An acquired retinal macroaneurysm (RAM) is a focal, abnormal dilation of a retinal arteriole wall, typically between 100 and 250 μm in diameter, occurring within the first three branch orders of the central retinal arterial tree in the posterior fundus. Unlike microaneurysms, which arise from capillaries and measure 15–100 μm, RAMs involve muscular arterioles and are often associated with arterial wall thinning, hyalinization, and surrounding exudation or hemorrhage due to arteriosclerotic changes. Patients may remain asymptomatic until complications—such as thrombosis, macular edema, or hemorrhage—impair vision, making early identification vital for both ocular and systemic management of underlying vascular risk factors. NCBILippincott Journals
Acquired Retinal Arterial Macroaneurysm (RAM) is an outpouching or focal dilation of a retinal arteriole, most often occurring in elderly patients with systemic vascular disease. These aneurysms measure approximately 100–250 µm in diameter and typically arise within the first three orders of the arterial bifurcation, most commonly along the superotemporal arcade AAOEyeWiki. RAMs can be classified anatomically as fusiform (uniform widening) or saccular (localized outpouching), and clinically as quiescent, hemorrhagic (with bleeding), or exudative (with leakage and edema) EyeWikiPubMed.
Types of Retinal Macroaneurysms
1. Fusiform RAM
A fusiform macroaneurysm features a spindle-shaped dilation that involves a segment of the arteriole uniformly. On fluorescein angiography, it appears as a gradual, elongated bulge along the arterial lumen. Fusiform RAMs tend to have a lower rupture rate than saccular types but can still cause chronic exudation and macular edema if untreated. Lippincott Journals
2. Saccular RAM
Saccular macroaneurysms present as a rounded, sac-like outpouching of the arteriole wall. They are more prone to rupture and hemorrhage—up to 72.7% of saccular lesions show bleeding—due to focal wall weakness. On angiography, they fill quickly and may leak profusely, often necessitating closer monitoring or intervention. Nature
3. Hemorrhagic RAM
Hemorrhagic RAMs are classified by the presence of intra-, sub-, or preretinal bleeding secondary to aneurysm rupture. Blood may accumulate in the macula or vitreous cavity, leading to sudden vision loss. These lesions often require prompt laser photocoagulation or anti-VEGF therapy to manage vision-threatening hemorrhage. Lippincott Journals
4. Exudative RAM
Exudative macroaneurysms leak plasma components—lipids and fluid—into the surrounding retina without frank hemorrhage. This leakage causes chronic macular edema and hard exudate deposition, resulting in gradual, painless vision decline. Optical coherence tomography (OCT) often reveals cystoid spaces and subretinal fluid. Lippincott Journals
5. Quiescent RAM
Quiescent RAMs show neither leakage nor hemorrhage. They are often incidental findings on routine fundoscopy. Although inactive, these lesions warrant periodic surveillance for transformation into hemorrhagic or exudative forms, especially in patients with poorly controlled vascular risk factors. Lippincott Journals
6. Simple vs. Complex RAM
– Simple RAM refers to isolated arterial ectasia without associated hemorrhage or exudation.
