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Corneal Ulcers

CORNEAL ULCERS

Corneal ulcers are open sores or epithelial defects with underlying inflammation on the cornea, the transparent front part of the eye that covers the iris and pupil.

These ulcers are often visible as grey to white opaque or translucent areas on the normally clear cornea. In some cases, they may be too small to detect without adequate magnification.

The cornea is useful in focusing light on the retina and protecting the inner eye structures. Corneal ulcers can be a serious condition leading to vision loss if not treated.

A Cornea ulcer will often appear as a grey to white opaque or translucent area on the normally clear and transparent cornea. Some corneal ulcers may be too small to see without adequate magnification.

Cornea is the structure in front of the eye. The cornea overlies the iris which is the coloured part of the eye and is separated from the iris by the aqueous fluid in the anterior chamber of the eye.

Causes of Corneal Ulcers

Infections:

Bacterial Infections: Commonly caused by bacteria like Staphylococcus and Pseudomonas. These bacteria can invade the cornea, especially if the surface is disrupted. Contact lens wearers are particularly at risk, especially with improper hygiene or prolonged wear.
Viral Infections: Herpes simplex virus (responsible for cold sores) and varicella-zoster virus (causing chickenpox and shingles) can lead to corneal ulcers. These viruses can cause recurrent infections, leading to chronic corneal ulceration.
Fungal Infections: These occur mainly due to improper contact lens care or prolonged use of corticosteroid eye drops. Fusarium and Candida species are common culprits.

Trauma:

Mechanical Injuries: Tiny cuts or scratches from metal, wood, glass, or any particle can damage the cornea, creating an entry point for infection. Even minor injuries can lead to significant complications if not treated properly.
Chemical Burns: Exposure to caustic chemicals or irritants can cause corneal burns, leading to ulceration. Alkali burns (from substances like ammonia or lye) are particularly dangerous because they penetrate deeper into the cornea.

Pre-existing Eye Conditions:

Dry Eye Syndromes: Conditions like keratoconjunctivitis sicca reduce the protective tear film, making the cornea more susceptible to injury and infection.
Eyelid Disorders: Conditions that prevent the eyelid from closing completely, such as Bell’s palsy, can leave the cornea exposed and prone to ulceration. Entropion (inward-turning eyelid) and trichiasis (ingrown eyelashes) can cause constant irritation and lead to ulcer formation.

Immunological Disorders:

Autoimmune Diseases: Conditions like rheumatoid arthritis and lupus can predispose individuals to corneal ulcers, either through direct inflammation or secondary infection. Immune-mediated conditions like scleritis can also contribute to ulcer formation.

Signs and Symptoms of Corneal Ulcers

Redness: The conjunctiva (the white part of the eye) and the anterior chamber may appear red due to dilated blood vessels.
Eye Pain: Ranges from mild to severe, often worsening with bright light exposure (photophobia).
Visual Disturbance: Blurred vision, especially if the ulcer is centrally located.
Tearing and Discharge: Excessive tearing, pus, or thick discharge from the affected eye.
Foreign Body Sensation: A constant feeling that something is in the eye.
Swelling: The eyelids may be swollen, and there may be noticeable edema around the ulcer.
Visible Ulcer: In some cases, a white or grey round spot on the cornea may be visible.

Investigations

Slit Lamp Examination: A slit lamp microscope is used to examine the eye in detail. A fluorescein dye is often applied to highlight the ulcer, making it more visible under blue light.
Microbial Cultures: Swabs or scrapings from the ulcer are sent for microscopy, culture, and sensitivity testing to identify the causative organism and guide treatment.
Corneal Sensitivity Test: This assesses the sensitivity of the cornea, which may be reduced in cases of viral ulcers or chronic conditions.

Management of Corneal Ulcers

Medical Treatment:

Anti-Infective Agents: Antibiotic, antiviral, or antifungal eye drops/ointments are used depending on the cause. For viral ulcers, oral antiviral medications may also be prescribed.
Cycloplegics: These are eye drops like cyclopentolate or atropine, used to dilate the pupil and relieve pain from ciliary muscle spasms.
Steroids: These may be used cautiously to reduce inflammation but only after the infectious cause is under control. They are usually prescribed by an ophthalmologist to avoid worsening the infection.

Surgical Management:

Eyelash Removal: If an ingrown eyelash is causing the ulcer, it may be removed along with its root. Recurrent cases may require electrolysis to destroy the hair follicle.
Eyelid Surgery: In cases where an inward-turning eyelid (entropion) is causing the ulcer, corrective surgery may be necessary.
Corneal Transplant (Keratoplasty): If the ulcer causes significant thinning of the cornea, a corneal transplant may be required to restore the integrity of the eye.

Preventive Measures

Eye Protection: Always wear protective eyewear when working with tools, chemicals, or in environments with flying debris.
Proper Contact Lens Care: Wash hands before handling lenses, avoid using saliva to wet lenses, never use tap water for cleaning, and do not wear lenses overnight unless they are specifically designed for extended wear.
Lubrication: Individuals with dry eyes or incomplete eyelid closure should use artificial tears to keep the cornea moist.
Early Treatment: Seek prompt medical attention for red or irritated eyes that do not improve with over-the-counter drops within 24 hours.

Complications

Corneal Scarring: A healed ulcer may leave a scar, leading to permanent visual impairment if the scar is centrally located.
Secondary Infections: An untreated ulcer can lead to secondary infections, worsening the prognosis.
Corneal Perforation: In severe cases, the ulcer may perforate the cornea, potentially leading to loss of the eye.
Endophthalmitis: This is a severe infection of the interior of the eye, which can result from untreated corneal ulcers.
Blindness: If not treated adequately, corneal ulcers can lead to significant vision loss or complete blindness.

Preventive Measures

Individuals should wear eye protective gears when using power tools or when they may be exposed to small particles that can enter the eye ( like particles from grinding wheel or a weed whacker)
Individuals who have dry eyes or whose lids do not close properly should use artificial teardrops to lubricate the eyes and keep them lubricated.
If an eye is red and irritated and worsens or does not respond to OTC ( Over the counter) eyedrops within a day contact an Ophthalmologist promptly.
People wearing contact lenses should be very careful about the way they clean and wear those lenses.
Always wash hands before handling those lenses.
Never use saliva to lubricate contact lenses because the mouth contains bacteria that can harm the cornea.
Remove lenses from the eyes every evening and clean them.
Never use tap water to clean the lenses
Never sleep with contact lenses not designed for overnight wear in the eyes.
Store lenses in disinfecting solutions overnight.
Remove lenses whenever the eyes are irritated and leave them out until there is no longer any irritation or redness.
Regularly clean the contact lens case, carefully read the instructions about contact lens care supplied by the lens maker, consider using daily disposable lenses.

Nursing Care Plan for Corneal Ulcer

Assessment	Nursing Diagnosis	Goals/Expected Outcomes	Interventions	Rationale	Evaluation
Observation of severe eye pain, redness, tearing, and photophobia	Acute pain related to inflammation and ulceration of the cornea as evidenced by patient verbalizing severe eye pain and sensitivity to light	To reduce eye pain and discomfort within 3 days	– Assess pain level using a pain scale and monitor changes – Administer prescribed analgesics and/or topical anesthetics as ordered – Apply cool compresses to the affected eye to alleviate discomfort – Encourage the patient to rest in a dimly lit room and avoid bright lights	– Pain assessment helps in evaluating the effectiveness of interventions – Analgesics and topical anesthetics help in reducing pain and providing relief – Cool compresses reduce inflammation and soothe the eye – Resting in a dimly lit room minimizes light exposure, reducing photophobia	– Patient reports a decrease in eye pain and discomfort, with less sensitivity to light
Presence of a white or grayish spot on the cornea and purulent discharge	Risk for infection related to bacterial or fungal invasion of the corneal ulcer.	To prevent the spread of infection and promote healing within 1 week	– Administer prescribed antibiotic or antifungal eye drops as ordered – Educate the patient on the importance of completing the full course of medication – Instruct the patient on proper hand hygiene before and after applying eye drops – Avoid the use of contact lenses until the ulcer has healed	– Antibiotics or antifungals are essential for treating the underlying infection and promoting healing – Completing the full course of medication ensures that the infection is fully eradicated – Proper hand hygiene reduces the risk of further contamination and spread of infection – Contact lenses can aggravate the ulcer and hinder healing
Assessment of visual acuity and patient’s ability to perform daily activities	Impaired vision related to corneal ulceration as evidenced by blurred vision and difficulty performing daily activities	To maintain or improve vision and functional ability within 2 weeks	– Perform visual acuity tests to monitor changes in vision – Educate the patient on the need to avoid activities that strain the eyes (e.g., reading, using screens) – Encourage the use of protective eyewear to shield the eye from dust and foreign particles – Arrange for assistance with daily activities as needed	– Visual acuity tests help in tracking the progression of the ulcer and its impact on vision – Avoiding eye strain supports the healing process and reduces discomfort – Protective eyewear prevents further injury and contamination of the affected eye – Assistance with daily activities ensures the patient’s safety and well-being during recovery	– Patient’s vision remains stable or improves, with no significant impairment in performing daily activities
Patient expresses concern about potential vision loss and the appearance of the eye	Anxiety related to fear of vision loss and changes in eye appearance as evidenced by the patient expressing concern about the condition	To reduce anxiety and improve the patient’s understanding of the condition within 1 week	– Provide information about corneal ulcers, their causes, treatment, and prognosis – Reassure the patient that early and appropriate treatment can prevent permanent vision loss – Offer emotional support and encourage the patient to express their fears and concerns – Refer the patient to a support group or counselor if anxiety persists	– Education empowers the patient with knowledge and reduces fear of the unknown – Reassurance helps the patient feel more confident in the treatment process – Emotional support fosters a therapeutic relationship and addresses the patient’s psychological needs – Support groups or counseling can provide additional emotional and psychological support	– Patient reports feeling less anxious and demonstrates understanding of the condition and treatment plan
Assessment of the patient’s adherence to treatment and follow-up care	Knowledge deficit related to unfamiliarity with the treatment regimen and follow-up care as evidenced by the patient asking questions about the medication and care plan	To ensure the patient understands and adheres to the treatment plan within 1 week	– Provide clear, step-by-step instructions on how to administer eye drops and medications – Educate the patient on the importance of attending follow-up appointments – Provide written materials or visual aids to reinforce teaching – Encourage the patient to ask questions and seek clarification about the treatment	– Clear instructions ensure proper medication administration and adherence to the treatment plan – Follow-up appointments are essential for monitoring healing and making necessary adjustments – Written materials or visual aids enhance understanding and retention of information – Encouraging questions ensures that the patient fully understands the treatment and care plan	– Patient demonstrates proper administration of eye drops and expresses confidence in managing the treatment plan

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Glaucoma

GLAUCOMA

Glaucoma is a group of disorder characterized by an abnormally high intraocular pressure , optic nerve dystrophy, and peripheral filed loss. (BRUNNER)

Glaucoma is a group of eye diseases which result in damage to the optic nerve and vision loss due to IOP.

It’s among the common causes of blindness.

Glaucoma occurs as a result of increased intraocular pressure (IOP) caused by a malformation or malfunction of the eyes drainage system.

The main cause of damage to the optic nerve is intraocular pressure (IOP), excessive fluid pressure within the eye, which can be due to various reasons including blockage of drainage ducts, and narrowing or closure of the angle between the iris and cornea.

Normal intraocular pressures average from 12-21 mm Hg. The increased pressure causes compression of the retina and the optic nerve, and causes progressive , permanent loss of eyesight if left untreated.

INCIDENCE

Globally 6 to 67 million.
More common in peoples older than 40 years.

Glaucoma has been called the “silent thief of sight” because the loss of vision usually occurs slowly over a long period of time. Worldwide, glaucoma is the second-leading cause of blindness after cataracts.

EYE ANATOMY ( Click here for eye anatomy)

Normal Pathway of Aqueous Humor

Aqueous fluid Circulation:

The aqueous fluid is a clear fluid produced in the Cilliary body then it will flow out through the Iris, lens, Pupil, Cornea, Anterior Chamber Trabecular Meshwork then to the Schlemm Canal.
The aqueous fluid flows nourishing the cornea and lens.
The eye has an internal fluid circulation system
Fluid is produced at the base of the iris
The fluid flows through the pupil to the front of the iris
The fluid exits the eye at the angle between the iris and the cornea where it drains through a spongy meshwork

The IOP is determined by:

Rate of aqueous production in the ciliary body
Resistance encountered by the aqueous as it flows out of the passages.

Causes/ Aetiology of Glaucoma

Glaucoma is a chronic eye disease that can lead to vision loss and blindness. We have primary causes of glaucoma which refers to the underlying mechanism or condition that directly leads to the development of glaucoma or secondary causes of glaucoma which refer to an underlying condition or factor that contributes to the development of glaucoma.

Primary Causes of Glaucoma:

Increased Eye Pressure: One of the major risk factors for glaucoma is elevated eye pressure. An abnormality in the eye’s drainage system can cause fluid to build up, leading to excessive pressure that damages the optic nerve.
Optic Nerve Damage: Glaucoma develops when the optic nerve becomes damaged. The exact reason for this nerve damage is not fully understood, but it is often related to increased eye pressure.
Fluid Buildup: The fluid inside the eye, known as aqueous humor, may not drain properly due to a malfunction in the drainage system. This can result in a gradual increase in eye pressure, leading to glaucoma.

Secondary Causes of Glaucoma:

Angle-Closure Glaucoma: This form of glaucoma occurs when the iris bulges and partially or completely blocks the drainage angle, preventing fluid circulation and increasing eye pressure.
Normal-Tension Glaucoma: In some cases, optic nerve damage occurs even when eye pressure is within the normal range. The exact cause of this type of glaucoma is unknown, but it may be related to reduced blood flow to the optic nerve.
Glaucoma in Children: Children can be born with glaucoma or develop it in the first few years of life. Blocked drainage, injury, or underlying medical conditions can cause optic nerve damage in children.
Pigmentary Glaucoma: In pigmentary glaucoma, pigment granules from the iris can block or slow fluid drainage from the eye, leading to increased eye pressure.
Inflammation of the Middle Layer of the Eye: Uveitis, which is inflammation of the middle layer of the pigmented vascular eye structure, can lead to uveitic glaucoma

Risk Factors for Glaucoma:

High Internal Eye Pressure: Elevated intraocular pressure is a significant risk factor for glaucoma.
Age: Glaucoma is more common in older adults, especially those over the age of 60.
Ethnicity: Individuals of Black, Asian, or Hispanic heritage have a higher risk of developing glaucoma.
Family History: Glaucoma tends to run in families, so having a close relative with glaucoma increases the risk.
Medical Conditions: Certain medical conditions, such as diabetes, migraines, high blood pressure, and sickle cell anemia, can increase the risk of glaucoma.
Thin Corneas: Having thin corneas is associated with a higher risk of glaucoma.
Extreme Nearsightedness or Farsightedness: Individuals with severe nearsightedness or farsightedness are at an increased risk of developing glaucoma.
Eye Injury or Surgery: Previous eye injuries or certain types of eye surgery can increase the risk of glaucoma.
Long-term Use of Corticosteroid Medications: Taking corticosteroid medicines, especially eye drops, for an extended period can increase the risk of glaucoma.

Pathophysiology of Glaucoma

The underlying cause of open-angle glaucoma remains unclear.

Excess production of aqueous humor, and decreased outflow of aqueous humor, are the key factors in the pathophysiology of glaucoma.

Excess production of aqueous humor can occur, leading to an increase in intraocular pressure. Additionally, there may be a decrease in the outflow of aqueous humor due to blockage or narrowing of the drainage pathways.

The increased intraocular pressure puts pressure on the optic nerve, compromising its blood supply and leading to ischemia. The optic nerve is responsible for transmitting visual information from the eye to the brain. When the optic nerve is damaged, it can result in the loss of vision.

Diagnosis of Glaucoma

Screening for glaucoma is usually performed as part of a standard eye examination performed by optometrists and ophthalmologists.

History taking: Examination for glaucoma also could be assessed with more attention given to sex, race, history of drug use, refraction, inheritance and family history.

Glaucoma tests;

Tonometry: This test measures the intraocular pressure (IOP) within the eye. The examiner will numb the eye with eye drops and then use a tonometer to measure the pressure. This can be done by applying a puff of warm air or using a tiny tool.
Gonioscopy: This test examines the angle where the iris meets the cornea. Eye drops are used to numb the eye, and a hand-held contact lens with a mirror is gently placed on the eye to visualize the angle between the cornea and iris.
Ophthalmoscopy (Dilated Eye Examination): This test examines the shape and color of the optic nerve. Eye drops are used to dilate the pupil, allowing the examiner to use a magnification device with a light to examine the optic nerve
Perimetry (Visual Field Test): This test assesses the complete field of vision. Patient is asked to look straight ahead while a light spot is presented in different areas of the peripheral vision. This helps create a map of the vision.
Pachymetry: This test measures the thickness of the cornea. A pachymeter is gently placed on the front of the eye to measure the corneal thickness. This measurement can help in understanding eye pressure readings.
Nerve Fiber Analysis: Imaging techniques such as optical coherence tomography, scanning laser polarimetry, and scanning laser ophthalmoscopy can be used to assess the thickness of the retinal nerve fiber layer.

Classification of Glaucoma.

Glaucoma has been classified into specific types:

Congenital Glaucoma

Congenital glaucoma is a rare form of glaucoma that is present at birth or develops shortly after birth.

It is characterized by abnormalities in the angle of anterior chamber obstructing the outflow of aqueous humour, leading to increased intraocular pressure and potential damage to the optic nerve.
Congenital glaucoma can manifest at birth ( True Congenital) before 3 years ( Infantile) or between 3-16 years Juvenile).

Clinical Feature of Congenital Glaucoma.

Age of onset: Congenital glaucoma presents in infants and young children, usually before the age of 3 years.
Triad of symptoms: The classic triad of symptoms associated with congenital glaucoma includes :

Watering (epiphora): Excessive tearing or watery eyes.
Photophobia: Sensitivity to light.
Blepharospasm: Involuntary contraction or twitching of the eyelids.

