Timolol


Article Author:
James Barnes


Article Editor:
Majid Moshirfar


Editors In Chief:
Dustin Constant
Donald Kushner


Managing Editors:
Avais Raja
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Carrie Smith
Abdul Waheed
Khalid Alsayouri
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Trevor Nezwek
Radia Jamil
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Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
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Heba Mahdy
Ahmad Malik
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Sarosh Vaqar
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Daniyal Ameen
Altif Muneeb
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes
Komal Shaheen
Sandeep Sekhon


Updated:
7/22/2019 11:31:16 AM

Indications

Timolol is a nonselective beta-blocker that available for both topical or systemic administration. Topical timolol is primarily used to reduce intraocular pressure in patients with open-angle glaucoma and ocular hypertension.[1] Topical timolol has also been shown to be effecting in treating and minimizing thin, superficial infantile hemangiomas.[2] Systemic administration of timolol can be part of a regimen managing hypertension, myocardial infarction, and migraine prophylaxis.[3][4][5] The use of timolol to treat adult atrial fibrillation is controversial.[6][7]

FDA-Labeled Uses of Topical Timolol:

Open-angle glaucoma

Ocular hypertension

Off-Label Uses of Topical Timolol:

Infantile hemangioma

FDA-Labeled Uses of Systemic Timolol:

Hypertension (not first-line)

Myocardial infarction

Migraine prophylaxis

Off-Label Uses of Systemic Timolol:

Atrial fibrillation (adult)

Open-angle glaucoma and Ocular Hypertension

Open-angle glaucoma characteristically presents with resistance to aqueous humor outflow via the trabecular meshwork.[8] This situation causes a gradual increase in intraocular pressure as the ciliary body continues to secrete aqueous humor. When the intraocular pressure increases beyond normal levels, it is ocular hypertension. If left untreated, this increase in pressure can lead to irreversible damage to the optic nerve and retinal ganglion cells, causing progressive vision loss.[8]

Beta-blockers such as timolol were once first-line treatment for open-angle glaucoma and ocular hypertension, but the recommendation now is that patients first be treated with a topical prostaglandin, such as latanoprost. Topical prostaglandins have demonstrated to be more effective in lowering intraocular pressure and carry a lower risk for systemic side effects when compared to beta-blockers.[9] Timolol is now usually prescribed to patients who may respond insufficiently or have a contraindication to topical prostaglandins. In many patients, timolol may be combined with prostaglandins for an enhanced reduction in intraocular pressure.[10]

Infantile Hemangiomas

Infantile hemangiomas are benign vascular tumors that occur in 4 to 10% of infants. These tumors characteristically have a proliferative phase, followed by involution. The resolution of infantile hemangiomas generally occurs before the age of 4.[2] Infantile hemangiomas are usually asymptomatic but may sometimes ulcerate, cause disfiguration, affect vision, or cause feeding difficulties depending on the location.[11] Topical ophthalmic timolol has been shown to be an effective way to treat thin, superficial infantile hemangiomas.[2] 

Hypertension

Although previously thought of as first-line therapy for the treatment of hypertension, recent reports have rejected beta-blockers, such as timolol, as a first-line treatment for hypertension in favor of more effective medications including diuretics, calcium-channel blockers, and renin-angiotensin system inhibitors.[12]

Myocardial Infarction

Myocardial infarction is defined as an ischemic infarction to the heart due to a blockage of one or more of the coronary arteries. Beta-blockers, such as timolol, have been shown to increase survival and improve long-term outcomes after myocardial infarction.[13]

Migraine Prophylaxis

Migraines characteristically present as recurrent moderate to severe headaches that can be accompanied by phonophobia, photophobia, and nausea. Migraines can cause severe, unilateral throbbing pain, and physical activity can be an aggravating factor. Timolol has been an effective method for migraine prophylaxis.[14] 

Atrial Fibrillation

Atrial fibrillation is a common rhythm abnormality of the heart. Patients with atrial fibrillation are at an increased risk for many cardiovascular events, including stroke, heart failure, thromboembolism, and cardiovascular-related hospitalizations. Although beta-blockers are among the most common agents used to control heart rate for patients with atrial fibrillation, timolol has not been FDA approved for this purpose, which is perhaps because although timolol is effective at regulating heart rate, it is unlikely to restore sinus rhythm.[15][6][7]

Mechanism of Action

Open-Angle Glaucoma

The exact mechanism of action by which timolol reduces the intraocular pressure in patients with open-angle glaucoma is unknown; however, the thinking is that timolol inhibits beta receptors on the ciliary epithelium. The ciliary epithelium normally functions to increase the production of aqueous humor. It has been proposed that through inhibition of beta receptors, timolol leads to a reduction in the production of aqueous humor and therefore, a reduction in intraocular pressure. Non-adrenergic pathways of timolol in the reduction of intraocular pressure have also been studied.[16][17][18][19]

Ocular Hypertension

Timolol’s exact mechanism in lowering the intraocular pressure in patients with ocular hypertension is unknown, but it is thought to be similar to its mechanism in lowering intraocular pressure for patients with open-angle glaucoma.[18][19][20]

