Carteolol (ophthalmic) - for open angle glaucoma

Carteolol is a non-selective beta-blocker that blocks both beta 1 and beta 2 receptors. It is available as a topical formulation for ophthalmic use in patients with a raised intraocular pressure or intraocular hypertension and chronic open angle Glaucoma.

Adult dose:

Use of Carteolol in the treatment of raised intraocular pressure (as in Glaucoma)

- Instill 1 drop in the affected eye(s) twice daily.

Dose in children:

It has not been studied in pediatric patients.

Pregnancy Risk Factor C

Since systemic absorption can occur, beta-blockers such as carteolol may be associated with bradycardia and fetal hypoglycemia.
To reduce the risk of birth defects, it is recommended that the lowest effective dose be used to treat glaucoma in pregnancy. This can be done with punctal Occlusion.

Carteolol use during breastfeeding

The effects of carteolol on nursing mothers and their excretion have not been investigated.
To reduce potential exposure to the nursing infant, it is recommended to use the minimum effective dose in conjunction with punctual obstruction.
Nursing mothers should use it with caution

Renal dose:

The manufacturer has not recommended any dose adjustments in patients with renal disease.

Dose in liver disease:

The manufacturer has not recommended any dose adjustments in patients with liver disease.

Common Side Effects Of Carteolol Include:

Ocular:
- Conjunctival hyperemia

Less Common Side Effects Of Carteolol Include:

Ocular:
- Anisocoria
- Corneal punctate keratitis
- Corneal staining
- Corneal sensitivity decreased
- Eye pain
- Vision disturbances

Contraindication to Carteolol include:

Allergy reactions to carteolol and any component of the formulation
Bradycardia
Atrioventricular (AV) block, second or third degree
Cardiogenic shock
Allergy Bronchial Asthma
Chronic obstructive pulmonary diseases (COPD) severe

Warnings and Precautions

Anaphylactic reactions
- Patients who have had an allergic reaction to beta-blockers in the past should not use it.
- Treatment with epinephrine can be ineffective if anaphylactic reactions occur.
Choroidal detachment:
- After filtration, choroidal detachment has been seen as a result of aqueous suppressive therapy that includes beta blockers.
Diabetes:
- Patients with diabetes mellitus might be able to use beta-blockade to reduce hypoglycemia.
Heart failure:
- Patients with severe heart disease should avoid beta-blockers.
- It could worsen an underlying myocardial injury.
Myasthenia gravis:
- Patients with myasthenia Gravis should not use it. It can worsen myasthenic symptoms such as weakness and ptosis.
Raynaud and peripheral vascular disease:
- Beta-blockers should be used with caution in patients with peripheral arterial disease or Raynaud's phenomenon.
Respiratory disease
- This should not be used in severe or moderate asthma. Patients with a history bronchial hyperreactivity should avoid it.
Thyroid disease:
- It can mask hyperthyroidism symptoms. A thyroid storm could result from the abrupt withdrawal of beta-blockers for patients with hyperthyroidism.

Carteolol (ophthalmic): Drug Interaction

Note: Drug Interaction Categories:

Risk Factor C: Monitor When Using Combination
Risk Factor D: Consider Treatment Modification
Risk Factor X: Avoid Concomitant Use

