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Acute Closed-angle Glaucoma

Disease Details

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Description: Acute closed-angle glaucoma is a medical emergency in which the drainage angle of the eye becomes suddenly blocked, leading to a rapid increase in intraocular pressure and potential vision loss.
Type: Acute closed-angle glaucoma, also known as acute angle-closure glaucoma, does not typically follow a specific pattern of genetic transmission. However, there can be a familial predisposition, indicating that genetic factors may play a role in an individual's susceptibility to the condition. It is considered a multifactorial disease, where both genetic and environmental factors contribute to its development.
Signs And Symptoms: Open angle glaucoma usually presents with no symptoms early in the course of the disease. However, it may gradually progress to involve difficulties with vision. It usually involves deficits in the peripheral vision followed by central vision loss as the disease progresses, but less commonly it may present as central vision loss or patchy areas of vision loss. On an eye examination, optic nerve changes are seen indicating damage to the optic nerve head (increased cup-to-disc ratio on fundoscopic examination).Acute angle closure glaucoma, a medical emergency due to the risk of impending permanent vision loss, is characterized by sudden ocular pain, seeing halos around lights, red eye, very high intraocular pressure, nausea and vomiting, and suddenly decreased vision. Acute angle closure glaucoma may further present with corneal edema, engorged conjunctival vessels and a fixed and dilated pupil on examination.Opaque specks may occur in the lens in glaucoma, known as glaukomflecken. The word is German, meaning "glaucoma-specks".
Prognosis: In open-angle glaucoma, the typical progression from normal vision to complete blindness takes about 25 years to 70 years without treatment, depending on the method of estimation used. The intraocular pressure can also have an effect, with higher pressures reducing the time until blindness.
Onset: The onset of acute closed-angle glaucoma is typically sudden and can be associated with rapid eye pain, blurred vision, headache, nausea, vomiting, and halos around lights. This condition is a medical emergency and requires immediate treatment to prevent permanent vision loss.
Prevalence: The prevalence of acute closed-angle glaucoma (also known as acute angle-closure glaucoma) varies geographically and demographically. It is more common in populations of East Asian descent and individuals with hyperopia (farsightedness). Acute angle-closure glaucoma is less common than open-angle glaucoma, affecting approximately 0.1% of individuals over 40 years old globally, but rates can be higher in specific high-risk groups.
Epidemiology: As of 2010, there were 44.7 million people in the world with open angle glaucoma. The same year, there were 2.8 million people in the United States with open angle glaucoma. By 2020, the prevalence is projected to increase to 58.6 million worldwide and 3.4 million in the United States.Both internationally and in the United States, glaucoma is the second-leading cause of blindness. Globally, cataracts are a more common cause. Glaucoma is also the leading cause of blindness in African Americans, who have higher rates of primary open-angle glaucoma. Bilateral vision loss can negatively affect mobility and interfere with driving.A meta-analysis published in 2009 found that people with primary open angle glaucoma do not have increased mortality rates, or increased risk of cardiovascular death.
Intractability: Acute closed-angle glaucoma can be considered intractable if not promptly treated, as it can lead to permanent vision loss. Immediate medical intervention is crucial in managing the condition to prevent irreversible damage. However, with timely treatment, including medications and surgical procedures, it can often be managed effectively.
Disease Severity: Acute closed-angle glaucoma is a medical emergency characterized by sudden and severe elevation of intraocular pressure, which can lead to rapid vision loss if not treated promptly. It requires immediate medical intervention to prevent permanent damage to the optic nerve and loss of vision.
Healthcare Professionals: Disease Ontology ID - DOID:13862