Buphthalmos: Congenital glaucoma can cause enlargement of the eyeball, known as buphthalmos or “ox eye or bull’s eye” . This occurs due to increased intraocular pressure (IOP) and rapid expansion of the eye.
Corneal changes: The elevated IOP in congenital glaucoma can lead to corneal enlargement and clouding. This can result in corneal edema and opacification, which may cause visual impairment.
Haab striae: Horizontal or oblique breaks in Descemet membrane, known as Haab striae, can be seen in congenital glaucoma. These striae are a result of the stretching of the cornea due to increased IOP.
Optic nerve damage: If left untreated or uncontrolled, congenital glaucoma can lead to optic nerve damage. This can result in vision loss.
Variable presentation: The severity and presentation of congenital glaucoma can vary. Some cases may be unilateral (affecting one eye) while others may be bilateral (affecting both eyes).
Blepharospasm (involuntary forceful closure of eyes): In congenital glaucoma, blepharospasm is a common clinical feature that refers to the involuntary and forceful closure of the eyelids.
Excessive lacrimation: Excessive tearing or lacrimation is another common symptom of congenital glaucoma since the increased pressure in the eye can cause the tear ducts to produce more tears than usual.
Enlarged and edematous cornea: The cornea, the clear front part of the eye, can become enlarged and edematous in congenital glaucoma. The increased pressure in the eye can lead to fluid accumulation in the cornea, causing it to swell which can result in cloudiness and opacification of the cornea.
Thin and blue sclera: The sclera, the white outer layer of the eye, may appear thin and blue in congenital glaucoma, due to increased pressure in the eye. The blue color is due to the visibility of the underlying choroid layer through the thin sclera.
Deep anterior chamber: Congenital glaucoma can cause a deepening of the anterior chamber, which is the space between the cornea and the iris. The increased pressure in the eye can push the iris backward, resulting in a deeper anterior chamber.
Flat lens: In congenital glaucoma, the lens of the eye may appear flat. The increased pressure in the eye can affect the shape and position of the lens. This can lead to changes in the focusing ability of the eye.
Optic disc atrophy: Optic disc atrophy, which refers to the degeneration and loss of nerve fibers in the optic disc, can occur in congenital glaucoma. The increased pressure in the eye can cause damage to the optic nerve.

Management of Congenital Glaucoma

The management of congenital glaucoma involves a combination of medical therapy and surgical interventions.

The main Aims of management is to lower intraocular pressure (IOP) and prevent further damage to the optic nerve.

Medical Therapy:

Medical therapy is often used as a temporary measure to control IOP and clear the cornea before surgery.
Medications such as topical beta-blockers like timolol, betaxolol, or prostaglandin analogs, and carbonic anhydrase inhibitors may be prescribed to reduce IOP.

Surgical Interventions:

1. Angle Surgery: The mainstay of treatment for congenital glaucoma is angle surgery, which aims to improve aqueous outflow and lower IOP.

Goniotomy: In this procedure, an incision is made across the trabecular meshwork to improve drainage of aqueous humor.
Trabeculotomy: This surgery involves incising the trabecular meshwork to create a new drainage pathway for aqueous humor.

2. Trabeculectomy: If angle surgery is not successful in controlling IOP, trabeculectomy may be performed. This procedure involves creating a new drainage channel to bypass the trabecular meshwork.

3. Glaucoma Implant Surgery: In cases where other surgical options fail, glaucoma implant surgery may be considered. This involves the placement of a drainage device, such as a Molteno, Baerveldt, or Ahmed implant, to regulate the flow of aqueous humor and lower IOP.

Follow-up and Monitoring:

Regular follow-up visits with an ophthalmologist are essential to monitor IOP, assess the effectiveness of treatment, and detect any potential complications or disease progression.
Ongoing management may involve adjustments to medication dosages, additional surgical interventions if necessary, and monitoring for potential long-term complications such as refractive errors or amblyopia.

ACQUIRED GLAUCOMA

Acquired glaucoma refers to glaucoma that develops later in life due to various factors such as age, genetics, underlying medical conditions, or trauma.

It is a chronic and progressive condition that requires ongoing management to control IOP and preserve vision.

It is further divided into;

PRIMARY GLUCOMA.

Primary Open angle glaucoma.
Primary angle closure Glaucoma
Chronic angle closure glaucoma.

SECONDARY GLAUCOMA

Lens induced glaucoma
Glaucoma due to uveitis
Neurovascular Glaucoma
Glaucoma associated with intraocular tumor
Steroid induced glaucoma.

PRIMARY OPEN-ANGLE GLAUCOMA (POAG)

Primary Open-Angle Glaucoma (POAG) also called as open angle glaucoma or chronic simple glaucoma or simple complex glaucoma results from the overproduction of aqueous humour through trabecular mesh work resulting into increased IOP and damage to optic nerve, resulting into loss of vision.

In this type there in no narrowing of the anterior chamber BUT there is resistance in the trabecular meshwork to aqueous flow resulting in gradual increase in IOP along with cupping of the optic disc and visual fields defects.

Predisposing factors for primary glaucoma include:

Cigarette smoking.
Diabetes Mellitus and Hypertension diseases.
Myopia (nearsightedness).
Old age.

Clinical features of primary glaucoma may include:

Asymptomatic in the early stages.
Mild headache and pain in the eye.
Difficulty in reading.
Delayed dark adaptation.
Alteration in vision sites.
Mild ache in the eyes
Increased IOP ( more than24 mmhg)
Loss of Peripheral vision
Reduced visual acquity at night.
Corneal edema
Visual field deficit.

Investigations for primary glaucoma include:

Tonometry: To measure intraocular pressure (IOP). In glaucoma, IOP may remain permanently high in the late stages and fluctuating in the early stages.
Gonioscopy: To assess the angle of the anterior chamber. Narrowing of the angle may be observed in glaucoma.
Fundus examination: Done with the use of ophthalmoscopy and a slit lamp biomicroscope to look for disc changes.
Perimetry: To assess changes in the visual field.

Treatment options for primary glaucoma include:

Medical treatment: This is the first choice for open-angle glaucoma.

Topical beta blockers: These drugs lower the production of aqueous fluid, thereby reducing IOP. Examples include Timolol mealate: (2.5-5 mg B.D), Betaxolol 25mg B.D, Levabunolol 2.5-5% B.D it has a longer effect
Dorzolamide(2%): It lowers IOP by decreasing the production of aqueous fluid.
Latanoprost(0.5): It decreases the flow of aqueous fluid.
Pilocarpine: It contracts the ciliary muscle and opens the trabecular meshwork, allowing increased outflow of aqueous humor.
Adrenergic group: Drugs like epinephrine hydrochloride decrease aqueous production through vasoconstriction.

Surgical treatment: Surgery is considered when there is a failure to respond to maximal medical therapy.

Laser therapy: Laser trabeculoplasty (ALT) may be performed if the patient does not respond to medical treatment
Filtering surgery: Trabeculectomy is a surgical procedure that creates an opening in the white of the eye to allow fluid to leave the eye.
Drainage tubes: Small tubes may be inserted in the eye to drain excess fluid and lower IOP.
Minimally invasive glaucoma surgery (MIGS): These procedures have less risk and require less postoperative care compared to traditional surgeries

PRIMARY ANGLE CLOSURE GLAUCOMA

Primary angle closure glaucoma, also known as primary closed angle glaucoma, narrow angle glaucoma, pupil block glaucoma, or acute congestive glaucoma, is a type of glaucoma characterized by a rapid onset and is considered an ophthalmic emergency. If not treated promptly, it can lead to blindness within a few days.

It is the type of glaucoma where the IOP is raised due to narrowing of the angle of anterior chamber it is more common in female with nervous personality.

Causes and Risk Factors:

Abnormality of the structures in front of the eyes, resulting in obstruction to the outflow of aqueous humor.
Narrow angle glaucoma due to factors such as a large-sized lens, bigger-sized ciliary body, smaller diameter of the cornea, or a small eyeball.
Anteriorly placed iris.
Hypermetropic eyes (related to far-sightedness).
Precipitating factors: Dim light, Emotional stress/anxiety and Mydriatic drugs like ( atropine, tropicamide, cyclopentolate)

Clinical Features:

The course of the disease can be divided into two types: subacute glaucoma and acute congestive glaucoma.

Subacute Glaucoma:

Gradual onset with transient attacks of blurring vision and mild headache.

Temporary increase in intraocular pressure (IOP) during the attacks, which last for a few seconds to minutes or hours.
Dilated pupils, shallow anterior chamber, and mild corneal edema during the attacks.
Symptoms resolve on their own.

Acute Congestive Glaucoma:

Abrupt increase in IOP due to sudden closure of the anterior chamber.

Symptoms include severe eye pain, defective vision, redness of the eye, photophobia, lacrimation, nausea, and vomiting.
Dilated pupils that are non-reactive to light and edematous optic disc.

Treatment Options:

The main goals of treatment for primary angle closure glaucoma are to prevent progression of angle closure and to control IOP.

Laser Iridotomy:

The conventional treatment for primary angle closure glaucoma is laser iridotomy (LI).
Laser iridotomy eliminates pupillary block and widens the angles by reducing the pressure differential between the anterior and posterior chambers.
Stepped-up standard glaucoma medications may be added if IOP remains high despite laser iridotomy .

“Stepped-up standard glaucoma medications” refers to the progression of treatment options for glaucoma patients that involves starting with the most commonly prescribed and effective medications and then adjusting or adding additional medications if necessary to achieve the desired reduction in intraocular pressure (IOP) and prevent further progression of the disease.

The following are some of the commonly used stepped-up standard glaucoma medications:

Prostaglandin analogs: Prostaglandin analogs, such as latanoprost (Xalatan), are often the first-line treatment choice for glaucoma. They are prescribed as eye drops and work by increasing the outflow of fluid from the eye, thereby reducing IOP.
Beta blockers: Beta blockers, such as timolol (Timoptic) and levobunolol (Betagan), are another class of medications used to treat glaucoma. They reduce IOP by decreasing the production of fluid in the eye. Beta blockers can be nonselective or selective, and they may have side effects such as burning/stinging, blurred vision, and systemic effects like decreased heart rate and bronchospasm.
Miotics: Miotics, such as pilocarpine (Isopto Carpine), work by constricting the pupil and increasing the outflow of fluid from the eye. They can be used as eye drops and may cause side effects such as blurred vision, sweating, and gastrointestinal symptoms.
Carbonic anhydrase inhibitors: Carbonic anhydrase inhibitors, such as dorzolamide (Trusopt) and brinzolamide (Azopt), reduce IOP by decreasing the production of fluid in the eye. They are available as eye drops and may cause side effects such as burning, bitter taste, and ocular allergies.
Sympathomimetics: Sympathomimetics, such as dipivefrin (Propine), work by reducing IOP through various mechanisms, including increasing the outflow of fluid and decreasing its production. They are available as eye drops and may cause side effects such as burning, increased blood pressure, and tremor.
Alpha-2 adrenergic agonists: Alpha-2 adrenergic agonists, such as brimonidine (Alphagan) and apraclonidine (Iopidine), reduce IOP by decreasing the production of fluid and increasing its outflow. They are available as eye drops and may cause side effects such as conjunctival blanching, headache, and drowsiness.

Surgical Options:

Trabeculectomy: Effective for primary angle closure glaucoma, but associated with a higher risk of complications such as filtration failure, shallow anterior chamber, and malignant glaucoma/aqueous misdirection.
Lens Extraction: Lens extraction, either alone or in combination with trabeculectomy, has been shown to significantly increase anterior chamber depth and widen the drainage angle, leading to IOP reduction.
Clear lens extraction (CLE) has been found to be highly effective in reducing IOP and improving quality of life in angle-closure glaucoma patients.
Phacoemulsification alone or combined with trabeculectomy may be considered depending on the patient’s condition.

CHRONIC CLOSED-ANGLE GLAUCOMA

Chronic closed-angle glaucoma is a condition characterized by elevated intraocular pressure (IOP) and damage to the optic nerve.

When this angle is narrowed or closed, pressure increases over time, causing damage to the optic nerve and leading to blindness. This will lead to Absolute Glaucoma.

Treatment Options for Chronic Closed-Angle Glaucoma:

Medical Therapy; This is used to lower the IOP in emergency cases as a temporary measure before surgery

This includes:

Parenteral analgesic to relieve pain
IV Mannitol and Acetazolamide 250mg TDS to lower IOP
Pilocarpine eye drops (2%) instilled every 30 minutes for 2 hours later hourly
Eye drops may include Beta blockers like Timolol mealate (5%) BD, prostaglandin analogs, alpha agonists, carbonic anhydrase inhibitors, or a combination of these medications.
Corticosteroid eye drops to reduce inflammation

Surgery:

Laser Iridotomy: In chronic closed-angle glaucoma, laser iridotomy is often performed to reopen the blocked drainage angle. This procedure involves creating a small hole in the iris to allow the fluid to flow freely and reduce IOP.
Trabeculectomy: Trabeculectomy is a surgical procedure that creates a new drainage channel to lower IOP. It involves creating a small flap in the sclera (white part of the eye) to allow the fluid to drain out.
Glaucoma Drainage Device: In some cases, a glaucoma drainage device, also known as a tube shunt, may be implanted to help drain the excess fluid and reduce IOP.
Cyclophotocoagulation: Cyclophotocoagulation is a laser procedure that targets the ciliary body, which produces the fluid in the eye. By reducing the production of fluid, it helps lower IO.

Absolute glaucoma

Absolute glaucoma is the final stage or end stage of all types of glaucoma, characterized by permanent vision loss or blindness due to increased intraocular pressure.

The eye has no vision, absence of pupillary light reflex and pupillary response, and has a stony appearance. Severe pain is present in the eye. The primary focus of treatment for absolute glaucoma is to reduce pain and keep the eye comfortable.

The treatment of absolute glaucoma is a destructive procedure like

Risk factors:

Include elevated intraocular pressure, IOP fluctuation, male gender, pseudoexfoliation syndrome, worsening visual fields, optic disc hemorrhage, migraine, systemic diseases (hypertension, diabetes, myopia), and low socioeconomic status.

Causes:

Absolute glaucoma can occur due to various reasons, including uncontrolled raised ocular pressure, non-compliance with glaucoma medication, trauma, intraocular surgery (especially cataract extraction), and association with certain syndromes like aniridia, Lowe syndrome, or Sturge-Weber syndrome.

Symptoms:

In the final stage of glaucoma, patients may experience severe eye pain, a stone-like appearance of the eye, tearing, photophobia, lost pupillary reflex, and no pupillary response.

In absolute glaucoma :

The pain can be relieved by retrobulbular injection of alcohol.
The IOP may be reduced by destroying the ciliary epithelium by cryphotocoagulation.
If the pain is not relieved by the conservative approaches then the painful blind eye is enucleated.

SECONDARY GLAUCOMA

Secondary glaucoma is a type of glaucoma that occurs as a result of underlying diseases or conditions within the eyes.

It can be caused by various factors such as uveitis (inflammation), trauma, intraocular hemorrhage, previous surgeries, diabetes, and the use of steroid medications.

Types of Secondary Glaucoma

Lens-induced glaucoma: This type of glaucoma occurs due to trabecular blockage caused by the lens. It can happen when the lens material clogs the trabeculae, leading to increased intraocular pressure (IOP).
Glaucoma due to uveitis: Inflammation associated with uveitis can lead to increased IOP. The inflammatory material can clog the trabecular meshwork and cause trabeculitis, resulting in elevated pressure within the eye.
Neurovascular glaucoma: This is a less common type of glaucoma that is difficult to treat. It is caused by proliferative diabetic retinopathy, which affects the blood flow to the eyes. Individuals with poor blood flow to the eyes are at a higher risk of developing this condition.
Glaucoma associated with intraocular tumors: Intraocular tumors, such as retinoblastoma and malignant melanoma, can cause an increase in IOP.
Steroid-induced glaucoma: Some individuals may develop glaucoma as a result of sensitivity to steroid medications. Sudden rises in IOP can occur, but appropriate use of steroids can help prevent this.
Pigmentary glaucoma: This is a rare condition where pigment cells slough off from the back of the iris and float around in the aqueous humor. It can lead to increased IOP.

Treatment of secondary glaucoma depends on the underlying cause and may involve a combination of medical management, laser therapy, or surgical intervention.

Nursing care for patients with glaucoma

Recognize and assess signs and symptoms of glaucoma.
Monitor intraocular pressure (IOP) and optic nerve function.
Administer prescribed medications, such as eye drops, to manage intraocular pressure.
Educate patients about glaucoma, including risk factors, treatment options, and the importance of regular eye exams.
Provide support and guidance on strategies to optimize eye health and prevent disease progression.
Coordinate referrals to ophthalmologists or glaucoma specialists for further evaluation and management.
Offer emotional support and counseling to patients adjusting to the diagnosis of glaucoma.
Assess for gradual loss of peripheral vision.
Monitor for increased intraocular pressure.
Assess for blurred or hazy vision, halos around lights, vision loss, headaches, or eye strain.
Implement measures to assist patients in managing visual limitations, such as reducing clutter, arranging furniture out of the travel path, and correcting for dim light and problems of night vision.
Demonstrate administration of eye drops, including counting drops, adhering to the schedule, and not missing doses.
Assist with the administration of medications as indicated, such as topical myotic drugs or other prescribed medications.
Provide sedation and analgesics as necessary, especially during acute glaucoma attacks associated with sudden pain.

Nursing Diagnosis for Glaucoma.

Impaired Visual Sensory Perception related to increased intraocular pressure and optic nerve damage.

Assess the patient’s visual acuity and field.
Monitor for changes in visual perception.
Provide education on strategies to optimize visual function.

Risk for Injury related to visual impairment and decreased peripheral vision.

Assess the patient’s mobility and safety awareness.
Implement measures to reduce environmental hazards.
Educate the patient on fall prevention strategies.

