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Anatomy and Physiology of the Musculo-skeletal System

The muscular-skeletal system is the system that is mainly important in locomotion, body support and makes bodies’ frame work

It consists of skeletal muscles, bones and joints

The skeletal muscle

The muscle consists of bundles of myocytes containing actin and myosin molecules. These molecules integrate and form myofibrils which cause muscle contraction in the same way as myocardial muscle.

Myocyte/sarcomere is elongated surrounded by cell membrane called sarcolemma with nuclei beneath and oxygen binding substance (myoglobin that store oxygen).

Myocyte is surrounded by a connective tissue called endomysium, a group of muscle fibres (fascicle) is surrounded by another connective tissue called perimysium and the whole muscle is surrounded by another connective tissue called epimysium

The three connective tissue forms a tendon which attaches a muscle to the bone surface (enthesis).

A muscle fascia is a fibrous tissue that surrounds the epimysium and tendon

Physiology of a skeletal muscle

Sarcomere is the functional unit of muscle contraction

When a muscle contracts light (actin) filaments and dark (myosin) filaments in a muscle come closer i.e. they interact to shorten the length of the muscle cell.

Many knobs (heads) like projection in myosin form cross-bridges with actin stimulating the muscle to contract, the cross bridge move pulling the filaments pass each other

When the cross bridge has moved as far as it can, it releases the actin and return to original position. The cross bridge is attached to actin of another place

When ATP is absent a muscle is an able to contract continuously (muscle fatigue) leading to muscle cramp.

Control of muscle contraction

The muscle is connected to CNS by motor neuron. Impulses from this neuron contract the muscle.

The point of contact between the motor neuron and muscle is called neuromuscular junction. Vesicle at the axon terminal release acetylcholine an important neurotransmitter

Impulses cause release of calcium ions within the cell which affect regulatory protein that allow actin and myosin to interact and form cross-bridges. A muscle cell will remain in a state of contraction until acetylcholine production stops

Acetylcholinesterase enzyme produced at the neuromuscular junction to destroy acetylcholine that permits re-absorption of calcium into the muscle cell and terminates contraction

Intensity of contraction depends on what you are trying to accomplish. The frontal lobe of the cerebrum decide what and how many muscle cells need to contract

Bones

These form the bodies frame work i.e shape and form of the body They give attachment of muscle and ligaments.
They also protect vital organs, store calcium, form blood elements and allow movement of the body as a whole

The function unit of a bone is an osteocyte

The bony matrix is produced by osteoblasts and comprises of colloids, mineral, carbohydrates and proteins

Various hormones are needed in maintain bony tissue i.e. thyroid hormones, growth hormones, calcitonin, parathyroid hormone and adrenal hormones

Joints

This is where two or more bones met. Joints allow flexibility and movement of the skeleton.

Types of joints

There are three types of joints

Fibrous joints

These are joints in which articulating surfaces of bones are connected by a fibrous tissue. Examples include sutures, middle radioulnar joint and joints between teeth.

There are three types of fibrous joints:

(1) Sutures are nonmoving joints that connect bones of the skull. These joints have serrated edges that lock together with fibers of connective tissue.

(2) The fibrous articulations between the teeth and the mandible or maxilla are called gomphoses and are also immovable.

(3) A syndesmosis is a joint in which a ligament connects two bones, allowing for a little movement (amphiarthroses). The distal joint between the tibia and fibula is an example of a syndesmosis.

Cartilaginous joints

The bone ends are united by a cartilage for example intervertebral joints, pubic symphysis and costochondral joints.

There are two types of cartilaginous joints:

(1) A synchrondosis is an immovable cartilaginous joint. One example is the joint between the first pair of ribs and the sternum.

(2) A symphysis consists of a compressable fibrocartilaginous pad that connects two bones. This type of joint allows for some movement. The hip bones, connected by the pubic symphysis, and the vertebrae, connected by intervertebral discs, are two examples of symphyses.

Synovial joints

These joint articular bony ends are lined by synovial membrane with synovial fluid to permit free movement. These include the ball and socket joints e.g. Hip and the hinge joints e.g. interphalangeal, knee joint etc

Synovial joints are characterized by the presence of an articular capsule between the two joined bones. Bone surfaces at synovial joints are protected by a coating of articular cartilage. Synovial joints are often supported and reinforced by surrounding ligaments, which limit movement to prevent injury. There are six types of synovial joints:

(1) Gliding joints move against each other on a single plane. Major gliding joints include the intervertebral joints and the bones of the wrists and ankles.

(2) Hinge joints move on just one axis. These joints allow for flexion and extension. Major hinge joints include the elbow and finger joints.

(3) A pivot joint provides rotation. At the top of the spine, the atlas and axis form a pivot joint that allows for rotation of the head.

(4) A condyloid joint allows for circular motion, flexion, and extension. The wrist joint between the radius and the carpal bones is an example of a condyloid joint.

(5) A saddle joint allows for flexion, extension, and other movements, but no rotation. In the hand, the thumb’s saddle joint (between the first metacarpal and the trapezium) lets the thumb cross over the palm, making it opposable.

(6) The ball-and-socket joint is a freely moving joint that can rotate on any axis. The hip and shoulder joints are examples of ball and socket joints.

Hyaline cartilage

It forms the articular surface and is vascular. It relies on diffusion from synovial fluid for its nutrition. It is rich in type II collagen that forms a mesh work enclosing giant macro – molecular aggregates or proteoglycans

DISEASES AFFECTING SKELETAL MUSCLES

MYASTHENIA GRAVIS

This is another autoimmune disease predominantly affecting females. There is un usual fatigue due to lack of acetylcholine receptor at the myoneural junctions which impair muscle contraction.

Signs and symptoms

The onset is gradual.
Excessive fatigue particularly towards end of the day with drooping of eye lids
Frequent falls
Difficult in chewing and swallowing
Involvement of respiratory muscles may lead to respiratory failure
A weak cough reflex may lead to accumulation of secretions and infections

Treatment and management

Short acting anticholine esterase drugs like edrophonium
Long acting ant cholinesterase drugs e.g. neostigmine or pyrisostigmine
Thymectomy and steroids also provide relief.
Exercises

MYOSITIS (MYOPATHY)

Myositis or myopathy refers to a group of primary diseases of muscles; Myositis (inflammation of muscles) can be genetically diseases.

Progressive muscular atrophy is a group of hereditary disorder characterized by progressive delegation of muscles without involvement of bones.

The wasting and weakness of muscles is symmetrically without any sensory loss. The affected muscles are large, firm but weak.

The child walks with a waddling giant like that of the duck

When rising from a supine lying position, in bed, the child rolls on his face (prone position) and then uses his arms to push his body up (tripod sign). Death in second decade is usual due to involvement of respiratory muscles.

Fibrositis – rheumatism (fibrocystic)

Fibrositis and muscular Rheumatism are terms used to describe recurring pains, stiffness in the muscles or the back, various parts of the body being involved from time to time.

The disease does not progress and such vague symptoms are attributable to emotional stress.

Treatment

Is usually symptomatic, heat and massages may be helpful and aspirin or one of the NSAIDS can be prescribed.