Risk Factor C (Monitor therapy).
Acetylcholinesterase inhibitors	Beta-Blockers may increase the bradycardic effects.
Alpha1-Blockers	Beta-Blockers can increase the orthostatic hypotensive effects of Alpha1Blockers. Ophthalmic products are less likely to be a risk than systemic ones.
Amiodarone	Beta-Blockers may increase bradycardic effects. Possible to cause cardiac arrest. Amiodarone could increase serum Beta-Blockers.
Antipsychotic Agents (Phenothiazines).	Beta-Blockers may increase hypotensive effects. Beta-Blockers can decrease the metabolism Antipsychotic Agents (Phenothiazines). The metabolism of Beta-Blockers may be affected by Antipsychotic Agents (Phenothiazines).
Barbiturates	May lower the serum level of Beta-Blockers.
Bradycardia-Causing Agents	May increase the bradycardic effects of Bradycardia-Causing agents.
Bretylium	May increase the bradycardic effects of Bradycardia Causing Agents. Patients receiving AV blocking drugs may experience a reduction in AV blockade due to Bretylium.
Bupivacaine	Beta-Blockers can increase serum Bupivacaine concentrations.
Calcium Channel Blockers (Nondihydropyridine)	BetaBlockers may increase the hypotensive effects. Also, signs of heart disease and Bradycardia have been reported. Calcium Channel Blockers (Nondihydropyridine), may increase serum Beta-Blockers. Exceptions: Bepridil.
Cardiac Glycosides	Beta-Blockers can increase the bradycardic effects of Cardiac Glycosides.
Cholinergic Agonists	Beta-Blockers could increase the toxic/adverse effects of Cholinergic Agonists. Particular concerns are the possibility of cardiac conduction abnormalities or bronchoconstriction. Administration: Use these agents with caution and monitor for conduction problems. Due to the possibility of additive bronchoconstriction, avoid methacholine and any beta-blocker.
Dipyridamole	Beta-Blockers may increase the bradycardic effects.
Disopyramide	Beta-Blockers may increase the bradycardic effects. Disopyramide may have a negative inotropic effect that Beta-Blockers can enhance.
EPINEPHrine (Nasal)	Beta-Blockers (Nonselective), may increase the hypertensive effects of EPINEPHrine.
EPINEPHrine (Oral Inhalation)	Beta-Blockers (Nonselective), may increase the hypertensive effects of EPINEPHrine Oral Inhalation.
Epinephrine (Racemic)	Beta-Blockers (Nonselective), may increase the hypertensive effects of Epinephrine, (Racemic).
EPINEPHrine Systemic	Beta-Blockers (Nonselective), may increase the hypertensive effects of EPINEPHrine Systemic.
Insulins	Beta-Blockers can increase the hypoglycemic effects of Insulins.
Ivabradine	Bradycardia-Causing agents may increase the bradycardic effects of Ivabradine.
Lacosamide	Bradycardia-Causing Agents can increase the AV-blocking effects of Lacosamide.
Lidocaine (Systemic)	Beta-Blockers can increase serum levels of Lidocaine (Systemic).
Lidocaine (Topical)	Beta-Blockers can increase serum Lidocaine (Topical).
Mepivacaine	Beta-Blockers can increase serum levels of Mepivacaine.
Methoxyflurane	May increase the hypotensive effects of Beta-Blockers.
Midodrine	May increase the bradycardic effects of Bradycardia Causing Agents.
NIFEdipine	May increase the hypotensive effects of Beta-Blockers. NIFEdipine could increase the negative inotropic effects of Beta-Blockers.
Nonsteroidal Anti-Inflammatory Drugs	BetaBlockers may have a lower antihypertensive impact.
Opioids (Anilidopiperidine)	Beta-Blockers may increase the bradycardic effects. Anilidopiperidine and other opioids may increase the hypotensive effects of Beta-Blockers.
Regorafenib	Beta-Blockers may increase the bradycardic effects.
Reserpine	May increase the hypotensive effects of Beta-Blockers.
Ruxolitinib	May increase the bradycardic effects of Bradycardia-Causing Agents. Management: Ruxolitinib Canadian product labels recommend that bradycardia-causing agent be avoided to the greatest extent possible.
Sulfonylureas	Beta-Blockers can increase the hypoglycemic effects of sulfonylureas. Nonselective beta blockers may be more dangerous than cardioselective betablockers. As an initial sign of hypoglycemia, all beta-blockers seem to be able to mask tachycardia. Ophthalmic beta blockers are likely to be associated with a lower risk than systemic drugs.
Terlipressin	May increase the bradycardic effects of Bradycardia Causing Agents.
Tofacitinib	May increase the bradycardic effects of Bradycardia Causing Agents.
Risk Factor D (Consider therapy modifications)
Alpha2-Agonists	Beta-Blockers may have an AV-blocking effect that is greater. It is possible to increase the risk of sinus node dysfunction. Beta-Blockers can increase the rebound hypertensive effect Alpha2Agonists. This can happen if the Alpha2-Agonist abruptly withdraws. Treatment: Monitor your heart rate closely while you are taking clonidine and beta blockers. When possible, stop taking beta blockers a few days before you begin clonidine withdrawal. Also, monitor your blood pressure carefully. We do not have any recommendations for alpha2-agonists. Apraclonidine is an exception.
Ceritinib	Bradycardia-Causing agents may increase Ceritinib's bradycardic effects. Management: If the combination is not possible, monitor patients for signs of bradycardia and closely track blood pressure and heart beat during therapy. Separate monographs will discuss exceptions.
Dronedarone	Beta-Blockers may increase bradycardic effects. Dronedarone could increase Beta-Blockers' serum levels. This is likely to be true only for agents that are metabolized via CYP2D6. Management: Lower initial beta-blocker doses are recommended. ECG findings should confirm that the patient is able to tolerate the combination.
Ergot Derivatives	Beta-Blockers can increase the vasoconstricting effects of Ergot Derivatives. Nicergoline is an exception.
Fingolimod	Fingolimod may increase the bradycardic effects of beta-blockers. If possible, avoid the use of beta-blockers and fingolimod together. Patients who require coadministration should be monitored for ECG changes overnight. Patients should be monitored for bradycardia.
Grass Pollen Allergen Extract (5 Grass Extract)	Beta-Blockers could increase the toxic/adverse effect of Grass Pollen Extract (5 Grass) Beta-Blockers can also inhibit the effectiveness of epinephrine to treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract). Other effects of epinephrine might not be affected or even increased by Beta-Blockers.
Siponimod	Bradycardia-Causing Drugs can increase Siponimod's bradycardic effects. Management: Siponimod should not be taken with bradycardia-causing drugs.
Theophylline Derivatives	Beta-Blockers (Nonselective), may decrease the bronchodilatory effects of Theophylline Derivates.
Risk Factor X (Avoid Combination)
Beta2-Agonists	Beta-Blockers (Nonselective), may decrease the bronchodilatory effects of Beta2Agonists.
Floctafenine	Beta-Blockers may have an adverse/toxic effect that can be increased.
Methacholine	Beta-Blockers can increase the toxic/adverse effects of Methacholine.
Rivastigmine	Beta-Blockers may increase the bradycardic effects.

Monitoring parameters:

Monitor the Intraocular pressure, blood pressure, and other systemic effects of beta blockers.

How to administer:

is available for topical ophthalmic use only.
The patient should be advised to wash the hands and avoid touching the dropper tip with any surface including the hands and eyes (to avoid contamination).
Remove contact lenses prior to administration and wait for at least 15 minutes prior to reinserting it.

Mechanism of action of Carteolol:

It blocks both beta 1 and 2 adrenergic receivers. It lowers intraocular pressure by decreasing aqueous humor output and/or increasing the flow of aqueoushumor. The ophthalmic dose contains approximately 25%.absorbedIt is done systemically. It is.MetabolizedThe liver via CYP2D6 has a half-life eliminationMaximum 5 hours TheTime to reach the summitPlasma concentration takes 15 minutes. It isexcretedBy the kidneys.

International brands: