COAL WORKER’S PNEUMOCONIOSIS – Causes, Pathophysiology, Signs and Symptoms, Diagnostic Evaluation and Management

• Coal worker’s pneumoconiosis (CWP) can be defined as the accumulation of coal dust in the lungs and the tissue’s reaction to its presence
• Pneumoconiosis, also known as Black Lung Disease, is an occupational lung disease caused by inhaling coal dust. There are two types of pneumoconiosis – simple, known as coal worker’s pneumoconiosis (CWP) and complicated, known as progressive massive fibrosis (PMF)

CAUSES

• Type of dust: more silica increases the risk of fibrosis. Coal rankings are as follows:

High: this coal is older and has the least amount of volatile matter (e.g. anthracite coal)

Medium: this coal is of moderate age and has a greater amount of volatile matter (e.g. bituminous coal)

Low: this coal is younger and has the greatest amount of volatile matter (e.g. lignite coal)

• Age at first exposure
• Length of time spent underground
• Smoking
• Size of dust particles
• Type of job: certain job requires more exposure to dust. Most dust is found at the coal face; therefore, individuals who work directly on the cutting of the coal have the highest exposure. The following list details dust exposure related to job title, beginning with the highest exposure:

Cutting-machine operator: this worker cut coal directly at the face. Respirable dust levels are highest here

Roof bolters: these individuals drill through rock and thus also exposed to silica. The continuous mine operator, loading machine operator, and shot firer are also exposed to higher amounts of respirable dust

Train operators: they drop sand onto the tracks for traction and may, therefore, develop silicosis

Motormen, brakemen, drivers and shuttle care operators: these individuals have less dust exposure because the coal has already been cut by the time they work with it, thus decreasing their exposure to respirable dust.

Mechanics, electricians and maintenance personnel: they have the least amount of dust exposure

PATHOPHYSIOLOGY

Coal dust that enters the lungs can neither be destroyed nor removed by the body —- the particles are engulfed by resident alveolar or interstitial macrophages —- remain in the lungs, residing in the connective tissue or pulmonary lymph nodes —- coal dust provides a sufficient stimulus for the macrophages to release various products, including enzymes, cytokines, oxygen radicals, and fibroblast growth factors —- aggregations of carbon-laden macrophages can be visualized under a microscope as granular, black areas. In serious cases, the lung may grossly appear black —- these aggregations can cause inflammation and fibrosis, as well as the formation of nodular lesions within the lungs —- the centers of dense lesions may become necrotic due to ischemia, leading to large cavities within the lung

SIGNS AND SYMPTOMS

• First stage is called simple pneumoconiosis, which is characterized by chronic cough, fever, expectoration and dyspnea on exertion. This is associated with little ventilator impairment. This stage will develop after 10-12 years of exposure
• Second stage is called progressive massive fibrosis: it is irreversible and continues even after cessation of the exposure. Prognosis is not good.

DIAGNOSTIC EVALUATION

• History of exposure
• Lung function test: varies from normal to obstructive or restrictive or combination of both. Diffusion decreased. Dyspnea on exertion. X-ray chest: small nodules, 1-10 mm in upper lung zones, and ground glass appearance of the lung
• Radiograph of CWP
• Pulmonary function tests: used to test the ability of the lungs to take in air (inspiration). Often used in conjunction with the X-ray chest. Forced vital capacity (FVC) and FEV1 (forced expiratory volume in one second) are used to diagnose lung disease

MANAGEMENT

Corticosteroids, pulmonary lavage, lung transplant

Prevention and Control

• Preplacement and periodic medical examination of workers
• Use of protective equipment by the workers
• Use of dust suppression measure
• Gravimetric dust sampling in dusty areas
• Exhaust ventilation

COMPLICATIONS

• Respiratory: pneumothorax, chronic obstructive pulmonary disease, cor pulmonale
• Infectious diseases: tuberculosis, vascular diseases

NURSING MANAGEMENT

Nursing Diagnosis

1. Impaired gas exchange related to cough and pain from incision:

• Open the airway with headtilt, chinlift, jaw thrust
• Set the position to maximize ventilation
• Use tools airway
• Perform chest physiotherapy
• Teach breathing deeply and coughing effectively
• Perform suction
• Auscultation of breath sounds
• Give bronchodilators (collaboration)

Oxygenation therapy

• Provide humidification system of oxygen equipment
• Monitor the flow of oxygen and the amount given
• Monitor signs of oxygen toxicity

• Risk for hemorrhage related to transplant procedure:

• Monitor pulse rate
• Monitor central venous pressure
• Provide sterile dressing on wound
• Give vitamin K as per doctor’s advice

• Pain related to surgical condition as evidenced by verbal communication

• Assess for the presence of pain, the scale, and intensity of pain
• Teach the client about pain management and relaxation with distraction
• Secure the chest tube to restrict movement and avoid irritation
• Assess pain-reduction measures
• Provide analgesics as indicated

ASBESTOSIS – Etiology, Symptoms, Pathophysiology, Diagnosis and Treatment

Asbestosis is a chronic inflammatory and fibrotic medical condition affecting the parenchymal tissue of the lungs caused by the inhalation and retention of asbestos fibers.

ETIOLOGY

Tiny asbestos fibers can get stuck deep inside the lungs. Inhaling asbestos fibers can cause scar tissue to form inside the lungs. This scar tissue does not expand and contract normally, which interferes with breathing. Asbestos fibers may remain in the lungs for a lifetime. In some cases, the fibers might damage the lungs or the membrane covering the lungs, leading to illness and even death

SYMPTOMS OF ASBESTOSIS

• Dry inspiratory crackles: which are clicking or rattling noises made by the lungs during inhalation
• ‘Clubbing of the fingers’: which may include softening of the fingernail beds, and bulging and of the end of the finger
• Misshapen nails: caused by a decrease of oxygenated blood flow to the extremities
• Shortness of breath
• A persistent dry cough
• Loss of appetite with weight loss
• Chest tightness or pain

OTHER SYMPTOMS OF ASBESTOSIS

• Coughing
• Chest pain
• Blood in the sputum
• Swelling in the neck or face
• Difficulty swallowing
• Loss of appetite
• Weight loss

PATHOPHYSIOLOGY

Asbestos is the scarring of lung tissue around terminal bronchioles and alveolar ducts —- resulting from the inhalation of asbestos fibers —- when such fibers reach the alveoli in the lung, where oxygen is transferred into the blood —- activation of the lung’s local immune system —- provoke an inflammatory reaction —- a slow ongoing progression of the immune system —- attempt to eliminate the foreign fibers —- macrophages phagocytose the fibers, releasing cytokines —- which eventually form a fibrous mass —- the result is interstitial fibrosis —- the fibrotic scar tissue causes alveolar walls to thicken —- which reduces elasticity and gas diffusion, reducing oxygen transfer to the blood as well as the removal of carbon dioxide

DIAGNOSIS

• Complete physical examination
• Chest X-ray
• Lung function tests
• A lung biopsy, in which tissue is removed by surgery, is the most reliable way to confirm the presence of microscopic asbestos fibers because X-rays cannot detect asbestos fibers in the lungs

TREATMENT

• Oxygen therapy to relieve shortness of breath
• Respiratory physiotherapy to remove secretions from the lungs
• Medications to thin secretions and relieve pain

RETINAL DETACHMENT – Types and Causes, Risk Factors, Signs and Symptoms, Diagnostic Evaluation and Management  

The retina is a light-sensitive membrane located at the back of the eye. When retina is detached from its pigmented epithelium is called retinal detachment. It is characterized by partial or total loss of vision.