Anatomy and Physiology of the Musculo-skeletal System Read More »

Hydrocele

HYDROCELE

A hydrocele is a fluid collection within the tunica vaginalis of the scrotum or along the spermatic cord.

A hydrocele is accumulation of serous fluid within the tunica vaginalis that produces swelling in the inguinal region or scrotum.

It often presents as painless swelling in the scrotum. Provided there is no hernia present, hydrocoeles below the age of 1 year usually resolve spontaneously.

In infants it is usually as a result of incomplete closure of the processus vaginalis. It may or may not be associated with inguinal hernia. In older boys and men it may be idiopathic.

Anatomy of the Scrotum.

Scrotum, is a thin external sac of skin that is divided into two compartments; each compartment contains one of the two testes, the glands that produce sperm, and one of the epididymis, where the sperm is stored.

The function of the scrotum is to protect the testes and to keep them at a temperature below the normal body temperature. The scrotum thus protrudes from the body wall. When contracted, it conserves heat; while relaxed it is smooth and elongated, permitting the circulation of air that effects cooling. The relatively cool temperature of the scrotum is thought to be important for the production of viable sperm.
A vertical septum of subcutaneous tissue in the center divides it into two parts, each containing one testis.
Smooth muscle fibers, called the dartos muscle, in the subcutaneous tissue contract to give the scrotum its wrinkled appearance. When these fibers are relaxed, the scrotum is smooth.
The cremaster muscle consists of skeletal muscle fibers and controls the position of the scrotum and testes. When it is cold or a man is sexually aroused, this muscle contracts to pull the testes closer to the body for warmth.

Etiology/Causes of a Hydrocele

The causes of hydrocele can be categorized into four main factors:

Excessive production of fluid within the sac: This occurs when there is an overproduction of fluid within the sac surrounding the testicle e.g. in acute/chronic epididymo-orchitis.
Defective absorption of fluid: This refers to a situation where the normal absorption of fluid within the sac is impaired, leading to the accumulation of fluid e.g. in testicular tumors, Hematocele.
Interference with lymphatic drainage of scrotal structures: Certain conditions, such in case of elephantiasis, torsion of testis, can disrupt the normal drainage of lymphatic fluid from the scrotal area, resulting in the development of a hydrocele.
Connection with a hernia of the peritoneal cavity: In the congenital variety, a hydrocele may be associated with a hernia of the peritoneal cavity, leading to the presentation of a hydrocele of the cord e.g. in patent tunica vaginalis.

Risk Factors

Direct Injury or inflammation of the testes
Prematurity
Testicular tumors
Infections in the testicle or the epididymitis

Pathophysiology

During the seventh month of fetal development, the testicles move from the abdomen into the scrotum.
When the testicle travels downward, a remnant piece of peritoneum wrapped around the testicle, called the tunica vaginalis and this allows fluid present in the abdominal cavity to surround the testicle.
This sac usually closes before birth, preventing additional fluid from going from the abdomen into the scrotum, and the fluid is gradually absorbed within the first year of life.
When the sac remains open tunica vaginalis is patent and connects with the general peritoneal cavity leading to development of a communicating Hydrocele.
The communication is usually too small to allow herniation of intra-abdominal contents. Digital pressure on the Hydrocele does not usually empty it, but the Hydrocele fluid may drain into the peritoneal cavity when the child is lying down.

Types of hydrocele

Non-communicating Hydrocele

Here there is no connection between the abdominal cavity and the sac around the testicle in the scrotum.
This type of Hydrocele is often found in newborns and these often resolve or go away over time.
It may take up to one year for this to happen, but as long as the swelling is decreasing, it can be safely observed.

Communicating Hydrocele

Here the sac does not close and this means that the fluid around the testicle can flow back up into the abdomen.
It is noticeable that the Hydrocele looks smaller early in the day and larger in the evening; the pressure changes cause the fluid to flow back into the abdomen.

CLASSIFICATIONS OF HYDROCELES

Primary hydrocele: A primary hydrocele is characterized by a soft, painless swelling that is usually large in size and makes it difficult to feel the testis. Transillumination can demonstrate the presence of fluid. Although these hydroceles are often asymptomatic, their large size can cause inconvenience and, if left untreated, may lead to atrophy of the testis due to compression or obstruction of blood supply. Early diagnosis during a complete physical examination may reveal small hydroceles in which the testis can be easily palpated within a lax hydrocele. However, in cases where the hydrocele sac is dense, ultrasound imaging is necessary to visualize the testis and reveal any underlying abnormalities. Primary hydroceles are usually painless, similar to testicular tumors.

A common method of diagnosing a primary hydrocele is through transillumination, where shining a strong light through the enlarged scrotum will pass light in the case of a primary hydrocele, while a tumor will not, except in the case of a malignancy with reactive hydrocele.

Its subdivided into four types.

Congenital Hydrocele:

Occurs when the processus vaginalis, a tube-like structure connecting the abdomen to the scrotum, remains open and communicates with the peritoneal cavity.
This allows peritoneal fluid to move, but the opening is usually too small to allow intra-abdominal contents to herniate through.
When pressure is applied to the hydrocele, it usually does not empty, but the fluid may drain into the peritoneal cavity when the individual is lying down.
The swelling cannot be felt above the inguinal ring, resembling a hernia.

Infantile Hydrocele:

Occurs when the processus vaginalis becomes closed at the level of the deep inguinal ring, but the portion beyond it remains open, allowing fluid to accumulate.
This condition is not exclusive to infants and can also occur in adults.
The swelling cannot be felt above the inguinal ring.

Encysted Hydrocele of the Cord:

In this type, both the proximal and distal portions of the processus vaginalis become closed off, while the central portion remains open, leading to the accumulation of fluid within it.
This results in a smooth oval swelling near the spermatic cord, which can be mistaken for an inguinal hernia.
When the testis is gently pulled downwards, the swelling moves downwards and becomes less mobile.

Vaginal Hydrocele (in females):

In females, a related condition known as a “hydrocele of the canal of Nuck” can occur.
This occurs when the canal of Nuck, the equivalent structure to the processus vaginalis in males, fails to close properly, leading to the development of a hydrocele.
This condition may present as a swelling in the groin or labia majora.

Secondary hydrocele: A secondary hydrocele arises from an underlying condition, such as infections (e.g., filariasis, tuberculosis of the epididymis, syphilis), trauma or injury (e.g., post herniorrhaphy hydrocele or malignancy).

Secondary hydroceles are generally smaller, with the exception of those caused by filariasis, which can lead to very large hydroceles.
Testicular infarction, microlithiasis of the testicle, and lithiasis of tunica vaginalis can also contribute to the development of secondary hydroceles.
Testicular diseases, including cancer, trauma (e.g., hernia), and orchitis (inflammation of the testis), can result in secondary hydroceles. They may also occur in infants undergoing peritoneal dialysis. It is important to note that a hydrocele is not a cancerous condition, but clinical evaluation is needed if a testicular tumor is suspected, as there are no documented cases associating hydroceles with testicular cancer in the world literature.

Secondary hydroceles are most commonly linked with acute or chronic epididymo-orchitis and are also observed with testicular torsion and certain testicular tumors. Commonly, a secondary hydrocele is soft and moderately sized, and the underlying testis can be felt. The secondary hydrocele usually resolves when the primary condition is treated.

