What everyone needs to know about Stroke

“Stroke is a medical emergency that strikes suddenly and it should be treated immediately to prevent neurological deficit and permanent disability.” Stroke results from an alteration in normal blood to the brain. Stroke is a term used to describe neurological changes caused by an interruption in blood supply to a part of the brain.

Define Stroke:-

“Stroke is a medical emergency that strikes suddenly and it should be treated immediately to prevent neurological deficit and permanent disability.” Stroke results from an alteration in normal blood to the brain.

“Cerebrovascular accident (CVA) is a medical condition in which poor blood flow to the brain results in brain cells die.”

“Stroke is a term used to describe neurological changes caused by an interruption in blood supply to a part of the brain.”

Causes and Types of Stroke:-

  • Ischemic Stroke:- An acute ischemic stroke caused by blockage of a cerebral artery by either thrombus or embolism.
    • Thrombotic Stroke:- Stroke that is caused by blood clots or a thrombus. A thrombotic stroke is an account for more than half of all stroke. It is commonly associated with atherosclerosis, arthritis, or vasculitis.
    • Embolic Stroke:- An embolic stroke is caused by a traveling thrombus or a group of thrombin that breaks off from one area of the body and travels through the cerebral artery via the carotid artery. It is caused by or associated with arterial fibrillation, rheumatic heart disease, myocardial infarction, ischemic heart disease, or atherosclerosis.
  • Hemorrhagic Stroke:- In this hemorrhagic stroke blood vessel’s integrity is interrupted and bleeding occurs into the brain tissues and the space surrounding the brain commonly intracerebral hemorrhage and subarachnoid hemorrhage.
    • Intracerebral Hemorrhage:- Bleeding into the brain cerebral tissue which is generally resulting from hypertension.
    • Subarachnoid Hemorrhage:- It is much more common and results from bleeding into the subarachnoid space. This type of stroke caused by a ruptured aneurysm or arteriovenous malformation.

Risk factors of Stroke:-

  • Age (above 60 years).
  • Gender (male has 30% more chances then female).
  • Family History.
  • Head Injury.
  • History of migraine or Headache.
  • Sickle cell disease.
  • Smoking, chronic alcoholism.
  • Tobacco using.
  • Drug abuse (cocaine).
  • Obesity.

Pathophysiology of Stroke:-

1. Ischemic Condition:-

Due to Ischemic condition — lack or loss of blood supply to brain tissue — Brain tissue ceases to function (within 60 second) — cell death and permanent changes with 3-10 minutes (after approximately 2-3 hours irreversible injury possible occur) — Altered central metabolism — Infarction — Neuronal injury — Penumbra (infarcted area or area of hypoperfusion in the brain) — coma or death.

2. Hemorrhagic Condition:-

Due to hemorrhage — rupture of vessels and bleeding — Haematoma — Tissue injury by compression of tissues from hematoma — Pressure of hematoma leads to loss of blood supply — Infarction — Neuronal injury — Penumbra — Coma or death.

Clinical Manifestation of Stroke:-

1.General Problems or Symptoms:-

  • Headache.
  • Change in mental status.
  • Vomiting.
  • Seizures.
  • Fever.

2. Early Warning Signs:-

  • F = Facial drooping.
  • A = Arms weakness.
  • S = Speech difficulty.
  • T = Time to call emergency services.

3. Ischemic Stroke:-

  • Transient Hemiparesis.
  • Hemiplegia.
  • Loss of speech and sensory loss.

4. Hemorrhagic Stroke:-

  • Occipital or neutral headache.
  • Syncope (sudden fall down).
  • Vertigo.
  • Paraesthesia (something is pinning to patient or pricking).
  • Transient paralysis.
  • Epistaxis (bleeding from the nose).
  • Retinal hemorrhage.

5. Cognitive Manifestation:-

  • Aphasia:- Communication disorder or deficit in the ability to communicate in all aspects like speaking, writing, reading, and understanding.
  • Alexia/Dyslexia:- Difficulty in reading or learning to read.
  • Agraphia:- writing difficulty or disorder.
  • Acalculia:- Inability to calculate.

6. Motor Changes:-

  • Hemiplegia.
  • Hemiparesis.
  • Apraxia:- Inability to perform correct movements.
  • Ataxia:- Failure of muscle co-ordination leads to unsteadiness in standing and walking.
  • Dysphasia.
  • Dysarthria.

7. Sensory Changes:-

Decreases senses typically occur on the affected site of the body.

