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Mental retardation is a generalized, triarchic disorder, characterized by subaverage cognitive functioning and deficits in two or more adaptive behaviors with onset before the age of 18. Once focused almost entirely on cognition, the definition now includes both a component relating to mental functioning and one relating to the individual’s functional skills in their environment.

Mental Retardation is a part of a broad category of developmental disability; it is defined by the American Association of Mental Deficiency as significantly subaverage general intellectual functioning existing concurrently with deficits in adaptive behavior and manifested during the developmental period (18 years of age). Adaptive behaviors include communication, self-care, work, leisure, health, and safety.

Etiology:

A diagnosis of mental retardation cannot be made on the basis of intellectual ability alone; there must be both intellectual and adaptive (personal independence and social responsibility) impairment.

Causes of mental retardation are genetic, biochemical, viral, and developmental.

• Prenatal Infection and intoxication
• Trauma or physical agent (e.g. lack of oxygen)
• Metabolic Disturbance
• Inadequate Prenatal Nutrition
• Gross postnatal brain disease (e.g. Neurofibromatosis or tuberous sclerosis)
• Chromosomal abnormalities
• Prematurity
• Low birth weight
• Autism
• Environmental deprivation

Associated Factors Include:

• Maternal Lifestyle (e.g. Poor nutrition, smoking, and substance abuse)
• Chromosomal disorders (most related to Down Syndrome)
• Specific Disorders such as fetal alcohol syndrome
• Cerebral Palsy, microencephaly or infantile spasms

Pathophysiology:

The Pathophysiology of Mental Retardation depends on the cause; early diagnosis and prompt treatment may particularly important in cases involving an identifiable and possibly correctable cause such as phenylketonuria (PKU), malnutrition, or child abuse.

Diagnosis usually is made after a period of suspicion. Diagnosis may be made at birth from recognition of specific syndromes such as Down Syndrome. Diagnosis and classification are based on standard IQ test scores.

Clinical Manifestations:

Findings may vary depending on the classification or degree of retardation.

Treatment:

• By most definitions mental retardation is more accurately considered a disability rather than a disease.
• Mental Retardation can be distinguished in many ways from mental illness, such as schizophrenia or depression.
• Currently, there is no “cure” for an established disability, though with appropriate support and teaching, most individuals can learn to do many things.
• Although there is no specific medication for mental retardation, many people with developmental disabilities have further medical complications and may take several medications.
• Beyond that there are specific programs that people with developmental disabilities can take part in wherein they learn basic life skills.
• These “goals” may take a much longer amount of time for them to accomplish, but the ultimate goal is independence.
• This may be anything from independence in tooth brushing to an independent residence.
• People with developmental disabilities learn throughout their lives and can obtain many new skills even late in life with the help of their families, caregivers, clinicians and the people who coordinate the efforts of all of these people.

Nursing Management:

1. Assess all children for signs of developmental delays.

2. Administer prescribed medications for associated problems such as anticonvulsants for seizure disorders, and methylphenidate (Ritalin) for attention deficit hyperactivity disorder.

3. Support the family at the time of initial diagnosis by actively listening to their feelings and concerns and assessing their composite strengths.

4. Facilitate the child’s self-care abilities by encouraging the parents to enroll the child in an early stimulation program, establishing a self-feeding program, initiating independent toileting, and establishing an independent grooming program (all developmentally appropriate).

5. Promote optimal development by encouraging self-care goals and emphasize the universal needs of children, such as play, social interaction and parental limit setting.

6. Promote anticipatory guidance and problem solving by encouraging discussions regarding physical maturation and sexual behaviors.

7. Assist the family in planning for the child’s future needs (e.g. Alternative to home care, especially as the parents near old age); refer them to community agencies.

8. Provide child and family teaching

• Identify normal developmental milestones and appropriate stimulating activities including play and socialization.
• Discuss the need for patience with the child’s slow attainment of developmental milestones.
• Inform parents about stimulation, safety and motivation.
• Supply information regarding normal speech development and how to accentual nonverbal cues, such as facial expression and body language, to help cue speech development.
• Explain the need for discipline that is simple, consistent and appropriate to the child’s .
• Review an adolescent’s need for simple, practical sexual information that includes anatomy, physical development and conception.
• Demonstrate ways to foster learning other than verbal explanation because the child is better able to deal with concrete objects than abstract concepts.
• Point out the importance of positive self-esteem, built by accomplishing small successes in motivating the child to accomplish other tasks.

9. Encourage the prevention of mental retardation

• Encourage early and regular prenatal care.
• Provide support for high risk infants.
• Administer immunizations, especially rubella immunization.
• Encourage genetic counselling when needed.
• Teach injury prevention �?? both intentional and unintentional.