Pathophysiology: The main effect of glaucoma is damage to the optic nerve. Eventually, this damage leads to vision loss, which can deteriorate with time. The underlying cause of open-angle glaucoma remains unclear. Several theories exist on its exact etiology. However, the major risk factor for most glaucomas and the focus of treatment is increased intraocular pressure. Intraocular pressure is a function of production of liquid aqueous humor by the ciliary processes of the eye, and its drainage through the trabecular meshwork. Aqueous humor flows from the ciliary processes into the posterior chamber, bounded posteriorly by the lens and the zonules of Zinn, and anteriorly by the iris. It then flows through the pupil of the iris into the anterior chamber, bounded posteriorly by the iris and anteriorly by the cornea.
From here, the trabecular meshwork drains aqueous humor via the scleral venous sinus (Schlemm's canal) into scleral plexuses and general blood circulation.In open/wide-angle glaucoma, flow is reduced through the trabecular meshwork, due to the degeneration and obstruction of the trabecular meshwork, whose original function is to absorb the aqueous humor. Loss of aqueous humor absorption leads to increased resistance and thus a chronic, painless buildup of pressure in the eye.In primary angle closure glaucoma, the iridocorneal angle is narrowed or completely closed obstructing the flow of aqueous humor to the trabecular meshwork for drainage. This is usually due to the forward displacement of the iris against the cornea, resulting in angle closure. This accumulation of aqueous humor causes an acute increase in pressure and damage to the optic nerve.The pathophysiology of glaucoma is not well understood. There are several theories regarding the mechanism of the damage to the optic nerve in glaucoma. The biomechanical theory hypothesizes that the retinal ganglion cell axons (which form the optic nerve head and the retinal nerve fiber layer) are particularly susceptible to mechanical damage from increases in the intraocular pressure as they pass through pores at the lamina cribrosa. Thus increases in intraocular pressure would cause nerve damage as seen in glaucoma. The vascular theory hypothesizes that a decreased blood supply to the retinal ganglions cells leads to nerve damage. This decrease in blood supply may be due to increasing intraocular pressures, and may also be due to systemic hypotension, vasospasm or atherosclerosis. This is supported by evidence that those with low blood pressure, particularly low diastolic blood pressure, are at an increased risk of glaucoma.The primary neurodegeneration theory hypothesizes that a primary neurodegenerative process may be responsible for degeneration at the optic nerve head in glaucoma. This would be consistent with a possible mechanism of normal tension glaucoma (those with open-angle glaucoma with normal eye pressures) and is supported by evidence showing a correlation of glaucoma with Alzheimer's dementia and other causes of cognitive decline.
Both experimental and clinical studies implicate that oxidative stress plays a role in the pathogenesis of open-angle glaucoma as well as in Alzheimer's disease.Degeneration of axons of the retinal ganglion cells (the optic nerve) is a hallmark of glaucoma. The inconsistent relationship of glaucomatous optic neuropathy with increased intraocular pressure has provoked hypotheses and studies on anatomic structure, eye development, nerve compression trauma, optic nerve blood flow, excitatory neurotransmitter, trophic factor, retinal ganglion cell or axon degeneration, glial support cell, immune system, aging mechanisms of neuron loss, and severing of the nerve fibers at the scleral edge.
Carrier Status: Acute closed-angle glaucoma is related to eye anatomy and fluid dynamics rather than genetic inheritance. There is no carrier status for this condition. It occurs when the drainage angle of the eye becomes suddenly blocked, leading to a rapid increase in intraocular pressure. This can cause severe eye pain, blurred vision, headache, and nausea, and requires immediate medical attention to prevent vision loss.
Mechanism: Acute closed-angle glaucoma, also known as acute angle-closure glaucoma, is a medical emergency characterized by a rapid increase in intraocular pressure (IOP) due to a sudden closure of the anterior chamber angle, where the iris meets the cornea. This angle is crucial for aqueous humor to drain out of the eye through the trabecular meshwork. When this angle closes abruptly, the outflow is blocked, leading to a rapid increase in IOP.