Anxiety related to the fear of vision loss and the chronic nature of the disease as evidenced by patient asking alot of questions about the diagnosis.

Assess the patient’s anxiety level and coping mechanisms.
Provide emotional support and counseling.
Teach relaxation techniques to help manage anxiety.

Deficient Knowledge related to glaucoma diagnosis and treatment as evidenced by the patient asking alot of questions.

Assess the patient’s understanding of glaucoma.
Provide education on the disease process, treatment options, and the importance of regular eye exams.
Encourage the patient to ask questions and clarify any misconceptions.

Noncompliance related to difficulty adhering to medication regimen as evidenced by the patient verbalizing problems in eye drop self administration.

Assess the patient’s understanding of the prescribed medications.
Identify barriers to medication adherence.
Provide education on the importance of medication compliance and strategies to improve adherence.

Disturbed Body Image related to changes in visual appearance and functional limitations as evidenced by the patient wearing black glasses.

Assess the patient’s perception of body image and self-esteem.
Provide emotional support and counseling.
Encourage the patient to express feelings and concerns about body image changes.

Preventive measures for glaucoma

Regular Eye Exams: Schedule regular comprehensive eye exams, especially if you are at a higher risk for glaucoma. Early detection and treatment can help prevent vision loss.
Medication Adherence: If you have been diagnosed with glaucoma or are at risk, it is important to take prescribed medications as directed by your healthcare provider. These medications help in reducing intraocular pressure and preventing further damage to the optic nerve.
Know Your Risk Factors: Be aware of the risk factors associated with glaucoma, such as age, family history, race (African Americans are at higher risk), and certain medical conditions like diabetes. If you fall into any high-risk category, it is important to be vigilant and take appropriate preventive measures.
Lifestyle Modifications:

Healthy Diet: Include a diet rich in leafy green vegetables, colored fruits, berries, and vegetables. These foods contain vitamins and minerals that are beneficial for eye health.
Regular Exercise: Engage in regular exercise at a moderate pace, as it can help lower eye pressure and improve overall health. However, avoid intense exercises that significantly raise your heart rate, as they may increase eye pressure.
Eye Protection: Wear protective eyewear during sports or activities that may pose a risk of eye injury.
Avoid Head-down Positions: If you have glaucoma or are at high risk, avoid prolonged head-down positions, as they can significantly raise eye pressure.
Sleep Position: Avoid sleeping with your eye against the pillow or on your arm, especially if you have obstructive sleep apnea (OSA), as it may increase the risk or severity of glaucoma.
Sun Protection: Wear quality polarized sunglasses and a hat to protect your eyes from harmful UV rays.
Oral Hygiene: Maintain good oral hygiene by brushing and flossing your teeth regularly, as there may be a link between gum disease and optic nerve damage in glaucoma.
Blood Pressure Management: Inform your ophthalmologist about your blood pressure medication, as low blood pressure during sleep can worsen glaucoma damage.

Complications of glaucoma

Vision Loss: Glaucoma can cause gradual and irreversible vision loss, starting with peripheral vision and eventually affecting central vision.
Blindness: If left untreated or poorly managed, glaucoma can lead to permanent blindness. It is one of the leading causes of irreversible blindness worldwide.
Optic Nerve Damage: Glaucoma causes damage to the optic nerve, which is responsible for transmitting visual information from the eye to the brain. This damage can result in permanent vision impairment.
Increased Intraocular Pressure: Elevated intraocular pressure can cause discomfort, pain, and headaches. It can also lead to corneal damage and changes in the shape of the eye.
Secondary Cataracts: Some types of glaucoma, such as angle-closure glaucoma, can lead to the development of secondary cataracts.
Macular Edema: In some cases, glaucoma can lead to macular edema, which is the accumulation of fluid in the macula, the central part of the retina. This can cause blurred or distorted central vision.
Visual Field Defects: Glaucoma can result in the loss of peripheral vision, leading to blind spots and difficulty with activities such as driving or navigating crowded spaces.
Corneal Damage: Increased intraocular pressure can cause corneal thinning and damage, leading to vision disturbances and discomfort.
Emotional and Psychological Impact: Glaucoma can have a significant emotional and psychological impact on individuals, causing anxiety, depression, and a decreased quality of life.

Glaucoma Read More »

Eye Trauma

Eye Trauma (Ocular Trauma)

Eye trauma is an injury to the eye that may result in visual impairment.

Ocular trauma refers to any injury to the eye or its surrounding structures caused by physical, chemical, thermal, or radiation agents.

It can range from minor irritations to severe injuries affecting vision or structural integrity. Commonly injured structures include the cornea, sclera, lens, retina, vitreous, optic nerve, and orbital tissues.

Types of eye injuries

Corneal Abrasions: A corneal abrasion is a scratch or injury to the cornea, the clear, dome-shaped surface that covers the front of the eye.
Chemical burns: Chemical burns occur when the child gets any type of chemical in his or her eye. Chemical burns are a medical emergency, and your child should receive immediate medical care. Chemical burns can result in a loss of vision and even a loss of the eye itself, if not treated promptly and accurately. Household cleaning agents are a common cause of this type of injury.
Hyphemia: This refers to blood in the anterior chamber of the eye. The anterior chamber is the front section of the eye’s interior where fluid flows in and out, providing nourishment to the eye and surrounding tissues. A hyphema is usually caused by an injury to the eye, and blood is seen in the eyeball. This is a medical emergency, and immediate medical care is necessary.
Bruising or Black Eye (Ecchymosis): Ecchymosis, more commonly known as a “black eye,” usually occurs from some type of injury to the eye, causing the tissue around the eye to become bruised.
Fractures of the orbit: The orbit is the bony structure around the eye. When one or more bones surrounding the eye are broken, the condition is called orbital fracture. An orbital fracture usually occurs after some type of injury or a strike to the face. Depending on where the fracture is located, it can be associated with severe eye injury and damage.
Eyelid lacerations: Eyelid lacerations are cuts to the eyelid caused by injury. The physician will examine the eye closely to make sure there is no damage to the eye itself.
Foreign bodies. Click here for more on foreign bodies of the eyes

Corneal Abrasion

Corneal abrasion is defined as a superficial injury that disrupts the integrity of the corneal epithelium, typically caused by trauma, physical irritation, or external mechanical forces.

Corneal abrasion is one of the most frequent types of eye injuries and can result from various causes. Although most cases heal rapidly without long-term effects, deeper injuries can lead to complications such as facet formation or stromal scarring, which may impair vision.

Causes of Corneal Abrasion

Corneal abrasions occur when the corneal surface is physically scraped or disrupted. The following are common causes:

Contact Lenses: Prolonged use, improper fit, or poor hygiene can irritate the cornea, causing abrasions.
Eyelashes: Misaligned (trichiasis) or ingrown eyelashes can repeatedly rub against the cornea.
Foreign Bodies: Small objects such as dust, dirt, sand, or metal fragments can scratch the cornea when lodged under the eyelid.
Eye Surface Dryness: Dehydration of the corneal surface due to poor tear production or exposure to wind can predispose to abrasion.
Chemical Irritants: Exposure to chemicals like cleaning agents or fumes may lead to epithelial disruption, increasing the risk of abrasion.

Signs and Symptoms

Corneal abrasion presents with noticeable symptoms that may significantly affect a patient’s comfort and ability to keep the eye open. These include:

Photophobia: Sensitivity to light, causing reluctance to open the affected eye.
Excessive Tearing: Reflex tearing occurs due to irritation and stimulation of the lacrimal glands.
Severe Eye Pain: The cornea is highly innervated, so even small abrasions cause significant discomfort.
Redness (Conjunctival Injection): Inflammation of the conjunctiva due to irritation or injury.
Blurred Vision: If the abrasion affects the visual axis, it may temporarily interfere with clarity of vision.

Clinical Diagnosis

History Taking: A detailed history is essential to identify the cause and assess risk factors, such as:

Use of contact lenses.
Exposure to environmental irritants (e.g., debris, chemicals).
Past history of similar episodes or underlying eye conditions.
Any known drug allergies.

Examination:

Record Visual Acuity: Test both eyes separately to assess the extent of visual impairment.
Use of Slit Lamp: Employ a slit lamp for high magnification to examine the corneal surface for epithelial defects. Fluorescein staining may be applied to highlight the abrasion under cobalt blue light.
Check for Discharge: Evaluate the eye for signs of infection, such as purulent discharge.
Rule Out Foreign Bodies: Carefully evert the eyelids and inspect for retained debris or lashes causing irritation.

Management of Corneal Abrasion

Treatment aims to promote healing, reduce pain, and prevent infection.

Antibiotic Prophylaxis:

Apply Chloramphenicol Eye Ointment:

Dosage: Twice daily for 5 days.
Purpose: Prevent bacterial infection during the healing process.

Alternatives: Fusidic acid or fluoroquinolone eye drops for contact lens-related abrasions.

Cycloplegic Eye Drops:

Administer Cyclopentolate (1%):

Use one drop if the patient experiences photophobia.
Purpose: Relieves pain by paralyzing the ciliary muscle and reducing spasm.

Pain Management:

Prescribe oral or topical analgesics for severe discomfort.
Avoid over-the-counter anesthetic eye drops, as they delay healing and mask symptoms.

Foreign Body Removal:

If a foreign object is present, gently remove it using sterile instruments or irrigation.

Follow-Up:

Patients should return for reassessment if symptoms persist beyond 48 hours or worsen, as deeper corneal injuries or infections may require additional interventions.

Chemical Burns

Chemical burns are serious ocular injuries caused by the exposure of the eye to harmful chemicals, which can damage the cornea, conjunctiva, and deeper ocular structures.

They are often considered ophthalmic emergencies requiring immediate attention to minimize vision loss. Depending on the type and extent of exposure, chemical burns can range from minor irritation to extensive tissue damage, including permanent scarring and blindness.

Types of Chemical Burns

Chemical burns can be broadly classified based on the nature of the chemical agent involved:

1. Alkali Burns:

Alkalis (e.g., ammonia, lime, lye, bleach) cause more severe injuries as they penetrate tissues rapidly, leading to extensive damage.
They saponify cell membranes and dissolve the stroma, resulting in deeper penetration.
Common sources: Cleaning agents, fertilizers, cement, and industrial chemicals.

2. Acid Burns:

Acids (e.g., sulfuric acid, hydrochloric acid, nitric acid) tend to cause coagulative necrosis, forming a barrier that limits further penetration.
The damage is usually less severe than alkali burns but still can result in significant ocular injury.
Common sources: Car batteries, glass polishing solutions, and chemical labs.

3. Irritants:

Substances such as detergents or pepper spray may cause irritation without penetrating tissues deeply.
The damage is commonly superficial but can be painful and temporarily debilitating.

Causes of Chemical Burns

Chemical burns are typically caused by exposure to industrial, household, or agricultural chemicals. Common sources include:

Household Cleaners: Ammonia-based cleaners, drain cleaners, and bleach are common culprits.
Industrial Chemicals: Cement, fertilizers, solvents, and laboratory chemicals pose occupational hazards.
Accidents: Splashes from car batteries or exposure to acid-based solutions during industrial processes.
Self-Harm or Assault: Intentional chemical exposure, often involving strong acids or alkalis.
Chemical Weapons: Tear gas, pepper spray, and other irritants used in law enforcement or conflicts.

Signs and Symptoms

Chemical burns to the eye present with symptoms that depend on the type, concentration, and duration of exposure to the chemical. Common signs and symptoms include:

Immediate Pain: Severe burning sensation and discomfort.
Photophobia: Sensitivity to light due to corneal irritation.
Tearing (Epiphora): Reflex tearing to flush out the chemical irritant.
Redness (Conjunctival Injection): Intense redness due to inflammation and vascular dilation.
Blurred Vision: Corneal edema or damage can interfere with vision clarity.
Swelling: Swelling of the eyelids (chemosis) and conjunctiva.
Corneal Haze or Opacity: Indicative of stromal damage, which is more common in alkali burns.
Severe Cases: Ischemia (whitening of the conjunctiva), perforation, or loss of corneal integrity.

Management of Chemical Burns

Chemical burns require immediate intervention to prevent irreversible damage. Treatment includes the following steps:

1. Immediate Irrigation:

Goal: Dilute and remove the chemical as quickly as possible.
Flush the eye thoroughly with copious amounts of water, saline, or Ringer’s lactate for at least 15-30 minutes.
Use an irrigation device (e.g., Morgan lens) if available.
Ensure eyelids are fully everted to remove any trapped chemical or debris.
Alkali Burns: Continue irrigation longer as they penetrate more deeply.

2. History Taking:

Identify the chemical agent if possible (e.g., safety data sheets, packaging).
Ask about the time of exposure and initial management attempts.

3. Assessment of pH:

Use pH paper to assess the tear film after irrigation.
Normal pH is 7.0-7.4; continue irrigation until pH normalizes.

4. Comprehensive Examination:

Visual Acuity: Test both eyes separately to document baseline vision.
Slit Lamp Examination: Assess corneal integrity, conjunctival damage, and anterior chamber involvement. Apply fluorescein dye to detect epithelial defects.
Eyelid and Conjunctiva: Check for burns, ischemia, or necrosis.

5. Medical Management:

Topical Antibiotics: Apply Chloramphenicol or Ciprofloxacin eye drops to prevent secondary infection.
Cycloplegic Drops: Administer Cyclopentolate (1%) or Atropine (1%) to relieve ciliary spasm and reduce pain.
Topical Steroids: Use cautiously to minimize inflammation but avoid long-term use as it may delay epithelial healing.
Artificial Tears: Provide lubrication to promote epithelial regeneration and comfort.
Ascorbic Acid and Citric Acid: Administered to promote collagen synthesis and minimize corneal ulceration.
Tetracycline or Doxycycline: May be prescribed to inhibit collagenase activity and prevent corneal melting.

6. Surgical Management: For severe cases, surgical intervention may be required:

Debridement: Removal of necrotic tissue to facilitate healing.
Amniotic Membrane Grafts: Promote epithelial recovery in severe damage.
Limbal Stem Cell Transplantation: Necessary for extensive limbal ischemia.

7. Follow-Up: Monitor the patient regularly for complications such as:

Persistent epithelial defects.
Corneal ulcers or thinning.
Secondary infections or glaucoma.

Penetrating Eye Trauma

Penetrating eye trauma is a severe ocular injury where an object pierces the eye, resulting in a full-thickness wound to the cornea, sclera, or both. This type of trauma often involves a high risk of vision loss, infection, and other complications if not treated promptly. It is a true ophthalmic emergency requiring immediate assessment and intervention.

Definition and Key Features

Penetrating Eye Trauma: A full-thickness injury caused by a sharp or high-velocity object that creates a single-entry wound.
Distinguished from perforating trauma, where there are both entry and exit wounds.
Commonly associated with other ocular injuries such as lens damage, vitreous hemorrhage, or retinal detachment.

Common Causes of Penetrating Eye Trauma

Penetrating eye injuries often result from accidents, occupational hazards, or violent incidents. Typical causes include:

Sharp Objects: Knives, scissors, needles, or glass shards.
High-Velocity Projectiles: Metal fragments, nails, or bullets.
Industrial or Construction Accidents: Tools like drills or saws, especially in environments without protective eyewear.
Agricultural Work: Injuries from sharp plant material or equipment in farming.
Assault or Violence: Stabbing or intentional harm.
Household Incidents: Injuries caused by mishandling tools or broken objects.

Signs and Symptoms

Penetrating eye trauma presents with distinctive signs and symptoms that require urgent medical attention:

Pain: Severe, acute pain in the affected eye.
Vision Loss: Blurred vision, reduced visual acuity, or complete loss of vision, depending on the injury’s severity.
Visible Wound: Laceration or puncture site visible on the cornea or sclera.
Protrusion of Internal Structures: Uveal prolapse (iris or ciliary body visible outside the wound).
Hyphema: Blood pooling in the anterior chamber.
Vitreous Hemorrhage: Blood in the vitreous humor, often causing visual obscuration.
Decreased Intraocular Pressure (IOP): Often due to globe rupture or leakage of intraocular contents.
Signs of Foreign Body: Visible or detected foreign object within the eye or orbit.
Eye Misalignment: Strabismus or restricted movement due to injury to extraocular muscles.
Seidel’s Test Positive: Fluorescein dye leak indicating aqueous humor leakage.

Management of Penetrating Eye Trauma

Penetrating eye trauma is a medical emergency, requiring immediate and meticulous management to prevent complications.

1. First Aid at the Scene:

Avoid Eye Manipulation: Do not attempt to remove the foreign object or apply pressure to the injured eye.
Protect the Eye: Shield the eye with a rigid eye shield (e.g., a plastic cup) to prevent further injury.
Do Not Instill Drops: Avoid placing any medications or liquids until assessed by a specialist.
Prompt Transport: Arrange for immediate transfer to a healthcare facility specializing in eye trauma.

2. History and Examination:

History Taking:

Mechanism of injury, time of occurrence, and presence of a foreign body.
Assess tetanus vaccination status.

Examination:

Record visual acuity in both eyes before intervention.
Use a slit lamp to assess the anterior segment, if possible.
Perform a Seidel’s test to check for aqueous leakage.

Avoid Pressure on the Eye:

Do not press the globe while examining.

3. Imaging:

X-ray or CT Scan:

To detect and localize intraocular or orbital foreign bodies.
Preferred imaging modality: CT scan (without contrast) to visualize metallic or radiopaque objects.

Ultrasound (B-scan):

For posterior segment evaluation, only if globe rupture is ruled out.

4. Medical Management:

Antibiotics: Administer systemic antibiotics (e.g., cefazolin + ciprofloxacin) to prevent endophthalmitis.
Tetanus Prophylaxis: Provide tetanus immunoglobulin or booster based on the patient’s vaccination history.
Pain Relief: Systemic analgesics for pain management.
Cycloplegics: Cyclopentolate or atropine drops to reduce ciliary spasm and pain.
Avoid Topical Steroids: Steroids are contraindicated until epithelial healing begins.