Infantile Hemangioma

The mechanism of how timolol can treat infantile hemangiomas has yet to be fully elucidated. However, it is postulated that timolol’s effect likely involves antagonism of beta-adrenergic receptors causing multiple processes including vasoconstriction, stimulation of apoptosis, and inhibition of angiogenesis.[21]

Hypertension

The sympathetic nervous system is very important in the regulation of blood pressure. In normal physiology, beta-1 and beta-2 receptors are activated by endogenous catecholamines. Once these receptors are activated, they stimulate their associated G-protein, thereby activating adenylyl cyclase and leading to an increase in cyclic-AMP (cAMP).[22] This secondary messenger can cause a cascade of reactions in the body, one of them being vasoconstriction and an elevation in blood pressure. Non-selective beta-blockers, such as timolol, block interactions between endogenous catecholamines and prevent the G-protein cascade from occurring, leading to decreased sympathetic tone and therefore decreased blood pressure.[12]

Myocardial Infarction[23][24][25][26]

There are many mechanisms by which beta-blockers can reduce morbidity and mortality in patients after myocardial infarction. For example, beta-blockers can reduce the myocardial demand for oxygen and relieve ischemic chest pain. By blocking the sympathetic receptors in the heart, heart rate will decrease. This induced bradycardia can lengthen diastole and increase perfusion of the heart. Beta-blockers can inhibit platelet aggregation, thromboxane synthesis, and decrease the rate of atherosclerosis and thromboembolism. They also inhibit cardiac remodeling after myocardial infarction.

Migraine Prophylaxis[14]

The exact mechanism of timolol as migraine prophylaxis is unknown. It is likely that it exhibits its effects through a variety of processes. One proposed mechanism is that a blockage of beta-adrenergic receptors decreases the synthesis and release of norepinephrine, an important intermediate in the pathophysiology of migraines. Another pathway that could contribute to timolol’s migraine prophylactic properties is that beta-blockers can regulate the neuronal firing of periaqueductal gray matter using GABA. Timolol is also thought to play a part in regulating the serotonergic system by inhibiting 5-HT, another important mediator in the pathophysiologic pathway of migraines. This modulation of serotonin’s effects is also thought to contribute beta-blockers’ ability to reduce the sensitivity of the auditory system, reducing the frequency of migraine attacks. It is also hypothesized that beta-blockers play a significant role in reducing the excitability of the visual system in patients with migraines. Beta-blockers, such as timolol, are also thought to reduce the spread of signals through the brain including the cortical spread as well as the excitability of the ventroposteromedial thalamic nucleus.

Atrial Fibrillation

The autonomic nervous system plays a consequential role in the development of atrial fibrillation. Aberrant sympathetic tone can stimulate myocyte contraction and promote irregular rhythms in susceptible patients.[27][28] Beta-blockers help maintain the regular rhythm of the heart by decreasing the autonomic tone, and therefore decreasing sympathetic stimulation, of the cardiac myocytes.[7]

Administration

Topical Ophthalmic Drop

Ocular Hypertension and Open-Angle Glaucoma

The topical ophthalmic form of timolol comes as a gel or as a solution. When using the gel form, one drop is administered daily to the affected eye. Available doses are 0.25% and 0.5%. When using the solution, one drop of the 0.25% solution is applied to the affected eye twice daily. If the response is inadequate, then the concentration is increased to 0.5% twice daily in the affected eye. Once the intraocular pressure is under control, the patient may decrease the dose to one drop daily.

Infantile Hemangiomas

One drop of 0.5% timolol gel is applied to the affected area 2 to 3 times a day. Treatment continues until improvement is stable.

Systemic

Hypertension

For the treatment of hypertension, 10 mg of oral timolol is given twice daily. If the patient’s response is inadequate, then the dose can be increased incrementally to a maximum of 60 mg per day.

Myocardial Infarction

For the secondary treatment of myocardial infarction, 5 mg of oral timolol is given twice daily. Dosing can be increased to 10 mg twice daily.

Migraine Prophylaxis

For the prophylactic treatment of migraines, the patient may take 10 mg of oral timolol twice daily. If the response is inadequate, then the dose can be increased to a maximum of 30 mg per day.

Atrial Fibrillation

Timolol can be used to treat atrial fibrillation with an initial dose of 10 mg twice daily. It can then be increased incrementally to a maximum of 30 mg twice daily.

Adverse Effects

Ocular Side Effects:

  • Burning
  • Stinging
  • Irritation
  • Dryness
  • Itching
  • Watery eyes
  • Conjunctival hyperemia
  • Blurry vision

Systemic Side Effects[10][29][30]:

  • Bronchospasm
  • Bronchoconstriction
  • Bradycardia
  • Depression
  • Fatigue
  • Confusion
  • Hair loss
  • Sexual impotence
  • Disorientation
  • Increased low-density cholesterol levels
  • Headache
  • Dizziness

Contraindications

The use of timolol is contraindicated in patients with a history of asthma, chronic obstructive pulmonary disease (COPD), and other pre-existing pulmonary conditions.[30] Other contraindications for timolol include underlying cardiovascular conditions, including bradycardia, heart block, or syncope.[31]

Monitoring

Ocular pressure, systemic effects of beta-blockade, blood pressure, heart rate, apical pulses, and radial pulses all require monitoring while a patient is on timolol.