  • Agnosia:- It is a disturbance or inability to recognize familiar objects or things, the most common types are visual and auditory.
  • Hemianopia (Homonymous Hemianopia):- It is the visual loss on the same half of the visual field of each eye so that client has half or normal vision.
  • Horner’s Syndrome:- It is the paralysis of sympathetic nerves to eyes causing sinking of the eyeball, ptosis, myosis (constricted pupils), and lack of tearing in eyes.

8.Unilateral Neglect:-

In this the client is unaware of the existence of his/her paralysed site. manifestation of unilateral neglect include:-

  • Failure to attempt to one side of the body.
  • Failure to respond to stimuli on one side of the body.
  • Failure to Use one extremity.
  • Failure to orient the head and eye to one side.
  • Incontinence (bowel or bladder).

Stroke Investigation:-

  • Physical Examination.
  • CET.
  • MRI.

Stroke Medical Management:-

1.Fibrinolytic or Thrombolytic Therapy:-

Example:- rt-PA (recombinant tissue plasminogen activator).

This drug is used for the treatment of acute ischemic stroke. rt-PA degrade thrombus by breaking down fibrin. [dose;- The dose of rt-PA for ischemic stroke is 0.9 mg/kg administered intravenously over 1 hour] after thrombolytic therapy the client is sent to ICU for careful monitoring of vital signs nutrition status and bleeding.

2.Endovascular Management:-

It include intra-arterial thrombolysis or mechanical thrombectomy or embolectomy.

Stroke Nursing Management:-

  • Altered cerebral tissue perfusion.
    • Goal:- to maintain tissue perfusion.
    • Assess factor related to individual situation for decrease cerebral perfusion and potential for increased ICP.
    • Monitor the vital sign.
    • Position with head slightly elevated of in neutral position.
    • Prevent straining of sterile and holding breath.
  • Impaired Physical Mobility.
    • Goal:- To ensure proper physical mobility.
    • Assess extend for impairment initially and on a regular basis.
    • Use aron sling form when patient is in upright position as indicated.
    • Place pillow under axilla to abduct arm to prevent abduction of shoulder or flexion of a elbow.
    • Encourage exercise such as quadriceps exercise, squeezing rubber ball, extension of finger.
  • Impaired verbal Communication.
    • Goal:- To establish method of communication in which need can be expressed.
    • Assess extend of disfunction pattern cannot understand words or has trouble speaking or making self understood.
    • Listen for errors in conversations and provide feedback.
    • Ask patient to follow simple comments.
    • Point to object to ask patient to name them to test for aphasia.
    • Provide alternative method of communication writing and pictures.
  • Altered sensory perception.
    • Goal:- To maintain visual level of consciousness of perceptual functioning.
    • Establish and maintain communication with patient to set up a sample method of communicated basic needs.
    • Eliminate external noise and stimuli as necessary with sensory overload.
    • Orient patient frequently to environment staff procedures as it assists patients to identify in conscious in reception and may release perceptual disorientation of reality.
    • Stimulate sense of touch give patient object to touch and hold.

Why You Need To Stop Ignoring Cataract

A cataract is opacity or cloudiness of the lens of the eye that may cause the loss of visual acuity. In the cataract color and structure of the lens is destruct and change in the milky white colors. Cataracts rank as it were behind arthritis and heart disease as a leading cause of disability in more seasoned grown-ups. Cataracts influence about 20.5 million Americans who are 40 a long time of age or more seasoned or approximately one in every six individuals in this age run. By age 80, more than half of all Americans have cataracts. Concurring to the World Health Organization, cataract is the driving cause of visual impairment within the world.

Introduction to Cataract:-

A cataract is opacity or cloudiness of the lens of the eye that may cause the loss of visual acuity. In the cataract color and structure of the lens is destruct and change in the milky white colors. Cataracts rank as it were behind arthritis and heart disease as a leading cause of disability in more seasoned grown-ups. Cataracts influence about 20.5 million Americans who are 40 a long time of age or more seasoned or approximately one in every six individuals in this age run. By age 80, more than half of all Americans have cataracts. Concurring to the World Health Organization, cataract is the driving cause of visual impairment within the world.

Cataract Causes and Risk factor:-

Lens Degeneration
  • Age:- Incidence increase After 50 years.
  • Ultravoilet radiation / rays.
  • Diabetes.
  • Long term use of corticosteroids.
  • Myopia.
  • Trauma.
  • Cigarette smoking.
  • Dehydration.
  • Intro ocular infection.