– Complex RAM involves additional retinal changes—hemorrhage, exudation, or thrombotic occlusion—requiring more aggressive management. asrs.org
Causes of Acquired Retinal Macroaneurysm
Each of these factors contributes to arteriolar wall weakening or increased hemodynamic stress, predisposing to aneurysmal dilation:
1. Systemic Hypertension
Chronic high blood pressure exerts increased shear stress on retinal arterioles, accelerating arteriosclerotic changes and wall thinning, which facilitate aneurysm formation. Approximately 75% of RAM patients have long-standing hypertension. NCBIPMC
2. Atherosclerosis
Lipid deposition and intimal thickening in retinal arteries compromise vessel wall integrity. Atherosclerotic changes—common in elderly patients—lead to focal wall weakening and aneurysmal dilation at branch points. NCBIScienceDirect
3. Age-Related Vascular Degeneration
Advancing age causes cumulative oxidative damage, reduced elastin content, and increased collagen cross-linking in arterial walls, impairing their resilience and promoting macroaneurysm development. PMC
4. Hyperlipidemia
Elevated serum cholesterol and triglycerides accelerate atherosclerotic plaque formation in retinal arterioles, fostering focal wall weakening and aneurysm risk. NCBINumber Analytics
5. Cardiovascular Disease
Systemic vascular diseases—such as coronary artery disease—reflect widespread arteriosclerosis, including in retinal vessels, predisposing to macroaneurysm formation. NCBIasrs.org
6. Diabetes Mellitus
Although primarily a microvascular disease, chronic hyperglycemia induces basement membrane thickening and pericyte loss in retinal vessels, contributing to abnormal arteriolar remodeling and occasional macroaneurysm formation. Number Analytics
7. Smoking
Tobacco-related oxidative stress and endothelial dysfunction accelerate arteriosclerosis in retinal vessels, increasing the likelihood of focal outpouching and aneurysm formation. Number Analytics
8. Female Gender (Postmenopausal)
Approximately 70% of RAMs occur in women, particularly in their sixth and seventh decades, possibly due to hormonal changes affecting vascular collagen and elastin balance. EyeWikiPMC
9. Genetic Predisposition
Family history of aneurysmal vascular disorders or connective tissue diseases (e.g., Ehlers–Danlos syndrome) may increase the risk of retinal arterial wall fragility. JournalAgent
10. Inflammatory Vasculopathies
Conditions like giant cell arteritis or polyarteritis nodosa cause vessel wall inflammation and destruction, weakening arteriolar structure and promoting aneurysmal dilation. PMC
11. Polycythemia
Elevated hematocrit increases blood viscosity and intraluminal pressure, aggravating shear stress on arterioles and predisposing to aneurysm formation. PMC
12. Coagulation Disorders
Antiphospholipid syndrome or anticoagulant therapy may lead to microthrombi and localized ischemia, impairing arteriolar wall repair mechanisms and resulting in aneurysm. PMC
13. Ocular Trauma
Blunt or penetrating eye injury can directly damage arterial walls, causing focal weakening and subsequent aneurysmal dilation during the healing process. JournalAgent
14. Radiation Retinopathy
Therapeutic radiation to the head or orbit may induce vascular endothelial damage and fibrosis, compromising arteriolar integrity and fostering aneurysm formation years later. JournalAgent
15. Hyperhomocysteinemia
Elevated homocysteine levels promote endothelial dysfunction and smooth muscle cell apoptosis in arterioles, increasing susceptibility to macroaneurysm development. JournalAgent
Symptoms of Retinal Macroaneurysm
Although many RAMs are asymptomatic, the following symptoms may arise when complications occur:
1. Sudden Vision Loss
Rupture-induced hemorrhage into the macula or vitreous can abruptly block the visual axis, causing profound, sudden vision impairment. JournalAgent
2. Blurred or Distorted Vision
Leakage of fluid and lipids into the macula leads to cystoid macular edema and hard exudates, producing blurred central vision and metamorphopsia. JournalAgent
3. Floaters
Preretinal or vitreous hemorrhage may manifest as tiny, moving dark spots in the visual field as red blood cells float within the vitreous gel. JournalAgent
4. Photopsia
Mechanical traction on the retina by blood clots or exudates can cause flashing lights or shimmering sensations, often preceding hemorrhage. JournalAgent
5. Scotomas
Local retinal damage from edema or hemorrhage can create blind spots (scotomas) in the central or peripheral visual field. JournalAgent
6. Micropsia or Macropsia
Distortion of retinal architecture by fluid accumulation may alter the perceived size of objects, making them appear smaller (micropsia) or larger (macropsia). JournalAgent
