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

Nephrolithiasis is also called the renal calculi, are hard, usually small stones that form somewhere in the renal structure. The stones are masses of crystals and protein that form when the urine became supersaturated with a salt capable of forming solid crystals.

Symptoms occur when the stone become impacted in the urinary tract. When stones are found in the kidneys, the condition is called nephrolithiasis.

ETIOLOGY

• Hypercalcemia and hypercalciuria caused by hyperparathyroidism
• Chronic dehydration, poor fluid intake and immobility
• Chronic infection with urea-splitting bacteria (proteus vulgaris)
• Chronic obstruction with stasis of urine, foreign bodies within the urinary tract

RISK FACTORS

• Metabolic: abnormalities that result in increased urine levels of calcium, oxaluric acid, uric acid or citric acid
• Climate: warm climate that cause increased fluid loss, low urine volume and increased solute concentration in the urine
• Diet

Large intake of dietary proteins that increases uric acid excretion

Excessive amounts of tea or fruit juices that elevate urinary level

Large intake of calcium and oxalate

Low fluid intake that increases urinary concentration

• Genetic factors: family history of stone formation, cystinuria, gout, or renal acidosis
• Lifestyle: sedentary occupation, immobility

PATHOPHYSIOLOGY

Due to any cause —- slow urine flow —- resulting supersaturation of the urine with the particular element —- first become crystallized —- later become stone

TYPES

• Calcium oxalate, calcium phosphate, or mixture

Incidence: 90%

Feature: account for two-third of stones. Small, rough, and hard. Shaped like needles, colors vary from gray to white

Possible causes:

Excessive calcium. Excessive urea. Hyperparathyroidism, Cushing’s disease, immobility, etc

Predisposing factors: idiopathic hypercalciuria, hyperoxaluria, independent of urinary pH, family history

• Struvite – magnesium ammonium phosphate

Incidence: 2%

Features: second most common type of stone. Calculi crumble easily. Stones have a yellow color

Causes: infection by urea splitting microbes, usually proteus. May cause abscess formation in the kidney

Predisposing factors: urinary tract infection

• Uric acid stones

Incidence: 2%

Features: dye enhancement needed for x-ray visualization. Small, hard and color varies from yellow to red

Causes: gout, high uric acid levels, decreased fluid intake

Predisposing factors: gout, acid urine, inherited condition

• Cystine stones:

Incidence: rare

Feature: small, smooth calculi, waxy stones

Causes: cystine-containing crystals appear in the urine

Predisposing factors: acid urine

SIGNS AND SYMPTOMS

• Costovertebral angle pain
• Groin pain
• Renal colic because renal stones produce an increase in hydrostatic pressure and distention of the renal pelvis and proximal ureters causing renal colic. Pain relief is immediate after stone passage
• Flank pain radiating to genitalia
• Hematuria
• Anuria
• Restlessness
• Pallor
• Temperature
• Nausea vomiting, diarrhea, abdominal discomfort due to renointestinal reflexes

DIAGNOSTIC EVALUATION

• History collection
• Physical examination
• Kidney radiography may show stone
• IVP (intravenous pyelogram), retrograde pyelogram is used to localize the degree and site of obstruction or to confirm the presence of a radiolucent stones, such as uric acid or cystine calculus
• Urinalysis: may indicate gross or microscopic hematuria and could indicate abrasion of the urinary tract
• Ultrasonography can be used to identify a radiopaque or radiolucent calculus in the renal pelvis, calyx, or proximal ureters. But it is less useful when attempting to locate stones trapped in the midureter
• A CT scan may be used to differentiate a non-opaque stone from the tumor
• Lab test: serum calcium, phosphorus, sodium, potassium, bicarbonate, uric acid, BUN and creatinine levels are also measured

MANAGEMENT

Medical Management

• The goals of management are to eradicate the stone, determine the stone type, prevent nephrons destruction, control infection, and relieve any obstruction that may be present
• The immediate objective of treatment of renal colic is to relieve the pain until its cause can be eliminated
• Opioid analgesic agents are administered to prevent shock and syncope that may result from the excruciating pain
• Nonsteroidal anti-inflammatory drugs (NSAIDs) are effective in treating renal stone pain because they provide specific pain relief. They also inhibit the synthesis of prostaglandin E, reducing swelling and facilitating passage of the stone
• Hot baths or moist heat to the flank areas may also be helpful

Nutritional Therapy

• Nutritional therapy plays an important role in preventing renal stones
• Fluid intake is the mainstay of most medical therapy for renal stones
• Patient with renal stones should drink eight to ten ounce glasses of water daily or have IV fluids prescribed to keep the urine dilute
• A urine output exceeding 2 L/day is advisable

International Procedures

If the stone does not pass spontaneously if complications occur, common intervention includes endoscopic or other procedure. For example:

• Ureteroscopy
• Extracorporeal shock wave lithotripsy (ESWL)
• Endourologic (percutaneous) stone removal

Ureteroscopy

• It involves first visualizing the stone and then destroying it
• In this inserting an ureteroscope into the ureter and then inserting a laser, electrohydraulic lithotripter, or ultrasound device through the ureteroscope to fragment and remove the stones

Extracorporeal shock wave lithotripsy

• It is used for most symptomatic, nonpassable upper urinary stones. Electromagnetically generated shock waves are focused over the area of the renal stone
• The high energy dry shock waves pass through the skin and fragment the stone

Endourologic (Percutaneous) stone removal

• It is used for most symptomatic, nonpassable, upper urinary stones. Electromagnetically generated shock waves are focused over the area of the renal stone
• The high energy dry shock waves pass through the skin and fragment the stone

Endourologic (Percutaneous) stone removal

• It is used to treat the larger stones
• A percutaneous tract is formed and a nephroscope is inserted through it. Then the stone extracted or pulverized

Electrohydraulic lithotripsy

• It is a similar method in which an electrical discharge is used to create a hydraulic shock wave to break up the stone
• A probe is passed through the cystoscope and the tip  of lithotripter is placed near the stone
• This procedure is performed under topical anesthesia
• The most common complications are hemorrhage, infection and urinary extravasations

Chemolysis

• Stone dissolution using infusions of chemical solutions (e.g. alkylating agents, acidifying agents)

Surgical Management

• Today surgery is performed in only 1 to 2% of patients. It is indicated if the stone does not respond to other forms of treatment
• If the stone is in kidney, the surgery performed maybe a nephrolithotomy (incision into the kidney with removal of the stone) or a nephrectomy, if the kidney is nonfunctional secondary to infection
• Stones in the kidney pelvis are removed by pyelolithotomy

COMPLICATION

• Obstruction: from remaining stone fragments
• Infection: from dissemination of infected stone particles or bacteria resulting from obstruction
• Impaired renal function: from prolonged obstruction before treatment and removal
• Perirenal hematoma: from bleeding around the kidney caused by trauma of shock waves or laser treatments

Nursing Management

Nursing Assessment

• Obtain history focusing on family history of calculi, episodes of dehydration, prolonged immobility, UTI, dietary, bleeding history, and medication history
• Assess pain location and radiation; assess level of pain using a scale of 1 to 10. Observe for presence of associated symptoms nausea, vomiting, diarrhea, abdominal distension
• Monitor for signs and symptoms of UTI, such as chills, fever, dysuria, frequency. Examine urine for hematuria
• Observe for signs and symptoms of obstruction, such as frequent urination of small amounts, oliguria, anuria

Nursing Diagnosis

• Acute pain related to the presence of, obstruction or movement of a stone with in urinary system
• Impaired urinary elimination related to blockage of urine flow by stones
• Risk for infection related to obstruction of urine flow and instrumentation during treatment
• Anxiety related to hospitalization
• Fear related to deficient knowledge regarding the disease
• Deficient knowledge related to lack of knowledge about prevention of recurrence, diet and symptoms of renal calculi

1. Acute pain related in the presence of obstruction or movement of a stone with in urinary system

Interventions

• Ask severity, location and duration of pain using a pain scale. Pain is typically in the flank or costovertebral angle and may radiate to the pelvic, groin, or abdominal area
• Encourage fluid intake, unless contraindicated, to promote the passage of stone, dilute the urine, and reduce the risk of further stone formation
• Administer pain medication as ordered to promote comfort
• Apply heat to flank pain area to reduce pain and promote comfort

• Impaired urinary elimination related to blockage of urine flow by stones

Interventions

• Monitor total urine output and pattern of voiding. Report oliguria or anuria
• For outpatient treatment, patient may use a coffee filter to strain urine
• Help patient to walk, if possible because ambulation may help move the stone through the urinary tract
• Teach patient to drink eight ounces of liquid with meals, between meals and in early evening to provide fluids for hydration but not to an excess that may increase renal colic

• Risk for infection related to obstruction of urine flow and instrumentation during treatment

Interventions

• Administer parenteral or oral antibiotics, as prescribed during treatment, and monitor for adverse effects
• Assess urine for color, cloudiness, and odor
• Obtain vital signs, and monitor for fever and symptoms of impending sepsis (tachycardia, hypotension)

Health Education

• Encourage fluids to accelerate passing of stone particles
• Teach about analgesics that still may be necessary for colicky pain, which may accompany passage of stone debris
• Warn that some blood may appear in urine for several weeks
• Encourage frequent walking to assist in passage of stone fragments
• Teach patient to strain urine through a coffee filter or stone strainer and to save for analysis
• Teach patient to take alpha-adrenergic blockers to help dilate ureters, thus improve stone passage

DIABETES MELLITUS – Types, Signs and Symptoms, Diagnostic Evaluation and Management

Diabetes mellitus is a group of metabolic diseases in which a person has high blood sugar, either because the pancreas does not produce enough insulin, or because cells do not respond to the insulin that is produced. This high blood sugar produces the classical symptoms of polyuria (frequent urination), polydipsia (increased thirst) and polyphagia (increased hunger). Hyperglycemia does not cause symptoms until glucose values are significantly elevated-above 200 milligrams per deciliter (mg/dL).