Other predisposing factors for secondary hydroceles include acute/chronic epididymo-orchitis, testicular torsion, testicular tumors, hematocele, filarial hydrocele, post herniorrhaphy, and hydrocele of a herniated sac.

Diagnosis and Investigations

Through Clinical Presentation: A primary hydrocele is described as having the following characteristics/presentations.

Clinical Presentation.

Fluctuating Size: The swollen area may vary in size, being smaller in the morning and larger later in the day. This fluctuation is known as a positive fluctuation test.
Discomfort: Patients may experience discomfort due to the heaviness of the swollen scrotum.
Scrotal Swelling: Hydroceles can present as painless unilateral or bilateral scrotal swelling.
Transillumination: When examined with a focused beam of light, the scrotum transilluminates, displaying a uniform glow without any internal shadows. Transillumination positive.
Impulse on Coughing: In most cases, the impulse on coughing is negative, although it may be positive in congenital hydroceles.
Reducibility: Hydroceles are usually non-reducible, meaning they cannot be easily pushed back into the abdomen. Reducibility absent.
Palpable Fullness: Upon examination, hydroceles present as a soft, non-tender fullness within the scrotum, which can be felt. Testis cannot be palpated separately. (exception – funicular hydrocele, encysted hydrocele)

Investigations and Diagnostic Findings

Laboratory studies. laboratory studies may be indicated to exclude other surgical or medical conditions that may be in the differential diagnosis.
Ultrasonography. Ultrasonography provides excellent detail of the testicular parenchyma; spermatoceles can be clearly distinguished from hydroceles on sonograms, a testicular tumor can also be identified.
Duplex ultrasonography. Duplex studies provide information regarding testicular blood flow when a hydrocele may be associated with chronic torsion.
Plain abdominal radiography. Plain radiography may be useful for distinguishing an acute hydrocele from a hernia.

Management and Treatment of Hydroceles

Observation for Infants: Most hydroceles appearing in the first year of life often resolve without treatment and therefore require only observation.
Surgical Removal: Hydroceles that persist after the first year or occur later in life may require surgical removal through a procedure known as hydrocelectomy, as they have little tendency towards regression. The method of choice for surgical removal is an open operation under general or spinal anesthesia for adults, and general anesthesia for children. Local infiltration anesthesia is not recommended due to its inability to relieve abdominal pain caused by traction on the spermatic cord.
Aspiration Precautions: If a testicular tumor is suspected, a hydrocele should not be aspirated, as this can lead to the dissemination of malignant cells. Ultrasonography should be used to clinically exclude the presence of a tumor. If no tumor is present, the hydrocele fluid can be aspirated with a needle and syringe.
Post-operative Care: After surgery, the scrotum should be supported, and ice bags can be used to alleviate pain. Regular changes of surgical dressings, observation of drainage, and monitoring for complications are necessary to prevent re-operation.
Complications Management: In cases with the presence of complications, open operation with or without orchiectomy may be preferred, depending on the severity of the complications.
Jaboulay’s Procedure: After aspiration of a primary hydrocele, fluid reaccumulates over the following months, necessitating periodic aspiration or operation. For younger patients, operation is usually preferred, while the elderly or unfit can have aspirations repeated whenever the hydrocele becomes uncomfortably large. Sclerotherapy is an alternative method, involving the injection of 6% aqueous phenol with 1% lidocaine for analgesia, which can inhibit reaccumulation. Multiple treatments may be necessary.
Aspiration and Sclerosing Agents: Aspiration of the hydrocele contents and injection with sclerosing agents, sometimes with tetracyclines, can be effective but is often very painful. However, these alternative treatments are generally regarded as unsatisfactory due to the high incidence of recurrences and the frequent necessity for repetition of the procedure.

Surgical Management.

The surgical management of hydroceles can be approached in several ways, including inguinal, scrotal, and sclerotherapy methods.

Inguinal Approach: This method involves ligation of the processus vaginalis high within the internal inguinal ring and is mostly the preferred procedure for pediatric hydroceles. In cases where a testicular tumor is detected on testicular ultrasonography, an inguinal approach with high control/ligation of the cord structures is necessary.
Scrotal Approach: The scrotal approach includes excision or eversion and suturing of the tunica vaginalis and is recommended for chronic noncommunicating hydroceles. However, this approach should be avoided if there is any suspicion of underlying malignancy.
Sclerotherapy: An additional adjunctive, if not definitive procedure is scrotal aspiration and sclerotherapy of the scrotum using tetracycline or doxycycline solutions. It’s important to note that recurrence after sclerotherapy is common, as is significant pain and epididymal obstruction, making this treatment a last resort in poor surgical candidates with symptomatic hydroceles and in men in whom fertility is no longer an issue.
Hydrocelectomy: This surgical procedure aims to excise the hydrocele sac or reconfigure the remnant of the tunica vaginalis to allow lymphatic drainage via scrotal lymphatics. This method may be considered in cases where other surgical approaches have not been successful.

Nursing Interventions

The nursing interventions appropriate for the child are:

Health education. Provide preoperative education, including a visit with OR personnel before surgery when possible. Discuss anticipated things that may concern the patient, such as masks, lights, IVs, BP cuff, electrodes, the feel of oxygen cannula or mask on nose or face, autoclave and suction noises, and the possibility of the child crying. Additionally, involve the child in age-appropriate discussions about the surgical procedure and encourage the expression of feelings and concerns.
Pre, Intra and Post operative care:

Pre-Operative Care:

Patient Assessment: Conduct a thorough assessment of the patient’s medical history, current health status, and any allergies. This includes obtaining baseline vital signs, laboratory tests, and diagnostic imaging as required.
Education: Provide the patient with information about the upcoming surgery, including preoperative instructions, potential risks, and what to expect during the recovery period.
Medication Management: Review the patient’s current medications and ensure appropriate management, including any required adjustments or discontinuations prior to surgery.
Psychological Support: Offer emotional support and address any anxiety or concerns the patient may have about the surgery.
Preparing the Surgical Site: Ensure the surgical site is properly prepared and sterile, including hair removal if necessary.

Intra-Operative Care:

Patient Positioning: Assist with positioning the patient on the operating table to ensure optimal access for the surgical team.
Monitoring: Continuously monitor the patient’s vital signs, including heart rate, blood pressure, oxygen saturation, and ECG, and respond to any changes promptly.
Sterile Technique: Assist the surgical team in maintaining a sterile environment and provide the necessary equipment and supplies as required.
Anesthesia Management: Collaborate with the anesthesiologist to ensure the patient’s comfort and safety during the administration of anesthesia.
Communication: Facilitate effective communication between the surgical team and other healthcare professionals, and provide support and reassurance to the patient throughout the procedure.

Post-Operative Care:

Recovery Monitoring: Monitor the patient’s vital signs, pain levels, and consciousness as they recover from anesthesia.
Pain Management: Administer prescribed pain medications and assess the patient’s pain levels regularly, providing comfort measures as needed.
Wound Care: Monitor the surgical site for any signs of infection or complications, and provide appropriate wound care as directed by the surgical team.
Mobilization: Encourage early mobilization and assist the patient with repositioning to prevent complications such as deep vein thrombosis and pressure ulcers.
Patient Education: Provide the patient and their family with postoperative instructions, including information on medication management, activity restrictions, and signs of potential complications.
Emotional Support: Offer emotional support to the patient and their family, addressing any concerns and providing reassurance during the recovery process.

3. Reduce risk for infection. Verify that preoperative skin, scrotal, and bowel cleansing procedures have been completed as needed depending on the specific surgical procedure. Apply a sterile dressing to prevent environmental contamination of the fresh wound. Administer antibiotics as indicated and ensure proper hand hygiene and aseptic techniques during care.

4. Monitor fluid volume. Measure and record intake and output, including tubes and drains. Monitor vital signs, noting changes in blood pressure, heart rate and rhythm, and respirations. Gradually resume oral intake as indicated, ensuring the child remains well-hydrated.

5. Relief from pain. Regularly evaluate the child’s pain, noting its characteristics, location, and intensity on a 0–10 scale. Assess and address any anxiety or fear related to the procedure. Identify and address any causes of discomfort other than the operative procedure. Provide additional comfort measures, such as backrubs, heat or cold applications, and age-appropriate distraction techniques. Administer pain medication as prescribed and assess the effectiveness of pain relief measures. Encourage the child to communicate their pain and comfort needs.

6. Promote mobility. Encourage early mobilization and ambulation as tolerated postoperatively to prevent complications such as deep vein thrombosis and promote circulation and respiratory function.

7. Monitor for complications. Assess for signs of postoperative complications such as infection, bleeding, or adverse reactions to anesthesia or medications. Monitor surgical incision sites for signs of inflammation, drainage, or other abnormalities.

8. Encourage adequate nutrition. Provide the child with a balanced and nutritious diet to support the healing process. Offer small, frequent meals if the child’s appetite is reduced and encourage fluid intake to prevent dehydration.

9. Collaborate with the interdisciplinary team. Work closely with the surgical team, child life specialists, and other healthcare professionals to ensure comprehensive care for the child. Communicate any concerns or changes in the child’s condition promptly.

10. Provide age-appropriate activities. Offer age-appropriate activities and play opportunities to promote the child’s emotional well-being and assist with their recovery. Arrange for appropriate entertainment and distraction to alleviate anxiety and boredom during hospitalization.

Complications of Hydroceles

Hematocele Formation: Hematocele, a collection of blood within the sac, can occur due to spontaneous bleeding into the sac or as a result of trauma. If not drained, it may lead to the formation of a clotted hematocele.
Calcification of the Sac: The sac may calcify, leading to the formation of a clotted hydrocele, often resulting from a slow, painless ooze of blood into the tunica vaginalis. This can make it difficult to differentiate from a testicular tumor.
Postherniorrhaphy Hydrocele: A relatively rare complication of inguinal hernia repair, possibly due to disruption of the lymphatics draining the scrotal contents.
Infection and Pyocele: Infection may lead to the formation of pyocele, a collection of pus within the sac.
Testicular Atrophy: Long-standing cases of hydrocele may lead to atrophy of the testis.
Rupture: Rupture of the sac may occur due to trauma or spontaneously. In some cases, absorption of the fluid may lead to a cure.
Herniation: In long-standing cases, the hydrocele sac may herniate through the dartos muscle.

Test Questions

1. Which of the following applies to the defect emerging from residual peritoneal fluid confined within the lower segment of the processus vaginalis?

A. Inguinal hernia
B. Incarcerated hernia
C. Communicating hydrocele
D. Noncommunicating hydrocele

1. Answer: D. Noncommunicating hydrocele

Option D: With a noncommunicating hydrocele, most commonly seen at birth, residual peritoneal fluid is trapped within lower segment of the processus vaginalis (the tunica vaginalis). There is no communication with the peritoneal cavity and the fluid usually is absorbed during the first months after birth.
Option A: An inguinal hernia arises from the incomplete closure of the processus vaginalis leading to the descent of an intestinal portion.
Option B: Incarceration occurs when the hernia becomes tightly caught in the hernia sac.
Option C: A communicating hydrocele usually is associated with an inguinal hernia because the processus vaginalis remains open from the scrotum to the abdominal cavity.

2. An infant with hydrocele is seen in the clinic for a follow-up visit at 1 month of age. The scrotum is smaller than it was at birth, but fluid is still visible on illumination. Which of the following actions is the physician likely to recommend?

A. Massaging the groin area twice a day until the fluid is gone.
B. Referral to a surgeon for repair.
C. No treatment is necessary; the fluid is reabsorbing normally.
D. Keeping the infant in a flat, supine position until the fluid is gone.

2. Answer: C. No treatment is necessary; the fluid is reabsorbing normally.

Option C: A hydrocele is a collection of fluid in the scrotum that results from a patent tunica vaginalis; illumination of the scrotum with a pocket light demonstrates the clear fluid; in most cases, the fluid reabsorbs within the first few months of life and no treatment is necessary.
Options A and D: Massaging the area or placing the infant in a supine position would have no effect.
Option B: Surgery is not indicated.

3. Nurse Jeremy is evaluating a client’s fluid intake and output record. Fluid intake and urine output should relate in which way?

A. Fluid intake should be double the urine output.
B. Fluid intake should be approximately equal to the urine output.
C. Fluid intake should be half the urine output.
D. Fluid intake should be inversely proportional to the urine output.

3. Answer: B. Fluid intake should be approximately equal to the urine output.

Option B: Normally, fluid intake is approximately equal to the urine output. Any other relationship signals an abnormality.
Option A: Fluid intake that is double the urine output indicates fluid retention
Option C: Fluid intake that is half the urine output indicates dehydration.
Option D: Normally, fluid intake isn’t inversely proportional to the urine output.

4. When explaining to the parents of a child with hydrocele about the possible cause of the condition, the nurse bases this explanation on the interpretation that hydrocele is most likely the result of which of the following:

A. Blockage in the inguinal canal.
B. Failure of the upper part of the processus vaginalis to atrophy.
C. A patent processus vaginalis that results in the collection of fluid along the spermatic cord.
D. An obliterated processus vaginalis that allows fluid to accumulate in the scrotal sac.

4. Answer: C. A patent processus vaginalis that results in the collection of fluid along the spermatic cord.

Option C: A hydrocele is a fluid collection within the tunica vaginalis of the scrotum or along the spermatic cord.
Options A, B, C: These processes does not occur in hydrocele.

5. Shortly after an infant is returned to his room following hydrocele repair, the infant’s mother tells the nurse that the child’s scrotum looks swollen and bruised. Which of the following responses by type nurse is the most appropriate?

A. “Let me see if the doctor has ordered aspirin for him. If he did, I’ll get it right away.”
B. “Why don’t you wait in his room? Then you can ask me any questions when I get there.”
C. “What you are describing is unusual after this type of surgery. I’ll let the doctor know.”
D. “This is normal after this type of surgery. Let’s look at it together just to be sure.”

5. Answer: D. “This is normal after this type of surgery. Let’s look at it together just to be sure.”

Option D: Swelling and bruising of the surgical site is a usual occurrence right after the surgery. Elevation of the scrotal area and anti-inflammatory agents can be administered as ordered by the physician.
Option A: Aspirin is not the drug of choice given for pediatric patients.
Option B: Answering questions could relieve the anxiety felt by the family and the patient.
Option C: Swelling and bruising are normal occurrences for the patient after the surgery.

Hydrocele Read More »

Acute Glomerulonephritis

Acute glomerulonephritis refers to a specific set of renal diseases in which an immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, mesangium, or capillary endothelium.

Acute glomerulonephritis (GN) is an inflammatory process involving the glomerulus of the kidney.

It is inflammation of the glomerulus.

Acute glomerulonephritis is the most serious and potentially devastating form of the various renal syndromes. Acute glomerulonephritis progresses to chronic glomerulonephritis in about 30% of adults.

This condition usually results in a clinical syndrome consisting of:

Hematuria
Proteinuria
Hypertension
Renal insufficiency
Azotemia. (elevated urea and creatinine compounds)

Incidence

Glomerulonephritis can occur at any age; it has a higher incidence in males than in females.

It is common in the young ones and the peak age is 7-10 years. Adolescents and young adults are also commonly affected by the acute glomerulonephritis.

CLICK HERE for the Anatomy of the Urinary System

Risk Factors

Throat infection: Winter or early spring
Pyoderma : Risk of infection after pyoderma: 25%
Peak incidence in pre‐school children.
Clinically apparent GN
occurs in < 2% of children infected with strep infection

Etiology

Acute GN can be due to a primary renal disease or to a systemic disease:

Its onset is usually secondary to infection of the upper respiratory tract, most commonly caused by group A beta – hemolytic streptococci (post streptococcal infection)
Malaria parasites (falciparum malariae)

It may be a result of the primary infection elsewhere in the body and be caused by primary staphylococcus, pneumococcus or a virus

It is thought to be due to an abnormal immune reaction to infection

Non streptococcal postinfectious GN may also result from infection by other bacteria, viruses, parasites, or fungi. Bacteria besides group A streptococci that can cause acute GN include the following:

Staphylococci, Diplococci, Other streptococci, Mycobacteria, Salmonella Tryphosa, Brucella sues, Treponema pallidum, Corynebacterium bovis Actinobacilli e.t.c.
Viruses e.g. Cytomegalovirus (CMV), coxsackievirus, Epstein-Barr virus (EBV), hepatitis B virus (HBV)

Goodpasture syndrome, a group of diseases affecting the lungs and kidneys.

Rare diseases that inflame blood vessels like granulomatosis with polyangiitis (formerly Wegener’s disease) Granulomatosis with polyangiitis is an uncommon disorder that causes inflammation of the blood vessels in your nose, sinuses, throat, lungs and kidneys. Formerly called Wegener’s granulomatosis, this condition is one of a group of blood vessel disorders called vasculitis. It slows blood flow to some of your organs

Pathophysiology

Following an occurrence of a streptococcal infection which can either be sore throat or a skin infection, there follows an immune response which is mounted against the streptococcal infection (a specific antibody is produced against streptococci)
These antibodies destroy the glomerulus because it resembles the antigens of the streptococci.
This usually occurs 2-3 weeks after the streptococcal infection has taken place. This is characterized by diffused inflammation of the renal cortex (glomeruli) of both kidneys.
The destruction of the glomerulus permits the red blood cells which is passed in urine as haematuria and pus-cells, RBC casts.
The destruction further causes reduction in the filtration process
Reduced ultra filtration stimulates angiotensin I release which in turn is changed to angiotensin II which causes constriction of arterioles, hence increasing total arteriolar resistance, leading to elevation of blood pressure.
Angiotensin ii release further causes production of aldosterone which causes reabsorption of sodium and water, leading to increase in cardiac output and elevation of blood pressure.

Clinical Features of Acute Glomerulonephritis.

Most often, the patient is a boy, aged 2-14 years, who suddenly develops puffiness of the eyelids and facial edema in the setting of a poststreptococcal infection. The urine is dark and scanty, and the blood pressure may be elevated.

Onset of symptoms is usually abrupt.
Nonspecific symptoms include weakness, fever, abdominal pain, and malaise.
Usually sudden onset with history of sore throat or skin infection, elevated temperature, headache and vomiting.
Body swellings of the face and lower extremities which tends to become worse in the mornings on waking up with elevation of hypostatic pressure.
Costovertebral angle tenderness and flank pain likened to renal colic.
Hematuria is a universal finding, even if it is microscopic. Gross hematuria is reported in 30% of pediatric patients.
Oliguria
Edema (peripheral or periorbital) is reported in approximately 85% of pediatric patients; edema may be mild (involving only the face)
Hypertension often develops. In severe cases, it may be extremely high with severe headache, palpitations, easy fatigability, visual disturbances, vomiting and convulsions (hypertensive encephalopathy).
Features of cardiac failure
As the disease progresses, the patient experiences shortness of breath, lethargy and anorexia.
Headache may occur secondary to hypertension; confusion secondary to malignant hypertension may be seen in as many as 5% of patients.
Shortness of breath or dyspnea on exertion secondary to heart failure or pulmonary edema; usually uncommon, particularly in children.
Possible flank pain secondary to stretching of the renal capsule.
Urinary changes:

Decreased urinary output-oliguria
Microscopic haematuria making the urine to appear dark, concentrated and smoky
Albumin is always present in large amounts
Casts may be present and can be seen

Clinical Features Summary

Abrupt onset
• Age 4‐ 12 years, M>F
• Latent period : Throat infection : 1‐2 weeks
• Skin infection : 3‐6 weeks
HEMATURIA
• Smoky brown or Cola colored
• Glomerular: dysmorphic RBC, casts in freshly spun urine
PROTEINURIA
• Mild to moderate but nephrotic range is rare
OLIGURIA
• Transient – 50%, Anuria rare
EDEMA : 85%
– Mild : periorbital or pedal
– Severe : hypertension, pleural effusion or ascites
– Adolescents : more likely face and legs
HYPERTENSION: in 80%
– Headache, Somnolence
– Changes in mental status
– Anorexia, Nausea , Convulsions
• HYPERTENSIVE EMERGENCY: 10%
‐ BP > 30% increased for age and sex
‐ Evidence of encephalopathy
‐ Heart failure or pulmonary edema
• AZOTEMIA : varying degrees
• CIRCULATORY CONGESTION : 20%
‐ Dyspnea, Orthopnea
‐ Cough, Tachycardia, Gallop rhythm
‐ CCF, Pulmonary edema

Diagnosis

In the setting of a postinfectious acute nephritis, a latent period of up to 3 weeks occurs before onset of symptoms. However, the latent period may vary; typically 1-2 weeks for post pharyngitis cases and 2-4 weeks for cases of post dermal infection (i.e, pyoderma).