7. Dyschromatopsia
Macular involvement may transiently impair color discrimination, particularly red–green differentiation. JournalAgent
8. Photophobia
Light sensitivity can accompany retinal irritation from hemorrhage or inflammation around the aneurysm site. JournalAgent
9. Visual Field Defects
Larger hemorrhages or exudative lesions can block segments of the retina, producing quadrant- or hemifield defects. JournalAgent
10. Asymptomatic Findings
Incidentally discovered RAMs during routine exam—without any visual complaints—underscore the importance of fundoscopic screening in at-risk patients. EyeWiki
Diagnostic Tests for Retinal Macroaneurysm
Physical Exam
1. Visual Acuity Test
Standard Snellen or ETDRS charts measure central vision, detecting any reduction caused by macular edema or hemorrhage. EyeWiki
2. Pupillary Light Reflex Examination
Assessment of direct and consensual pupillary responses rules out afferent pathway defects due to macular involvement. EyeWiki
3. Confrontation Visual Field Testing
Gross screening for peripheral field defects helps identify scotomas from large hemorrhages or exudates. EyeWiki
4. Intraocular Pressure Measurement
Tonometry ensures there are no concurrent glaucomatous changes that could complicate management. EyeWiki
Manual Tests
5. Direct Ophthalmoscopy
A handheld ophthalmoscope provides initial identification of arterial dilations, hemorrhages, and exudates. EyeWiki
6. Indirect Ophthalmoscopy
Binocular indirect exam with a condensing lens offers a wider field view to localize peripheral RAMs and assess vitreous hemorrhage. EyeWiki
7. Slit-Lamp Biomicroscopy with Fundus Lens
High-magnification stereo view enables detailed evaluation of aneurysm morphology and surrounding retinal changes. EyeWiki
8. Amsler Grid Test
Patient-performed grid assessment detects metamorphopsia and central scotomas from macular involvement. EyeWiki
Lab and Pathological Tests
9. Complete Blood Count (CBC)
Evaluates for polycythemia or anemia, which can influence blood viscosity and hemorrhagic risk. PMC
10. Lipid Profile
Assesses cholesterol and triglyceride levels to identify hyperlipidemia contributing to arteriosclerosis. NCBI
11. Erythrocyte Sedimentation Rate (ESR) & C-Reactive Protein (CRP)
Markers of systemic inflammation may reveal underlying vasculitides weakening arteriole walls. PMC
12. Coagulation Profile (PT/INR, aPTT)
Detects coagulopathies or effects of anticoagulant therapy that can exacerbate hemorrhage. PMC
Electrodiagnostic Tests
13. Full-Field Electroretinography (ffERG)
Assesses global retinal function; significant changes may occur if widespread edema or hemorrhage affects photoreceptors. EyeWiki
14. Multifocal Electroretinography (mfERG)
Evaluates focal macular function, detecting subtle functional deficits from localized RAM-induced damage. EyeWiki
15. Electrooculography (EOG)
Measures the standing potential between cornea and retina; can indicate generalized retinal pigment epithelium dysfunction. EyeWiki
16. Visual Evoked Potential (VEP)
Assesses optic nerve pathway integrity, ruling out concurrent optic neuropathies in complex cases. EyeWiki
Imaging Tests
17. Fundus Photography
Color imaging documents aneurysm size, location, and hemorrhagic or exudative changes over time. EyeWiki
18. Fundus Fluorescein Angiography (FFA)
Dynamic angiography highlights aneurysm filling patterns, leakage, and capillary non-perfusion. NCBI
19. Indocyanine Green Angiography (ICGA)
Provides deeper choroidal vessel visualization, helping differentiate RAM from choroidal vascular lesions. NCBI
20. Optical Coherence Tomography (OCT)
Cross-sectional imaging reveals macular edema, subretinal fluid, and intraretinal hemorrhage morphology. NCBI
Non-Pharmacological Treatments
In RAM management, non-drug strategies aim to stabilize the lesion, reduce complications, and optimize systemic health.
A. Physiotherapy & Electrotherapy
Transcorneal Electrical Stimulation (TES)
Description: Noninvasive placement of contact-lens electrodes delivering weak electrical currents to the cornea.
Purpose: To promote retinal neuron survival and reduce edema.
Mechanism: Electrical stimulation enhances neurotrophic factor secretion and modulates inflammatory pathways in retinal tissue PMCJournal of Translational Medicine.Periocular Bioelectric Stimulation
Description: Surface electrodes around the orbit deliver pulsed currents.
Purpose: To improve microcirculation in the posterior segment.
Mechanism: Alters endothelial function, increasing nitric oxide release and vasodilation, reducing vessel wall stress Journal of Translational Medicine.Low-Level Light Therapy (LLLT)
Description: Near-infrared light applied externally.
Purpose: Antioxidant and anti-inflammatory effects.