Sources:

Lippincott Review Series

http://wikipedia.org

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Nursing Care Plan - Chicken Pox

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Nephrotic syndrome has small pores in the podocytes, large enough to permit proteinuria (and subsequently hypoalbuminemia, because some of the protein albumin has gone from the blood to the urine) but not large enough to allow cells through (hence no hematuria). By contrast, in nephritic syndrome, RBCs pass through the pores, causing hematuria.NURSING CARE PLAN - Nephrotic Syndrome

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1. The primary site of CSF formation is believed to be the choroid plexusus of the lateral ventricles. CSF flows from the lateral ventricles through the foramen of Monro to the third ventricle, then through the aqueduct of Sylvius into the fourth ventricle through the foramen of Luschka and the midline foramen of Magendie into the cisterna magna. From there it flows to the cerebral and cerebellar subarachnoid spaces where ti is absorbed.
2. Causes of Hydrocephalus are varied but result in either impaired absorption of CSF within the arachnoid space (formerly referred to as communicating hydrocephalus) or obstruction to the flow of CSF through the ventricular system (formerly referred as noncommunicating hydrocephalus.
3. Most cases of obstruction are the result of developmental malformations; other causes include neoplasms, infection and trauma. Obstruction to the normal flow can occur at any point in the CSF pathway, which produces increased pressure and dilation of the pathways proximal to the site of obstruction.
4. Impaired absorption can result form meningitis, prenatal maternal infections, meningeal malignancy (secondary to leukemia or lymphoma), an arachnoid cyst, and tuberculosis.

Nursing Care Plan - Hydrocephalus

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Hydrocephalus is a condition caused by an imbalance in the production and absorption of CSF in the ventricular system. When production exceeds absorption, CSF accumulates, usually under pressure, producing dilation of the ventricles.

It is a term derived from the Greek words “hydro” meaning water, and “cephalus” meaning head, and this condition is sometimes known as “water on the brain”.

People with hydrocephalus have abnormal accumulation of cerebrospinal fluid (CSF) in the ventricles, or cavities, of the brain. This may cause increased intracranial pressure inside the skull and progressive enlargement of the head, convulsion, and mental disability.

Usually, hydrocephalus does not cause any intellectual disability if recognized and properly treated. A massive degree of hydrocephalus rarely exists in typically functioning people, though such a rarity may occur if onset is gradual rather than sudden.

Hydrocephalus occurs with a number of anomalies, such as NTD�??s.

Etiology:

Congenital hydrocephalus usually results from defects, such as Chairi malformations. It is also associated with spina bifida.

Acquired hydrocephalus usually results from space-occupying lesions, hemorrhage, intracranial infections or dormant development defects.

Classification of Hydrocephalus:

Hydrocephalus can be caused by impaired cerebrospinal fluid (CSF) flow, reabsorption, or excessive CSF production.

• The most common cause of hydrocephalus is CSF flow obstruction, hindering the free passage of cerebrospinal fluid through the ventricular system and subarachnoid space (e.g., stenosis of the cerebral aqueduct or obstruction of the interventricular foramina - foramina of Monro secondary to tumors, hemorrhages, infections or congenital malformations).
• Hydrocephalus can also be caused by overproduction of cerebrospinal fluid (relative obstruction) (e.g., papilloma of choroid plexus).

Based on its underlying mechanisms, hydrocephalus can be classified into communicating, and non-communicating (obstructive). Both forms can be either congenital, or acquired.

Communicating

· Communicating hydrocephalus, also known as non-obstructive hydrocephalus

· It is caused by impaired cerebrospinal fluid resorption in the absence of any CSF-flow obstruction.

· It has been theorized that this is due to functional impairment of the arachnoid granulations, which are located along the superior sagittal sinus and is the site of cerebrospinal fluid resorption back into the venous system.

· Various neurologic conditions may result in communicating hydrocephalus, including subarachnoid/intraventricular hemorrhage, meningitis, Chiari malformation, and congenital absence of arachnoidal granulations (Pacchioni’s granulations).