### Mechanism
The primary mechanism of acute closed-angle glaucoma involves the displacement of the peripheral iris toward the trabecular meshwork, blocking the drainage of aqueous humor. Factors that can contribute to this displacement include:

1. **Pupillary Block**: When the pupil is mid-dilated, the iris can bunch up and obstruct the flow of aqueous humor from the posterior to the anterior chamber.
2. **Plateau Iris**: A structural abnormality where the ciliary processes push the peripheral iris forward.
3. **Lens-Induced Mechanisms**: Large or anteriorly positioned lens can push the iris forward.

### Molecular Mechanisms
The molecular mechanisms contributing to acute closed-angle glaucoma are less well-defined compared to the anatomical factors, but some molecular factors include:

1. **Genetic Factors**: Mutations and polymorphisms in genes involved in ocular development and structure, such as the MYOC gene and CYP1B1, have been implicated.
2. **Intraocular Pressure Regulation**: Proteins and signaling pathways that regulate aqueous humor production and outflow, including those in the trabecular meshwork, like signaling via transforming growth factor-beta (TGF-β) and matrix metalloproteinases (MMPs), may play roles.
3. **Inflammatory Mediators**: Local inflammation, potentially involving cytokines like interleukins and TNF-alpha, can contribute to changes in the trabecular meshwork and iris, exacerbating angle closure.

Understanding the exact molecular and genetic contributions requires more research, but these factors collectively play a role in the pathogenesis of acute closed-angle glaucoma. Prompt medical intervention is crucial to prevent irreversible vision loss.
Treatment: The modern goal of glaucoma management is to decrease the intraocular pressure (IOP), thus slowing the progression of glaucoma and preserving the quality of life for patients, with minimal side-effects. This requires appropriate diagnostic techniques and follow-up examinations, and judicious selection of treatments for the individual patient. Although IOP is only one of the major risk factors for glaucoma, lowering it via various pharmaceuticals and/or surgical techniques is currently the mainstay of glaucoma treatment.
The IOP should be reduced to a target level at which the disease progression is controlled protecting the visual field and improving life quality. The target level is set individually depending on multiple factors including the pretreatment IOP, the severity and rate of the disease progression, and the side effects of the medications. In general, the target IOP is equal or lower than 18mmHg in mild, 15mmHg in moderate and 12mmHg in severe stage glaucoma. After setting the target IOP, regular follow-up should be done assessing the IOP and the disease progression.
Vascular flow and neurodegenerative theories of glaucomatous optic neuropathy have prompted studies on various neuroprotective therapeutic strategies, including nutritional compounds, some of which may be regarded by clinicians as safe for use now, while others are on trial. Mental stress is also considered as consequence and cause of vision loss which means that stress management training, autogenic training and other techniques to cope with stress can be helpful.
Compassionate Use Treatment: Acute closed-angle glaucoma is a medical emergency requiring immediate treatment. Standard treatment typically includes medications to lower intraocular pressure, such as topical beta-blockers, alpha agonists, and systemic carbonic anhydrase inhibitors. If these are insufficient, intravenous mannitol or oral glycerin may be used.

In terms of compassionate use, off-label, or experimental treatments:

1. **Compassionate Use**: Medications not yet approved for acute closed-angle glaucoma but allowed via compassionate use programs may include investigational drugs currently in clinical trials. These are typically accessed in severe cases where standard treatments have failed.

2. **Off-label Treatments**: Some medications approved for other forms of glaucoma or ocular conditions might be used off-label. Examples include certain prostaglandin analogs or newer carbonic anhydrase inhibitors that are primarily approved for open-angle glaucoma but can be used off-label when necessary.

3. **Experimental Treatments**: Research is ongoing into novel approaches for managing acute closed-angle glaucoma. These may include new pharmacological agents targeting different pathways of intraocular pressure regulation, laser-based procedures, or advanced surgical techniques currently under investigation in clinical trials. However, access to these treatments is generally restricted to clinical trial participants.

Always consult a healthcare provider for specific medical advice and treatment options tailored to individual patient needs.
Lifestyle Recommendations: Here are some lifestyle recommendations for managing acute closed-angle glaucoma:

1. **Regular Eye Exams**: Get regular eye check-ups to monitor eye pressure and overall eye health.
2. **Medications Compliance**: Follow the prescribed treatment plan, including medications and eye drops, to prevent pressure increases.
3. **Adequate Hydration**: Limit the intake of caffeinated beverages that can increase eye pressure.
4. **Healthy Diet**: Eat a diet rich in fruits, vegetables, and omega-3 fatty acids to support overall eye health.
5. **Manage Chronic Conditions**: Keep conditions like diabetes and hypertension under control, as they can affect eye health.
6. **Avoid Certain Activities**: Limit activities that involve straining or lifting heavy weights, which can increase eye pressure.
7. **Protect Your Eyes**: Use protective eyewear in situations that pose a risk to your eyes.
8. **Stress Management**: Practice stress-reduction techniques such as yoga, meditation, or deep-breathing exercises to reduce overall stress levels.
9. **Avoiding Medications**: Certain medications, such as decongestants or some antihistamines, can increase eye pressure; consult your doctor before taking them.