Cataract Pathophysiology:-

  • Various crystals, Glucose, and any other factors accumulate on the lens.
  • Resulting in the structure and color of the lens is totally changed.
  • Due to the opacity of the lens, the rays are net transmit towards the retina.
  • Resulting blurred vision and blindness is occur.

Types of Cataract:-

The there most common types of cataracts are defined by their location in the lens, Nuclear, Cortical, and posterior subcapsular.

  1. Nuclear Cataract:- A nuclear cataract tends to have a substantial genetic component that causes a central opacity in the lens. It is associated with myopia (nearsightedness).
  2. Cortical Cataract:- It involves the anterior Posterior or equatorial cortex of the lens. Vision is worse in very bright light. Sunlight exposure is a risk factor in cortical cataract formation.
  3. Posterior subcapsular cataract:- It occurs in front of the posterior capsule. It typically develops in younger people and is associated with prolonged corticosteroid, Use, diabetes, or ocular trauma. Near vision is diminished and the eye is increasingly sensitive to glare from bright light.

Cataract Clinical Feature:-

  • Cataract is painless.
  • Difficulty in vision in the bright light.
  • Sensitivity to glare.
  • Reduce visual acuity.
  • Blurred vision.
  • Double vision (Diplopia).
  • Decrease colours vision.
  • Light scattering.
  • Anxiety.
  • Blindness.

Cataract Diagnostic Evaluation:-

  • Snellen Visual Acuity test.
  • Ophthalmoscopy.
  • Slit-lamp biomicroscopic examination.

Cataract Management:-

Cataract Surgical Management:-

Surgery is definitive treatment for cataract. Two type of surgeries:-

1.Extra Capsular Cataract Extraction:-

It consist of removing of lens and the anterior portion of lens capsule manually. The posterior capsule is left nitact to support the intraocular lens (IOL).

Phacoemulsification:-

In this method of extracapsular cataract surgery, a portion of the anterior capsule is removed, allowing extraction of the lens nucleus and cortex while the posterior capsule is left intact to support an intraocular lens. An ultrasound device is used to liquefy the nucleus and cortex, which are then suctioned out through a tube.

Implantation of Intraocular Lens:-

After removing the cataract an Intraocular lens is usually implanted into the eye either through a small incision using a foldable intraocular lens. The lens implanted is inserted through the incision into the capsular back.

Intraocular lens implant after cataract surgery.

2.Intracapsular Cataract Extraction:-

An ICCE Instrument is used to remove the entire lens and capsule manually. From the late 1800s until the 1970s, the procedure of choice for cataract extraction was intracapsular cataract extraction (ICCE). The whole lens (ie, nucleus, cortex, and capsule) is evacuated, and fine sutures close the incision. ICCE is infrequently performed nowadays; however, it is indicated when there’s a need to remove the complete focal point, such as with a subluxated cataract (ie, partially or completely dislocated lens).

Nursing Management For Cataract:-

Nursing Assessment:-

Assess the patient’s distance and close visual acuity. In the event that the patient is planning to have surgery, particularly note the visual acuity in the patient’s unoperated eye. Utilize this data to determine how visually compromised the patient may be while the operative eye is healing. In addition, evaluate the psychosocial impact of the patient’s visual disability and the level of knowledge regarding the disease process and therapeutic options. Postoperatively, assess the patient’s level of comfort and capacity to follow the postoperative regimen.

Pre operative Nursing Care for Cataract:-

  • History taking and physical examination.
  • Monitor and record the vital sign of the patient.
  • Explain the surgery to the patient and his family members and relatives.
  • Instruct the patient not to have food for approximately 6-8 hours.
  • Instillate the eye drops 2-3 times in a day for any inflammation.
  • Prepare the client psychologically and physically for the surgery.
  • Take the written concern from the client or family members.
  • If the Intraocular pressure is increased then immediately administered the mannitol to normalize the Intraocular pressure.

Post Operative Care for Cataract:-

  • Closely observe the client for an anesthetic effect.
  • Elevate the head side up to 30-45 to prevent the increased intraocular pressure and intracranial pressure.
  • Keep the sterile dressing under doctor’s orders.
  • Avoid any work and provide the proper rest to the client.
  • Maintain the intake and output.
  • Finally when the dressing is removed then place the eye patches on the affected eye for several hours.
  • Encourage the patient to wear eyeglasses during the day after surgery or to prevent exposure to bright light.
  • Encourage the patient to wear an eye shield at night to protect the operated eye.
  • Avoid lifting, pushing, or pulling objects or do heavy exercise.
  • Avoid lying on the side of the affected eye.
  • Keep activity light (Walking, reading, watching T.V.), etc.

Home Care For Intraocular Lens Implant:-

  • Wear glasses or metal eye shields at all times following surgery as instructed by the physician.
  • Always wash hands before touching or cleaning the postoperative eye.
  • Clean the postoperative eye with a clean tissue; wipe the closed eye with a single gesture from the inner canthus outward.
  • Bathe or shower; shampoo hair cautiously or seek assistance.
  • Avoid lying on the side of the affected eye the night after surgery.
  • Keep activity light (eg, walking, reading, watching television). Resume the following activities only as directed by the physician: driving, sexual activity, unusually strenuous activity.
  • Remember not to lift, push, or pull objects heavier than 15 lb.
  • Avoid bending or stooping for an extended period.
  • Be careful when climbing or descending stairs.
  • Know when to call the physician.*

References:-

  1. Brunner and Suddarth’s, Textbook of Medical-Surgical Nursing, 10th edition, SENSORINEURAL FUNCTION.
  2. Lewis Dirksen Heitkemper Bucher, Medical Surgical Nursing, Assessment and Management of Clinical Problems, Ninth Edition, SECTION 4 Problems Related to Altered Sensory Input.

Glaucoma A Silent Cause of Vision Loss

Glaucoma is a group of eye disease which is characterized by increase intraocular pressure. Increase IOP damages the Optic nerve and nerve fiber layer. A glaucoma is a group of ocular conditions characterized by optic nerve damage. The optic nerve damage is related to the intraocular pressure (IOP) caused by congestion of aqueous humor in the eye. There is a range of pressures that have been considered “normal” but that may be associated with vision loss in some patients. Glaucoma is more prevalent among people older than 40 years of age, and the incidence increases with age. It is also more prevalent among men than women and in the African American and Asian populations.
There are two types of glaucoma Primary glaucoma which include Open angle glaucoma and angle closer glaucoma, and another one is Secondary glaucoma.

Introduction:-

Glaucoma is a group of eye disease which is characterized by increase intraocular pressure. Increase IOP damages the Optic nerve and nerve fiber layer. A glaucoma is a group of ocular conditions characterized by optic nerve damage. The optic nerve damage is related to the intraocular pressure (IOP) caused by congestion of aqueous humor in the eye. There is a range of pressures that have been considered “normal” but that may be associated with vision loss in some patients. Glaucoma is one of the leading causes of irreversible blindness in the world and is the leading cause of blindness among adults in the United States. It is estimated that at least 2 million Americans have glaucoma and that 5 to 10 million more are at risk (Margolis et al.,2002). Glaucoma is more prevalent among people older than 40 years of age, and the incidence increases with age. It is also more prevalent among men than women and in the African American and Asian populations.

Glaucoma

Glaucoma Causes:-

  • Genetic factors:- Family history of glaucoma.
  • Old age:- age for more than 45 years.
  • Hypertension.
  • Diabetes.
  • Myopia ( nearsightedness ).
  • Eye trauma.
  • Prolong use of topical or systemic corticosteroids.
  • Cardiovascular disease.

Types of Glaucoma:-

There are several types of glaucoma. Whether glaucoma is known as open-angle or angle-closure glaucoma depends on which mechanisms cause impaired aqueous outflow. Glaucoma can be primary or secondary, depending on whether associated factors contribute to the rise in intraocular pressure (IOP).

Glaucoma is divided into two type:-

  1. Primary Glaucoma:- Primary glaucoma are two types. those are Primary Open-angle Glaucoma and Primary Angle Closer (Pupillary block) Glaucoma.
  2. Secondary Glaucoma.

Primary Glaucoma:-

Open angle Glaucoma:-

It is the most common type of glaucoma. It is usually bilateral and slowly progressive occur without discomfort and pain. In this type of glaucoma, the trabecular meshwork is obstructed so the aqueous humor outflow is further obstructed and the Intraocular pressure (IOP) increases.

In open-angle glaucoma the outflow of aqueous humor is obstructed at trabecular meshwork.

Clinical Manifestation:-

Sign and symptoms or clinical manifestations of open-angle glaucoma are different according to different subtypes. those symptoms of subtypes are:-

  • Chronic open-angle glaucoma (COAG):- Optic nerve damage, visual field defects, Intraocular pressure (IOP) >21 mm Hg. May have fluctuating IOPs. Usually no symptoms but possible ocular pain, headache, and halos.
  • Normal-tension glaucoma:- Intraocular pressure (IOP) ≤ 21 mm Hg. Optic nerve damage, visual field defects.
  • Ocular Hypertension:- Elevated intraocular pressure (IOP). Possible ocular pain or headache.
  • Other Sign and symptoms are:-
    • Gradual onset.
    • Painless.
    • Mild Headache.
    • Frequent visual changes.
    • Mild itching.
    • Loss of peripheral vision (Tunnel vision).
    • Increase Intraocular Pressure.

Angle closer Glaucoma:-

The primary close angle glaucoma occurs to the anatomically narrow-angle between the iris and cornea, so the aqueous humor outflow is inhibited and the intraocular pressure is increase. Obstruction in aqueous humor outflow due to the complete or partial closure of the angle from the forward shift of the peripheral iris to the trabecula. The obstruction results in an increased IOP.

Clinical Manifestation:-

SIgn and symptoms of angle closer glaucoma are different according different subtypes. those symptoms are:-

  • Acute angle closer Glaucoma (AACG):-
    • Rapidly progressive visual impairment, periocular pain, conjunctival hyperemia, and congestion.
    • Pain may be associated with nausea, vomiting, bradycardia, and profuse sweating.
    • Reduced central visual acuity, severely elevated IOP, corneal edema.
    • The pupil is vertically oval, fixed in a semi dilated position, and unreactive to light and accommodation.
  • Subacute angle closer glaucoma:-
    • The transient blurring of vision, halos around lights; temporal headaches, and/or ocular pain; pupil may be semi-dilated.
  • Chronic Angle closer Glaucoma:-
    • Progression of glaucomatous cupping and significant visual field loss; IOP may be normal or elevated; ocular pain and headache.
  • Other Symptoms are:-
    • Rapid Onset.
    • Halos around Light.
    • Blurred vision.
    • Severe pain and redness in the eye.
    • Nausea and vomiting were due to an increase in intraocular pressure.
    • Headache.

Secondary Glaucoma:-

When the Intraocular Pressure is increased due to the trauma, diabetes, corticosteroid use, congenital abnormalities, sepsis, tumor then this type of glaucoma called Secondary glaucoma.

Glaucoma Diagnostic Evaluation:-

  1. Patient ocular and medical history collection.
  2. Tonometry by the tonometry to increase the Intraocular pressure.
  3. Ophthalmoscopy to inspect the optic nerve.
  4. Gonioscopy to asses irido corneal angle.
  5. Slit-lamp examination.
  6. Central visual field testing.

Glaucoma Management:-

Glaucoma Medical management:-

  • Cholinergic agent:- These agents increase aqueous fluid outflow by contracting the ciliary muscle and constrict the pupil.
  • Carbonic Anhydrase inhibitor:- These agent decreases aqueous humor production.
  • Steroidal eye drops to reduce the inflammation.
  • Osmatic Diuretics:- Use to treat an acute form of glaucoma.

Glaucoma Surgical Management:-

  1. Laser Peripheral Iridotomy. In peripheral for pupillary block glaucoma, an opening is made in the iris to eliminate the pupillary blockage and to allow fluid to drain.
  2. Surgical Iridectomy. In this procedure, the iris is surgically removed for the proper flow of the aqueous humor. It is an invasive procedure.
  3. Laser Trabeculoplasty. In this procedure laser burns are applied to the inner surface of the trabecular meshwork to open the intertrabecular space and widen the canal of scheming, therapy promoting outflow of aqueous humor and decrease intraocular pressure.
  4. Trabeculectomy. In this procedure, the part of iris and trabecular meshwork is totally removed by surgery.

Glaucoma Nursing management:-

  • Instruct the client for the uses of medication life long.
  • Instruct the client any changes in the vision and eye pain then the immediate report.
  • If the patient has any surgery of the eye then time to time dressing with the strict aseptic technique should be applied.
  • Asses the Intraocular pressure and de[th of the anterior chamber.
  • Record the vital sign in every 2 hours until the effect of anesthesia.
  • Instruc the patient mot to touch the eye to decrease the chance of infection.
  • Position the patient on the unoperated site with the head of the bed is 30 degrees elevated.
  • Check the eye for any leakage from the surgical site if occur then immediately inform the doctor.
  • Encourage the patient to wear an eye shield at night to protect the operated eye from injury.
  • Encourage the patient to wear dark glasses after eye dressing is removed.
  • Administer the medication as prescribed by the doctor.

Glaucoma Patient Education for Home care:-

Know your intraocular pressure (IOP) measurement and the desired range. • Be educated almost the degree of your vision loss and optic nerve damage. • Keep a record of your eye pressure estimations and visual field test results to screen your claim progress. • Review all your medications (including over-the-counter and herbal drugs) together with your ophthalmologist, and mention any side effects each time you visit. • Ask about potential side impacts and drug interactions of your eye medications. • Inquire whether non-specific or less expensive shapes of your eye medications are available. • Survey the dosing plan together with your ophthalmologist and inform him or her in case you have got inconvenience complying with the schedule. • Participate in the decision-making process. Let your doctor know what dosing plan works for you and other inclinations with respect to your eye care. Have the Nurse watch you instilling eye medication to decide whether you are administering it properly. Be mindful that glaucoma drugs can cause unfavorable effects if utilized improperly. Eyedrops are to be administered as prescribed, not when eyes feel irritated. • Ask your ophthalmologist to send a report to your primary care doctor after each appointment. • Keep all follow-up appointments.

What do you mean by Otosclerosis?

Otosclerosis is a condition in which there is abnormal bone growth inside the middle ear cavity. It includes symptoms of otosclerosis, otosclerosis causes, surgery for otosclerosis, Stapedectomy for otosclerosis, and treatment for otosclerosis.

Introduction to Otosclerosis:-

Otosclerosis is a condition in which there is abnormal bone growth inside the middle ear cavity. Otosclerosis is a condition that results from the formation of new abnormal spongy bone around the oval window with the resulting fixation of the steps.

Otosclerosis is a heredity disorder. Otosclerosis is a common cause of hearing loss i young adult. In otosclerosis the stapes begins to fused with surrounding bones, eventually becoming fixed to it, so stapes can not vibrate. This means sound no longer transmitted into the inner ear efficiently.

A. Otosclerosis Normal Anatomy

What causes Otosclerosis?

Exact cause of Otosclerosis is unknown. But there are some risk factors of Otosclerosis those are-

  • 50% of cases hereditary. this is the main cause of Otosclerosis.
  • Otosclerosis is more common in females in pregnancy.
  • Otosclerosis can cause if a person to have a family history of hearing loss.

What are the Sign and symptoms of Otosclerosis?

The sign and symptoms of Otosclerosis are –

  • In Otosclerosis hearing loss may be Unilateral or Bilateral.
  • Tinnitus.
  • Vertigo.
  • Postural Imbalance.
  • Pinkish discoloration (Red color tympanic membrane) known as Schwartz sign which indicates vascular changes in-ear.
(B) Arrow points to the sclerotic process at the foot
of the stapes. (C) Stapes are broken away surgically from its diseased base. The hole in the footplate provides an area where
an instrument can grasp the plate. (D) The footplate is removed from its base. Some otosclerotic tissue may remain,
and tissue is placed over it. (E) Robinson stainless-steel prosthesis in position

How is Otosclerosis Diagnosis?

  • Otoscopic Examination.
  • Audiometry.
  • Hearing test.

How is Otosclerosis is Treated?

Otosclerosis Management:-

Otosclerosis Non-Surgical:-

There is no known non-surgical treatment for Otosclerosis. But some physicians believe that by giving Sodium fluoride can mature abnormal spongy bone growth and prevent the breakdown of the bone tissue. Amplification with a hearing aid can also help.

Otosclerosis Surgical Management:-

A Stapedectomy For Otosclerosis. It is the surgical removal of stapes and a prosthesis or metal wire is connected between the incus and oval window. A stapedectomy, performed through the canal, includes removing the stapes superstructure and portion of the footplate and embeddings a tissue join and an appropriate prosthesis. A few surgeons elect to evacuate as it was a little portion of the stapes footplate (ie, stapedotomy). Notwithstanding the strategy utilized, the prosthesis bridges the gap between the incus and the inner ear, giving better sound conduction. Stapes surgery is exceptionally effective in improving hearing. Adjust unsettling influence or genuine vertigo, which seldom occurs in other middle ear surgical methods, can happen for a short time after stapedectomy.

Otosclerosis Post Operative care:-

  • Do not blow nose for 2-3 weeks after surgery.
  • Avoid contact with people who have respiratory and other infections.
  • Avoid activity that causes a sudden pressure change in the ear such as Scuba diving, flying, driving into the mountain.
  • Assess for facial nerve damage and muscle weakness.
  • Avoid bending, lifting, straining. It may cause dizziness.
  • Administer antivertigo, and antiemetic.

Reference:-

  1. Brunner and Suddarth’s, Textbook of Medical-Surgical Nursing, 10th edition, Assessment and Management of Patients With Hearing and Balance Disorders.

What do you mean by Brain Abscess?

Brain abscess (or cerebral abscess) is an abscess caused by inflammation and collection of infected material, coming from local (ear infection, dental abscess, infection of paranasal sinuses, infection of the mastoid air cells of the temporal bone, epidural abscess) or remote (lung, heart, kidney, etc.) infectious sources, within the brain tissue. The infection may also be introduced through a skull fracture following head trauma or surgical procedures. Brain abscess is usually associated with congenital heart disease in young children. It may occur at any age but is most frequent in the third decade of life. Although brain abscess is relatively rare, it is a complication encountered increasingly in patients whose immune systems have been suppressed either through therapy or disease.

Introduction:-

Brain abscess (or cerebral abscess) is an abscess caused by inflammation and collection of infected material, coming from local (ear infection, dental abscess, infection of paranasal sinuses, infection of the mastoid air cells of the temporal bone, epidural abscess) or remote (lungheartkidney, etc.) infectious sources, within the brain tissue. The infection may also be introduced through a skull fracture following head trauma or surgical procedures. Brain abscess is usually associated with congenital heart disease in young children. It may occur at any age but is most frequent in the third decade of life. Although brain abscess is relatively rare, it is a complication encountered increasingly in patients whose immune systems have been suppressed either through therapy or disease.

What is the Pathophysiology of Brain Abscess?

A brain abscess could be a collection of irresistible fabric inside the tissue of the brain. It may happen by the coordinate attack of the brain from intracranial injury or surgery; by the spread of infection from nearby destinations, such as the sinuses, ears, and teeth (paranasal sinus infections, otitis media, dental sepsis); or by the spread of infection from other organs (lung abscess, infective endocarditis) (Hickey, 2003). To anticipate brain abscess, otitis media, mastoiditis, sinusitis, dental contaminations, and systemic diseases ought to be treated promptly.

What are the Signs and Symptoms or Clinical Manifestations of Brain Abscess?

The clinical signs of a brain abscess result from modifications in intracranial flow (edema, brain move), contamination, or the area of the abscess. Cerebral pain, ordinarily worse in the morning, is the foremost winning side effect. Vomiting is also common. Focal neurologic signs (weakness of an extremity, diminishing vision, seizures) may happen, depending on the location of the abscess. There may be a alter in mental status, as reflected in lethargic, befuddled, crabby, or muddled behavior. Fever may or may not be displayed.

Symptoms of Brain Abscess:-

Frontal Lobe:-

  • Hemiparesis.
  • Aphasia ( Expressive ).
  • Seizures.
  • Frontal Headache.

Temporal Lobe:-

  • Localized Headache.
  • Change in vision.
  • Facial weakness.
  • Aphasia.

Cerebellar Abscess:-

  • Occipital Headache.
  • Ataxia (inability to coordinate movements).
  • Nystagmus (Rhythmic, involuntary movements of the eye).

What is the Diagnostic Evaluation of Brain Abscess?

In the condition of brain abscess Repeated neurologic examinations and proceeding evaluation of the patient is essential to decide the area of the abscess. A computed tomography (CT) check is important in finding the site of the boil, After the advancement and determination of suppurative lesions, and in deciding the ideal time for surgical mediation. A magnetic resonance imaging (MRI) scan is valuable to obtain pictures of the brain stem and posterior fossa in the event that an abscess is suspected in these regions.

Explain the Management of Brain Abscess?

Brain Abscess Medical Management:-

Brain sore is treated with antimicrobial therapy and surgical incision or aspiration. On the off chance that the abscess is encapsulated, CT-guided stereotactic needle aspiration beneath local anesthesia may be performed. Antimicrobial treatment is prescribed to dispense with the causative organism or decrease its virulence. Penicillin G (20 million U) and chloramphenicol (Chloromycetin) (4 to 6 g/day given intravenously in separated measurements) are usually prescribed because anaerobic streptococci and Bacteroides are the foremost common causative organisms (Hickey, 2003). Large IV doses are usually prescribed preoperatively to enter the blood-brain boundary and reach the abscess. The treatment proceeds postoperatively. Corticosteroids may be endorsed to help reduce the inflammatory cerebral edema in the event that the patient shows evidence of an expanding neurologic deficit. Antiseizure medicines (phenytoin, phenobarbital) may be endorsed to prevent seizures. Numerous abscesses may be treated with suitable antimicrobial therapy alone, with close monitoring by CT scans.

Brain Abscess Nursing Management:-

Nursing care focuses on ongoing assessment of the neurologic status, administering medications, assessing the response to treatment, and providing supportive care.

Continuous neurologic evaluation alerts the nurse to changes in ICP, which may show a requirement for more aggressive intervention. The nurse also assesses and records the reactions to drugs. Blood laboratory test results, particularly blood glucose and serum potassium levels, ought to be closely checked when corticosteroids are endorsed. Medical intervention may be required to return these values to typical or satisfactory levels.

Patient security is additionally a key nursing responsibility. Damage may result from a decreased level of awareness and falls related to motor weakness or seizures.

The patient with a brain abscess is greatly sick, and neurologic deficits may stay after treatment, such as hemiparesis, seizures, visual deficits, and cranial nerve palsies. Focal seizures are the foremost common sequelae, happening in almost 30% of patients (Hickey, 2003). The nurse must assess the family’s ability to express their trouble at the patient’s condition, adapt to the patient’s illness and deficits, and get support.

Reference:-

  1. Brunner and Suddarth’s, Textbook of Medical-Surgical Nursing, 10th edition, Management of Patients With Neurologic Infections, Autoimmune Disorders, and Neuropathies.

What the Heck Is Mastoiditis?

One of the foremost vital structures in your inner ear is the mastoid bone. In spite of the fact that it’s called a bone, the mastoid doesn’t have the commonplace structure associated with other bones within the human body. It’s made to air sacs and resembles a sponge, instead of being solid and unbending like most bones. It is an infection of the mastoid air cells caused by untreated or inadequately treated otitis media. Infection can be acute or chronic.

One of the foremost vital structures in your inner ear is the mastoid bone. In spite of the fact that it’s called a bone, the mastoid doesn’t have the commonplace structure associated with other bones within the human body. It’s made to air sacs and resembles a sponge, instead of being solid and unbending like most bones.

It is an infection of the mastoid air cells caused by untreated or inadequate treated otitis media. Infection can be acute or chronic.

Mastoiditis Cause:-

The most common cause of mastoiditis is Middle ear infection if it is left untreated or inadequately treated otitis media. This can cause the mastoid bone to begin to disintegrate.

Mastoiditis Symptoms or Clinical Manifestation:-

  • Mastoid tenderness ( Swelling behind the ear ).
  • Pain behind the ear.
  • Redness behind the ear.
  • Purulent ear discharge.
  • Fever, malaise, anorexia.
  • Hearing loss.
  • Tympanic perforation.

Mastoiditis Investigation:-

  • Otoscopic Examination:- A red thick immobile eardrum with or without perforation.
  • C.T. Scan ( Fluid in mastoid air cells ).
  • Culture of ear drainage.
  • Physical examination.

Mastoiditis Management:-

Mastoiditis Surgical Management:-

  1. Mastoidectomy:- It is the surgical removal of all the impacted tissues so infection does not spread to other structures.
  2. Tympanoplasty:- It is the reconstruction of eardrum and ossicles to improve the hearing.
  • Tympanoplasty 1st (Myringoplasty):- A graft ( muscle fascia, skin, or venous tissue ) is placed over a perforation in the tympanic membrane and other middle ear structures are normal.
  • Tympanoplasty 2nd (Ossiculoplasty):- The matter which has become displaced/disconnected from the tympanic membrane is grafted to reconnect the structures. (The patient cartilage, or bone, cutover ossicles, stainless steel, wires are used to repair or replace ossicles ).

Mastoiditis Surgical Approach of the Ear:-

  • Trans canal Approach.
  • Endaural approach.
  • Post auricular approach ( It is used for the more extensive repair of the middle ear and inner ear structure).

Mastoiditis Surgery Pre-operative Care:-

  • Give systemic antibiotics to reduce infection.
  • Before surgery irrigates the ear with a solution of equal parts of vinegar and sterile water to maintain normal pH.
  • Avoid contact with people with upper respiratory tract surgery.
  • Assure the patient that hearing loss after surgery is normal.
  • Teach deep breathing exercises after surgery.

Mastoiditis Surgery Post-operative Care:-

  • An antiseptic soft gauze packed in the ear canal.
  • If the skin incision is used a dressing placed over it.
  • Keep dressing dry and clear using sterile training.
  • Regular observe incision sight for signs of incision or hemorrhage.
  • Keep the patient flat with the head turned to the side and the operative side of ear facing up for at least 12 hours after surgery.
  • Avoid physical activity.
  • Give prescribed antibiotics.