• Normal pressure hydrocephalus (NPH) is a particular form of communicating hydrocephalus, characterized by enlarged cerebral ventricles, with only intermittently elevated cerebrospinal fluid pressure. The diagnosis of NPH can be established only with the help of continuous intraventricular pressure recordings (over 24 hours or even longer), since more often than not, instant measurements yield normal pressure values. Dynamic compliance studies may be also helpful. Altered compliance (elasticity) of the ventricular walls, as well as increased viscosity of the cerebrospinal fluid, may play a role in the pathogenesis of normal pressure hydrocephalus.
• Hydrocephalus ex vacuo also refers to an enlargement of cerebral ventricles and subarachnoid spaces, and is usually due to brain atrophy (as it occurs in dementias), post-traumatic brain injuries and even in some psychiatric disorders, such as schizophrenia. As opposed to hydrocephalus, this is a compensatory enlargement of the CSF-spaces in response to brain parenchyma loss - it is not the result of increased CSF pressure.

Non-communicating

Non-communicating hydrocephalus, or obstructive hydrocephalus, is caused by a CSF-flow obstruction (either due to external compression or intraventricular mass lesions).

• Foramen of Monro obstruction may lead to dilation of one or, if large enough (e.g., in colloid cyst), both lateral ventricles.
• The aqueduct of Sylvius, normally narrow to begin with, may be obstructed by a number of genetically or acquired lesions (e.g., atresia, ependymitis, hemorrhage, tumor) and lead to dilatation of both lateral ventricles as well as the third ventricle.
• Fourth ventricle obstruction will lead to dilatation of the aqueduct as well as the lateral and third ventricles.
• The foramina of Luschka and foramen of Magendie may be obstructed due to congenital failure of opening (e.g., Dandy-Walker malformation).
• The subarachnoid space surrounding the brainstem may also be obstructed due to inflammatory or hemorrhagic fibrosing meningitis, leading to widespread dilatation, including the fourth ventricle.

Congenital

• The cranial bones fuse by the end of the third year of life. For head enlargement to occur, hydrocephalus must occur before then. The causes are usually genetic but can also be acquired and usually occur within the first few months of life, which include 1) intraventricular matrix hemorrhages in premature infants, 2) infections, 3) type II Arnold-Chiari malformation, 4) aqueduct atresia and stenosis, and 5) Dandy-Walker malformation.
• In newborns and toddlers with hydrocephalus, the head circumference is enlarged rapidly and soon surpasses the 97th percentile. Since the skull bones have not yet firmly joined together, bulging, firm anterior and posterior fontanelles may be present even when the patient is in an upright position.
• The infant exhibits fretfulness, poor feeding, and frequent vomiting. As the hydrocephalus progresses, torpor sets in, and the infant shows lack of interest in his surroundings. Later on, the upper eyelids become retracted and the eyes are turned downwards (due to hydrocephalic pressure on the mesencephalic tegmentum and paralysis of upward gaze). Movements become weak and the arms may become tremulous. Papilledema is absent but there may be reduction of vision. The head becomes so enlarged that the child may eventually be bedridden.
• About 80-90% of fetuses or newborn infants with spina bifida�??often associated with meningocele or myelomeningocele�??develop hydrocephalus.

Acquired

• This condition is acquired as a consequence of CNS infections, meningitis, brain tumors, head trauma, intracranial hemorrhage (subarachnoid or intraparenchymal) and is usually extremely painful.

Pathophysiology of Hydrocephalus:

Clinical Manifestations:

1. Abnormal rate of head growth
2. Bulging fontanelle
3. Tense anterior fontanelle (often bulging and nonpulsatile)
4. Dilated scalp veins
5. Macewen�??s sign (�??cracked pot�??)
6. Frontal bossing
7. Setting sun sign
8. Sluggish and unequal pupils
9. Irritability and lethargy with varying LOC
10. Abnormal infantile reflexes
11. Possible cranial nerve damage

Manifestations in children include possible signs of increased ICP, which include headache on awakening with improvement following emesis, papilledema, strabismus, ataxia, irritability, lethargy, apathy and confusion.

Laboratory and Diagnostic Study Findings:

1. Level II ultrasonography of the fetus will allow a prenatal diagnosis. (Transuterine placement of ventriculoamniotic shunts during late pregnancy is still being developed as a treatment modality).
2. CT scan will diagnose most cases postnatally.
3. MRI can be used if a complex lesion is suspected.

Nursing Management:

1. Teach the family about the management required for the disorder

a. Treatment is surgical by direct removal of an obstruction and insertion of shunt to provide primary drainage of the CSF to an extracranial compartment, usually peritoneum (ventriculoperitoneal shunt)

1. The major complications of shunts are infections and malfunction

2. Other complications include subdural hematoma caused by a too rapid reduction of CSF, peritonitis, abdominal abscess, perforation of organs, fistulas, hernias and ileus.

b. A third ventriculostomy is a new nonshunting procedure used to treat children with hydrocephalus.