Onset of nephritis within 1-4 days of streptococcal infection suggests preexisting renal disease.
Urine: protein, microscopy for pus cells, red blood cells, red blood cell casts, proteins positive, glucose positive.
Blood: urea and Creatinine levels, and electrolytes
Ultrasound scan of the kidneys
Blood pressure
Throat and skin swab where indicated for C&S
Blood cultures: Indicated in patients with fever, immunosuppression, intravenous drug use history, indwelling shunts, or catheters.
Antinuclear antibody (systemic lupus erythematosus)
Renal biopsy is required for definitive diagnosis, particularly in primary renal diseases. Renal Biopsy is indicated only in;
• Hepatitis B infection
• Nephritis
• Infective endocarditis
• Associated with HSP(Henoch-Schonlein purpura (also known as IgA vasculitis) is a disorder that causes the small blood vessels in your skin, joints, intestines and kidneys to become inflamed and bleed)

Management

Admission is recommended for patients with anuria, nephrotic syndrome, massive proteinuria, significant hypertension, or pulmonary symptoms.
Salts (sodium restriction)

Should not be used in cooking or added to food (salt free diet).
If oedema is severe, no salt diet should be given.
Avoid or use with caution any drugs excreted in by the kidney
The disease is usually self-limiting and the majority of patients may recover spontaneously.

3. Rest:

The patient should be nursed in a bed rest in a warm well-ventilated room. Ambulation is encouraged in an attempt to reduce oedema and DVT.

4. Dietary regulations (Diet regimen)

Proteins in the diet, about 20 – 40g of protein daily will be adequate.
Adequate calorie from carbohydrates and fats ensures minimum protein breakdown.

5. Fluids and electrolytes

Assess the patient frequently for signs and symptoms of fluid overload.
Daily weighing of the patient.
Fluids must be encouraged2-3lires in24hours to increase urinary output.
An intake and output chart must be kept and the urine examined daily for albumin, RBCs and casts.
Correction of electrolyte abnormalities (ie, hypocalcemia, hyperkalemia) and acidosis, if present
Restrict fluids in patients with significant edema.
Loop diuretics are indicated for patients with nephrotic syndrome (4% of patients) or massive proteinuria.
Eradicate streptococcal causes by oral antibiotic therapy; Penicillin is indicated in nonallergic patients e.g. Phenoxy methyl penicillin 500mg qid. Child: 10 – 20mg per dose Or Amoxicillin 500mg tds. Child: 15mg/kg per dose. If allergic to penicillin give erythromycin every 6hours. Child: 15mg/kg per dose

6. Prophylactic treatment: penicillin every month or erythromycin to minimize reoccurrence.

7. Agents useful in treating hypertension include calcium channel blockers e.g. nifedipine, amlodipine and nitroprusside sodium.

8. Dialysis incase of;
– Fluid overload
– Severe azotemia
– Electrolyte abnormalities

9. Pulmonary edema
– Aggressive diuresis , Oxygen, Morphine, Ventilation

10. Hyperkalemia
– Oral/iv Restriction, Potassium binding resins
– Nebulized Salbutamol, Glucose insulin
– Calcium infusion

Prognosis

Is always poor with acute glomerulonephritis than with nephritic syndrome

Nursing Diagnosis

Ineffective breathing pattern related to the pulmonary edema or cardia failure as evidenced by shortness of breath.
Altered urinary elimination related to decreased bladder capacity or irritation secondary to infection as evidenced by oliguria.
Excess fluid volume related to a decrease in regulatory mechanisms (renal failure) as evidenced by edema.
Risk for infection related to a decrease in the immunological defense.
Imbalanced nutrition less than body requirements related to anorexia, nausea, vomiting.
Risk for impaired skin integrity related to edema and pruritus.
Hyperthermia related to the ineffectiveness of thermoregulation secondary to infection as evidenced by a thermometer reading above normal ranges.
Dialysis in case of;
– Fluid overload
– Severe azotemia
– Electrolyte abnormalities
Pulmonary edema
– Aggressive diuresis , Oxygen, Morphine, Ventilation
Hyperkalemia
– Oral/iv Restriction, Potassium binding resins
– Nebulized Salbutamol, Glucose insulin
– Calcium infusion

Nursing Care Planning and Goals

Nursing care planning goals for a child with acute glomerulonephritis are:

Excretion of excessive fluid through urination.
Demonstration of behaviors that would help in excreting excessive fluids in the body.
Improvement of distended abdominal girth.
Improvement of respiratory rate.
Participation and demonstration of various ways to achieve effective tissue perfusion.

Nursing Interventions

Activity. Bed rest should be maintained until acute symptoms and gross hematuria disappear.
Prevent infection. The child must be protected from chilling and contact with people with infections.
Monitor intake and output. Fluid intake and urinary output should be carefully monitored and recorded; special attention is needed to keep the intake within prescribed limits.
Monitor Blood Pressure. Blood pressure should be monitored regularly using the same arm and a properly fitting cuff.
Monitor urine characteristics. The urine must be tested regularly for protein and hematuria using dipstick tests.

Evaluation

Goals are met as evidenced by:

Excretion of excessive fluid through urination.
Demonstration of behaviors that would help in excreting excessive fluids in the body.
Improvement of distended abdominal girth.
Improvement of respiratory rate.
Participation and demonstration of various ways to achieve effective tissue perfusion.

Prevention

Early treatment of throat and skin infections
Avoid overcrowding
Adequate ventilation in dwellings.

Complications

Renal failure
Nephritic syndrome
Hypertensive encephalopathy
Heart failure
Pulmonary edema.
The patient may have both nephritic syndrome and acute glomerulonephritis and they are called to have nephritic nephritis and the prognosis is poor.

Acute Glomerulonephritis Read More »

Cataract

Cataract refers to the clouding or opacity of the eye’s lens, leading to impaired vision. This condition occurs when proteins in the lens clump together, causing light to scatter as it passes through the lens. This prevents a sharply defined image from forming on the retina, resulting in blurred or diminished vision.

Cataracts can develop in one or both eyes but do not spread from one eye to the other.
The loss of transparency, or opacity formation is called Cataract.

WHEN EYES WORK PROPERLY

In a healthy eye, light passes through the cornea and pupil, and the lens focuses this light to produce clear, sharp images on the retina. When a cataract forms, the lens becomes cloudy, which disrupts this process. The light becomes scattered, and the image that reaches the retina is blurred. As a cataract progresses, it can severely impact vision, making daily tasks like reading, driving, and recognizing faces difficult.

Light passes through the cornea and the pupil to the lens.
The lens focuses light and produces clear, sharp images on the retina.
As a cataract develops, the lens becomes clouded, which scatters the light and prevents a sharply defined image from reaching the retina. As a result, vision becomes blurred.
Cataract can occur to one eye or both

Risk Factors for Cataracts in Adults

Cataracts are primarily associated with aging, but several other factors can increase the risk:

Age: The most significant risk factor, with cataracts being prevalent in older adults.
Sunlight (UV light) Exposure: Prolonged exposure to ultraviolet radiation from the sun can increase the risk.
Smoking: Tobacco smoke contains harmful chemicals that can damage the lens.
Diabetes: High blood sugar levels can cause changes in the lens, leading to cataracts.
Trauma: Both blunt and penetrating injuries to the eye can cause cataracts.
Family History: A genetic predisposition can increase the likelihood of developing cataracts.
Corticosteroid Therapy: Long-term use of corticosteroids can contribute to cataract formation.
Radiation Exposure: Exposure to radiation, including X-rays and other forms of ionizing radiation, can increase the risk.
Electrical Injury: Electric shocks can cause cataracts due to the energy damaging the lens.
Myotonic Dystrophy: This genetic disorder can lead to early-onset cataracts.
Ocular Inflammation (Uveitis): Chronic inflammation of the uvea can damage the lens and lead to cataract formation.

Causes of Cataracts

Aging: The most common cause, leading to changes in the lens over time.
Ocular Diseases: Conditions like diabetes mellitus and uveitis can cause cataracts.
Previous Ocular Surgery: Surgery for conditions like glaucoma can increase the risk of cataracts.
Systemic Medications: Prolonged use of steroids and phenothiazines can contribute to cataract formation.
Trauma: Injuries to the eye, including those involving intraocular foreign bodies, can lead to cataracts.
Ionizing Radiation: Exposure to X-rays and UV rays can damage the lens.
Congenital Factors: Some infants are born with cataracts due to maternal illnesses like rubella or genetic conditions.
Inherited Abnormalities: Conditions like myotonic dystrophy, Marfan syndrome, and high myopia can predispose individuals to cataracts.
Dehydration: Severe dehydration, such as that seen in cholera victims, can increase the risk, as noted in some cases in India.

Types of Cataracts

1. Acquired Cataracts

Age-Related Cataract: The most common type, typically developing after age 40.
Presenile Cataract: Occurs in individuals younger than the typical age range for cataracts.
Traumatic Cataract: Results from an injury to the eye.
Drug-Induced Cataract: Caused by prolonged use of certain medications, such as corticosteroids.
Secondary Cataract: Develops as a result of other medical conditions like diabetes or ocular inflammation.

2. Congenital Cataracts

Inborn Cataract: Present at birth and often associated with genetic conditions or maternal infections.

Classifications of Cataracts

Age-Related Cataract Classification

A. Morphological Classification

NUCLEAR CATARACT

Nuclear Cataract: Occurs in the central nucleus of the lens, often leading to a yellowing or browning of the lens. This type can progress slowly over years. Most common.

CORTICAL CATARACT

Cortical Cataract: Occur on the outer edge/layer of the lens (cortex). Begins on the outer edge of the lens, characterized by white, wedge-shaped opacities that spread towards the center. This type often causes issues with glare.

SUBCAPSULAR CATARACT

Occur just under the capsule of the lens.
Starts as a small, opaque area.
It usually forms near the back of the lens, right in the path of light on its way to the retina.
It’s interferes with reading vision
Reduces vision in bright light
Causes glare or halos around lights at night.

POSTERIOR SUBCAPSULAR CATARACTS

Posterior Subcapsular Cataracts: Begins at the back of the lens (posterior pole) and spreads to the periphery or edges of the lens. It can be developed when: Part of the eye is chronically inflamed or Heavy use of some medications (steroids).
Affects vision more than other types of cataracts because the light converges at the back of the lens. Dilating drops are useful in this type by keeping the pupils large and thus allow more light into the eye.

B. Maturity Classification

IMMATURE CATARACT

Immature Cataract: The lens is partially opaque, with some areas remaining clear. Vision is still possible but may be significantly impaired.

MATURE CATARACT

Mature Cataract: The lens is completely opaque, leading to a significant reduction in vision. The lens may appear pearly white.
Lens appears pearly white
Mature cataract, with obvious white opacity at the Centre of pupil.

HYPERMATURE CATARACT ( Morgagnian)

Hypermature Cataract (Morgagnian): The lens cortex becomes liquefied, and the lens nucleus may sink within the capsule. This can lead to a wrinkled anterior capsule and potentially severe complications.

Intumescent: The proteins in the lens break down and the lens absorbs water and becomes swollen, appearing milky white.
Liquefactive/Morgagnian Type: Cortex undergoes auto-lytic liquefaction and turns uniformly milky white. The nucleus loses support and settles to the bottom.

CONGENITAL CATARACT

Congenital Cataract Classification

Occur in about 3:10000 live births.
2/3 of case are bilateral (half of the cause can be identified)
The most common cause is genetic mutation usually.
It can cause amblyopia(lazy eye) in infants.

It is divided to:

1. Systemic Association

Metabolic Disorders: Conditions like galactosemia and galactokinase deficiency can cause cataracts in infants.
Prenatal Infections: Infections like congenital rubella can lead to cataract formation in newborns.
Chromosomal Abnormalities: Genetic syndromes such as Down syndrome, Patau syndrome, and Edward syndrome are associated with a higher risk of congenital cataracts.

2. Non-Systemic Association

Idiopathic Cases: In some cases, the cause of congenital cataracts is unknown.

Clinical Presentation of Cataracts

Blurred Vision: Gradual loss of clarity, leading to difficulty in seeing fine details.
Reduced Visual Acuity: Difficulty in seeing both near and distant objects.
Night Vision Problems: Increased difficulty seeing in low light or at night.
Glare Sensitivity: Bright lights, such as sunlight or car headlights, may cause discomfort or halos.
Halos Around Lights: Rings of light may appear around bright sources.
Double Vision: Seeing two images of a single object, typically in one eye.
Color Distortion: Colors may appear faded or yellowed.

Differential Diagnosis

Glaucoma: Increased intraocular pressure leading to optic nerve damage.
Diabetic Retinopathy: Damage to the retinal blood vessels due to diabetes.
Hypertensive Retinopathy: Retinal damage caused by high blood pressure.
Age-Related Macular Degeneration: Deterioration of the central part of the retina.
Retinitis Pigmentosa: A group of genetic disorders causing retinal degeneration.
Trachoma: A bacterial infection leading to roughening of the inner eyelid.
Onchocerciasis (River Blindness): A parasitic infection that can cause blindness.
Vitamin A Deficiency: Can lead to night blindness and, in severe cases, total blindness.

Clinical Findings / Investigations

• The most common objective finding associated with cataracts is decreased visual acuity.
• This is measured with an office wall chart or near-vision card.

VISUAL ACUITY

Acuity refers to the sharpness of vision or how clearly you see an object.
• In this test, the doctor checks to see how well you read letters from across the room
• Eyes are tested one at a time, while the other eye is covered.
• Using the chart with progressively smaller letters from top to bottom, to determine the level of vision.

2. SLIT LAMP EXAM (SLE)

• SLE allows the ophthalmologist to see the structures of the eye under
magnification.
• The microscope is called a slit lamp because it uses an intense slit of light to illuminate your cornea, iris, and lens.
• These structures are viewed in small sections to detect any small
abnormalities.

3. DILATED EXAM

• Dilating drops are placed in the eyes to dilate the pupils wide and provide a better view to the back of the eyes.
• It allows the ophthalmologist to examine the lens for signs of a cataract and, if needed, determine how dense the clouding is.
• It also allows for examination of the retina and the optic nerve.
• Dilating drops usually keep your pupils open for a few hours before
their effect gradually wears off.

4. REFRACTION

$“Which is clearer?” “One or two?” Learning Manifest Refraction$

• This is performed by your doctor to see if the decrease in vision is simply
due for need for new glasses, or if there is another process at work that accounts for the decrease in visual acuity.

Treatment/Management of Cataracts

1. Non-Surgical Management.

Glasses: Cataracts alter the refractive power of the natural lens, so glasses can help maintain good vision.
Make sure that eyeglasses or contact lenses are the most accurate prescription possible.
Patient Advice:

Lighting: Improve home lighting with more or brighter lamps.
Sunglasses: Wear sunglasses outdoors to reduce glare.
Night Driving: Limit night driving.

2. Surgical Management.

Indications:

Changes in eyeglasses no longer improve vision.
Quality of life is significantly impacted.
Cataract removal is likely to improve vision (when visual acuity cannot be improved with glasses).

Surgical Techniques:

Phacoemulsification:

Procedure: A tiny, hollowed tip uses high-frequency (ultrasonic) vibrations to break up the cloudy lens (cataract). The same tip is used to suction out the lens.
Advantages: Minimally invasive, precise, and generally results in faster recovery.

Extracapsular Cataract Extraction (ECCE):

Procedure: The nucleus and cortex are removed from the capsule, leaving behind the intact posterior capsule, peripheral anterior capsule, and zonules.
Advantages: Preserves the capsular bag, reducing the risk of complications like vitreous prolapse.

Intracapsular Cataract Extraction:

Procedure: The entire lens (nucleus, cortex, and capsule) is removed as a single piece after breaking the zonules.
Advantages: Eliminates the risk of posterior capsular opacification (after-cataract).
Disadvantages: Increased risk of complications like vitreous prolapse and retinal detachment.

3. Pre-Operative Assessment:

General Health Evaluation:
- Blood pressure check.
- Assessment of patient’s ability to cooperate with the procedure and lie flat during surgery.
Eye Drop Instillation Instruction: Teach patients how to instill eye drops correctly.
Reassurance and Consenting: Provide reassurance and obtain informed consent.
Intraocular Pressure: Ensure normal intraocular pressure or adequate control of pre-existing glaucoma.

4. Post-Operative Care:

Discharge: Patients are usually discharged home the same day.
Follow-Up: Patients are seen in the office the next day, the following week, and then again after a month to monitor healing progress.
Patient Advice:
- Discomfort: Mild discomfort is normal for a couple of days after surgery.
- Eye Patch/Shield: Wear an eye patch or protective shield the day of surgery.
- Exertion: Avoid strenuous exertion to prevent increased pressure in the eyeball.
- Trauma: Avoid ocular trauma.
Medications: The doctor may prescribe medications to prevent infection and control eye pressure:
- Steroid drops: To reduce inflammation.
- Antibiotic drops: To prevent infection.

Complications of Cataract Surgery

Infective Endophthalmitis: A rare but severe infection that can lead to vision loss.
Suprachoroidal Hemorrhage: Severe intraoperative bleeding that can cause permanent vision loss.
Uveitis: Inflammation of the uvea, more common in patients with diabetes or a history of ocular inflammation.
Ocular Perforation: A rare but serious complication.
Refractive Error: Incorrect intraocular lens power can lead to residual vision problems.
Posterior Capsular Rupture and Vitreous Loss: Can increase the risk of retinal detachment.

Nursing Care Plan for Cataracts

Assessment	Nursing Diagnosis	Goals/Expected Outcomes	Interventions	Rationale	Evaluation
Patient reports blurred vision, difficulty seeing at night, and sensitivity to glare	Disturbed Sensory Perception related to cataract formation as evidenced by blurred vision, difficulty seeing at night, and sensitivity to glare	To improve visual acuity and reduce sensory disturbances within 2 weeks	– Assess visual acuity using a Snellen chart or other appropriate tools – Educate the patient about cataract symptoms and the impact on vision – Advise on environmental modifications, such as using brighter lights and reducing glare – Encourage the patient to use magnifying aids or reading glasses as needed	– Regular assessment of visual acuity helps in monitoring the progression of cataracts – Patient education empowers the patient with knowledge about their condition – Environmental modifications can help manage symptoms and improve quality of life – Magnifying aids can assist in daily activities and reading	– Patient reports improved ability to see clearly and manage symptoms with environmental modifications
Patient expresses concern about vision loss and the need for surgery	Anxiety related to vision loss and surgical intervention as evidenced by patient expressing concern and fear about the procedure	To reduce anxiety and improve the patient’s understanding of the treatment plan within 1 week	– Provide information about cataract surgery, including the procedure, risks, and benefits – Reassure the patient that cataract surgery is a common and effective treatment – Discuss postoperative care and recovery expectations – Offer emotional support and address any specific concerns or fears	– Providing information helps alleviate fear and confusion about the surgery – Reassurance and education can reduce anxiety and increase patient comfort – Understanding postoperative care and recovery helps prepare the patient for the process – Emotional support fosters a positive therapeutic relationship	– Patient reports feeling less anxious and demonstrates understanding of the surgical procedure and recovery process
Assessment of preoperative and postoperative visual acuity and any changes	Ineffective Health Maintenance related to inadequate knowledge of postoperative care as evidenced by patient’s lack of understanding of care instructions	To ensure proper adherence to postoperative care and monitor visual changes within 1 week	– Provide detailed instructions on postoperative care, including eye drop administration, avoiding eye strain, and recognizing signs of complications – Schedule follow-up appointments to monitor recovery and visual acuity – Educate the patient on signs of infection or complications, such as increased redness, pain, or vision changes – Review the importance of attending follow-up appointments and adhering to care instructions	– Detailed instructions help prevent complications and promote proper healing – Follow-up appointments are crucial for monitoring progress and addressing any issues – Early recognition of complications can prevent further problems and improve outcomes – Adherence to care instructions ensures optimal recovery and visual improvement	– Patient demonstrates proper postoperative care practices and reports no signs of complications – Visual acuity improves as expected and follow-up appointments are attended
Patient reports difficulty performing daily activities and decreased quality of life due to vision changes	Impaired Functional Ability related to decreased visual acuity as evidenced by difficulty performing daily activities and decreased quality of life	To enhance functional ability and quality of life through improved visual acuity within 4 weeks	– Assess the impact of visual changes on daily activities and quality of life – Collaborate with an occupational therapist to address functional limitations and recommend adaptive strategies – Provide resources for low vision aids and support services – Encourage the patient to engage in activities they enjoy to improve overall well-being	– Assessment of impact helps tailor interventions to the patient’s specific needs – Occupational therapy can provide strategies and tools to improve daily functioning – Resources for low vision aids and support services can enhance independence and quality of life – Encouraging engagement in enjoyable activities supports emotional and psychological well-being	– Patient reports improved ability to perform daily activities and an enhanced quality of life
Patient has difficulty understanding and following medication regimens and postoperative care	Knowledge Deficit related to unfamiliarity with postoperative medication and care instructions as evidenced by patient’s questions and confusion	To improve patient understanding and adherence to the medication and care regimen within 1 week	– Provide clear, written instructions on medication administration and postoperative care – Demonstrate the proper technique for administering eye drops and caring for the eye – Use teach-back methods to confirm understanding and clarify any questions – Schedule a follow-up call or visit to review instructions and address any issues	– Written instructions reinforce verbal teaching and provide a reference for the patient – Demonstration ensures proper technique and reinforces learning – Teach-back methods confirm understanding and allow for clarification of doubts – Follow-up calls or visits provide additional support and address any remaining concerns	– Patient demonstrates correct medication administration and adherence to postoperative care instructions

Cataract Read More »

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

Corneal Ulcers Read More »

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.

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