Mechanism: Photobiomodulation enhances mitochondrial function, reducing oxidative stress in retinal cells.Transcutaneous Electrical Nerve Stimulation (TENS)
Description: Noninvasive cutaneous electrodes near the eye.
Purpose: Pain relief for associated headaches and ocular discomfort.
Mechanism: Gate-control of nociceptive signals and endorphin release.Ocular Massage Therapy
Description: Gentle manual pressure on closed eyelids.
Purpose: Promote transient reduction of intraocular pressure and enhance perfusion.
Mechanism: Cyclic compression–release improves microvascular flow.Infrared Diode Laser Reflexotherapy
Description: Low-power laser on orbital acupuncture points.
Purpose: Modulate autonomic regulation.
Mechanism: Neurovascular reflexes improve ocular blood flow.Microcurrent Ocular Stimulation
Description: Microampere currents delivered via eyelid pads.
Purpose: Neuroprotective and anti-edema.
Mechanism: Stimulates retinal glial cells to secrete growth factors.Electro-acupuncture
Description: Acupuncture needles around the orbit with electrical pulses.
Purpose: Vascular regulation and neuroprotection.
Mechanism: Modulates autonomic and neuroimmune responses.Pulsed Electromagnetic Field Therapy (PEMF)
Description: External electromagnetic coils.
Purpose: Reduce inflammation and edema.
Mechanism: Alters ion flux and cellular signaling in retinal vasculature.Vibro-ocular Stimulation
Description: Low-frequency vibration on eyelids.
Purpose: Improve lymphatic drainage of the orbit.
Mechanism: Mechanical stimulation clears interstitial fluid.
B. Exercise Therapies
Aerobic Exercise
Description: Brisk walking, cycling 30 min/day.
Purpose: Blood pressure reduction and vascular health.
Mechanism: Improves endothelial function and systemic hemodynamics AAO.Resistance Training
Description: Light to moderate resistance exercises twice weekly.
Purpose: Enhance circulatory efficiency and metabolic control.
Mechanism: Improves insulin sensitivity and arterial compliance.Isometric Handgrip Exercises
Description: Sustained grip at 30 % maximum strength for 2 min, 4 times/day.
Purpose: Lower resting blood pressure.
Mechanism: Vascular remodeling and autonomic adaptation.Yoga-Based Stretching
Description: Gentle poses focusing on relaxation.
Purpose: Stress reduction and blood pressure control.
Mechanism: Lowers sympathetic tone, reduces vascular resistance.
C. Mind-Body Therapies
Mindfulness Meditation
Description: Guided breathing and visualization for 20 min/day.
Purpose: Stress management to prevent blood pressure spikes.
Mechanism: Reduces cortisol and sympathetic activation.Progressive Muscle Relaxation
Description: Systematic tensing and relaxing of muscle groups.
Purpose: Lower systemic vascular resistance.
Mechanism: Autonomic balance shifts toward parasympathetic dominance.Biofeedback Training
Description: Real-time monitoring of physiological signals (e.g., heart rate).
Purpose: Teach self-regulation to maintain stable blood pressure.
Mechanism: Enhances awareness and voluntary modulation of vascular tone.
D. Educational Self-Management
Home Blood Pressure Monitoring
Description: Twice-daily readings with a validated cuff.
Purpose: Early detection and adjustment of hypertension.
Mechanism: Enables timely medication titration in collaboration with physician.Dietary Sodium Tracking
Description: Logging daily salt intake.
Purpose: Encourage adherence to < 2 g sodium/day.
Mechanism: Reduces volume-mediated blood pressure elevation.Vision Self-Monitoring Diary
Description: Daily record of visual changes (floaters, blur).
Purpose: Prompt early clinical evaluation.
Mechanism: Tracks progression or resolution of symptoms.
Pharmacological Treatments (Drugs)
Below are the 10 most evidence-based pharmacologic agents for RAM, including ocular and systemic medications:
Intravitreal Bevacizumab (Avastin®)
Class: Anti-VEGF monoclonal antibody
Dosage: 1.25 mg/0.05 mL intravitreal injection, monthly for 3 months then as needed BioMed Central.
Administration Time: Office-based injection.
Side Effects: Endophthalmitis, elevated intraocular pressure, vitreous hemorrhage.