2. Provide preoperative nursing care

a. Assess head circumference, fontanelles, cranial sutures, and LOC; check also for irritability, altered feeding habits and a high-pitched cry.

b. Firmly support the head and neck when holding the child.

c. Provide skin care for the head to prevent breakdown.

d. Give small, frequent feedings to decrease the risk of vomiting.

e. Encourage parental-newborn bonding.

3. Provide Postoperative nursing care (nursing interventions are the same as those for increased ICP)

a. Assess for signs of increased ICP and check the following; head circumference (daily), anterior fontanelle for size and fullness and behavior.

b. Administer prescribed medications which may include antibiotics to prevent infection and analgesics for pain.

c. Provide shunt care

1. Monitor for shunt infection and malfunction which may be characterized by rapid onset of vomiting, severe headache, irritability, lethargy, fever, redness along the shunt tract, and fluid around the shunt valve.

2. Prevent infection (usually from Staphylococcus epidermis or Staphylococcus aureus)

3. Monitor for shunt overdrainage (headache, dizziness and nausea). Overdrainage may lead to slit ventricle syndrome whereby the ventricle become accustomed to a very small or slitlike configuration, limiting the buffering ability to increased ICP variations.

4. Teach home care

a. Encourage the child to participate in age-appropriate activities as tolerated. Encourage the parents to provide as normal lifestyle as possible. Remind both the child and parents that contact sports are prohibited.

b. Explain how to recognize signs and symptoms of increased ICP. Subtle signs include changes in school performance, intermittent headache, and mild behavior changes.

c. Arrange for the child to have frequent developmental screenings and routine medical checkups.

Nursing Care Plan - Hydrocephalus

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Nursingcrib.com NURSING CARE PLAN - Hydrocephalus

According to the advisory, the Board has not announced any changes in the prevailing requirement of cases for the intra-partal, intraoperative and immediate care of the newborn.

The required number of OR/DR Cases remains to be 5, amidst some announcements made by some Nursing Schools that it was already reduced to 3.

The Board or Nursing would like to emphasize that they adhere to a �??NO RETROACTIVE APPLICATION OF ANY NEW POLICY �??, therefore if and when new promulgations are finally issued this will never be applied to �??graduating students�??. All related policy-changes that will be announced shall be in effect for those who will enroll for this coming June of 2009.

Applicants for the 2009-2010 Nursing Licensure Examination are directed to follow the PREVAILING PRESCRIPTIONS of five cases each with regards to O.R., D.R., and Cord Care requirements.

Nursing graduates of 2011 and 2012, meaning those enrolling in their 2nd and 3rd Academic Year shall be those who shall be affected by the new policy promulgations.

The BON Advisory

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Definition:

Down syndrome, Down’s syndrome, or trisomy 21 is a chromosomal disorder caused by the presence of all or part of an extra 21st chromosome. It is the most common chromosomal abnormality.

Background:

• It is named after John Langdon Down, the British doctor who described the   syndrome in 1866.
• The disorder was identified as a chromosome 21 trisomy by Jérôme Lejeune in 1959.
• The condition is characterized by a combination of major and minor differences in structure.
• Often Down syndrome is associated with some impairment of cognitive ability and physical growth as well as facial appearance.
• Down syndrome in a baby can be identified with amniocentesis during pregnancy or at birth.
• Individuals with Down syndrome tend to have a lower than average cognitive ability, often ranging from mild to moderate developmental disabilities.
• A small number have severe to profound mental disability.
• The incidence of Down syndrome is estimated at 1 per 800 to 1,000 births, although these statistics are heavily influenced by the age of the mother. Other factors may also play a role.
• Health concerns for individuals with Down syndrome include a higher risk for congenital heart defects, gastroesophageal reflux disease, recurrent ear infections, obstructive sleep apnea, and thyroid dysfunctions.
• Early childhood intervention, screening for common problems, medical treatment where indicated, a conducive family environment, and vocational training can improve the overall development of children with Down syndrome. Although some of the physical genetic limitations of Down syndrome cannot be overcome, education and proper care will improve quality of life.

Etiology:
The cause is unknown and multiple theories exist. The concept of multiple causality is most accepted.

• Cytogenetics of the disorder are well established.
• Approximately 92% to 95% of cases are attributed to an extra chromosome 21 hence the name trisonomy 21.
• About 3-6% of cases maybe caused by translocation of chromosomes 15 (21 or 22).
• From 1-3% of persons demonstrate mosaicsm (cells with both normal and abnormal chromosomes).
• Children with down syndrome are born to parents of all ages. Although there is a higher incidence among mothers over age 35, most are born to mothers under age 35 (80%).