5. Surgical Intervention: Surgical repair is essential for restoring ocular integrity and function:

Wound Closure: Repair corneal or scleral lacerations using sutures.
Removal of Foreign Body: Extract intraocular foreign bodies via pars plana vitrectomy or other techniques.
Addressing Secondary Injuries: Treat associated injuries like lens damage, retinal detachment, or hemorrhage.
Vitrectomy: Indicated in cases of vitreous hemorrhage or retinal injury.
Enucleation (if necessary): In severe, irreparable cases, to prevent sympathetic ophthalmia or infection.

6. Postoperative Care: Close monitoring for complications:

Endophthalmitis: Intraocular infection requiring aggressive treatment.
Glaucoma: Secondary increase in intraocular pressure.
Retinal Detachment: Delayed complication requiring surgical repair.

7. Follow-up: Regular follow-up to assess visual recovery and detect late sequelae.

Complications of Penetrating Eye Trauma

Endophthalmitis: Severe, sight-threatening intraocular infection.
Retinal Detachment: Due to posterior segment injury.
Sympathetic Ophthalmia: Autoimmune reaction affecting the uninjured eye.
Corneal or Scleral Scarring: Permanent scarring leading to visual impairment.
Globe Rupture: Extensive damage causing loss of globe integrity.
Blindness: Permanent vision loss if damage is extensive or complications arise.

Prevention

Protective Eyewear: Essential in high-risk environments such as construction, manufacturing, or sports.
Safety Protocols: Adherence to workplace safety guidelines to minimize risks.
Public Awareness: Education on the importance of eye safety and early medical intervention.

Blunt Trauma to the Eye

Blunt trauma to the eye refers to injuries caused by a non-penetrating force that impacts the eye and surrounding structures.

It is a common type of ocular trauma resulting from direct blows, sudden acceleration or deceleration forces, or high-energy impacts. These injuries can range from mild to severe, potentially leading to vision-threatening complications if not promptly addressed.

Definition and Mechanism of Injury

Blunt Trauma: Non-penetrating injuries caused by a forceful impact to the eye, leading to compression and sudden deformation of the globe.

The trauma can result in:

Anterior Segment Injuries: Corneal abrasions, hyphema, and lens dislocation.
Posterior Segment Injuries: Retinal detachment, choroidal rupture, and optic nerve damage.
Orbital Injuries: Fractures or damage to adjacent structures like the eyelids or lacrimal apparatus.

Common Causes of Blunt Eye Trauma

Sports Injuries: Injuries from balls (e.g., basketball, baseball), racquets, or physical contact in contact sports.
Assaults: Fists, punches, or other blunt objects during physical altercations.
Motor Vehicle Accidents: Airbag deployment, dashboard impact, or windshield collision.
Falls: Impact with hard surfaces during slips or falls.
Industrial Accidents: Blows from heavy machinery or tools without proper eye protection.
Explosive Blasts: Resulting from the shockwave of an explosion.

Signs and Symptoms

Blunt trauma presents a wide variety of symptoms depending on the severity of the injury and the structures involved:

General Symptoms:

Pain: Ranges from mild to severe, depending on the depth and location of the injury.
Blurred Vision: Visual impairment due to corneal, lens, or retinal involvement.
Photophobia: Sensitivity to light, especially in anterior segment injuries.
Periorbital Swelling or Bruising: “Black eye” or ecchymosis around the orbit.
Visible Deformity: In cases of orbital fractures or severe swelling.

Specific Clinical Signs:

Hyphema: Accumulation of blood in the anterior chamber.
Subconjunctival Hemorrhage: Blood pooling under the conjunctiva, giving a red appearance to the eye.
Corneal Abrasions or Edema: Scraping or swelling of the corneal epithelium.
Iris or Pupil Abnormalities: Traumatic mydriasis or irregularly shaped pupil due to sphincter damage.
Retinal Detachment: Flashes, floaters, or loss of peripheral vision due to retinal separation.
Globe Rupture: Severe globe deformity, decreased intraocular pressure (IOP), and prolapse of intraocular contents.
Orbital Fractures: Diplopia (double vision) and enophthalmos (sunken eye) due to damage to the orbital bones.

Management of Blunt Eye Trauma

Blunt trauma to the eye can lead to complex injuries requiring prompt, systematic management.

1. Initial Assessment:

History Taking:

Mechanism of injury, time of occurrence, use of protective eyewear, and associated symptoms.
Tetanus vaccination history if there are lacerations.

Visual Acuity Testing:

Assess vision in both eyes using a Snellen chart or pinhole test.

Comprehensive Examination:

Inspect for swelling, bruising, lacerations, and deformities.
Perform slit-lamp examination to evaluate corneal, anterior chamber, and lens injuries.
Measure intraocular pressure (if no globe rupture is suspected).

2. Imaging:

CT Scan (Preferred): Essential for detecting orbital fractures, intraocular foreign bodies, and posterior segment injuries.
Ultrasound (B-scan): To assess vitreous hemorrhage or retinal detachment, only if globe integrity is intact.
X-ray: May identify fractures but is less sensitive than CT.

3. Acute Medical Management:

Pain Management: Administer systemic analgesics for pain relief.
Cycloplegics: Cyclopentolate drops to reduce ciliary spasm and photophobia.
Topical Antibiotics: Prophylactic antibiotic eye drops or ointments to prevent infection.
Steroids: Considered in non-perforating injuries to reduce inflammation and swelling (under specialist guidance).
Elevate Head: Helps reduce intraocular pressure and manage hyphema.

4. Specialized Interventions:

Hyphema Management: Treat with bed rest, head elevation, and monitoring of intraocular pressure. Avoid NSAIDs (e.g., aspirin) as they may worsen bleeding.
Surgical Repair: Required for globe rupture, retinal detachment, or severe orbital fractures.
Orbital Decompression: Necessary for severe orbital fractures causing nerve or muscle entrapment.
Secondary Procedures: Removal of vitreous hemorrhage or scar tissue in delayed presentations

Complications of Blunt Trauma to the Eye

Blunt eye trauma can lead to acute and long-term complications, including:

Vision Loss: Temporary or permanent, depending on the severity of injury.
Glaucoma: Traumatic glaucoma due to elevated intraocular pressure.
Retinal Detachment: A sight-threatening complication requiring surgical repair.
Post-Traumatic Cataract: Opacification of the lens following trauma.
Sympathetic Ophthalmia: A rare autoimmune reaction affecting the uninjured eye.
Scarring or Deformities: Visible scars or orbital deformities impacting function and appearance.

Prevention

Protective Eyewear: Use safety goggles in high-risk environments such as sports, construction, or industrial work.
Public Awareness: Educate on the importance of eye safety and early medical evaluation.
Occupational Safety Measures: Follow workplace safety protocols to minimize the risk of injury.

Classification of Eye Injuries Based on BETTS

The Birmingham Eye Trauma Terminology System (BETTS) provides a systematic approach for classifying ocular trauma. It categorizes injuries based on whether the globe remains intact (closed globe) or is compromised (open globe).

Closed Globe Injuries

In closed globe injuries, the outer layers of the eye (cornea and sclera) remain intact, and the injury is confined within the eye.

A. Contusion: Caused by blunt trauma that compresses and damages ocular tissues without causing an open wound.

Features:

Hyphema: Blood in the anterior chamber.
Vitreous Hemorrhage: Bleeding into the vitreous humor.
Choroidal Rupture: Break in the choroid, visible on fundus examination.
Retinal Edema or Detachment: May result from force transmitted through the eye.

Examples: Punch to the eye, sports injuries (e.g., impact from a ball).

B. Lamellar Laceration: A partial-thickness wound where the outer layers of the cornea or sclera are disrupted but do not penetrate fully.

Features:

No communication between the external environment and the interior of the eye.
Symptoms include pain, tearing, and light sensitivity.

Causes: Sharp objects that lightly scrape the eye without full penetration.

Open Globe Injuries

Open globe injuries involve a full-thickness wound of the cornea or sclera, leading to exposure of intraocular structures.

A. Rupture: Caused by a blunt force that increases intraocular pressure, resulting in a burst injury at the weakest point of the globe.

Features:

Irregular globe shape due to prolapse of internal tissues.
Severe vision loss or no light perception.

Causes: Direct blows to the eye or accidents causing sudden, severe impact.

B. Laceration: A full-thickness wound caused by a sharp object cutting through the eye wall.

Subcategories:

1. Penetrating Injury:

A single-entry wound caused by a sharp object.
Example: Injury from a nail, knife, or pencil.

2. Perforating Injury:

Two wounds: an entry and an exit wound.
Example: Gunshot or sharp object passing entirely through the globe.

3. IOFB (Intraocular Foreign Body):

A foreign object enters the eye and remains lodged inside.
Examples: Metal shards, glass, or wood splinters.
Complications include infection (endophthalmitis) or chronic inflammation.

Key Differences in BETTS Terminology

Type	Key Characteristics	Examples
Closed Globe	Intact outer layers (no full-thickness wound).	Contusion, lamellar laceration.
Open Globe	Full-thickness wound of cornea or sclera.	Rupture, laceration, IOFB.
Contusion	Non-penetrating injury causing internal damage.	Hyphema, retinal detachment.
Lamellar Laceration	Partial-thickness wound.	Sharp objects causing abrasion.
Rupture	Burst injury due to increased intraocular pressure.	Blunt trauma from fist or object.
Laceration	Full-thickness cut with intraocular involvement.	Penetrating, perforating injuries.
IOFB	Retained foreign body inside the eye.	Metallic or glass fragments.

Injury by Ocular Structures

Structure	Injuries
Cornea	– Simple abrasions or epithelial damage. – Recurrent erosions. – Corneal opacity from trauma or edema.
Sclera	– Partial or full-thickness lacerations. – Associated with globe rupture in severe cases.
Anterior Chamber	– Hyphema (blood in the chamber). – Exudates from traumatic uveitis.
Iris and Pupil	– Traumatic miosis (pupil constriction). – Traumatic mydriasis (dilated, non-responsive pupil). – Iridodialysis (detachment of the iris root). – Aniridia (complete loss of the iris).
Lens	– Vossius ring: Pigment deposit on the lens capsule. – Concussion cataracts. – Lens dislocation.
Retina and Vitreous	– Commotio retinae (retinal whitening). – Retinal tears or detachment. – Vitreous hemorrhage.
Choroid	– Rupture seen as crescent-shaped whitish areas on fundus examination. – Choroidal hemorrhage or detachment.

General Nursing Interventions for Patients with Eye Trauma

1. Assess Visual Acuity

Intervention: Perform baseline and ongoing visual acuity testing using a Snellen chart or equivalent.
Rationale: Establishes the degree of visual impairment and helps monitor progression or recovery of vision.

2. Inspect the Eye for Injuries

Intervention: Examine the eye for lacerations, swelling, foreign bodies, or other visible abnormalities.
Rationale: Identifies the type and extent of injury, guiding appropriate care and treatment.

3. Apply Sterile Eye Dressing

Intervention: Cover the affected eye with a sterile eye patch or dressing if indicated.
Rationale: Protects the injured eye from further trauma, infection, or environmental irritants.

4. Maintain Head Elevation

Intervention: Position the patient with the head elevated at 30–45 degrees.
Rationale: Reduces intraocular pressure, minimizes edema, and assists in the management of hyphema or swelling.

5. Administer Prescribed Medications

Intervention: Administer antibiotics, cycloplegics, or anti-inflammatory eye drops as prescribed.
Rationale: Prevents infection, reduces pain, and controls inflammation to promote healing.

6. Avoid Eye Rubbing

Intervention: Educate the patient to avoid touching or rubbing the injured eye.
Rationale: Prevents further damage, infection, or aggravation of the injury.

7. Assess for Pain

Intervention: Monitor the patient’s pain level and administer analgesics as prescribed.
Rationale: Pain relief enhances comfort and compliance with treatment, facilitating recovery.

8. Use Cold Compresses for Swelling

Intervention: Apply a cold compress to the affected area if there is swelling (avoid direct pressure on the globe).
Rationale: Reduces inflammation and bruising in cases of blunt trauma.

9. Monitor for Signs of Infection

Intervention: Observe for redness, warmth, purulent discharge, or worsening pain.
Rationale: Early detection of infection allows for timely intervention to prevent complications.

10. Provide Emotional Support

Intervention: Reassure the patient and provide emotional support throughout treatment.
Rationale: Helps reduce anxiety and promotes trust, improving the patient’s cooperation and recovery.

11. Educate on Proper Medication Use

Intervention: Teach the patient how to administer eye drops or ointments correctly.
Rationale: Ensures effective use of medications and reduces the risk of further injury or contamination

12. Monitor for Vision Changes

Intervention: Frequently assess the patient for any new or worsening visual symptoms.
Rationale: Detects complications such as retinal detachment, glaucoma, or optic nerve damage early.

13. Protect the Unaffected Eye

Intervention: Advise the patient to limit activities that may strain the uninjured eye.
Rationale: Prevents sympathetic ophthalmia, a rare condition where the unaffected eye becomes inflamed.

14. Facilitate Diagnostic Testing

Intervention: Prepare the patient for imaging (e.g., CT scan, ultrasound) as ordered.
Rationale: Provides detailed information about the injury, aiding in accurate diagnosis and treatment planning.

15. Prepare for Surgical Intervention

Intervention: If surgery is required, educate and prepare the patient for the procedure.
Rationale: Ensures the patient is informed and reduces preoperative anxiety, improving surgical outcomes.

Eye Trauma Read More »

Foreign body in the Eye

FOREIGN BODY IN THE EYE

Foreign object in the eye is something that enters the eye from outside the body.

A foreign body in the eye refers to any external object or substance that enters and remains within the ocular structures, causing discomfort, irritation, or injury.

It can be anything that does not naturally belong there, and may include a speck of dust, wood chip, metal shaving, grass clipping, insect or a piece of glass.

Most foreign bodies are found under the eyelid or on the surface of the eye. When a foreign object enters the eye it will most likely affect the cornea or the conjunctiva.

It can be EXTRA OCCULAR: Lid, sclera conjunctiva cornea or
It can be INTRAOCCULAR: Angle of the anterior chamber, iris lens, Vitreous, Retina.

Find the anatomy of the eye by clicking here

MORBID ANATOMY:

The cornea is a clear doom that covers the front surface of the eye. It serves as a protective covering from the front of the eye. Light enters the eye through the cornea. It also helps to focus light on the retina at the back of the eye.

The conjunctiva is the thin mucous membrane that covers the sclera, or the white of the eye. The conjunctiva runs to the edge of the cornea. It also covers the moist area under the eyelids.

A foreign object that lands on the front part of the eye can not get lost behind the eye ball, but they can cause scratches on the cornea. These injuries usually are minor. However some types of foreign objects can cause infection or damage the vision.

Causes of Foreign Bodies in the eye.

Foreign bodies commonly enter the eye as a result of everyday activities, environmental factors, or accidents. While most are superficial and easily removable, high-velocity objects present the greatest danger due to their potential to penetrate deeper structures.

Foreign Objects at High Speed: Objects like metal or glass particles are often propelled into the eye during explosions, drilling, or hammering. These pose a high risk of injury due to their velocity and sharp edges.
Natural Causes:

Eyelashes: Often fall into the eye and cause irritation.
Dried Mucus: Flakes of dried mucus can lodge on the eye’s surface.

Environmental Debris:

Dirt and Sand: Typically blown into the eyes by wind or falling debris, these materials are common in outdoor settings.
Sawdust: Often occurs during woodworking or construction activities.

Sharp Particles:

Metal Fragments: A common occupational hazard in welding, machining, or using power tools.
Glass Fragments: May result from car accidents, breaking glass, or explosions.

Cosmetics: Mascara, eyeliner, or powder-based cosmetics can accidentally enter the eye, especially during application.
Chemicals: Cleaning agents, industrial chemicals, or sprays can irritate or damage the cornea when they come into contact with the eye.
Contact Lenses: Damaged lenses or improper handling may leave particles in the eye, causing discomfort or injury.

Signs and Symptoms of foreign bodies in the eye.

Foreign bodies in the eyes can present with various symptoms and signs, depending on their location, size, and nature.

A. Corneal Foreign Body

Pain: The cornea is highly innervated, making even small foreign bodies excruciatingly painful.
Foreign Body Sensation: The patient often describes feeling like something is in the eye, even when the object is not visible.
Photophobia (Light Sensitivity): Corneal irritation triggers light sensitivity, as the inflammation affects the pupillary reflex.
Tearing: Excessive tearing is a protective mechanism to wash away the irritant.
Blurred Vision: May occur if the cornea’s central area is involved, interfering with light transmission.
Ciliary Injection: Redness concentrated around the limbus (the junction of the cornea and sclera) indicates corneal irritation or inflammation.
Hypopyon: Accumulation of pus in the anterior chamber suggests severe infection or inflammation.

B. Conjunctival Foreign Body

Mild Discomfort: Less painful compared to corneal foreign bodies because the conjunctiva has fewer nerve endings.
Gritty Sensation: Described as feeling like sand in the eye.
Visible Foreign Body: The object is often seen on the conjunctiva upon inspection.
Redness and Swelling: Conjunctival injection and mild edema may accompany irritation.
Localized Irritation: Irritation is often limited to the area in contact with the foreign body.

C. Intraocular Foreign Body (Penetrating)

Severe Pain and Vision Loss: Indicate deeper damage to the eye’s structures.
Photophobia and Tearing: Reflex responses to protect the eye.
Hyphema: Blood in the anterior chamber is a sign of significant trauma to the iris or ciliary body.
Retinal Damage or Detachment: May present as flashes of light, floaters, or sudden loss of peripheral vision.
Nausea and Vomiting: These symptoms may accompany severe trauma, possibly due to vagus nerve stimulation.

D. Chemical Foreign Bodies

Burning Pain: Often severe, depending on the chemical’s nature (alkali burns cause deeper damage than acidic burns).
Tearing and Redness: Immediate attempts by the eye to flush out the irritant.
Corneal Opacification: The cornea may become cloudy in severe cases, affecting vision.
Conjunctival Injection: Intense redness from irritation or damage.