Intravitreal Ranibizumab (Lucentis®)
Class: Anti-VEGF Fab fragment
Dosage: 0.5 mg/0.05 mL monthly BioMed Central.
Side Effects: Conjunctival hemorrhage, floaters, IOP rise.
Intravitreal Aflibercept (Eylea®)
Class: VEGF-trap fusion protein
Dosage: 2 mg/0.05 mL every 8 weeks after three monthly loading doses PMC.
Side Effects: Ocular hypertension, endophthalmitis.
Intravitreal Triamcinolone Acetonide (Kenalog®)
Class: Corticosteroid
Dosage: 4 mg/0.1 mL single injection Wikipedia.
Side Effects: Cataract progression, steroid-induced glaucoma.
Dexamethasone Implant (Ozurdex®)
Class: Biodegradable corticosteroid implant
Dosage: 0.7 mg intravitreal implant, repeat every 4–6 months as needed.
Side Effects: IOP elevation, ocular discomfort.
Amlodipine Besylate (Norvasc®)
Class: Dihydropyridine calcium channel blocker
Dosage: 5–10 mg orally once daily MedlinePlus.
Side Effects: Peripheral edema, flushing, palpitations.
Lisinopril (Zestril®)
Class: ACE inhibitor
Dosage: 10–20 mg orally once daily.
Side Effects: Dry cough, hyperkalemia, renal impairment.
Atorvastatin (Lipitor®)
Class: HMG-CoA reductase inhibitor
Dosage: 20–40 mg orally once daily Specialty Vision.
Side Effects: Myalgia, elevated liver enzymes.
Aspirin (Low-Dose)
Class: Antiplatelet agent
Dosage: 75–100 mg orally once daily.
Side Effects: Gastrointestinal bleeding, hemorrhagic stroke risk.
Oral Prednisolone
Class: Systemic corticosteroid
Dosage: 0.5–1 mg/kg/day tapered over 4–6 weeks.
Side Effects: Hyperglycemia, immunosuppression, osteoporosis.
Dietary Molecular Supplements
These 10 supplements support retinal vascular health and may reduce progression of exudation or hemorrhage:
Lutein (5–20 mg/day): A macular carotenoid that filters blue light and is antioxidant Drugs.comHealthline.
Zeaxanthin (2 mg/day): Complements lutein in macular pigment protection WebMDVerywell Health.
Docosahexaenoic Acid (DHA) (500–1000 mg/day): Omega-3 fatty acid; reduces inflammation and supports photoreceptor integrity.
Eicosapentaenoic Acid (EPA) (500 mg/day): Omega-3; modulates inflammatory cytokines.
Vitamin C (500 mg twice daily): Antioxidant; scavenges free radicals in microvasculature.
Vitamin E (400 IU/day): Lipophilic antioxidant protecting cell membranes.
Zinc (80 mg/day): Cofactor for antioxidant enzymes in retina; included in AREDS2 formula Wikipedia.
Copper (2 mg/day): Prevents copper-deficiency anemia in zinc supplementation Wikipedia.
Bilberry Extract (80 mg twice daily): Rich in anthocyanins; improves capillary strength.
Astaxanthin (4 mg/day): Carotenoid with potent antioxidant and anti-inflammatory effects.
Advanced Therapeutics (Drugs)
Emerging or off-label 6 agents in specialized categories:
Alendronate (70 mg weekly): Bisphosphonate; inhibits osteoclasts via apoptosis Mayo ClinicWikipedia.
Zoledronic Acid (5 mg IV annually): Potent bisphosphonate with similar mechanism.
Palucorcel (CNTO 2476): Human umbilical tissue-derived cells, subretinal injection of ~200,000 cells; provides paracrine neurotrophic support PMC.
Autologous Bone-Marrow MSCs: Intravitreal 10 ×10⁶ cells; paracrine secretion of growth factors WJGNet.
Sodium Hyaluronate (Healon®): Intracameral viscoelastic (1 mL); maintains anterior chamber during surgery and may protect endothelium.
MSC-Derived Exosomes: Intravitreal ~50 µg protein; deliver miRNAs and growth factors for retinal repair.
Surgical & Laser Interventions
Indirect Laser Photocoagulation
Procedure: Focal argon laser directed at macroaneurysm with mild burns MDPI.