Pathophysiology:
The degree of cognitive and physical impairment is related to the percentage of cells with the abnormal chromosome makeup.

Clinical Manifestations:
1.    Separated sagittal suture
2.    Oblique palpebral fissures
3.    Small nose
4.    Depressed nasal bridge
5.    High-arched palate
6.    Skin excess laxity
7.    Wide space and plantar crease between the big and second toe.
8.    Hyperextensible and lax joints
9.     Muscle weakness
Other common findings include a small penis, short, broad hands (transverse (simian) palmar crease), a protruding tongue, small ears, Brushfield spots, and dry skin.

Associated problems and features:

• Intelligence varies from severely retarded to low normal but is usually in the mild to moderate range.
• Social development may be 2 to 3 years beyond mental age; temperament range is similar to normal children, with a trend toward the easy child.
• Congenital anomalies include congenital heart disease (especially septal defects), renal agenesis, duodenal atresia. Hirschsprung disease, tracheoesophageal fistula, and skeletal deformities.
• Sensory problems include strabismus, nystagmus, myopia, hyperopia, excessive tearing and cataracts, and conductive hearing loss.

Other physical disorders inlcudes:

• Respiratory infections, leukemia, and thyroid dysfunction.
• Growth is reduced and there is rapid weight gain.
• Sexual development maybe delayed, incomplete or both. Male genitalia and secondary characteristics are underdeveloped. Breast development is mild to moderate with menarche at appropriate age. Women may be fertile, men are infertile.

Nursing Management:

1. Assess for associated problems.
2. Administer medications which maybe prescribed for associated problems.
3. Implement a plan of care that is the same as for mental retardation. Include planning and intervention strategies for associated problems and features.
4. Encourage genetic counseling.
5. Explain hypertonicity and joint hyperextensibility to parents, and that the child’s resultant lack of clinging is physiologic and not a sign of detachment.
6. Prevent respiratory infections by clearing the nose with a bulb syringe, using a cool mist vaporizer, performing chest physiotherapy when needed, providing good handwashing and avoiding exposure to infection.
7. When feeding infants and young children, use a small, straight-handled spoon to push food to the side and back of the mouth. Feeding difficulties occur due to a protruding tongue and hypotonia.
8. Encourage fluids and foods rich in fiber. Constipation results from decreased muscle tone, which affects gastric motility.
9. Provide good skin care because the skin is dry and prone to infection.

Source:

Lippincott Review Series

http://wikipedia.org

Image by: Lucina Foundation

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Results from separation of the sensory layer of the retina containing the rod and cones from the pigmented epithelial layer beneath.

Assessment:

1. Initially, the patient complains of flashes of light, floating spots or filaments in the vitreous, or blurred, �??sooty�?? vision. Most of these phenomena result from traction between the retina and vitreous.
2. If detachment progresses rapidly, the patient may report a veil-like curtain or shadow obscuring portions of the visual field. The veil appears to come from above, below, or from one side; the patient may initially mistake the obstruction for a drooping eyelid or elevated cheek.
3. Straight-ahead vision may be unaffected in early stages but, as detachment progresses, there will be loss of central as well as peripheral vision.

Diagnostic Evaluation:

1. Ophthalmoscopy or slit-lamp examination with full pupil dilation shows retina as gray or opaque in detached areas. The retina is normally transparent.

Surgical Interventions:

1. Surgical intervention aims to reattach the retinal layer to the epithelial layer and has a 90% to 95% success rate.

Techniques include:

a. Photocoagulation, in which a laser or xenon are �??spot welds�?? the retina to the pigment epithelium.

b. Electrodiathermy, in which a tiny hole is made in the sclera to drain subretinal fluid, allowing the pigment epithelium to adhere to the retina.

c. Cryosurgery or retinal cryopexy, another �??spot weld�?? technique that uses a super cooled probe to adhere the pigment epithelium to the retina.

d.  Scleral buckling, in which the sclera is shortened to force the pigment epithelium closer to the retina; commonly accompanied by vitrectomy.

Nursing Interventions:

1. 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 medications as ordered.

2. 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.

3. Encourage ambulation and independence as tolerated.

4. Administer medication for pain, nausea, and vomiting as directed.

5. Provide quiet diversional activities, such as listening to a radio or audio books.

6. Teach proper technique in giving eye medications.

7. Advise patient to avoid rapid eye movements for several weeks as well as straining or bending the head below the waist.

8. Advise patient that driving is restricted until cleared by ophthalmologist.

9. Teach the patient to recognize and immediately  report symptoms that indicate recurring detachment, such as floating spots, flashing lights, and progressive shadows.

10. Advise patient to follow up.

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