Additional Clinical Signs

Lid Edema: Swelling of the eyelids may occur with significant irritation or trauma.
Subconjunctival Hemorrhage: Blood under the conjunctiva may indicate minor trauma or chemical irritation.
Anterior Chamber Reaction: Inflammatory cells or blood in the anterior chamber suggest deeper penetration or severe irritation.
A Feeling of Pressure or Discomfort: The object’s presence creates a constant sense of heaviness or pressure in the eye.
Sensation of a Foreign Body: Patients often feel like something is stuck in their eye, even when the object is not visible.
Rubbing of Eyes: Patients instinctively rub their eyes in an attempt to dislodge the object, which can worsen abrasions or push the object deeper.
Eye Pain: Pain intensity varies depending on the location and type of foreign body. Corneal foreign bodies are particularly painful due to the cornea’s dense innervation.
Extreme Tearing: Reflexive tearing occurs as the eye tries to flush out the irritant naturally.
Photophobia (Pain When Looking at Light): Inflammation and irritation make the eye sensitive to light, causing additional discomfort.
Excessive Blinking: The eye blinks frequently as a natural protective mechanism.
Redness or Bloodshot Appearance: Dilation of conjunctival blood vessels causes visible redness.
Discharge of Fluid or Blood: Seen in penetrating injuries, this is a sign of structural damage or rupture.

Classification of Foreign Bodies in the Eye

Classification Based on Toxicity

Type

Description

Examples

Clinical Relevance

Toxic Foreign Bodies

Substances that can cause chemical burns, systemic toxicity, or significant tissue damage.

– Metallic: Iron, nickel, copper, mercury.

– Non-Metallic: Organic (plant, wood) or inorganic (plastic, glass).

– May cause severe inflammation or infection (e.g., plant matter harboring bacteria).

– Metals like copper and mercury can lead to systemic toxicity.

Inert Foreign Bodies

Generally non-toxic materials causing irritation or mechanical injury rather than chemical damage.

– Metallic: Gold, silver, platinum.

– Non-Metallic: Glass, carbon, rubber.

– Often well-tolerated (e.g., gold) but may cause irritation or abrasion if embedded.

Classification Based on Material Properties

Type	Examples	Clinical Relevance
Metallic Magnetic	Iron, steel, nickel.	– Easily removed using magnets. – Can rust, causing toxic corneal rust rings requiring removal (Alger brush).
Non-Magnetic	Copper, aluminum, mercury, zinc.	– Copper: Can cause chalcosis (severe inflammation). – Mercury: Highly toxic, potential for systemic absorption. – Zinc: Tissue irritation and inflammation.
Non-Metallic Organic	Wood, thorns, plant material, insect parts.	– High risk of infection (bacteria or fungi).
Inorganic	Glass, plastic, stone, porcelain, rubber.	– Less reactive but can cause significant mechanical damage depending on size and sharpness.

Classification Based on Location

Location	Description	Examples	Clinical Relevance
Superficial	Foreign body located on the surface of the cornea or conjunctiva.	Dust, sand, small metal shavings.	Easily accessible and removed, but may cause corneal abrasions if not treated promptly.
Embedded	Partially or fully lodged in the cornea, sclera, or conjunctiva.	Plant thorns, glass shards, metallic particles.	Can lead to scarring, infection, or tissue damage if not removed properly.
Intraocular	Foreign body penetrating the globe, possibly reaching deeper structures.	High-velocity metal fragments, sharp objects.	Medical emergency; may cause hyphema, retinal detachment, or loss of vision if untreated.

Classification Based on Mechanism of Entry

Type	Description	Examples	Clinical Relevance
Blunt Trauma	Impact without penetration; foreign body may remain on the surface or cause abrasions.	Dirt, dust, small particles.	Can cause significant irritation, tearing, and superficial corneal injuries.
Sharp Trauma	Penetrating injuries caused by sharp objects that may embed foreign bodies deeply in ocular tissues.	Needles, plant thorns, glass shards.	Increased risk of intraocular infection, retinal damage, or structural complications like perforation.
High Velocity	Objects propelled at high speeds, often during industrial accidents.	Metal fragments during welding, explosions.	High risk of intraocular penetration, hyphema, and globe rupture. Requires urgent specialist intervention.

Management of Foreign

Management of foreign bodies in the eyes includes emergency care, hospital care, and preventive measures.

A. Emergency Management (Pre-Hospital)

Wash Hands: Ensure hands are clean to prevent infection when managing the affected eye.
Inspect the Eye in Bright Light: Use a flashlight or other bright light for better visualization.
Avoid Eye Pressure: Do not press or rub the eye to prevent further injury.
Do Not Use Tools: Avoid using tweezers or swabs on the eye’s surface, as this can push the object deeper.
Restrict Eye Movement: Minimize eye movement by instructing the patient to keep both eyes still.
Do Not Remove Contact Lenses: Unless there is swelling or a chemical injury, leave lenses in place to avoid additional trauma.
Bandage the Eye: Use a clean cloth or sterile gauze to cover the injured eye gently.
Cover the Uninjured Eye: This helps reduce sympathetic movement of the injured eye.
Refer to Hospital: Ensure the patient gets professional medical care promptly.

B. Hospital Management

10. Topical Anesthesia:

Proparacaine or Tetracaine: To numb the eye for painless examination and removal.

11. Fluorescein Staining:

A fluorescent dye highlights corneal abrasions or objects under a cobalt blue light.

12. Inspection and Removal:

Use a magnifier or slit lamp to locate and remove foreign objects.
Moistened Cotton Swab: For superficial conjunctival foreign bodies.
Irrigation: Sterile saline may flush out loose debris.
Special Instruments: Tools like an Alger brush or fine forceps may be required for embedded objects.

13. Management of Corneal Abrasions:

Antibiotic Ointments: Prevent infection (e.g., Ciprofloxacin, Moxifloxacin).
Cycloplegics: Eye drops like cyclopentolate or homatropine keep pupils dilated, reducing painful spasms.

14. Pain Management:

Acetaminophen or NSAIDs: For larger abrasions or persistent discomfort.

15. Advanced Imaging:

CT Scan: Used to detect intraocular foreign bodies or fractures in orbital bones.

16. Treatment of Complications:

Corneal Rust Rings: Removed using an Alger brush under magnification.
Hyphema Management: Elevate the head, apply cold compresses, and refer for specialized care.

C. Prevention

Protective Eyewear: Wear goggles or safety glasses when:

Working with tools like saws, grinders, or hammers.
Handling chemicals or engaging in welding activities.

Hygiene and Awareness:

Avoid touching the eyes with dirty hands.
Be cautious in environments prone to airborne debris.

Complications of Foreign Bodies in the Eye

Foreign bodies in the eye, if untreated or improperly managed, can lead to a range of complications. These complications depend on factors such as the type, size, and location of the foreign body, as well as the speed and manner in which it entered the eye.

1. Rust Ring: Iron or steel foreign bodies can oxidize upon contact with eye fluids, leaving a rust ring on the cornea.

This can lead to persistent irritation, delayed healing, and requires removal using specialized tools like an Alger brush.

2. Corneal Abrasions and Erosions: Superficial scratches caused by the foreign body or attempts to remove it.

May result in recurrent corneal erosions, chronic pain, or blurred vision if not treated properly.

3. Infectious Keratitis: Infection of the cornea, commonly seen with organic foreign bodies like wood or plant material.

Can progress to corneal ulcers or abscesses, potentially leading to vision loss if untreated.

4. Endophthalmitis: A severe intraocular infection caused by penetrating injuries introducing pathogens into the globe.

Requires urgent treatment to prevent blindness or loss of the eye.

5. Hyphema: Bleeding into the anterior chamber caused by trauma from a penetrating or high-velocity foreign body.

Can lead to increased intraocular pressure, corneal staining, or secondary glaucoma.

6. Iritis or Anterior Uveitis: Inflammation of the iris or anterior uveal tract due to trauma or irritation.

Causes pain, photophobia, redness, and may lead to long-term complications such as synechiae (adhesions between the iris and lens).

7. Scleral or Corneal Scarring: Permanent scarring due to embedded foreign bodies or complications from abrasions and infections.

Can cause significant visual impairment if the scar obstructs the central visual axis.

8. Globe Rupture: Penetrating foreign bodies or severe blunt trauma can lead to rupture of the eye’s outer layers.

Medical emergency requiring surgical intervention, often resulting in partial or total vision loss.

9. Retinal Detachment: High-velocity foreign bodies can damage the retina, leading to its separation from the underlying tissue.

Presents as flashes of light, floaters, or curtain-like vision loss and requires urgent surgical repair to prevent permanent blindness.

10. Sympathetic Ophthalmia: A rare immune-mediated inflammatory response affecting both eyes, triggered by trauma to one eye.

Can cause bilateral vision loss if not identified and treated early.

11. Increased Risk of Glaucoma: Secondary glaucoma may develop due to chronic inflammation, hyphema, or scarring in the anterior chamber.

Can result in gradual vision loss due to elevated intraocular pressure.

12. Subconjunctival Hemorrhage: Bleeding under the conjunctiva, often seen in blunt trauma.

Usually resolves without treatment but may mask more severe injuries.

13. Persistent Foreign Body Sensation: Residual irritation after removal due to incomplete removal of debris or secondary abrasions.

May lead to chronic discomfort, requiring further evaluation and management.

14. Anterior Chamber Foreign Bodies: Small foreign bodies can settle in the anterior chamber, causing inflammation or secondary infection.

May require advanced surgical techniques for removal.

15. Cataract Formation: Penetrating injuries that disrupt the lens capsule may lead to traumatic cataracts.

Requires surgical intervention to restore vision.

Nursing Interventions for a Child with a Foreign Body in the Eye

The interventions aim to minimize the child’s pain and anxiety, prevent complications, and ensure timely and effective treatment while educating caregivers on prevention.

1. Assess the Child’s Condition.

Intervention: Conduct a thorough assessment of the child’s eye, documenting signs such as redness, tearing, swelling, or visible foreign body.
Rationale: Early assessment helps determine the severity of the injury and guides immediate care.

2. Ensure Safety and Comfort.

Intervention: Calm and reassure the child, keeping them still to prevent further eye movement.
Rationale: Reducing anxiety minimizes reflexive rubbing or blinking, preventing further injury.

3. Educate the Caregiver.

Intervention: Instruct the caregiver to avoid touching or attempting to remove the foreign body themselves.
Rationale: Improper handling can worsen the condition or cause secondary trauma.

4. Position the Child Properly.

Intervention: Position the child upright and instruct them to avoid lying flat, especially in cases of suspected penetration.
Rationale: Upright positioning reduces intraocular pressure and minimizes the risk of fluid leakage.

5. Restrict Eye Movement.

Intervention: Cover both eyes with a sterile dressing or eye shield to restrict ocular movement.
Rationale: Moving one eye causes the other to move reflexively, which can exacerbate the injury.

6. Perform Gentle Irrigation (If Appropriate).

Intervention: Irrigate the affected eye with sterile saline solution if the foreign body is superficial and safe to remove.
Rationale: Irrigation helps flush out loose debris without causing further trauma.

7. Administer Prescribed Topical Anesthesia.

Intervention: Apply prescribed topical anesthetics (e.g., proparacaine) to numb the eye for examination or treatment.
Rationale: Reduces pain and allows easier inspection and removal of the foreign body.

8. Monitor for Signs of Complications.

Intervention: Observe for signs of infection, vision changes, or increased swelling and redness.
Rationale: Prompt detection of complications like infection or hyphema ensures timely intervention.

9. Provide Pain Management.

Intervention: Administer prescribed pain relievers, such as acetaminophen, to manage discomfort.
Rationale: Relieving pain helps keep the child calm and cooperative during treatment.

10. Facilitate Ophthalmology Referral.

Intervention: Arrange for immediate referral to an ophthalmologist for advanced care, especially for penetrating or embedded foreign bodies.
Rationale: Specialized care is necessary to prevent complications such as corneal scarring or vision loss.

11. Support Emotional Well-being.

Intervention: Use age-appropriate communication to explain procedures to the child and involve caregivers in comforting them.
Rationale: Addressing fear and anxiety improves cooperation and builds trust.

12. Educate on Prevention.

Intervention: Teach the child and caregivers about using protective eyewear during activities such as playing with sharp objects, using tools, or engaging in outdoor activities.
Rationale: Preventive measures reduce the risk of future injuries.

Foreign body in the Eye Read More »

Stye (Hordeolum).

Stye Lecture Notes for Nurses

Stye or Hordeolum

A stye is a painful, red lump that forms on the edge of the eyelid. It is an acute infection of a small gland in the eyelid, most commonly caused by the bacterium Staphylococcus aureus. The medical term is Hordeolum.

A stye is a localized infection of the hair follicles or sebaceous glands of the eyelids.

A stye is a staphylococcal abscess that may occur on either the external or internal margin of the eyelids.

Types of Stye

External Stye (Hordeolum Externum)

This is the most common type, appearing on the outer edge of the eyelid. It is an infection of an eyelash follicle or a gland of Zeis or Moll. External styes are generally more painful than internal styes because they form on the surface of the eyelid, often along the lash line, involving many nerve endings, making them tender and noticeable.

Location: Outer edge of the eyelid, at the lash line.
Cause: Acute bacterial infection of an eyelash follicle or a sebaceous gland (Gland of Zeis or Moll).
Pain Level: Typically more acutely painful, sharp, and localized tenderness.
Appearance: Often resembles a small, red, tender pimple or boil, sometimes with a visible head.

Internal Stye (Hordeolum Internum)

This forms on the inner surface of the eyelid and is an infection of a Meibomian gland (an oil-producing gland within the eyelid). Unlike external styes, the pain from an internal stye is often described as a more generalized ache or pressure rather than sharp, localized pain, and they tend to be less acutely painful. However, they can cause more significant and diffuse swelling of the entire eyelid. Internal styes may sometimes require medical intervention for drainage as they are less likely to rupture on their own and tend to recur.

Location: Inner surface of the eyelid, often causing swelling across the entire eyelid.
Cause: Acute bacterial infection of a Meibomian gland.
Pain Level: Less acutely painful than external styes, often a generalized ache or pressure.
Appearance: Can cause significant, diffuse swelling of the eyelid; the lump may be felt or seen when the eyelid is everted.

Chalazion

A chalazion is not a type of stye, but rather a chronic, non-infectious lump in the eyelid. It often develops when an internal stye doesn't fully resolve, or when a Meibomian gland becomes blocked and its contents (oil) are released into the surrounding tissue, causing sterile inflammation. Unlike styes, chalazia are typically painless once the initial inflammation subsides, although they can cause cosmetic concerns or, if large enough, temporary blurred vision by pressing on the cornea.

Location: Usually forms deeper in the eyelid, away from the lid margin.
Cause: Blocked Meibomian gland, leading to sterile inflammation; often a sequela of an untreated internal stye.
Pain Level: Generally painless and non-tender after the initial inflammatory phase subsides.
Appearance: A firm, round, non-tender lump in the eyelid; typically no acute redness unless secondarily infected.

Clinical Features (Signs and Symptoms)

The signs and symptoms of a stye are very distinct. You will see and hear the following from your patient:

A visible lump: A noticeable red lump appears on the top or bottom eyelid.
Swelling and Redness: The area is red and swollen. Sometimes a small area is affected, but sometimes the entire eyelid swells up.
Pain and Tenderness: The lump is painful, and it is tender when touched.
Itching and Burning: Patients often complain of itching in the early stages, as well as a burning sensation in the eye.
Pus Formation: A tiny, yellowish spot (pus point) develops at the center of the swollen area after 2-3 days, right before it may burst spontaneously.
Eye Discomfort: Patients feel a gritty sensation, as if a foreign body is in the eye. There is also discomfort during blinking.
Watering and Discharge: The eye may water excessively (tearing) and can have mucous discharge. This can lead to crusting of the eyelid margins, especially upon waking.
Sensitivity to Light (Photophobia): The eye becomes very sensitive to bright light.
Blurred Vision: In some cases, vision may be temporarily blurred due to the swelling or discharge.

In summary,

Redness on the affected area

Pain

Tenderness

Itching

Photophobia

Pus formation

Yellowish swelling 3 days b4 opening spontaneously

May burst spontaneously

Itching in the early stages

A lump on the top or bottom eyelid

Swelling, pain & tenderness

Pus formation

Watering of the eye

Eye is sensitive to light

Small area of the eyelid is swollen but sometimes the entire eyelid swells up

Tiny, yellowish spot develops at the center of the swollen area

Discomfort during blinking

Sensation of a foreign body in the eye

Mucous discharge in the eye

Blurred vision

Crusting of the eyelid margins

Burning in the eye

Management of a Stye

The goals are to

relieve pain, promote drainage, and prevent the spread of infection. Most styes will heal spontaneously with simple care.

Usually the stye will heal spontaneously
Avoid rubbing the eye as this might spread the infection
Apply a warm/ hot compress to the eye for 10 minutes
Apply tetracycline eye ointment 1% 2-4 times daily until 2 days after symptoms have disappeared
Remove the eye lash when it’s loose
When the forms in one of the deeper glands of the eyelid a condition is called internal hordeolum
The pain and other symptoms are usually more severe.
Because this type of the stye rarely ruptures by it self, a doctor may have to open it to drain the pus

Immediate and Home Care (Conservative Management)

Warm Compresses: This is the most important treatment. Apply a clean cloth soaked in warm water to the closed eye for 10-15 minutes, 3-4 times a day. This helps drainage.
Lid Hygiene: Gently clean the eyelid margins to remove crusts and bacteria.
Important Advice: Tell the patient to NEVER squeeze or rub the stye, as this can spread the infection deeper.
Eyelash Removal: You can gently remove an eyelash if it is loose and coming directly from the center of the stye, as this can help it drain.

Medical Management

Topical Antibiotics: A clinician may prescribe Tetracycline 1% eye ointment or Chloramphenicol eye ointment, applied 2-4 times daily until 2 days after symptoms have disappeared.
Pain Relief: Simple analgesics like Paracetamol can be used for pain.
Oral Antibiotics: These are reserved for severe infections or if the infection spreads to the surrounding skin (preseptal cellulitis).

Surgical Management

Incision and Drainage (I&D): This procedure is performed if resolution does not begin in the next 48 hours after warm compresses are started, especially for a painful internal hordeolum.
Procedure: The procedure consists of the doctor numbing the area, making a very small incision on the inner or outer surface of the eyelid, and draining the pus. Very small sutures may be used to close the lesion.

Nursing Interventions

Your role as a nurse is central to effective management and prevention.

Assess and Differentiate: Conduct a thorough assessment of the patient’s eye, taking a good history to differentiate between a stye and other conditions like a chalazion or cellulitis. Assess pain using a pain scale.

Educate on Warm Compresses: Demonstrate the correct technique for warm compresses—using a clean cloth, ensuring the water is warm (not hot), and applying for the right duration and frequency.

Reinforce the "No Squeeze" Rule: Emphatically explain why squeezing or rubbing is dangerous and can lead to a much worse infection like cellulitis.

Promote Eyelid Hygiene: Teach the patient and their family how to gently clean the eyelids with warm water and a clean cotton ball to remove crusts and reduce bacterial load.

Administer Medications Safely: If prescribed, teach the patient the correct way to apply eye ointment or drops without contaminating the tube/bottle tip and without touching the eye itself.

Implement Infection Control Measures: Stress the importance of rigorous hand washing before and after touching the eye. Advise against sharing towels, pillowcases, and facecloths.

Monitor for Complications: Continuously assess for signs of worsening infection, such as increased swelling, severe pain, changes in vision, or fever. Know the red flags for referring to a doctor immediately.

Provide Pain and Comfort Management: Administer prescribed analgesics and reassure the patient that styes are common and usually resolve with proper care. This reduces anxiety.

Offer Nutritional Advice: Suggest a healthy diet rich in vitamins A and C to support immune function and promote healing.

Provide Clear Discharge and Prevention Advice: Give clear, simple instructions on how to prevent recurrence, focusing on makeup hygiene, not rubbing eyes, and managing underlying conditions like blepharitis.

Document Everything: Accurately document all assessments, interventions, patient education provided, and the patient's response to treatment in the nursing notes.

Nursing Care Plan

Assessment	Nursing Diagnosis	Planning (Goals)	Implementation: Interventions	Implementation: Rationale	Evaluation
Subjective: Patient states, "My eyelid is very sore." Objective: Localised, red, swollen, tender lump on the upper eyelid margin.	Acute Pain related to the inflammatory process and pressure from abscess as evidenced by patient's verbal report and tenderness on palpation.	Patient will report a reduction in pain within 24 hours. Patient will demonstrate correct application of warm compress.	1. Teach and demonstrate application of warm compresses for 10-15 mins, 4x daily. 2. Administer prescribed analgesics. 3. Advise patient to avoid touching the stye.	1. Heat promotes drainage, which relieves pressure and pain. 2. Analgesics provide systemic pain relief. 3. Pressure worsens pain and risks spreading infection.	Goal Met. Patient reports pain has decreased and correctly shows how to apply a warm compress.
Objective: Patient wears contact lenses and heavy eye makeup. Asks, "Why do I keep getting these?"	Deficient Knowledge related to disease process, self-care, and prevention strategies as evidenced by patient's question and identified risk factors.	By end of session, patient will verbalize 3 key preventive measures.	1. Educate on strict hand hygiene. 2. Instruct on not sharing cosmetics/towels. 3. Advise to remove makeup nightly and discard old products. 4. Instruct to avoid wearing contact lenses until healed.	1. Reduces bacterial transfer to the eye. 2. Prevents cross-contamination. 3. Empowers patient to modify risk factors and prevent recurrence. 4. Prevents trapping bacteria and irritating the eye.	Goal Met. Patient correctly lists hand washing, not sharing makeup, and removing makeup as preventive measures.
Objective: Pus point is visible on the stye. Patient lives in close quarters with siblings.	Risk for Infection related to the presence of an active bacterial lesion and potential for poor hygiene.	Patient and family will remain free from signs of spreading infection throughout the illness.	1. Emphasize that personal items (towels) must not be shared. 2. Instruct to wash hands after touching the eye or applying medication. 3. Teach correct application of antibiotic ointment if prescribed.	1. Staph bacteria are easily transmitted via contaminated items. 2. Prevents auto-inoculation and spreading to others. 3. Topical antibiotics treat the local infection and reduce bacterial load.	Goal Met. The stye resolved without spreading. No other family members developed styes.

Complications

Chalazion: An internal stye may heal and leave a painless lump.
Preseptal Cellulitis: The infection spreads to the whole eyelid. This needs urgent antibiotic treatment.
Orbital Cellulitis: A medical emergency where the infection goes behind the eye. Refer immediately.
Recurrence: Styes can come back, especially with poor hygiene.

Prevention

Good Personal Hygiene: Proper and regular hand washing is the most important preventive measure.
Face Washing: Keep the face, especially the eye area, clean.
Makeup Hygiene: Never share cosmetics or eye makeup tools. Remove all makeup every night. Discard old or contaminated eye makeup (every 3-6 months).
Do Not Share Personal Items: Avoid sharing towels, flannels, or pillowcases.

Good personal hygiene,Proper hand washing
Regular washing of the face
Remove any loose eyelashes
it is recommended to never share cosmetics or cosmetic eye tools with other people
It is also recommended to remove makeup every night before going to sleep and discard old or contaminated eye makeup.

Stye (Hordeolum). Read More »

Trachoma

Trachoma is contagious infection of the conjunctiva and cornea characterized by formation of granulation and scarring

Trachoma is a contagious bacterial infection which affects the conjunctival lining covering of the eye, the cornea and the eyelids.
Is a Greek word meaning “ Roughness”

Etiology

Trachoma is caused by the Chlamydia trachomatis bacteria and is essentially preventable and curable.
It is the leading infectious cause of blindness in the world and it spreads very easily.

Predisposing Factors to Trachoma

Poor sanitation (lack of latrines, rubbish pit)
Unclean water supply/ even lack of water.
Living in dry and dusty environment.
Overcrowding with unhygienic conditions.
Reduced personal and community hygiene allow the bacteria to infect and reinfect the eyes of the individuals living in endemic areas.

Risk Factors of Trachoma

Dirty face
Improper hand hygiene
Ignorance about personal hygiene and environmental sanitation.
Inadequate housing and lack of functional housing
Crowded living conditions e.g. children sharing beds.
Poor water supply.
Swimming in water
Poor nutrition
Age
Occupation

Risks for Mode of Spread: 6D’s

Dry
Dusty
Dirty
Density
Dung
Discharge

Mode of Transmission: 5F’s

Fingers
Flies
Feaces
Face
Fomites

Incubation period

5- 21 days

Mode of infection

Direct spread (e.g. direct personal contact)
Vector transmission (e.g. bush fly, house fly)
Material transfer (e.g. shared towels clothes)

Clinical Features of Trachoma.

The signs and symptoms will depend on the presence/ absence of secondary infection, incase of a bacterial infection the signs resemble bacterial conjunctivitis.
Conjunctiva appears congested.
Irregular scarring of the conjunctiva
The cornea shows superficial keratitis
Later corneal opacity and corneal ulcer may occur.
Eye irritation
Redness and itching
Mucoid Discharge
Swelling of the eyelids
Inflammation inside the upper eyelid
Scarring of the upper lid
Distortion of the upper eyelid
Development of eyelashes that turns into the eye lid then rub on the cornea causing entropion
Abnormal growth of corneal blood vessels
Foreign body sensations
Stickiness of the lids
Keratitis
Conjunctival congestion
Herbert follicles and Herbert pits develop
Conjunctival scarring
Corneal ulcer
Corneal opacity

WHO classification of Trachoma (FISTO)

Trachomatis Follicular inflammation (TF)

This is an active phase of the disease at least with 5 or more follicles already forming in the upper margin and there size is larger than 0.5mm in diameter.

Trachomatis inflammation (TI)

The inflammation is very active with thickening of the upper conjunctiva.

Trachomatis Scarring: (TS)

- Trachomatis scarring in the tarsal conjunctiva seen as a white bands or threads of fibrosis.

Trachomatis trichiasis(TT)

When at least 1 eyelash rubs on the ocular surface. (atleast one trichiasis lash)

Trachomatis corneal opacity (C.O)

Corneal opacity: when there is visible corneal opacity in the eye pupillary area and a visual acuity less than 6/18

DIAGNOSIS :

History
Physical examination
Investigation: Pus swab

Management of Trachoma

Aims

To prevent spread
To Relieve symptoms
To prevent complications

Admission
Isolation
History taking
Reassurance
Observation : physical examination and specific examination
Inform the ophthalmologist
Investigations are done
Medical history is taken
Medical Treatment.

T= tetracycline

E = Erythromycin

S=Sulfacetamide

T= Topical

Medical management.

Topical application of antibiotics like 1% Tetracycline ointment 3 times daily for six weeks.
Erythromycin, azromycin eyedrops is instilled 4 times daily for six weeks.
Systemic steroids can be given to reduce the inflammation/congestion like predisolone or dexamethasone.
Alternatively doxycycline may be given for 2-3 weeks ( dose is given according to age of the patient).

Surgical management

Surgery is performed for in turned eyelids (entropion)
Electrolysis: insertion of a probe into the follicle to pull it out.
Cyrotherapy : Using cold freeze thaw to squeeze the follicle
Argon laser treatment: The follicle will be destroyed.

Nursing Care

Regular cleaning of the eyes
Disinfect equipments used
Ironing and cleaning linens
Encourage hand washing
Barrier nursing measures
Nutrients e.g. proteins and vitamins
Rest and sleep
Reassurance

Advice on discharge

Health education on environmental change
Drug compliance
Increase access to clean water and sanitation.

Nursing Diagnosis for Trachoma

Acute pain: eye related to swelling of the lymph nodes, photophobia and inflammation.
Disturbed Sensory Perception: Visual related to damage to the cornea.
Risk for infection, the spread related to lack of knowledge.
Body image disorders related to loss of vision.

Complications.

Trichiasis (inward growth of eyelashes that rub on the cornea, conjunctiva)
Entropion (eyelid rolled inward against eyeball by muscle spasm by scarring of the conjunctiva)
Keratitis(inflammation of the cornea)
Ptosis(abnormal low lying or drooping of the upper eyelid)
Secondary glaucoma
Corneal opacity, blindness.

Preventive Measures

Avoid physical contact with a person suffering from trachoma
Personal cleanliness especially the face and hands
Washing hands and face frequently with soap and water
Keep separate towels, handkerchiefs, linens for each member of the family
Use latrines to dispose off faeces covered with lid
Avoid crowded places
Wash , hang , dry and iron all linens
Good hygiene during deliveries
Avoid eye makeup
Spray flies
clean compounds to keep away flies
Early diagnosis and treatment

Prevention ( SAFE) Strategy by WHO.

S= Surgery (Surgery for trchiasis/entropion/corneal opacity)
A=Antibiotics (Azithromycin 500mg single dose)
F= Facial cleanliness
E= Environmental Improvement.

Trachoma Read More »

Hypoxic Ischemic Encephalopathy

Hypoxic Ischemic Encephalopathy (HIE) is a type of newborn brain damage caused by oxygen deprivation and limited blood flow.

Hypoxic Ischemic Encephalopathy is when the brain does not get enough oxygen, permanent brain damage can result. Hypoxic Ischemic Encephalopathy is a type of birth injury; this is a broad term used to refer to any harm that a baby experiences at or near the time of birth. Other terms used for HIE include birth asphyxia, perinatal asphyxia, and neonatal encephalopathy.

Hypoxic Ischemic Encephalopathy falls under the Broad term “Encephalopathy“

Encephalopathy

Encephalopathy is a general term used to describe damage or disease affecting brain function. The causes are varied and can be related to infection, liver conditions, drug toxins, and more.

Some of the major types include the following:

Chronic Traumatic Encephalopathy: This condition occurs due to direct injury to the brain, leading to nerve damage. This type is commonly found in athletes.
Hepatic Encephalopathy: Often caused by liver cirrhosis, when the liver is not able to filter and function properly, toxins accumulate in the blood and brain.
Glycine Encephalopathy: This type of encephalopathy is genetic with symptoms appearing after birth.
Toxic Metabolic Encephalopathy: This type of encephalopathy results from toxins, infections, or organ failure. When chemical composition in the body becomes imbalanced, it can impact the brain’s normal function.
Hypoxic-Ischemic Encephalopathy: When the brain does not get enough oxygen, permanent brain damage can result.
Hypertensive Encephalopathy: Prolonged hypertension that is not treated can cause the brain to swell resulting in neurological damage.
Uremic Encephalopathy: If the kidneys are not functioning properly, they cannot filter harmful substances. The buildup of uremic toxins can cause confusion and other symptoms.

Etiology of Hypoxic Ischemic Encephalopathy

Pathologically, any factors which interfere with the circulation between maternal and fetal blood exchange in form of maternal factors, delivery factors and fetal factors.

Maternal factor:

hypoxia,
anemia,
diabetes,
hypertension,
smoking,
nephritis,
heart disease,
too old or too young,etc

Delivery condition:

Abruption of placenta,
placenta previa,
prolapsed cord,
premature rupture of membranes,etc

Fetal factor:

Multiple birth,
congenital or malformed fetus,etc

High Risk Factors

Mismanagement of a high-risk pregnancy: Women with conditions such as preeclampsia and gestational diabetes require more extensive monitoring and treatment.
Umbilical cord complications: The umbilical cord is like a lifeline between mother and baby, supplying oxygen and nutrients and removing fetal waste. Anything that compresses the cord or reduces its function puts the baby at risk of HIE.
Placental or uterine complications: The placenta and uterus also play very important roles in providing oxygenated blood to the baby. Examples of placental and uterine issues that may cause HIE include:
- Placental abruption: when the placenta separates from the uterus before the baby is born
- Placenta previa: when the placenta attaches too close to the cervix; this can cause dangerous bleeding and oxygen deprivation during delivery
- Placental insufficiency: when the placenta is unable to deliver enough blood to the baby
- Uterine rupture: when the uterus tears, partially or completely

Infections: Infections in the mother can spread to the baby during labor and delivery, especially if the medical team do not take adequate precautions (such as doing indicated infection screening and prescribing antibiotics when needed).
Improper fetal heart monitoring: If a baby shows signs of fetal distress on the fetal heart monitor, doctors and nurses can often intervene so that their oxygen supply is restored. If necessary, this may involve an emergency C-section. However, if monitoring is sporadic or does not occur, important signs of danger may be missed.
Failure to prevent a premature birth: Premature babies are at higher risk for HIE and other birth injuries because their lungs are so underdeveloped. Therefore, it is very important that doctors do what they can to prevent premature birth, such as performing a cervical cerclage (a stitch placed in the cervix to stop it from opening too early) or providing progesterone treatment.
Allowing prolonged labor to continue: Labor is stressful for babies because uterine contractions compress the placenta and umbilical cord that supply their oxygen. If something is preventing labor from progressing, and physicians do not offer intervention (such as an emergency C-section), this is negligence. Prolonged labor is more likely to occur when a baby is larger than normal, or the mother’s pelvis is smaller than normal.
Medication problems: Sometimes physicians prescribe medications such as Pitocin and Cytotec in order to induce or enhance labor. Unfortunately, these medications can also cause uterine contractions to become so strong and frequent that the baby is dangerously deprived of oxygen.
Mismanagement of a neonatal condition: Hypoxic-ischemic injury can be caused by complications during the neonatal period, i.e. a baby’s first month of life. Problems such as respiratory distress, jaundice, and neonatal hypoglycemia can all contribute to an HIE diagnosis, especially if mismanaged.

Clinical Features of Hypoxic Ischemic Encephalopathy

Breathing problems
Feeding problems
Missing reflexes (for example, the baby does not respond to loud noises)
Seizures
Low Apgar scores
Low or high muscle tone
Altered level of consciousness (e.g. not alert)

Classification of Hypoxic Ischemic Encephalopathy

Clinical Classification

Mild(stage I): hyperalert, irritable, normal muscular tone & reflex, no seizure, normal EEG
Moderate(stage II): lethargy, hypotonia, weak sucking & Moro response, often seizure, EEG+
Severe(stage III): coma, absent muscular tone & reflex, persistent seizure, EEG++

Levene Classification

Feature	Mild	Moderate	Severe
CONSCIOUSNESS	Irritable	Lethargy	Comatose
TONE	Hypotonia	Marked	Severe
SEIZURE	No	Yes	Prolonged
SUCKING/ RESPIRATION	Poor Suck	Unable to Suck	Unable to maintain Spontaneous respiration

Sarnat Staging Classification

(Commonly used)

Sarnat staging is used alongside electroencephalogram findings to provide information about the prognosis for the infant.

	Grade I Mild	Grade II Moderate	Grade III Severe
Alertness	Hyperalert	Lethargy	Coma
Muscle tone	Normal or increased	Hypotonic	Flaccid
Seizures	None	Frequent	Uncommon
Pupils	Dilated, reactive	Small, reactive	Variable, fixed
Respiration	Regular	Periodic	Apnoea
Duration	< 24 Hours	2 – 14 Days	Weeks

electroencephalogram

Management of Hypoxic Ischemic Encephalopathy

This is a pediatrics emergency.

HIE is managed using a treatment called therapeutic hypothermia, where the baby’s brain or body is cooled down below normal temperatures to slow damage.
This allows the baby’s brain to recover and reduces the level of disability they may have as they grow. According to current guidelines, the treatment must be given within six hours of birth, not exceeding 24 hours.
The treatment of encephalopathy varies, depending on the underlying cause of the condition.

Generalized treatment:

Ventilation: CPAP(continuous positive airway pressure) , CMV(continuous mandatory ventilation), HFOV (High-frequency oscillatory ventilation )
Perfusion/Circulation: Dopamine/Dobutamine
Energy: normal glucose level maintained (50-110mg/dl): Hypo and hyperglycemia avoided
Fluid: 60-80ml/kg/d – restriction if SIADH(Syndrome of inappropriate hormone secretion)
Electrolytes- Sodium and Calcium should be monitored.
Avoid Polycythemia: If Hct>65-70, partial exchange transfusion is done to bring Het level to 55.
Control of seizures: HIE seizures are difficult to control ;
Phenobarbital loading dose 15-20mg/kg, iv maintenance dose 3-5mg/kg, iv
Phenytoin loading dose 15-20mg/kg, iv maintenance dose 5mg/kg, iv Midazolam: 0.1-0.3mg/kg, iv Leveracetam, Topiramate
EEG

Special Investigations

Continous AEEG- Amplified EEG used for cerebral function monitoring. Detects voltage pattern- burst, low voltage, isoelectric Detects electrical seizure activity
CT scan: only indicated in emergency

Prognosis

Depend on the severity of brain damage & medical treatment, usually:

Mild or moderate cases could be cured completely, but severe cases represent poor prognosis with high mortality or cerebral complications such as mental retardation & cerebral palsy.
Overall mortality – 20%
Overall incidence of sequele – 30%
Mild: 100% good prognosis
Moderate: 80% normal
Severe : 50% death, 50% sequele

Presence of seizure increases chance of Cerebral palsy by 50-70 times.

Prevention

Better Obstetric care
Skilled resuscitation teams and neonatal facilities.

Nursing Diagnosis

Acute Confusion related to Hypoxia ,Disturbance in cerebral metabolism ,Accumulation of toxins in the brain, Structural changes in the brain as evidenced by Cognitive dysfunction , Altered psychomotor performance , Tremors, Fluctuation in the level of consciousness, Agitation, Misperception, Neurobehavioral manifestations, Difficulty initiating purposeful behavior.
Impaired Memory related to Neurological disturbances related to encephalopathy, Inadequate intellectual stimulation, Changes in brain structure and processes, Irreversible brain damage, Depressive symptoms as evidenced by Reports experiences of forgetfulness, Consistently forgets to schedule or keep appointments , Difficulty recalling events, Difficulty recalling familiar names, objects, and words, Inability to learn or retain new skills or information, Inability to perform a previously learned skill.
Disturbed Thought Processes related to Insufficient oxygen supply to the brain secondary to encephalopathy, Head trauma related to encephalopathy, Infections as evidenced by Incorrect perception of stimuli, Difficulty performing activities of daily living , Difficulty communicating verbally, Impaired interpretation of events, Impaired judgment, Impaired decision making, Inadequate emotional responses, Disorientation

Hypoxic Ischemic Encephalopathy Read More »

Conjunctivitis

Conjunctivitis is an inflammation of the lining of the eye and eyelid caused by bacteria, viruses, chemicals or allergies, fungal, parasites.

It is characterized by dilatation of the conjunctival vessels, resulting in hyperemia and edema of the conjunctiva, typically with associated discharge.
It’s the most common cause of red eye usually painless and characterized by pussy or watery discharge.

Types of Conjunctivitis

Bacterial conjunctivitis :- caused by bacterium e.g. staphylococcus or streptococcus
Acute viral conjunctivitis:- e.g. herpes simplex
Allergic conjunctivitis:- caused by allergy e.g. smoke, cosmetic and medicines

Bacterial Conjunctivitis

Predisposing factors for bacterial conjunctivitis

Flies
Poor hygienic conditions
Hot dry climate
Poor sanitation
Dirty habits

Causes of Bacterial Conjunctivitis

Staphylococcus aureus is the most common cause of bacterial conjunctivitis
Pneumococcus.
Streptococcus pyogenes (haemolyticus) is virulent and usually produces pseudomembranous conjunctivitis.
Pseudomonas pyocyanea is a virulent organism, which readily invades the cornea.
Neisseria gonorrhoeae typically produces acute purulent conjunctivitis in adults and ophthalmic neonatorum in newborn
Neisseria meningitidis may produce muco-purulent conjunctivitis.
Corynebacterium diphtheriae causes acute membranous conjunctivitis

Mode of Infection

Conjunctiva may get infected from three sources:-

1.Exogenous infections may spread:

Directly through close contact
Vector transmission e.g., flies
Material transfer e.g. infected fingers of health workers, common towels,handkerchiefs & tonometers

Local spread may occur from neighbouring structures such as infected lacrimal sac, lids, and nasopharynx.
Endogenous infections may occur very rarely through blood, e.g., gonococcal and meningococcal infections.

Pathology

Pathological changes of bacterial conjunctivitis consist of:

Vascular response. It is characterized by congestion and increased permeability of the conjunctival vessels associated with proliferation of capillaries.
Cellular response. It is in the form of exudation of polymorphonuclear cells and other inflammatory cells into the substantia propria of conjunctiva as well as in the conjunctival sac.
Conjunctival tissue response. Conjunctiva becomes edematous. The superficial epithelial cells degenerate, become loose and even desquamate. There occurs proliferation of basal layers of conjunctival epithelium and increase in the number of mucin-secreting goblet cells.
Conjunctival discharge. It consists of tears, mucus, inflammatory cells, desquamated epithelial cells, fibrin and bacteria. If the inflammation is very severe, diapedesis of red blood cells may occur and discharge may become blood stained.

Acute Bacterial Conjunctivitis

Acute bacterial conjunctivitis is characterized by marked conjunctival hyperemia and mucopurulent discharge from the eye.
It is the most common type of bacterial conjunctivitis.
Common causative bacteria are: Staphylococcus aureus, Pneumococcus and Streptococcus.

Infectious period

The time during which an infected person can infect others thus while the eye discharge is present.

Clinical Presentation

Typically there is conjunctival infection, especially in the fornices where the blood supply is rich.
Discharge is variable, but typically is present in the mornings, and on waking the eye is difficult to open because the eyelids are stuck together.
The eyelids may be red and inflamed.
The condition may be unilateral or bilateral.
The vision is always unaffected and there is usually no pain.
The patient may complain of a gritty or foreign body sensation, some discomfort and very occasionally very mild photophobia.
Slight blurring of vision due to mucous flakes in front of cornea.
Flakes of mucopus seen in the fornices, canthi and lid margins is a critical sign

Clinical course and diagnosis

Mucopurulent conjunctivitis is usually bilateral, although one eye may become affected 1–2 days before the other.
The disease usually reaches its height in three to four days. If untreated, in mild cases the infection may be overcome and the condition is cured in 10–15 days

Diagnosis

It is by clinical and/or microscopic examination and culture of discharge from the eye.
It is usually not possible to tell whether the conjunctivitis is caused by bacteria or viruses without laboratory tests.

Management of bacterial Conjunctivitis

Clean the eyes and apply topical antibiotics
Bacterial conjunctivitis usually resolves without treatment
Topical antibiotics may be needed only if no improvement is observed after 3 days
Dark goggles should be used to prevent photophobia.
No bandage should be applied in patients with mucopurulent conjunctivitis. Exposure to air keeps the temperature of conjunctival cul-de-sac low which inhibits the bacterial growth
No steroids should be applied, otherwise infection will flare up and bacterial corneal ulcer may develop.
Topical Antibiotics:
Therefore, treatment may be started with chloramphenicol (1%), or gentamicin (0.3%), or tobramycin 0.3% or framycetin 0.3% eye drops 3–4 hourly in day and ointment used at night will not only provide antibiotic cover but also help to reduce the early morning stickiness.
Quinolone antibiotic drops such as ciprofloxacin (0.3%), ofloxacin (0.3%), gatifloxacin (0.3%) or moxifloxacin (0.5%) may be used as alternative in severe cases

Chronic Bacterial Conjunctivitis

Chronic bacterial conjunctivitis also known as ‘Chronic catarrhal conjunctivitis’ or ‘simple chronic conjunctivitis’ is characterized by mild catarrhal inflammation of the conjunctiva.

Viral Conjunctivitis

Viral causes include:

Adenovirus
Herpes simplex virus
Poxvirus
Mycovirus and Paramyxovirus

Signs of Viral conjunctivitis

Red/pink eye.
Chemosis, if severe.
Follicles may be present on the palpebral conjunctiva.
Bleeding from conjunctival vessels in severe adenoviral conjunctivitis.

Management/Treatment

Supportive treatment for amelioration of symptoms is the only treatment required and includes:

Apply cold compresses
If photophobia is present, advise patient to wear dark glasses
Artificial lubricant can be prescribed for patient comfort.

Topical antibiotics help to prevent superadded bacterial infections.
Topical antiviral drugs are not beneficial in adenoviral conjunctivitis.
Topical steroids should not be used during active inflammation as these may enhance viral replication and extend the period of infectivity.

Weak steroids such as fluorometholone or loteprednol (0.5%) are indicated in patients with subepithelial infiltrates, and in those with membrane formation.

Full explanation of the condition to increase patient awareness and reduce discomfort.

Preventive measures include:

Frequent hand washing
Relative isolation of infected individual
Avoiding eye rubbing and common use of towel or handkerchief sharing
Disinfection of ophthalmic instruments and clinical surfaces after examination of a patient is essential.

Allergic Conjunctivitis

It is the inflammation of conjunctiva due to allergic or hypersensitivity reactions which may be immediate (humoral) or delayed (cellular).

Types

Simple allergic conjunctivitis

Seasonal allergic conjunctivitis (SAC)
Perennial allergic conjunctivitis (PAC)

Vernal keratoconjunctivitis (VKC)
Atopic keratoconjunctivitis (AKC)

Simple Allergic Conjunctivitis

It is a mild, nonspecific allergic conjunctivitis characterized by itching, hyperaemia and mild papillary response.

Etiology

Simple allergic conjunctivitis, is a type-I immediate hypersensitivity reaction mediated by IgE.

Types

Seasonal allergic conjunctivitis (SAC). SAC is a response to seasonal allergens such as tree and grass pollens. It is of very common occurrence and may be associated with allergic rhinitis.
Perennial allergic conjunctivitis (PAC) is a response to perennial allergens such as house dust, animal dander and mite. The onset is subacute, the condition is chronic in nature and occurring all through the year.

Clinical Features

Symptoms

Intense itching and burning sensation in the eyes associated with watery mucus and mild photophobia.

Signs

Hyperaemia and chemosis which give a swollen juicy appearance to the conjunctiva.
Oedema of lids is often present.

Diagnosis

Diagnosis is made from:

Typical symptoms and signs,
Normal conjunctival flora, and
Presence of abundant eosinophils in the discharge.

Treatment

Elimination of allergens if possible.
Topical vasoconstrictors like naphazoline, antizoline and tetrahydrozoline provide immediate decongestion.
Artificial tears like carboxymethyl cellulose provide soothing effect. As they sometimes relieve discomfort in mild cases
Mast cell stabilizers such as sodium cromoglycate and nedocromil sodium are very effective in preventing recurrences in atopic cases.
Steroids, if condition is severe
Cool water poured over the face with the head inclined downward constricts capillaries.

Other forms of Conjunctivitis

Fungal conjunctivitis

it is caused by Candida albicans. Babies can be affected during birth through an infected birth canal.

Fine white plaques are apparent on the conjunctiva.
The treatment is with nystatin drops and ointment.

Parasitic conjunctivitis

In hot climates, parasites causing onchocerciasis (river blindness) and schistosomiasis (bilharzia) can induce conjunctivitis.

Prevention

Exclude people with conjunctivitis from public places until discharge from the eyes has ceased.
Good personal hygiene must be followed. Careful hand washing, using soap and warm water.
Do not share towels and wash clothes

Conjunctivitis Read More »

Eye Anatomy and Physiology

Eye Anatomy.

Eye is the organ for sight. The globe-shaped eyeball occupies the anterior part of the orbit/eye socket. The eyeball is embedded in the orbital cavity.

The eye contains the receptors for vision and a refracting system that focuses light rays on the receptors in the retina.

Diagram Showing the structure of the Eye.

The Structure of the Eye

The eye is spherical in shape and the diameter of an adult eye is approximately 2.5cm.
Internally, the eye is divided into 2 chambers.
The lens, suspensory ligaments and ciliary body separate the 2 chambers;

Anterior and posterior chamber

Anterior chamber. It is filled with a clear watery fluid called aqueous humour.

This chamber is in front of the lens.
It is further divided into 2 cavities ie anterior and posterior cavities.

Posterior chamber. It is filled with a jelly like substance called vitreous humour (vitreous body). This chamber is behind the lens.

There are three main layers of tissue in the walls of the eye:

The outer fibrous layer consisting of sclera and cornea
The middle vascular layer or uveal tract consisting of the choroid, ciliary body and iris
The inner nervous tissue layer consisting of the retina.

The outer fibrous layer

This consists of sclera and cornea.

The sclera or white of the eye forms the outermost layer of the posterior and lateral aspects of the eyeball.

It is continuous anteriorly with a clear transparent epithelial membrane, the cornea.

The cornea is transparent due to its vascularity and the regular arrangement of its fibres.

Its surface is lined by the conjunctiva.
It is well supplied with nerve endings from the trigeminal nerve.
It consists of a firm fibrous membrane that maintains the shape of the eye.
This membrane gives attachment to the extrinsic muscles of the eye.
Light rays pass through the cornea to reach the retina.
The cornea is convex anteriorly.
It is involved in refracting (bending) light rays to focus them on the retina.

The middle vascular layer

The middle vascular layer is also known as the uveal tract.
This layer consists of the choroid, ciliary body and iris.

The choroid lines sclera in the posterior compartment of the eye.

The choroid is rich in blood supply and is chocolate brown in colour.

The ciliary body is an anterior continuation of the choroid which is inserted into suspensory ligaments.

These ligaments extend to the lens and hold it in position.
The ciliary body is supplied by the 3rd cranial nerve (Oculomotor).
The ciliary body also consists of;
Ciliary muscles. Contraction and relaxation of these smooth muscles determine the size and thickness of the lens.
Secretory epithelial cells (Ciliary glands). These secrete aqueous humour which nourishes structures in the anterior chamber.

The iris is the visible coloured ring at the front of the eye.

The iris extends anteriorly from the ciliary body lying behind the cornea and in front of the lens.
It divides the anterior chamber of the eye into anterior and posterior cavities.
It contains both circular and radiating muscle fibres which control the size of the pupil.
The colour of iris is genetically determined and depends on the number of pigment cells present.
NB: The Oculomotor nerve supplies the muscles of the iris and ciliary body (intrinsic eye muscles).

The inner nervous tissue layer

The inner layer of the eye ball is the retina.
It is the light sensitive (photosensitive) part of the eye.
It contains several millions of sensory photo receptor cells.
These cells are responsible for converting light into nerve impulses.

The retina consists of two layers;

The pigmented outer layer which lines choroid.
The inner most neural layer which is in contact with the vitreous humour.
The light sensitive layer consists of sensory receptor cells ie rods and cones.
These contain photosensitive pigments that convert light rays into nerve impulses.
Rod cells pre-dominate in the periphery and function best in dim light. These cells are much more numerous.
Cone cells pre-dominate near the centre of the retina. These are adapted for bright light and colour vision.
Near the posterior of the retina is a part called macula lutea or yellow spot.
The greatest concentration of cone cells is at a small area in the yellow spot called the fovea centralis.
It is the most vital part of retina for high definition or vision.
The optic disc or blind spot is a small area where the optic nerve leaves the eye.
The blind spot does not have light sensitive cells.

Parts of the Eye and functions.

Eyebrows-protect eyeball from sweat, dust and other foreign bodies.

Eyelids –movable folds acting as curtains, preventing injuries. Meet at palpebral fissure(both eyelids meet). It contains sebaceous glands, sweat glands and accessory lacrimal glands all aligned with conjuctival material.

Conjunctiva-clear, delicate mucous membrane. it lines the eyelids and is highly vascularised. It protects the eye against infections. It also acts as a physical barrier, and produces mucin (goblet cells)which lubricates the eye ball.

Sclera-is a fibrous tissue of the eye(white),is tough and contains collagen fibres, and covers 5/6 of the eyeball. It protects inner structures maintains the shape of the eyeball. It also acts as a passage of blood vessels and nerves

Cornea-covers 1/6 of the eyeball. Its clear, transparent and has 5 layers.

Its functions include;

protection of the eye as it’s very
Refractive media of the and
Prevents aqueous from coming out of the eye Anterior chamber

Is just behind the cornea and its functions include;

Refractive media
Maintains shape and structure of the eyeball
Bathes/nourishes the

Production and flow of aqueous humor.

Aqueous Humor is secreted by the epithelial cells of the ciliary body. it passes through suspensory ligaments into the posterior chamber, then flow through the pupil into the anterior chamber. From anterior chamber it drains through trabecular meshwork into the canal of schlemm (scleral venous sinus) then goes to the general circulation

Iris-is the thin visible, contractile, and coloured part of the eye, with a central aperture known as the pupil. It divides the anterior segment of the eye into anterior and posterior chambers. It controls amount of light entering the eye and plays a role in accommodation.

Ciliary body-Is continuous with choroid(middle layer of eyeball). It suspends the lens which is important during accommodation, and produces aqueous.

Choroid-Is the soft brown part behind the eye. Is most vascularized, and nourishes the retina.

Lens-is the transparent, highly elastic biconvex body, that lies immediately behind the pupil/front of the vitreous body. Its thickness is controlled by ciliary muscle through the suspensory ligaments.

Its functions include:

Refractive media
Absorbs ultra violet rays

Retina-Innermost layer of eyeball where images are formed. It has macula, optic disk, rods and cones. It consists of 2 layers.

Epithelial
Nervous layer
It absorbs
Stores and releases vitamin

Vitreous body-is transparent, jelly like media.

It maintains the shape of eyeball and acts as refractive

Blood and Nerve supply to the eye

The blood supply of the eye is from the ciliary and central retinal arteries.
These are branches of ophthalmic artery which is also a branch of the internal carotid artery.
Venous drainage is by the central retinal vein.
These vessels run alongside the optic nerve.
Nerve supply is by the optic nerve which is the 2nd cranial nerve.
The retinal nerve fibres originate in the retina.
These fibres converge to form the optic nerve at the optic disc.

