follow up to his cataract extraction. (His drop regimen was currently prednisolone and ofloxacin 0.3% [Ocuflox] q.i.d. OS, and brimonidine ophthalmic solution [Alphagan P] t.i.d. OS.) His BCVA was consistent at 20/20-2 OD and 20/70-1 OS. Goldmann applanation tonometry revealed IOPs of 14 mmHg and 28 mmHg for OD and OS respectively. all other slit lamp findings were the same except for grade 1+ cells in the anterior chamber OS, which was now deep. The cornea OS showed trace temporal edema near the incision. A posterior chamber IOL appeared centered and in good position. The drop regimen was unchanged and I requested a follow up for two days to recheck the IOP.

Cataract surgical follow up

During the next week of postop care, G.N.'s uncorrected vision measured 20/50-2 OS with a consistent IOP of 12 mmHg. Slit lamp exam showed a significant reduction in post-op inflammation. I tapered prednisolone drops to b.i.d. and had G.N. discontinue the ofloxacin.

FOLLOW-UP #7 After several additional follow-ups and one month after cataract extraction OS, G.N.'s IOP was still well controlled, measuring 13 mmHg OU. For convenience, I had him switch from brimonidine t.i.d. to bimatoprost (Lumigan) q.h.s.

FOLLOW-UP #8 A follow up five months later revealed an IOP of 14 mmHg OD and 8 mmHg OS.

Know what to look for

Angle-closure glaucoma accounts for approximately 6% of all patients who have glaucoma, or nearly 0.6% of the general population.The incidence in females is roughly three times that for males. Studies have also shown the relative risk in Asians as three times greater compared with other racial groups.

Elevated IOP induced by acute angle closure produces the characteristic clinical findings of pain, blurred vision, frontal headache, closed angles, elevated TOP, corneal edema, shallow anterior chambers, conjunctival injection and fixed, mid-dilated pupil. It's easy to diagnose acute angle closure, but the distinction between acute or chronic angle closure may not initially be evident because there's often an overlap in the clinical presentation.

More importantly, the distinction between a primary angle closure resulting from pupillary block and secondary angle closure or mixed-mechanism glaucoma can often prove challenging - especially in the absence of a patent iridotomy. The more posterior the level at which the angle closure occurs, the more complex the diagnosis and treatment, especially for angle closure resulting from multiple levels, as with mixed-mechanism glaucoma.

The extent of peripheral anterior synechiae in G.N.'s eyes was difficult to establish. ?-scan ultrasound imaging revealed equal axial lengths and lens thickness in each of G.N.'s eyes. The only difference evident was a more anterior position of the lens of the glaucomatous eye, typical of unilateral angle closure glaucoma patients. Considering this information and the anatomical dimensions of G.N.'s eyes, I made a diagnosis of mixed mechanism glaucoma involving both a pupillary block component, eliminated via iridotomy, and a phacomorphic component, resulting in persistent narrow angles and elevated IOP, post-iridotomy. (Phacomorphic glaucoma is a secondary angle-closure glaucoma typically resulting from an intumescent, cataractous lens.)

There is no universal agreement on the best way to treat the combination of cataract and angle closure glaucoma. In cases of chronic mixed mechanism angle closure glaucoma involving a significant cataractous lens contribution, the mechanism of angle closure may be principally related to an imbalance of a large and anteriorly positioned lens and a small anterior chamber. Thus, it seems reasonable that cataract extraction could improve IOP control in these patients.

Studies have suggested extracapsular cataract extraction and posterior chamber lens implantation as a useful management option, especially in patients with severe glaucomatous neuropathy and visual field defects at presentation. Modern cataract extraction techniques, involving phaco-emulsification; foldable IOL implantation; and, small, clear corneal incisions, have been shown to increase anterior chamber width and depth, normalize IOP and prevent synechiae formation.

Studies have shown 40% to 65% of angle closure glaucoma patients require no medical IOP control at all, post cataract extraction. This treatment has also been suggested for cases of acute primary angle closure glaucoma, especially in Asian (narrow angle) patients, where a mixed mechanism is likely. However, cataract extraction as treatment for chronic angle closure glaucoma may be limited. Lai, et al. demonstrated that removal of a cataractous lens alone could not open an angle that is permanently closed by peripheral anterior synechiae. They recommended concurrent goniosynechialysis in these cases, which involves surgical breakage of the peripheral anterior synechiae.

Additional treatment possibilities include laser peripheral iridotomy, argon laser peripheral iridoplasty, surgical goniosynechialysis, filtration surgery and various combinations of each. However, long-term results in Asian patients with combined iridotomy and iridoplasty indicate failure to prevent subsequent IOP elevation and synechial angle closure development. Reclosure of the angle is also common with goniosynechialysis as a sole treatment. This may, however, be a useful adjunct to cataract surgery. Filtration surgery, although effective at IOP reduction, is associated with serious complications, multiple surgical interventions, and often, deterioration of visual function. Specifically, patients with angle closure glaucoma are at risk of developing a flat anterior chamber after filtering surgery.

In this case, after cataract extraction and IOL implantation, excellent IOP control was achieved in G.N.'s left eye during the critical first six months post-op period. His visual outcome was stable and limited by established glaucomatous optic nerve damage. Findings in several large studies indicate that 50% to 75% of ipsilateral eyes in patients who suffer an acute angle closure attack will develop an attack within five years. Considering this risk and his surgically induced antisometropia, G.N. was counseled and scheduled for a cataract extraction OD.

Know how to proceed

Angle-closure glaucoma is the most prevalent form of glaucoma in the Asian population and is a significant cause of blindness worldwide. This case demonstrates the clinical presentation and management options for patients who have mixed-mechanism, angle-closure glaucoma. The high rate IOP control failure post iridotomy, especially in Asian patients, indicates a need for close follow up. When a patient presents with significant glaucomatous damage, consider early surgical intervention.

Scott Williams, O.D.

Larry R. Henry, O.D.

by Scott Williams, O.D., and Larry R. Henry, O.D.

Dr. Williams recently completed his Ocular Disease Residency at BVA Advanced Surgical Eyecare in Edmond, Okla. He is currently in private practice in Victoria, British Columbia.

Dr. Henry is clinical director for BVA Advanced Surgical Eyccare. He also serves as adjunct professor and residency supervisor for Northeastern State University College of Optometry.

Copyright Boucher Communications, Inc. Feb 2004
Provided by ProQuest Information and Learning Company. All rights Reserved

Return to Diamox
Home Contact Resources Exchange Links ebay