These lifestyle changes can help manage and potentially reduce the risk of acute closed-angle glaucoma progression.
Medication: There are several pressure-lowering medication groups that could be used in lowering the IOP, usually eyedrops. The choice of medication usually depends on the dose, duration and the side effects of each medication. However, in general, prostaglandin analogues are the first-line treatment for glaucoma.Prostaglandin analogues, such as latanoprost, bimatoprost and travoprost, reduce the IOP by increasing the aqueous fluid outflow through the draining angle. It is usually prescribed once daily at night. The systemic side effects of this class are minimal. However, they can cause local side effects including redness of the conjunctiva, change in the iris color and eyelash elongation.There are several other classes of medications that could be used as a second-line in case of treatment failure or presence of contraindications to prostaglandin analogues. These include:

Topical beta-adrenergic receptor antagonists, such as timolol, levobunolol, and betaxolol, decrease aqueous humor production by the epithelium of the ciliary body.
Alpha2-adrenergic agonists, such as brimonidine and apraclonidine, work by a dual mechanism, decreasing aqueous humor production and increasing uveoscleral outflow.
Less-selective alpha agonists, such as epinephrine, decrease aqueous humor production through vasoconstriction of ciliary body blood vessels, useful only in open-angle glaucoma. Epinephrine's mydriatic effect, however, renders it unsuitable for closed-angle glaucoma due to further narrowing of the uveoscleral outflow (i.e. further closure of trabecular meshwork, which is responsible for absorption of aqueous humor).
Miotic agents (parasympathomimetics), such as pilocarpine, work by contraction of the ciliary muscle, opening the trabecular meshwork and allowing increased outflow of the aqueous humour. Echothiophate, an acetylcholinesterase inhibitor, is used in chronic glaucoma.
Carbonic anhydrase inhibitors, such as dorzolamide, brinzolamide, and acetazolamide, lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.Each of these medicines may have local and systemic side effects. Wiping the eye with an absorbent pad after the administration of eye drops may result in fewer adverse effects. Initially, glaucoma drops may reasonably be started in either one or in both eyes.The possible neuroprotective effects of various topical and systemic medications are also being investigated.
Repurposable Drugs: Repurposable drugs for acute closed-angle glaucoma include:

1. **Acetazolamide:** Originally used as a diuretic and for altitude sickness, acetazolamide reduces the production of aqueous humor, thereby decreasing intraocular pressure.
2. **Timolol:** A beta-blocker initially used for hypertension and arrhythmias, timolol reduces intraocular pressure by decreasing aqueous humor production.
3. **Pilocarpine:** Primarily used to treat dry mouth, pilocarpine can constrict the pupil and open the angle in the eye, facilitating aqueous humor outflow.
4. **Glycerol:** Used to reduce intracranial pressure, glycerol can also help lower intraocular pressure by dehydrating the vitreous body.

These medications can provide rapid reduction of intraocular pressure and symptomatic relief in acute closed-angle glaucoma.
Metabolites: Acute closed-angle glaucoma involves a sudden increase in intraocular pressure due to the obstruction of the drainage angle of the eye. Key metabolites involved in ocular processes may include aqueous humor components such as glucose, lactate, and ascorbic acid. Accumulation and imbalance of these substances can affect intraocular pressure mechanisms. However, the term "nan" is not clear in this context and does not pertain to known metabolites or specific measurements in glaucoma.
Nutraceuticals: Nutraceuticals are natural products with potential health benefits or therapeutic effects. No specific nutraceuticals are proven to effectively treat or prevent acute closed-angle glaucoma. Management of this condition primarily involves medical and surgical interventions to lower intraocular pressure and prevent optic nerve damage. Always consult with a healthcare professional for appropriate diagnosis and treatment options.
Peptides: For acute closed-angle glaucoma, peptide-based therapies are not commonly used in clinical practice. Current treatments primarily focus on reducing intraocular pressure (IOP) quickly to prevent optic nerve damage. These treatments include medications such as topical beta-blockers, alpha-agonists, carbonic anhydrase inhibitors, and prostaglandin analogs. In urgent situations, oral or intravenous hyperosmotic agents may be used. There is ongoing research into various therapeutic approaches, including peptides, but they are not standard treatments at this time.