Toxicity

Because timolol is a beta-blocker, its overdose symptoms are similar to those of other beta-blockers. Many metabolic and circulatory systems depend on the free circulation of catecholamines. Overdose of beta-blockers can cause catecholamine levels to decrease sharply. This effect can lead to a variety of symptoms, including hypotension, bradycardia, hypoglycemia, decreased myocardial contractility and oxygen consumption, tiredness, and fatigue. Clinicians should focus special attention to patients taking anticholinergics or medicines that are cardiotoxic, as these may potentiate timolol’s toxic effects.[32]

The first step in the management of beta-blocker overdose is to secure the airway and administer cardiac life support if needed. Oxygen and bronchodilators can be used to treat patients with bronchospasm. Atropine should be given to patients who are experiencing bradycardia or require rapid intubation. Sodium bicarbonate and magnesium sulfate may also prove useful in managing the patient’s cardiac symptoms. IV fluids, including dextrose, glucagon, and calcium salts can be used to treat the patient’s metabolic symptoms. Benzodiazepines can be a first-line treatment for any seizures the patient may experience. Gastrointestinal decontamination or administration of activated charcoal can be used to decrease absorption of the beta-blocker in the gut.[32]

Enhancing Healthcare Team Outcomes

Timolol is a common medication often used in the treatment of open-angle glaucoma and ocular hypertension. It is crucial for all members of the patient care team (primary care physician, emergency department, nurse practitioner, pharmacist, etc.) to be aware of the contraindications of timolol and its potential side effects. The ophthalmic nurse should also ensure that the medication is working by regularly monitoring the intraocular pressure. Any vision or pressure changes require communication with the ophthalmologist. Ideally, only the ophthalmologist should change the dosage and frequency. Pharmacists can weigh in with medication reconciliation, dose verification, and counseling regarding adverse effects, and communicate any concerns to the nurse or prescribing physician. Both the nurse and pharmacist are responsible for instruction on how to administer ocular formulations effectively.

The pharmacist should counsel the patient about the medication, the specific dose, and any side effects that may occur. Patients should be told to immediately seek help if they overdose or experience serious side effects.

While timolol is a common and generally well-tolerated medication, an interprofessional team approach to include physicians, specialists, specialty-trained nurses, and pharmacists, collaborating as a unit, will optimize therapeutic results and minimize adverse events. [Level V]


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Timolol - Questions

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A 70-year-old male with a prior history of cataract surgery, COPD, hypertension, and ulcerative colitis comes to your clinic complaining of progressive blurry vision. Physical examination is notable for ronchi in both lungs upon auscultation, a blood pressure of 135/96, and decreased visual acuity in the periphery of the visual field. Medications include albuterol, budesonide, and hydrochlorothiazide. The patient is referred to an ophthalmologist for examination and the ophthalmologist reports that the patient's intraocular pressure is 24 mm Hg (normal 12-22 mm Hg). Which medication used to treat this condition should be avoided?



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A 72-year-old female with a history of arthritis, hypertension, and previous LASIK surgery comes to the office complaining of progressive vision loss. Medications include oral prednisone, hydrochlorothiazide, and a daily multivitamin. Physical examination is notable for right knee tenderness, swelling, and erythema and decreased visual acuity in the periphery of the patient's visual field. Examination with an ophthalmoscope reveals abnormalities in the optic nerve. You decide to use a common beta-blocker to treat this condition. What is its mechanism of action?



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A 68-year-old African American male comes to the clinic for a routine eye exam. He has 20/400 vision and has a -6.75D prescription for glasses. His intraocular pressure is 24 mmHg (normal: 12-22 mmHg). Five years ago, he suffered a heart attack and now requires a pacemaker. He has had type 2 diabetes for the past 15 years and recently had knee surgery to repair a torn meniscus. Due to numerous risk factors, it is decided to start the patient on a medication that will lower his intraocular pressure. Which of the following medications is contraindicated in this patient?



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A pregnant patient with a history of asthma comes to the clinic for a routine eye exam. On examination, she has visual deficits in her periphery and abnormalities in her optic nerve. She is given a topical ophthalmic solution to treat her condition. The next day, the patient is rushed to the hospital due to severe asthmatic symptoms. Which of the following medications could have caused this?



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The starting shortstop of your local MLB team comes into your office during the midst of a hitting slump. He complains that he is having trouble seeing the ball as well as he used to. Upon examination, he demonstrates good visual acuity but decreased vision in the periphery of his visual field. He reports taking a daily steroid to help control his Crohn's Disease. You decided to measure his intraocular pressure and find that it is 24 mmHg (normal: 12-22 mmHg). You decide to treat his ocular symptoms with an ophthalmic solution of a common beta-blocker. Which of the following ocular structures is most likely to be targeted by this medication?



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Timolol - References

References

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