TYPES AND CAUSES

• Rhegmatogenous retinal detachment: it is characterized by tear or hole in retina. This allows fluid from within the eye to slip through the opening and get behind the retina. The fluid separates the retina from the membrane that provides it with nourishment and oxygen. The pressure from the fluid can push the retina away from the retinal pigment epithelium, causing the retina to detach.
• Tractional retinal detachment: it occurs when scar tissue on the retina’s surface contracts and causes the retina to pull away from the back of the eye. This is a less common type of detachment that typically affects people with diabetes
• Exudative detachment: this type of detachment is caused by retinal diseases such as inflammatory disorder or Coats disease, which causes abnormal development in the blood vessels behind the retina.

RISK FACTORS

Risk factors for retinal detachment include:

• Posterior vitreous detachment (PVD): a common condition in aging individuals, in which the fluid in the retina breaks down, putting strain on the retinal fibers
• Extreme nearsightedness
• Family history of retinal detachment
• Trauma to the eye
• Being over 40 years old
• Prior history of retinal detachment
• Complications from cataract surgery
• Diabetes

SIGNS AND SYMPTOMS

There is no pain associated with retinal detachment, but there are usually symptoms before the retina becomes detached. Primary symptoms include:

• Blurred vision
• Partial vision loss
• Flashes of light when looking to the side
• Areas of darkness in field of vision
• Suddenly seeing many floaters (small bits of debris that appear as black flecks or strings floating before the eye).

DIAGNOSTIC EVALUATION

• Tonometry: to evaluate the eye pressure
• Gonioscopy: to inspect the drainage angle of eye
• Ophthalmolscopy: to evaluate the optic nerve

SURGICAL MANAGEMENT

• Photocoagulation: it is a laser burn around the tear site and the resulted scar will fixes the retina to the back of the eye.
• Cryopexy: it consists of application of freezing probe to the tear site and the resulting scarring will help hold  the retina in place
• Retinopexy: in this doctor will put a gas bubble in eye to help the retina move back into place. Once the retina is back in place, with the help of laser the holes are sealed out
• Scleral buckling: in this the sclera is pulled near the retina by decreasing the diameter of sclera. A small piece of silicone maybe sutured on or around the eye in a fashion that indents the eyeball and brings the retinal break that caused the detachment again in contact with it. This allows the subretinal fluid to reabsorb and the retina to reattach. Sometimes an air or gas bubble is injected at the time of surgery to aid reattachment of the retina.
• Vitrectomy:  by making tiny incisions into the eyeball, instruments are able to remove all the vitreous and subretinal fluid and reattach the retina. The retinal tear or tears that caused the detachment are then treated with laser to cause a permanent adhesive scar in this area and prevent a future detachment. A gas bubble, or less frequently and oil bubble, is instilled in the eye at the end of surgery to maintain the retina in contact with the eye wall as the laser scar matures

NURSING MANAGEMENT

Nursing Diagnosis

• Anxiety related to possible vision loss
• Disturbed sensory perception related to visual impairment
• Ineffective health maintenance related to knowledge deficit
• Risk for injury related to impaired vision
• Self-care deficit related to impaired vision

Interventions

• Prepare the patient for surgery

Instruct the patient to remain quiet in prescribed (dependent) position, to keep the detached area of the retina in dependent position

Patch both eyes

Wash the patient’s face with antibacterial solution

Instruct the patient not to touch the eyes to avoid contamination

Administer preoperative medication as ordered

• Take measures to prevent postoperative complications

Caution the patient to avoid bumping head

Encourage the patient no to cough or sneeze or to perform other strain-inducing activities that will increase intraocular pressure

• Encourage ambulation and independence as tolerated
• Administer medication for pain, nausea and vomiting as directed
• Provide quiet diversional activities, such as listening to a radio or audio books
• Teach proper technique in giving eye medications
• Advise patient to avoid rapid eye movements for several weeks as well as straining or bending the head below the waist
• Advise patient that driving is restricted until cleared by ophthalmologist
• Teach the patient to recognize and immediately report symptoms that indicate recurring detachment, such as floating spots, flashing lights and progressive shadows
• Advise patient to follow-up

OSTEITIS DEFORMANS (PAGET’S DISEASE) – Etiology, Pathophysiology, Signs and Symptoms, Diagnostic Evaluations and Management

Paget’s disease of bone disrupts the body’s normal bone recycling process, in which old bone tissue is gradually replaced with new bone tissue.  Overtime, the affected bones may become fragile and weak. Page’t disease of bone most commonly occurs in the pelvis, skull, spine and legs. The involved bone can be soft, leading to weakness and bending of the pelvis, low back (spine), hips, thighs, head and arms.

ETIOLOGY

• Both genetic and environmental factors are thought to play a role
• About 15% of people with Paget’s disease have a family history
• Autosomal dominant inheritance has also been described in some families
• Mutations have been identified in four genes that cause Paget’s disease
• Mechanical stress may play a role
• Paramyxovirus infection (including measles and respiratory syncytial virus) has been suggested as a possible trigger but this has been disputed.

PATHOPHYSIOLOGY

The metabolic hyperactivity is the main feature of Paget’s disease —- the primary abnormality is believed to be an intense focal resorption of normal bone by abnormal osteoclasts, leading to creation of voids and cavities in the bone —- these osteoclasts are abnormal in size, activity, and quantity and have excess nuclei —- the physiological compensatory mechanism for repair results in the deposition of fibrotic tissue and even new bone in the cavities by osteoblasts —- the osteoblast activity is so rapid that newly formed bone is not organized and remains irregular and woven in nature —- the newly formed woven bone is less resistant and more elastic than typical lamellar bone, and hence prone to deformity and micro-fractures, especially in the weight-bearing extremities —- there is a high degree of vascularity in the pagetoid bone cause of pain

Paget’s disease Evolves Through three Distinct Phases

1. An initial, short-lived burst of multinucleate osteoclastic activity causing bone resorption
2. A mixed phase of both osteoclastic and osteoblastic activity, with increased levels of bone turnover leading to deposition of structurally abnormal bone
3. A final chronic sclerotic phase, during which bone formation outweighs bone resorption

SIGNS AND SYMPTOMS

Most people who have Page’s disease of bone experience no symptoms. When symptoms do occur, the most common complaint is bone pain which may includes:

• Pelvis: Paget’s disease of bone in the pelvis can cause hip pain
• Skull: an overgrowth of bone in the skull can cause hearing loss or headaches
• Spine: if spine is affected, nerve roots can become compressed. This can cause pain, tingling and numbness in an arm or leg
• Leg: as the bones weaken, they may bend. Enlarged and misshapen bones in legs can put extra stress on nearby joints, which may cause wear-and-tear arthritis in knee or hip.

DIAGNOSTIC EVALUATIONS

• Bone-specific alkaline phosphatase (BSAP) levels are raised
• Urinary excretion of deoxypyridinoline and N-telopeptide are elevated
• Serum calcium, phosphorus, and parathyroid hormone levels are usually normal but immobilization may lead to hypercalcemia
• X-rays may show a number of signs of both osteolysis and excessive bone formation occur
• Radionuclide bone scans can show the extent of the disease
• Bone biopsy may be needed if malignant change is suspected

MANAGEMENT

Treatment approaches can focus on providing physical assistance, including the addition of wedges in the shoe, walking aids and the administration of physical therapy and pharmacotherapy

Pharmacotherapy

• Nonsteroidal anti-inflammatory drugs (NSAIDs) and paracetamol may be effective for pain
• Anti-resorptive therapy is with either bisphosphonates or calcitonin
• Biphosphonates:

Oral or intravenous bisphosphonates are the main stay of treatment

They are thought to reduce bone turnover, improve bone pain, promote healing of osteolytic lesions and restore normal bone histology

Newer bisphosphonates such as zoledronic acid may help to better achieve metabolic control of the disease and so improve these statistics

Pamidronate, risedronate, and zoledronic acid are preferred

Any calcium and vitamin D deficiency needs to be corrected before starting a bisphosphonate to avoid hypocalcemia

All oral medications should be taken with a large glass of water (6-8 oz) upon arising in the morning. Patients should remain upright for the next 30 minutes and not eat until that time has passed. Any of these treatments can be repeated if necessary. Side effects of these medicines may involve heartburn and sometimes increasing bone pain for a short period of time

There are also injectable medications. Injectable medications that can be given for Paget’s include:

• Pamidronate: which is injected in the vein once a month or once every few months? The injection takes a few hours. Unusually, there can be inflammation of the eye or loss of bone around the teeth (osteonecrosis)
• Zoledronate: this is injected in the vein once a year
• Calcitonin, a hormone that is injected under the skin several times a week

COMPLICATIONS

Complications from Paget’s disease depend on the site affected and the activity of the disease:

• Bone pain
• Bone deformity, kyphosis, frontal bossing of the skull, an enlarged maxilla, an increase in head size
• Pathological fractures
• Osteoarthritis
• Deafness and tinnitus may be due to compression of cranial nerve VIII
• Spinal stenosis
• Nerve compression syndromes

NURSING MANAGEMENT

1. Acute pain related to nerve compression, muscle spasm

Interventions

• Assess complaints of pain, location, duration of attacks, precipitating factors which aggravate
• Maintain bedrest, semi-Fowler position to the spinal bones, hips and knees in a state of flexion, supine position
• Use logroll (board) during a change of position
• Auxiliary mounting brace
• Limit activity during the acute phase according to the needs
• Teach relaxation techniques
• Collaboration: analgesics, traction, physiotherapy

• Impaired physical mobility related to pain, muscle spasms, and damage neuro-muskulus restrictive therapy

Interventions

• Give patients to perform passive range of motion exercises and active
• Assist patients in ambulation activity progressively
• Provide good skin care, massage point pressure after rehap change of position. Check the state of the skin under the brace with a specific time period
• Note the emotional responses and behaviors in immobilizing
• Demonstrate the use of auxiliary equipment such as a cane
• Collaboration: analgesic

GLAUCOMA – Etiology and Risk Factors, Pathophysiology, Types, Signs and Symptoms, Diagnostic Evaluation and Management

Glaucoma is a disease of the major nerve of vision, called the optic nerve. Glaucoma is characterized by a particular pattern of progressive damage to the optic nerve that generally begins with a subtle loss of side vision.

ETIOLOGY AND RISK FACTORS

The most important risk factors include:

• Age
• Elevated eye pressure
• Thin cornea
• Family history of glaucoma
• Nearsightedness
• Past injuries to the eyes
• Steroid use
• A history of severe anemia or shock

PATHOPHYSIOLOGY

Ocular perfusion, metabolic demand, ocular blood flow, intraocular pressure —- vulnerability to change —- autoregulation dysfunction —- retinal ganglion cell death —- glaucoma

TYPES

• Open-angle glaucoma (chronic): chronic open-angle glaucoma is the most common form of glaucoma. The ‘open’ drainage angle of the eye can become blocked leading to gradual increased eye pressure. If this increased pressure results in optic nerve damage, it is known as chronic open-angle glaucoma. The optic nerve damage and vision loss usually occurs so gradually and painlessly
• Angle-closure glaucoma: angle-closure glaucoma results when the drainage angle of the eye narrows and becomes completely blocked. In the eye, the iris may close off the drainage angle and cause a dangerously high eye pressure. When the drainage angle of the eye suddenly becomes completely blocked, pressure builds up rapidly, and this is called acute angle-closure glaucoma
• Exfoliation syndrome: exfoliation syndrome is a common form of a open-angle glaucoma that results when there is a buildup of abnormal, whitish material on the lens and drainage angle of the eye. This material and pigment from the back of the iris can clog the drainage system of the eye, causing increased eye pressure.
• Pigmentary glaucoma: pigmentary glaucoma is characterized by the iris bowing backwards, and coming into contact with the support structures that hold the lens in place. This position disrupts the cells lining the back surface of the iris containing pigment, and results in a release of pigment particles into the drainage system of the eye. This pigment can clog the drain and can lead to an increase in eye pressure. 
• Low-tension glaucoma: this is another form that experts do not fully understand. Even though eye pressure is normal, optic nerve damage still occurs. Perhaps the optic nerve is over-sensitive or there is atherosclerosis in the blood vessel that supplies the optic nerve.

SIGNS AND SYMPTOMS

The signs and symptoms of primary open angle glaucoma and acute angle-closure glaucoma are quite different.

Signs and Symptoms of Primary Open-angle Glaucoma

• Peripheral vision is gradually lost. This nearly always affects both eyes
• In advanced stages, the patient has tunnel vision

Signs and Symptoms of Closed Angle Glaucoma

• Eye pain, usually severe
• Blurred vision
• Eye pain is often accompanied by nausea and sometimes vomiting
• Light appears to have extra halo-like glows around them
• Red eyes
• Sudden, unexpected vision problems, especially when lighting is poor.

Common Symptoms are:

• Unusual trouble adjusting to dark rooms
• Difficulty focusing on near or distant objects
• Squinting or blinking due to unusual sensitivity to light or glare
• Change in color of iris
• Red-rimmed, encrusted or swollen lids
• Recurrent pain in or around eyes
• Double vision
• Dark spot at the center of viewing
• Lines and edges appear distorted or wavy
• Excess tearing or ‘watery eyes’
• Dry eyes with itching or burning
• Sudden loss of vision in one eye
• Sudden hazy or blurred vision
• Flashes of light or black spots
• Halos or rainbows around light

DIAGNOSTIC EVALUATION

• Eye-pressure test: Tonometer, a device which measures intraocular pressure. Some anesthetic and a dye are placed in the cornea, and a blue light is held against the eye to measure pressure. This test can diagnose ocular hypertension; a risk factor for open-angle glaucoma.

Gonioscopy: this examines the area where the fluid drains out of the eye. It helps determine whether the angle between the cornea and the iris is open or blocked (closed)

Perimetry test: also known as a visual field test. It determines which area of the patient’s vision is missing. The patient is shown a sequence of light spots and asked to identify them. Some of the dots are located where the person’s peripheral vision is; the part of vision that is initially affected by glaucoma. If the patient cannot see those peripheral dots, it means that some vision damage has already occurred.

Optic nerve damage: the ophthalmologist uses instruments to look at the back of the eye, which can reveal any slight changes which may also point towards glaucoma onset

Visual acuity test: this eye chart test measures how well you see at various distances

Visual field test: this test measures peripheral (side vision)

Dilated eye exam: in this exam, drops are placed in eyes to widen, or dilate, the pupils. Eye care professional uses a special magnifying lens to examine retina and optic nerve for signs of damage and other eye problems.

MANAGEMENT

Medical Management

• Prostaglandin analogues: these medications have prostaglandin-like compounds as their active ingredient. They increase the outflow of the fluid inside the eye. Examples include Xalatan and Lumigan. (Beta blockers: these medications reduce the amount of fluid the eye produces. Some patients may experience breathing problems, hair loss, fatigue, depression, memory loss, a drop in blood pressure. Examples of such medications include timolol, betaxolol and metipranolol). (Carbonic anhydrase inhibitors: these also reduce fluid production in the eye. Side effects may include nausea, eye irritation, and dry mouth, frequent urination, tingling in the fingers or toes, and a strange taste in the mouth. Examples include brinzolamide and dorzolamide). (cholinergic agents: also known as miotic agents).

SURGERY

• Trabeculoplasty: a high-energy laser beam is used to unblock clogged drainage canals, making it easier for the fluid inside the eye to drain out. This procedure nearly always reduces inner eye pressure. However, the problem may come back.
• Filtering surgery (viscocanalostomy): if eyedrops and laser surgery are not effective in controlling eye pressure, trabeculectomy is required. This procedure is performed in a hospital or an outpatient surgery center. Patient receives a medication to help relax and usually an injection of anesthetic to numb eye. Using small instruments under an operating microscope, an opening is created in the sclera and removes a small piece of eye tissue at the base of cornea through which fluid drains from eye (the trabecular meshwork). The fluid in eye can now freely leave the eye through this opening. As a result, eye pressure will be lowered.
• Drainage implant (aqueous shunt implant): this option is sometimes used for children or those with secondary glaucoma. A small silicone tube is inserted into the eye to help it drain out fluids better.
• Laser cycloablation (ciliary body destruction, cyclophotocoagulation or cyclocryopexy) is another form of laser treatment generally reserved for patient with severe forms of glaucoma with poor visual potential. This procedure involves applying laser burns or freezing to the part of the eye that makes the aqueous fluid. This therapy destroys the cells that make the fluid, thereby reducing the eye pressure
• Aqueous shunt devices: they are artificial drainage devices used to lower the eye pressure. They are essentially plastic microscopic tubes attached to a plastic reservoir. The reservoir is placed beneath the conjunctival tissue. The actual tube is placed inside the eye to create a new pathway for fluid to exit the eye. This fluid collects within the reservoir beneath the conjunctiva creating a filtering bleb. This procedure maybe performed as an alternative to trabeculectomy in patients with certain types of glaucoma.

NURSING MANAGEMENT

Nursing Assessment

• Evaluate the patient for any of the clinical manifestations
• Assess patient’s level of anxiety and knowledge base
• Assess the patient’s knowledge of disease process

Nursing Diagnosis

• Pain related to increased to increased IOP
• Fear related to pain and potential loss of vision
• Self-care deficit related to visual deficit
• Anxiety related to lack of knowledge about the surgical and postoperative experience
• Risk for injury related to blurred vision
• Risk for infection related to trauma to incision
• Acute pain related to trauma to incision

Intervention

Relieving Pain

• Notify health care provider immediately
• Administer medications as directed
• Explain to patient that the goal of treatment is to reduce IOP as quickly as possible
• Explain procedures to patient
• Reassure patient that with reduction in IOP, pain and other signs and symptoms should subside

Relieving Fear

• Provide reassurance and calm presence to reduce anxiety and fear
• Prepare patient for surgery, if necessary

Relieving Anxiety

• Assess the degree and duration of visual impairment
• Orient the patient to new environment
• Explain the perioperative routines
• Push to perform daily living habits when able
• Encourage the participation of family

Prevention of Injury

• Provided a comfortable position to the patient
• Help the patient to set the environment
• Orient the patient in a room
• Discuss the need for use of goggles when instructed
• Do not put pressure over the affected eye trauma
• Used the proper procedures when providing eye drugs

Promoting Self-Care

• Cleared the all doubts of patient regarding the disease condition
• Maintained good IPR with the patient
• Provided calm cool environment to the patient
• Music therapy and pet therapy given to patient
• Relaxation therapy also provided to relieve the anxiety of patient

Improving Knowledge

• Provided adequate knowledge about a disease condition
• Provided the sunglasses to patient during exposure to sunlight
• Provided medications to patient on proper time
• Advised the patient to talk with doctor

COMPLICATIONS

If left untreated, glaucoma will cause progressive vision loss, normally in these stages:

• Blind spots in peripheral vision
• Tunnel vision
• Total blindness

EYE BANKING AND CORNEAL TRANSPLANTATION STEPS OR PROCEDURE

FUNCTIONS OF EYE BANK, CONTRAINDICATIONS FOR DONATION, RETRIEVAL PROCEDURE, ROLE OF NURSE DURING CORNEAL TRANSPLANTATION, AFTER SURGERY and HOME CARE INSTRUCTIONS

It is an organization that deals with the collection, storage and distribution of donor eyes for the purpose of corneal grafting

• Corned blindness is a major form of visual deprivation in developing countries. A high percentage of these individuals can be visually rehabilitated by corneal transplantation (keratoplasty), a procedure that has very high rate of success among organ transplants. Quality of donor cornea, the nature of recipient pathology and the availability of appropriate postoperative care are the factors that determine the final outcome of this procedure. In corneal grafting, this diseased and opaque cornea is replaced by a healthy transplant cornea taken from a donor eye.
• A corneal transplant can take one of two forms: a full-thickness penetrating keratoplasty, involving excision and replacement of the entire cornea, or a lamellar keratoplasty, which removes and replaces a superficial layer of corneal tissue.

FUNCTIONS OF EYE BANK

Procurement and supply of donor cornea to the corneal surgeons is the primary goal of eye banks.

• The eye bank collects the eyes of voluntary registered eye donors after their death of those deceased person when enlightened relatives agree to donate the eyes as a service to humanity. From hospital deaths and from postmortem cases, after obtaining the consent from the next of kin.
• These eyes are processed by the Eye Bank and are supplied to eye surgeons for corneal grafting and other sight restoring operations
• Before proceeding for recovery eye bank personnel should ascertain the following details: location, age of the donor, cause of death and time of death.

CONTRAINDICATIONS FOR DONATION

• All eye banks have age limits both minimum and maximum
• Previous corneal graft
• Death of unknown cause
• Dementia
• Creutzfeldt-Jacob disease
• Subacute sclerosing panencephalitis
• Congential rubella
• Reyes syndrome
• Active viral encephalitis or encephalitis of unknown origin
• Active septicemia
• Rabies
• Retinoblastomas, tumors of the anterior segment
• Active ocular infections
• Pterygia or other superficial disorders of the conjunctiva or corneal surface
• Certain intraocular or anterior segment surgeries
• Leukemia
• Active disseminated lymphomas
• Hepatitis B and C, HTLV-1 or 2, HIV, syphilis
• Behavioral and or social issues, i.e. homosexual or other high-risk sexual behavior within the last 5 years
• Intravenous drug use for nonmedical reasons within the last 5 years
• Exposure to infectious disease within the last year by contact with an open wound, needle stick, or mucous membrane
• Tattooing or piercing within the last 12 months using shared instruments

RETRIEVAL PROCEDURE

• Retrieval procedure could be either enucleation or corneal scleral rim excision
• Eye Bank team on arrival at the location should locate the next of kin and convey condolence and obtain death certificate
• In the absence of a death certificate the registered medical practitioner should satisfy self that life is extinct
• The eye bank team should obtain consent on a consent form from the legal custodian of the donor
• After obtaining consent the donor should be identified either through a tag or through the next of kin
• The eye bank team should then proceed to prepare the site
• Gross physical examination should be conducted with utmost respect for observations regarding build: average, healthy or emaciated
• Eye bank team should look out for needle marks on the arm, skin lesions, etc
• Eye bank team should look out for ulcers or gangrene in exposed areas
• Ocular examination should be conducted
• Medical records and medical information should be obtained
• Information for hemodilution should be obtained
• Social history of the donor should be obtained wherever possible from the next of kin

ROLE OF NURSE DURING CORNEAL TRANSPLANTATION

• Explain the transplant procedure to the patient and answer any questions he may have
• Advise him that healing will be slow and that his vision may not be completely restored until the sutures are removed, which may be in about a year
• Tell the patient that most corneal transplants are performed under local anesthesia and that he can expect momentary burning during injection of the anesthetic
• Explain to him that the procedure will last for about an hour and that the he must remain still until it has been completed
• Tell the patient that analgesics will be available after surgery because he may experience a dull aching
• Inform him that a bandage and protective shield will be placed over the eye
• As ordered, administer a sedative or an osmotic agent to reduce intraocular pressure
• Ensure that the patient has signed a consent form

AFTER SURGERY

• After the patient recovers from the anesthetic, assess for and immediately report sudden, sharp, or excessive pain, bloody, purulent, or clear viscous drainage or fever
• As ordered, instill corticosteroid eyedrops or topical antibiotics to prevent inflammation and graft rejection
• Instruct the patient to lie on his back or on his unaffected side, with the bed flat or slightly elevated as ordered. Also, have him avoid rapid head movements, hard coughing or sneezing, bending over, and other activities that could increase intraocular pressure; likewise, he should not squint or rub his eyes
• Remind the patient to ask for help in standing or walking until he adjusts to changes in his vision
• Make sure that all his personal items are within his field of vision

HOME CARE INSTRUCTIONS

• Teach the patient and his family to recognize the signs of graft rejection (inflammation, cloudiness, drainage, and pain at the graft site)
• Instruct them to immediately notify the doctor if any of these signs occur
• Emphasize that rejection can occur many years after surgery; stress the need for assessing the graft daily for the rest of the patient’s life. Also, remind the patient to keep regular appointments with his doctor
• Tell the patient to avoid activities that increase intraocular pressure, including extreme exertion, sudden, jerky movements, lifting or pushing heavy objects and straining during defecation
• Explain the photophobia, a common adverse reaction, gradually decreases as healing progresses
• Suggest wearing dark glasses in bright light
• Teach the patient how to correctly instill prescribed eyedrops
• Remind the patient to wear an eye shield when sleeping
• Tell the patient to consult with the surgeon before driving or participating in sports or other recreational activities

CATARACT – Risk Factors and Etiology, Pathophysiology, Signs and Symptoms, Diagnostic Evaluation and Management

A cataract is a clouding or opacity of the normally clear lens of eye. The patient may have a cataract in one or both the eyes. Cataract is the third leading cause of preventable blindness.

RISK FACTORS AND ETIOLOGY

• Increasing age
• Diabetes
• Drinking excessive amounts of alcohol
• Excessive exposure to sunlight
• Exposure to ionizing radiation, such as that used in X-rays and  cancer radiation therapy
• Family history of cataracts
• High blood pressure
• Obesity
• Previous eye injury or inflammation
• Previous eye surgery
• Prolonged use of corticosteroid medications
• Smoking

PATHOPHYSIOLOGY

Following are the various mechanisms involves in the occurrence of cataract:

• Caused by degeneration and opacification of existing lens fibers, formation of aberrant fibers or deposition of other material in their place.
• Loss of transparency occurs because of abnormalities of lens protein and consequent disorganization of the lens fibers
• Any factor that disturbs the critical intra and extra-cellular equilibrium of water and electrolytes, the colloid system within the fibers causing opacification
• Fibrous metaplasia of lens fibers occurs in complicated cataract
• Epithelial cell necrosis occurring in angle closure glaucoma leads to focal opacification of the lens epithelium
• Abnormal products of metabolism, drugs or metals can be deposited in storage diseases, metabolic diseases and toxic reactions

Three biochemical factors are evident in cataract formation:

1. Hydration: seen particularly in rapidly developing forms. Actual fluid droplets collect under the capsule forming lacunae between fibers, the entire tissue may swell and becomes opaque, and this process is reversible in early stage, as in juvenile insulin dependent diabetes. Hydration maybe due to osmotic changes in the lens or due to changes in the semipermeability of the capsule
2. Denaturation of lens protein: if the proteins are denatured with an increase in insoluble protein, a dense opacity is produced. This stage is irreversible and opacity does not clear, this change is seen in young lens or the cortex of the adult nucleus where metabolism is active
3. Sclerosis: inactive fibers of the nucleus suffer from degenerative change of slow sclerosis

Altered the metabolic process within lens —- reduction in oxygen uptake —- increase in water content followed by dehydration —- protein in the lens undergoes numerous age related changes —- causes the formation of cataract

TYPES OF CATARACT

• Nuclear cataracts: a nuclear cataract may at first causes more nearsighted. But with time, the lens gradually turns more densely yellow and further cloudy. As the cataract slowly progresses, the lens may even turn brown. Advanced yellowing or browning of the lens can lead to difficulty distinguishing between shades of color.
• Cortical cataracts: a cortical cataract begins as whitish, wedge-shaped opacities or steaks on the outer edge of the lens cortex
• Posterior subcapsular cataracts: a posterior subcapsular cataract starts as a small, opaque area that usually forms near the back of the lens, right in the path of light on its way to the retina
• Congenital cataracts (Aphakia): some people are born with cataracts or develop them during childhood. Such cataracts maybe the result of the mother having an infection during pregnancy
• Hypermature shrunken cataract: when cortex disintegrates and transform into mass. The lens become inspissated and shrunken, the anterior capsule becomes thickened
• Morgagnian Hypermature Cataract: sometimes cortex becomes liquefies and nucleus sink into the bottom. The liquefied cortex become milky and nucleus is seen as brown mass, visible as semicircular line in pupillary area altering its position with change in position of the head

SIGNS AND SYMTPOMS

• Clouded, blurred or dim vision
• Increasing difficulty with vision at night
• Sensitivity to light and glare
• Seeing ‘halos’ around lights
• Frequent changes in eyeglass or contact lens prescription
• Fading or yellowing of colors
• Double vision in a single eye

DIAGNOSTIC EVALUATION

• Visual acuity test: a visual acuity test uses an eye chart to measure how well an eye can read a series of letters
• Slit-lamp examination: with this examination, the eye can be visualizing at large scale by magnifying the eye. The microscope is called a slit lamp; it uses an intense line of light, a slit, to illuminate cornea, iris, lens and the space between iris and cornea
• Retinal examination: to visualize the retina

Other tests:

• Snellen visual acuity test
• Opthalmoscopy
• Slit lamp bimicroscopic examination
• Glare testing
• Keratometry
• Ocular examination
• Perimetry: to determine the scope of visual fields

MANAGEMENT

Objective of Cataract Surgery

• The objective of cataract surgery is to remove the opacified lens
• Successful treatment of acute attack and prompt alleviation of manifestations
• Prevention of complications and further attacks
• Rehabilitation and education of the clients and significant others

Pharmacologic Therapy

• Beta carotene
• Vitamin C and E
• Antioxidant supplements
• Selenium
• Multivitamin supplements
• Contact lenses
• Strong bifocals
• Glasses
• Mydriatics: Phenylephrine HCL acid
• Cyloplegics: Tropicamide
• Homatropine
• Atropine

Surgical Management

• Phacoemulsification: in this method, surgery can usually be performed in less than 30 minutes and usually requires only minimal sedation. Numbing eyedrops or an injection around the eye is used and, in general, no stitches are used to close the wound, and often no eye patch is required after surgery
• Extracapsular cataract extraction surgery: this procedure is used mainly for very advanced cataracts where the lens is too dense to dissolve into fragments. This technique requires a larger incision so that the cataract can be removed in one piece without being fragmented inside the eye. An artificial lens is placed in the same capsular bag as with the phacoemulsification technique. This surgical technique requires a various number of sutures to close the larger wound, and visual recovery is often slower. Extra capsular cataract extraction usually requires an injection of numbing medication around the eye and an eye patch after surgery
• Intracapsular cataract surgery: this surgical technique requires an even larger wound than extracapsular surgery, and the surgeon removes the entire lens and the surrounding capsule together. This technique requires the intraocular lens to be placed in a different location, in front of the iris
• Aphakia: (absence of the lens) is corrected by the use of eyeglasses, contact lenses

NURSING MANAGEMENT

Nursing Assessment

• Assess knowledge level regarding procedure

Assess the level of fear and anxiety

Determine visual limitations

Postoperative Assessment

• Assess pain level

Sudden onset: maybe due to ruptured vessel or suture and may lead to hemorrhage

Severe pain: accompanied by nausea and vomiting maybe caused by intraocular pressure

Assess visual acuity in unoperated eye

Assess patient’s ability to ambulate

Assess patient’s level of independence

Nursing Diagnoses

• Self-care deficit related to visual deficit
• Anxiety related to lack of knowledge about the surgical and postoperative experience
• Risk for injury related to blurred vision
• Risk for infection related to trauma to incision
• Acute pain related to trauma to incision

Nursing Intervention

Relieving Pain

• Give medication to reduce pain as analgesics
• Give cold compression demand for blunt trauma
• Encourage to the use of sunglasses in strong light
• Vital signs must assess frequently
• Physical rest in bed with backrest elevated to provide comfort

Relieving Anxiety

• Assess the degree and duration of visual impairment
• Orient the patient to new environment
• Explain the preoperative routines
• Push to perform daily living habits when able
• Encourage the participation of family

Prevention of Injury

• Provided a comfortable position to the patient
• Help the patient to set the environment
• Orient the patient in a room
• Discuss the need for use of goggles when instructed
• Do not put pressure over the affected eye trauma
• Used the proper procedures when providing eye drugs

Promoting Self-Care

• Cleared the all doubts of patient regarding the disease condition
• Maintained good IPR with the patient
• Provided calm cool environment to the patient
• Music therapy and pet therapy given to patient
• Relaxation therapy also provided to relieve the anxiety of patient

Improving Knowledge

• Provided adequate knowledge about a disease condition
• Provided the sunglasses to patient during exposure to sunlight
• Provided medications to patient on proper time
• Advised the patient to talk with doctor
• Followed the recommendations that ensure regular eye checkup by the ophthalmologist

Health Education

• Advised the patient to wear sunglasses during exposure
• Advised the patient to take analgesics to reduce pain
• Advised the patient to take proper diet
• Advised the patient to take care of eyes after surgery
• Advised patient to prevent eyes from dirt and dust
• Advised patient to preventing eyes from trauma
• Advised patient to report to doctor for early complications
• Advise patient to increase activities gradually as directed by health care provider
• Caution against activities that cause patient to strain
• Instruct patient and family in proper use of medications
• Advise patient to apply plastic shield over the eye at night to avoid accidental injury during sleep
• Infirm about fitting temporary corrective lenses for the first 6 weeks

COMPLICATIONS

• Capsular rupture
• Vitreous loss
• Endothalemitis
• Pseudoexfoliation
• Myopia

After Care

Before the patient goes home, may receive the following:

• A patch to wear over eye until the follow-up exam
• Eyedrops to prevent infection, treat inflammation, and help with healing
• Wear dark sunglasses outside after removing the patch
• Wash hands well before and after using eye drops and touching eye. Try not to get soap and water in eye when are bathing or showering for the few days

RHEUMATOID ARTHRITIS – Etiology and Risk Factors, Pathophysiology, Clinical Manifestations, Diagnostic Evaluations and Management

Rheumatoid arthritis is a chronic inflammatory disorder that typically affects the small joints in hands and feet.

It is an autoimmune disorder, it occurs when immune system mistakenly attacks own body’s tissues. In addition to causing joint problems, rheumatoid arthritis sometimes can affect other organs of the body – such as the skin, eyes, lungs and blood vessels.

ETIOLOGY AND RISK FACTORS

• The causes of rheumatoid arthritis are unknown
• It is believed that the tendency to develop rheumatoid arthritis may be genetically inherited (hereditary)

RISK FACTORS

• Age: risk increases with age
• Gender: women are more affected than men
• Genetic risk: there is a strong familial link in some cases

PATHOPHYSIOLOGY

Due to any cause —- synovitis —- increase in the lymphocytes and plasma cells —- articular cartilage destruction —- granulation tissue grows across the surface of cartilage (pannus) from the ending of joint —- articular surface shows loss of cartilage beneath the expanding pannus —- inflammatory pannus causes causes focal destruction of bones —- deformity and soft tissue swelling

CLINICAL MANIFESTATIONS

• Fatigue
• Anorexia
• Weight loss
• Stiffness
• Lack of appetite
• Low-grade fever
• Muscle and joint aches

Specific articular involvement is manifested

• Pain stiffness limitation of motion and signs of inflammation (heat swelling tenderness)

Extra-articular Manifestations

• Peripheral edema
• Peripheral neuropathy
• Myositis
• Tenocynovitis
• Rheumatoid vasculitis
• Sjorgen’s syndrome
• Amyloidosis
• Fetly syndrome

COMPLICATIONS

• Osteoporosis: rheumatoid arthritis itself, along with some medications used for treating rheumatoid arthritis, can increase the risk of osteoporosis – a condition that weakens bones and makes them more prone to fracture
• Carpal tunnel syndrome: if rheumatoid arthritis affects wrists, the inflammation can compress the nerve that serves most of hand and fingers
• Heart problems: rheumatoid arthritis can increase risk of hardened and blocked arteries, as well as inflammation of the sac that encloses heart
• Lung diseases: people with rheumatoid arthritis have an increased risk of inflammation and scarring of the lung tissues, which can lead to progressive shortness of breath

DIAGNOSTIC EVALUATION

• History collection
• Physical examination: check points for swelling, redness and warmth. Also check reflexes and muscle strength
• Laboratory tests

Complete blood count (CBC): people with rheumatoid arthritis tend to have an elevated erythrocyte sedimentation rate (ESR), which indicates the presence of an inflammatory process in the body.

• Radiographic studies of joint: X-rays help to track the progression of rheumatoid arthritis in your joints overtime
• Synovial fluid analysis

TREATMENT

• NSAIDs: are medications that can reduce tissue inflammation, pain, and swelling, e.g. brufen, etc
• Steroids: corticosteroids medications such as prednisone reduce inflammation and pain and slow joint damge
• Disease-modifying antirheumatic drugs (DMARDs): these drugs can slow the progression of rheumatoid arthritis and save the joints and other tissues from permanent damage. Common DMARDs include methotrexate, leflunomide, hydroxychloroquine and sulfasalazine
• Calcium and vitamin D supplements: to prevent thinning of the bones due to osteoporosis

Surgical Management

If medications fail to prevent or slow joint damage, surgery may help to restore ability to use joint

Rheumatoid arthritis surgery may involve one or more of the following procedures:

• Total joint replacement: during joint replacement surgery, surgeon removes the damaged parts of joint and inserts a prosthesis made of metal and plastic
• Tendon repair: inflammation and joint damage may cause tendons around joint to loosen or rupture. Repair the tendons around joint
• Joint fusion: surgically fusing a joint may be recommended to stabilize or realign a joint and for pain relief when a joint replacement is not an option

NURSING MANAGEMENT

Nursing Diagnosis

1. Chronic pain related to joint inflammation and overuse

Interventions

• Perform a comprehensive assessment of pain to include location characteristics, onset, duration, frequency, severity
• Evaluate with patient and health care team, effectiveness of past pain control measures that have been used
• Reduce or eliminate the factors that increase the pain experience (e.g. fear fatigue lack of knowledge)
• Teach use of nonpharmacological techniques (relaxation, distraction, massage)
• Provide optimal pain relief with prescribed analgesics

• Impaired physical mobility related to joint pain and stiffness

Interventions

• Determine the limitations of joint movement and affect on function to establish baseline plan of care
• Collaborate with physical therapy into establish exercises program to improve the joint function
• Explain the plan and purpose of exercises to the patient and family
• Initiate pain control measures before beginning of joint exercises (hot packs, warm shower)
• Assist patient to do active, passive joint movements (selection of proper footwear use of assistive devices)

• Self-care deficit related to disease progression, weakness

Interventions

• Monitor patient’s ability for independent self care
• Monitor patients need for hygiene, dressing, grooming, eating
• Establish a routine for self-care activities assist patient in accepting dependency needs to ensure all needs are meet
• Teach family to encourage independence and to intervene only when patient is unable

OSTEOMYELITIS – Causes and Risk Factors, Modes of Transmission, Pathophysiology, Signs and Symptoms, Diagnostic Evaluation and Management

Osteomyelitis is an infection of a bone caused by Staphylococcus aureus. Infection with a fungus is a rare cause.

MODES OF TRANSMISSION

If some bacteria settle on a small section of bone, they can multiply and cause infection. Bacteria can get to bone:

• Via the bloodstream: this is the most cause in children. Bacteria sometimes get into the blood from an infection in another part of the body and then travel to a bone
• Following an injury: bacteria can spread to bone if you have a deep cut on the skin. In particular, if you have a broken bone which you can see through the cut skin

PATHOPHYSIOLOGY

Infection from bacteria —- the initial response to infection is inflammation, increased vascularity, and edema —- after 2 or 3 days, thrombosis of the blood vessels occurs —- ischemia with bone necrosis —- if it is not treated properly, a bone abscess forms —- new bone growth (the involucrum) forms and surrounds the sequestrum —- produces recurring abscesses —- chronic osteomyelitis

CAUSES AND RISK FACTORS

Anyone at any age can develop osteomyelitis. However, one has an increased risk if:

• Have recently fractured (broken) a bone
• Have bone prosthesis (an artificial hip, a screw in a bone following surgery, etc)
• Have recently had surgery to a bone
• Have a poor immune system. For example, AIDS, taking chemotherapy, seriously ill with another disease, etc
• Have had a previous episode of osteomyelitis
• Have reduced skin sensation. This can lead to damage and infection of the skin which can spread to the blood or to local bone. For example, some people with diabetes have reduced sensation in their feet
• Have regular kidney dialysis

SIGNS AND SYMPTOMS

• Pain and tenderness over an area of bone
• A lump may develop over a bone, which is usually very tender
• Redness of overlying skin may then develop
• Feeling generally unwell with fever (high temperature) as the infection develops

DIAGNOSTIC EVALUATION

• X-ray
• CT scan

MEDICAL TREATMENT

Antibiotics

An antibiotic is usually started as soon as possible. The initial antibiotic chosen is one that is likely to kill the bacteria which commonly cause osteomyelitis. However, the antibiotic is sometimes changed to a different one when the results of the tests confirm which bacterium is causing the infection. The symptoms may settle quite quickly after taking an antibiotic. Penicillin and cephalosporin is the drug of choices

To control pain you may be given painkillers

Surgical Management

Surgery is required if:

• An abscess develops. The pus in an abscess needs to be drained.
• The infection presses on other important structures. For example, an infection in the spine may press on the spinal cord
• The infection has become chronic (persistent) and some bone has been destroyed. Dead and infected bone may need to be removed to allow the infection to clear. Sometimes, plastic surgery is needed at the same time to cover any wound to give the best chance of cure

Rarely, amputation of a foot or leg is needed if infection persists in a leg bone

NURSING MANAGEMENT

1. Acute pain related to inflammation and swelling
2. Assess the level of pain
3. The affected part may be immobilized with a splint to decrease pain and muscle spasm
4. Elevation reduces swelling and associated discomfort
5. Comfortable position is given
6. Analgesic given to treat pain

• Impaired physical mobility related to pain, use of immobilization devices, and weight-bearing limitations
• Assess the normal level of activity
• The joints above and below the affected part should be gently placed through their range of motion
• The nurse encourages full participation in ADLs within the physical limitations to promote general well-being
• Analgesics are given

• Deficient knowledge related to the treatment regimen
• Assess the level of knowledge by verbalization with the patient
• Answer each question of the patient
• Clarify all doubts of the patient

OSTEOMALACIA – Etiology, Signs and Symptoms, Pathophysiology, Diagnostic Evaluation and Management

Osteomalacia refers as a metabolic disease of bones, often caused by a vitamin D deficiency. Metabolic disorder characterized by inadequate or delayed mineralization of bone and it result from a defect in the bone-building process

ETIOLOGY

Body uses calcium and phosphate to build strong bones. Osteomalacia may occur if bodies do not get enough of these minerals in diet or if body does not absorb them properly. These problems may be caused by:

• Vitamin D deficiency: people who live in areas where sunlight hours are short or eat a diet low in vitamin D can develop osteomalacia. Vitamin D deficiency is a common cause of osteomalacia
• Certain surgeries: normally, the stomach breaks down food to release vitamin D and other minerals that are absorbed in the intestine. This process is disrupted if one has surgery like gastrectomy and may result in osteomalacia. Surgery to remove or bypass small intestine also can lead to osteomalacia
• Celiac disease: in this autoimmune disorder, the lining of small intestine is damaged by consuming foods containing gluten, a protein found in wheat, barley and rye. A damaged intestinal lining does not absorb nutrients, such as vitamin D, as well as a healthy one does
• Kidney or liver disorders: problems with kidneys or liver can interfere with ability to process vitamin D
• Drugs: drugs used to treat seizures, including phenytoin and Phenobarbital, can cause osteomalacia

SIGNS AND SYMPTOMS

• Bone pain
• Tenderness
• Difficulty in changing position
• Muscle weakness
• Bowing of bones
• Pathologic fractures

PATHOPHYSIOLOGY

Due to any cause —- decreased level of vitamin D —- decreased absorption of calcium and phosphorus from intestine —- serum level of calcium and phosphorus decreases —- activate parathyroid gland —- result in less of calcium and phosphorus from bones —- deformity of bones —- bone became soft and unable to bear stress and weight

DIAGNOSTIC EVALUATION

• Physical examination: check for skeletal deformity like spinal kyphosis, bowed legs
• Blood and urine tests: in cases of osteomalacia caused by vitamin D deficiency or by phosphorus loss, abnormal levels of vitamin D and the minerals calcium and phosphorus are often detected
• X-ray: slight cracks in bones that is visible on X-rays
• Bone biops: during a bone biopsy, doctor inserts a slender needle through skin and into bone to withdraw a small piece of bone for viewing under a microscope. This procedure is done after using a local anesthetic and takes only about a half-hour. Although a bone biopsy is very accurate in detecting osteomalacia

MANAGEMENT

• Vitamin D, phosphorus, calcium supplements are prescribed
• Exposure to sunlight is also advised to patient (for short period of time)
• Vitamin D rich diet (fortified milk and milk products, cereals, egg, etc) is given to the patient

NURSING MANAGEMENT

Nursing Diagnosis

1. Impaired physical mobility related to decalcification and stretching of the muscles

Interventions

• Encourage patient to do the daily activities
• If person is not able to perform daily routine then assist him
• Ask patient for some exercises but also ready with some pain control measures
• Provide supplements of calcium as prescribed by the physician

• Bone pain related to weakness and stretching of muscles

Interventions

• Assess the intensity, duration, onset of the pain
• Assess the measures use by the health care time previously
• Provide comfort devices
• Provide medications as prescribed by the physician
• Provide psychological support and assist while changing the position

• Risk for fractures related to calcium deficiency and muscle weakness

Interventions

• Assess for any cracks on the bones
• Encourage for vitamin D rich diet
• Provide calcium supplements to the patient as prescribed by physician