Benefits: Durable closure of aneurysm, reduces exudation.
Subthreshold Micropulse Laser
Procedure: Low-intensity, high-frequency diode laser pulses.
Benefits: Minimizes collateral retinal damage while reducing edema MDPI.
Pars Plana Vitrectomy with Pneumatic Displacement
Procedure: Core vitrectomy, intravitreal gas injection to displace submacular hemorrhage ResearchGate.
Benefits: Clears hemorrhage, improves visual recovery.
Vitreoretinal Surgical Techniques
Procedure: May include membrane peeling and subretinal injection of tPA.
Benefits: Removes preretinal hemorrhage, prevents fibrosis ResearchGate.
Neodymium:YAG Laser Hyaloidotomy
Procedure: Posterior hyaloidotomy to drain subhyaloid blood.
Benefits: Rapid clearance of premacular hemorrhage.
Prevention Strategies
Tight Blood Pressure Control (< 130/80 mm Hg) reduces RAM formation and rupture AAO.
Dyslipidemia Management with statins to prevent arteriosclerotic progression Specialty Vision.
Avoid Valsalva Maneuvers (heavy lifting, straining) to prevent aneurysm rupture PMC.
Maintain Healthy Diet rich in fruits, vegetables, and omega-3s (Mediterranean style) Verywell Health.
Regular Ophthalmic Examinations annually or with new symptoms for early detection.
Smoking Cessation to improve vascular health.
Weight Management (BMI 18.5–24.9 kg/m²) reduces cardiovascular stress.
Moderate Exercise (≥ 150 min/week) improves endothelial function AAO.
Alcohol Moderation (< 2 drinks/day men, < 1 drink/day women) to avoid blood pressure spikes.
Medication Adherence for antihypertensives, statins, and antiplatelets.
When to See a Doctor
Sudden Vision Loss or central scotoma PubMed.
New Floaters or Flashes indicating possible hemorrhage.
Metamorphopsia (visual distortion).
Persistent Ocular Pain or red eye.
No Improvement in symptoms after 2 weeks of observation.
What to Do & What to Avoid
Do:
Monitor vision daily with an Amsler grid.
Record blood pressure twice daily.
Adhere to prescribed medications.
Maintain a low-salt diet.
Attend all ophthalmology appointments.
Avoid:
Lifting > 10 kg or straining.
Smoking and second-hand smoke.
Unsupervised use of herbal supplements.
Excessive caffeine or alcohol.
Vigorous ocular rubbing.
Frequently Asked Questions
What causes acquired RAM?
Aging-related arteriosclerosis and hypertension weaken vessel walls, leading to focal dilations.Can RAM resolve on its own?
Yes—many quiescent RAMs thrombose and involute spontaneously over weeks to months.Is vision always affected?
No—quiescent RAMs may be asymptomatic; vision loss occurs with macular involvement.How is RAM diagnosed?
Fundus examination, fluorescein angiography, and OCT angiography confirm diagnosis and classification.Is anti-VEGF therapy standard?
Off-label but increasingly used for exudative RAMs threatening the fovea.What are the risks of laser treatment?
Potential for retinal scarring and local rupture if energy is excessive.Can controlling blood pressure reverse RAM?
It prevents new aneurysms and aids involution but does not reverse existing dilation.Are systemic steroids helpful?
Reserved for severe inflammatory complications; risk of side effects must be weighed.Do I need surgery for RAM?
Only for nonresolving hemorrhage or tractional complications; most are managed conservatively.Can supplements prevent RAM?
Antioxidant and vascular-supportive supplements may protect microvasculature but don’t replace blood pressure control.How often should I have eye exams?
At least annually for high-risk patients; sooner with new visual symptoms.Is RAM hereditary?
No clear genetic predisposition; strongly linked to systemic vascular disease.Can exercise worsen RAM?
Mild to moderate exercise is beneficial; avoid heavy straining that provokes Valsalva.What is the prognosis?
Generally good if diagnosed early and managed with blood pressure control; risk of permanent vision loss if macula is involved.Will RAM recur?
New RAMs can develop, especially if hypertension and dyslipidemia remain uncontrolled.
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: July 10, 2025.