Physiology of Sight

Light rays from objects are bent (refracted) as they pass through varying densities of the clear media of the eye to focus onto the retina.
In the eye, the biconvex shape of the lens refracts and focuses light rays on the retina.
Before reaching the retina, the light rays pass through the cornea.

The cornea also plays a role in the refractive power of the eyes.
The lens is elastic thus has ability to change shape. Change in shape varies the amount of refraction for clarity of focus. This is known as accommodation.
Accommodation is necessary in order for objects at different distances to be visualized with equal clarity.
The normal eye in its relaxed state brings rays of light from distant objects into sharp focus.
However for clear focusing on near objects, an autonomic reflex comes into play.
The reflex involves accommodation, miosis and convergence as follows;

Accommodation. This refers to the increase in the refractive power of the lens in order to focus light rays from near objects on the retina. The ciliary muscle contracts and changes shape of the lens to bulge increasing its convexity and refractive power.

Miosis. This is also known as constriction of pupils.

It accompanies accommodation.
It ensures that light rays are concentrated to pass through the centre of the lens and focus on the retina.

Convergence (movement of the eyeballs). This refers to bilateral movement of the eyes at the same time in order to focus on a nearby object eg focusing the tip of one’s nose.

The light sensitive layer in the retina containing sensory photo receptor cells (rods and cones) convert light rays into nerve impulses.
These are transmitted through the visual pathways to the visual area in occipital lobe of cerebrum.
Here, they are interpreted as sensation of light form.

They are processed into images of objects which are given meaning by other cerebral areas.
This process involves interaction with information stored as memory in the association areas of the brain.

NB: The images refracted on the retina are upside down.

The brain adapts to this early in life so that objects are perceived as upside/upright.

Accessory Organs of the Eye

The eye is a delicate organ on the body and it is protected by several structures.

These include;

(1). The eye brows:

These are numerous hairs that project from the skin at the supra orbital margins of the frontal bone.
These protect the eye from sweat, dust and other foreign bodies.

(2). Eyelids and eyelashes:

These are two movable folds of tissue above and below the front of each eye.
There are sebaceous glands, some open into the hair follicles of the eye lids.

The eyelids contain two muscles.

These include;
Levator palpebrae superioris which raises the upper eyelid
Orbicularis oculi which closes the eyelids.
The hair on the eye lid is called eye lashes.
The eyelids have a lining (mucous membrane) of the conjunctiva.
This lining is a fine transparent membrane that is on the inner surface of the eyelid.
This layer also covers the eyeball. Where it lines the eyelids, there is a highly vascularized columnar epithelium The corneal conjunctiva has avascular stratified epithelium.
This means that the conjunctiva has epithelium without blood vessels at the cornea.
The medial and lateral angles where the eyelids come together are called medial and lateral canthus respectively.
At the edges of the eyelids, are eyelid margins that have numerous sebaceous glands.
These are modified and secrete an oily material (meibum) spread over the conjunctiva by blinking.
The material delays evaporation of the tears.
- Protect the eye from injury
- Blinking at about 3 to 7 seconds interval spreads tears and oily secretions over the cornea. This prevents drying of the eyeball.
  - Function of the eyelids and eyelashes

(3). Lacrimal apparatus:

The lacrimal apparatus consists of the structures that secrete tears and drain them from the front of the eyeball.
These include;
1 lacrimal gland and its ducts
2 lacrimal canaliculi ie superior and inferior to the caruncle of the eye.
1 lacrimal sac
1 nasolacrimal duct
Each eye has a lacrimal gland behind the supra orbital margin.
Lacrimal glands are exocrine glands.
They secrete tears which are composed of water, mineral salts, antibodies and bactericidal enzymes.
The tears leave the lacrimal glands by several small ducts.
They then pass over to the front of the eye under the eyelids towards the medial canthus where they drain into two lacrimal canaliculi.
The opening of canaliculi on each side is called punctum.
The canaliculi lie above one another separated by a red body called caruncle.
The tears then drain into the lacrimal sac which is the upper expanded part of the nasolacrimal duct
When foreign bodies or other irritants enter the eye, secretion of tears is greatly increased and the conjunctival blood vessels dilate.
Secretion of tears is also increased in emotional states like crying and laughing.
Excess tears are drained from the eye via the lacrimal apparatus into the lacrimal sac and then into the nasolacrimal duct.
Functions of the lacrimal apparatus.
It has a fluid which is filled into the conjunctival sac.
This fluid consists of tears and oily (meibum) secretions of meibomian/tarsal glands.
The fluid is spread over the cornea by blinking.
This mixture washes away irritants eg dust.
It provides oxygen and nutrients to the avascular corneal conjunctiva and drains off wastes.
Bactericidal enzyme lysozyme protects the eye by preventing microbial infection.
The oiliness nature of the fluid delays its evaporation and prevents drying/friction of the conjunctiva.
The fluid also prevents the eyelids from sticking together while sleeping.
Main function of tears / tear fluid
To lubricate the eye to facilitate oxygen and carbon dioxide exchange.
To produce an optically smooth cornea surface.
To cleanse the eye with a bactericidal enzyme lysozyme.
To prevent the conjunctiva from drying.

(4). Extrinsic muscles :

These are also called extrinsic muscles.
They are 6 in number and include the following;
Medial rectus which rotates the eyeball inwards.
Lateral rectus which rotates the eyeball outwards
Superior rectus which rotates the eyeball upwards
Inferior rectus which rotates the eyeball downwards

Function of the muscles

They protect the eye through the flexible movement of the types of muscles.
These movements help us to see in all directions of the eyeball movement.
Hence they also play a protective function ie protecting the eye and the whole body.

Eye Anatomy and Physiology Read More »

Intracranial Hemorrhage

INTRACRANIAL HEMORRHAGE

An intracranial hemorrhage is a type of bleeding that occurs inside the skull (cranium).

Bleeding around or within the brain itself is known as a cerebral hemorrhage (or intracerebral hemorrhage).

Bleeding caused by a blood vessel in the brain that has leaked or ruptured is called a hemorrhagic stroke.

All bleeding within the skull is referred to as intracranial hemorrhage.

Causes of Intracranial Hemorrhage.

Head Trauma: Injury to the head from falls, car accidents, sports incidents, or seizures.
Hypertension: High blood pressure leading to damage in blood vessel walls, causing leakage or rupture.
Blood Clot: Blockage of a brain artery by a clot formed in the brain or traveling from another body part.
Cerebral Aneurysm: Rupture of a weak spot in a blood vessel wall, forming a balloon-like bulge that bursts.
Malformed Arteries or Veins: Leaking of improperly formed arteries or veins.
Bleeding Tumors: Hemorrhage from tumors causing bleeding.
Pregnancy-Related Conditions: Conditions linked to pregnancy or childbirth, including eclampsia, difficult delivery, and assisted delivery.
Coagulopathy or Anticoagulation Medicine: Blood clotting disorders, use of anticoagulants like warfarin or heparin, or bleeding disorders like hemophilia and thrombocytopenia.
Child Abuse Syndrome: Shaken baby syndrome as a result of child abuse.
Postsurgical Causes: Hemorrhage occurring after surgeries like craniotomy or shunting.

Pathophysiology:

The brain relies on a network of blood vessels to supply oxygen and nutrients. Intracranial hemorrhage disrupts this supply, preventing oxygen from reaching brain tissue. The pooled blood from the hemorrhage increases pressure on the brain, further limiting oxygen delivery.

During a hemorrhage or stroke, if oxygen deprivation persists for more than three or four minutes, brain cells begin to die. This results in damage to affected nerve cells and the related functions they control. The interruption of blood flow around or inside the brain is a critical factor leading to cellular damage and dysfunction.

Types of Intracranial Hemorrhage

Epidural hematoma
Subdural hematoma
Subarachnoid hemorrhage
Intra cerebral hemorrhage

Epidural Hematoma (Subgalea hemorrhage.

Subgaleal hemorrhage occurs when emissary veins between the skull and intracranial venous sinuses tear, leading to blood collection between the dura/apo-neurosis and periosteum of the skull.

High-pressure bleeding is a prominent feature. An epidural hematoma, may briefly lead to lose consciousness and then consciousness is regained latter.

Epidural hematoma is accumulation of blood between the Dura and the skull following fracture of the skull

Most commonly from rupture of middle meningeal artery.
The hematoma expands rapidly since accumulating blood is arterial in origin and causes compression of the Dura and flattening of underlying gyri
The patient develops progressive loss of consciousness if hematoma is not drained early.

Signs and symptoms

Swelling of the ears
Increasing head circumference as bleeding expands into this space. (hydrocephalus)
Hypovolemic shock,
Tachycardia,
Hypotension

Diagnosis

Subgaleal hemorrhage may present as a large, boggy fluid collection palpable on the head’s surface. Characteristic of a subgaleal hemorrhage is that it is not restricted by suture lines and may shift with movement. This is in contrast to the more common cephalohematoma, a superficial collection of blood restricted to the space between the periosteum and skull, which is contained along suture lines.
Neonates with subgaleal hemorrhage are at high risk for rapid decompensation; the subgaleal space can expand to collect a newborn’s entire intravascular blood volume if bleeding continues unrecognized.

Subdural hematoma (SDH)

A subdural hemorrhage occurs when bridging veins carrying blood through the dura mater to the arachnoid mater of the meninges are torn.

This causes bleeding, with blood collecting below the dura and brain.

Presence of blood on the surface of the brain beneath its outer covering.

SDH is a collection of blood below the inner layer of the dura mater but external to the arachnoid membrane.

Subdural hematoma is accumulation of blood between the Dura and subarachnoid.
Develops most often from rupture of veins which cross the surface convexities of the cerebral hemispheres.

Subdural hematoma may be acute or chronic.

Acute subdural hematoma; develops following trauma and consists of clotted blood, often in the front parietal region. There is no significant compression of gyri. Since the accumulated blood is of venous origin, symptoms appear slowly and may become chronic with passage of time if not fatal.
Chronic subdural hematoma; occurs often with brain atrophy. Chronic subdural hematoma is composed of liquid blood. Separating the hematoma from underlying brain is a membrane composed of granulation tissue.

Diagnosis

Because subdural bleeders are located within the skull, there is often no physical sign on the scalp that reflects injury. Instead, the presence of hemorrhage may initially be unrecognized. For most neonates, subdural hemorrhage remains asymptomatic and resolves without consequence.
Clinical problems can arise in case of large volume hemorrhage or if bleeding slowly continues over hours or even days, as in cases of bleeding disorders.
Symptomatic neonates often present 24–48 hours after birth with nonspecific signs such as apnea, respiratory distress, altered neurologic state, or seizures.

Subarachnoid hemorrhage

Subarachnoid hemorrhage occurs when the veins of the subarachnoid villi are torn, leading to a collection of blood in the subarachnoid space.

There’s bleeding between the brain and the thin tissues that cover the brain. These tissues are called meninges.

A sudden, sharp headache usually comes before a subarachnoid hemorrhage. Typical symptoms also include loss of consciousness and vomiting.

Hemorrhage into the subarachnoid space is most common, caused by;
rupture of an aneurysm, and rarely, rupture of a vascular malformation.
Of the three types of aneurysms affecting the larger intracranial arteries—berry, mycotic and fusiform, berry aneurysms are most important and most common.
Berry aneurysms are saccular in appearance with rounded or lobulated bulge arising at the bifurcation of intracranial arteries and varying in size from 2 mm to 2 cm or more.
They account for 95% of aneurysms which are liable to rupture.
Berry aneurysms are rare in childhood but increase in frequency in young adults and middle life.
They are, therefore, not congenital anomalies but develop over the years from developmental defect of the media of the arterial wall at the bifurcation of arteries forming thin-walled saccular bulges.
Although most berry aneurysms are sporadic in occurrence, there is an increased incidence of their presence in association with congenital polycystic kidney disease and coarctation of the aorta.
In more than 85% cases of subarachnoid hemorrhage, the cause is massive and sudden bleeding from a berry aneurysm on or near the circle of Willis.

The four most common sites are;

In relation to anterior communicating artery.
At the origin of the posterior communicating artery from the stem of the internal carotid artery.
At the first major bifurcation of the middle cerebral artery.
At the bifurcation of the internal carotid into the middle and anterior cerebral arteries

Intracerebral hemorrhage

An intracerebral brain hemorrhage (ICH) is bleeding in the brain caused by the rupture of a damaged blood vessel in the head.

As the amount of blood increases, the build-up of pressure can lead to brain damage, unconsciousness or even death.

Intra cerebral hemorrhage is when there’s bleeding inside the brain.

This is bleeding into the brain’s ventricular system, where the cerebrospinal fluid is produced and circulates through towards the subarachnoid space. It can result from physical trauma or from hemorrhaging in stroke ( HTN). This is the most common type of ICH that occurs with a stroke. It’s not usually the result of injury.

Spontaneous intracerebral hemorrhage occurs mostly in patients of hypertension. Children with systemic diseases that manifest with HTN are at risk because they have micro aneurysms in very small cerebral arteries in the brain tissue.
Rupture of one of the numerous micro aneurysms is believed to be the cause of intracerebral hemorrhage
Not common to have recurrent intracerebral hemorrhages like is the case of subarachnoid hemorrhages
The common sites of hypertensive intracerebral hemorrhage are the region of the basal ganglia (particularly the putamen and the internal capsule), pons and the cerebellar cortex

Diagnosis

There are very few clinical symptoms of IcH. When present, signs may include an acute drop in hematocrit, new-onset hypotension, and lethargy.
However, these symptoms are often present in extremely low birth weight and prematures

Signs and Symptoms

A prominent warning sign is the sudden onset of neurological deficit. This is a problem with the brain’s functioning. The symptoms progress over minutes to hours and they include:

Headache accompanied by neck stiffness
Drowsiness
Difficulty speaking/crying
Nausea
Vomiting
Decreased consciousness
Seizure
Coma
Weakness in one part of the body
Elevated blood pressure
Cognitive dysfunction or memory loss
Sudden tingling, weakness, numbness, or paralysis of the face, arm or leg, particularly on one side of the body
Loss of balance or coordination in older children
Babies less than 12 months old may develop a swollen fontanel, or soft spot

Diagnosis

History taking
Computed temography (CT- scan) of head
MRI of head
CBC
Coagulation profile e.g. INR, PT
Physical examination e.g. glasgow coma scale (GCS):
- Eye Opening
- Verbal response
- Best motor response

GLASGOW COMA SCALE

Management

Admission in icu or surgical ward
Resuscitation (ABC); All patients with GCS < 8 should be intubated for airway protection
Surgical management

ICH is a medical emergency. Survival depends on getting treatment right away. It may be necessary to operate to relieve the pressure on the skull (craniotomy)

Craniotomy; to evacuate blood
Endovascular treatment; to occlude parent artery
Aneurysm coiling; obstruct aneurysm site with coil

MEDICAL MANAGEMENT

Steroids to Reduce Swelling: Steroids help reduce inflammation and swelling in the brain. Minimizing swelling is important to prevent further damage to delicate brain tissue.
Anticoagulants: Reduces clotting to prevent the formation of blood clots. Clots can exacerbate the existing hemorrhage and lead to complications like stroke.
Anti-Seizure Medications: Controls and prevents seizures. Seizures can further damage the brain and hinder the recovery process.
Medications to Counteract Anticoagulants: Reverses the effects of any blood thinners previously taken. Prevents excessive bleeding and facilitates clotting.
Blood Pressure Management: Maintain mean arterial pressure below 130 mm Hg. Helps control bleeding, but excessive hypotension should be avoided to ensure adequate blood flow to the brain.
Avoiding Hyperthermia: Prevents elevated body temperature. Elevated temperature can worsen brain damage; controlling it is essential for recovery.
Correction of Coagulopathy: Using interventions like fresh frozen plasma, vitamin K, or platelet transfusions. Correcting coagulation issues ensures proper blood clotting and reduces the risk of complications.
Anticonvulsant Initiation: Controls seizures. Seizures can cause additional harm to the brain and hinder recovery.
Transfer to Operating Room or ICU: Facilitates specialized care and monitoring. Swift transfer ensures prompt and appropriate management of the patient’s condition.
Consideration of Nonsurgical Management: For patients with minimal neurological deficits. Nonsurgical approaches may be appropriate in less severe cases, avoiding unnecessary interventions.
Dietary Measures: Initiating enteral feedings, possibly via nasogastric tube or percutaneous device. Ensures proper nutrition and supports the patient’s recovery.
Activity Management: Bed rest initially, followed by a progressive increase in activity. Balancing rest and activity promotes recovery without causing undue stress on the healing brain.

Nursing Concerns Intracranial Hemorrhage:

Risk for Increased Intracranial Pressure: Bleeding within the brain can lead to increased intracranial pressure, which can damage brain tissue.
Risk for Neurological Deficits: The hemorrhage can cause permanent neurological damage, such as paralysis, speech impairment, or cognitive decline.
Risk for Seizures: The hemorrhage can trigger seizures.
Risk for Complications of Immobility: The patient may be bedridden, increasing the risk of complications such as pneumonia, deep vein thrombosis, and pressure ulcers.
Risk for Anxiety and Fear: The patient and family may experience anxiety and fear about the diagnosis and prognosis.
Risk for Family Dysfunction: The patient’s illness can put a strain on family relationships.
Risk for Post-Traumatic Stress Disorder: The patient may experience PTSD after a traumatic brain injury.

Complications to Monitor:

Seizures: Can occur and require prompt management.
Paralysis: Possible impairment of motor functions.
Memory Loss: Cognitive deficits may arise.
Stroke: Hemorrhage can lead to a secondary stroke.
Permanent Brain Damage: A risk, especially if complications are not managed effectively.
Cerebral Coning: Herniation of brain tissue, a serious complication.
Depression: Emotional and psychological impact.
Bedsore: Potential complication due to immobility, requiring preventive measures.

Intracranial Hemorrhage Read More »