Diabetes mellitus is a group of chronic disorder of endocrine pancreas. This disease characterized by increased levels of glucose in blood (hyperglycemia) resulting from defects in insulin secretion, insulin action, both.

There are three main types of diabetes mellitus (Type-1 DM)

1. TYPE-1 Diabetes Mellitus: Type 1 DM results from the body’s failure to produce insulin, and currently requires the person to inject insulin or wear an insulin pump. It is also called ‘insulin-dependent diabetes mellitus’ (IDDM) or ‘juvenile diabetes’. The immune system mistakenly manufactures antibodies and inflammatory cells that are directed against and cause damage to patients’ own body tissues. In persons with type 1 diabetes, the beta cells of the pancreas, which are responsible for insulin production, are attacked by the misdirected immune system. Exposure to certain viral infections (mumps and coxsackie viruses) or other environmental toxins may serve to trigger abnormal antibody responses that cause damage to the pancreas cells where is made. Some of the antibodies seen in type 1 diabetes include anti-islet cell antibodies, anti-insulin antibodies and anti-glutamic decarboxylase antibodies
2. TYPE-2 Diabetes mellitus: Type 2 DM results from insulin resistance, also referred to as non-insulin-dependent diabetes mellitus (NIDDM) or ‘adult-onset diabetes.’ In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body’s needs. In many cases the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells)
3. Gestational diabetes: gestational diabetes, occurs when pregnant women without a previous diagnosis of diabetes develop a high blood glucose level. Gestational diabetes (or gestational diabetes mellitus, GDM) is a condition in which women without previously diagnosed diabetes exhibit high blood glucose levels during pregnancy (especially during their third trimester)

SIGNS AND SYMPTOMS

• Increased thirst (polydepsia)
• Frequent urination (polyuria)
• Increased hunger (polyphagia)
• Weight loss
• Fatigue
• Blurred vision
• Slow-healing sores or frequent infections
• Dark skin

DIAGNOSTIC EVALUATION

• Glycated hemoglobin test: this blood test indicates average blood sugar for the past two to three months. It measures the percentage of blood sugar attached to hemoglobin, the oxygen-carrying protein in red blood cells. A normal level is below 5.7 percent
• Random blood sugar test: a blood sample will be taken at a random time. Regardless of when you last ate, a random blood sugar level of 200 mg/dL (11.1 mmmol/L) or higher suggests diabetes, a blood sugar level less than 140 mg/dL (7.8 mmol/L) is normal.
• Fasting blood sugar test: a blood sample will be taken after an overnight fast. A fasting blood sugar level from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) is considered prediabetes. If it is 126 mg/dL (7 mmol/L) or higher on two separate tests, indicates diabetes.
• Oral glucose tolerance test: it is rarely used test for hyperglycemia, patient is asked to fast overnight, and the fasting blood sugar level is measured. Then drink a sugary liquid, and blood sugar levels are tested periodically for the next two hours. A blood sugar level less than 140 mg/dL (7.8 mmol/L) is normal. A reading of more than 200 mg/dL (11.1 mmol/L) after two hours indicates diabetes. A reading between 140 and 199 mg/dL (7.8 mmol/L and 11.0 mmol/L) indicates prediabetes.
• Urine glucose and ketone levels: these are not as accurate in monitoring, changes in blood glucose as serum or blood levels. The presence of glucose in urine indicates hyperglycemia.

COMPLICATIONS

• Cardiovascular disease
• Nerve damage (neuropathy)
• Kidney damage (nephropathy) or kidney failure
• Damage to the blood vessels of the retina (diabetic retinopathy), potentially leading to blindness
• Clouding of the normally clear lens (cataract)
• Feet problems caused by damaged nerves or poor blood flow that can lead to serious infections
• Bone and joint problems, such as osteoporosis
• Skin problems, including bacterial infections, fungal infections and non healing wounds
• Teeth and gum infections
• Dawn phenomenon: It is rise of blood glucose between 4 am to 8 am that is not a response to hypoglycemia. This condition occurs in people both DM1 and DM2. Cause is unknown but due to hormone variation.
• Diabetic ketoacidosis: diabetic ketoacidosis develops when there is too little insulin in body. Without enough insulin, sugar cannot enter in cells for energy. Blood sugar level rises and body begins to break down fat for energy. This process produces toxic acids known as ketones. Excess ketones accumulate in the blood and eventually ‘spill over’ into the urine. Diabetic ketoacidosis can lead to diabetic coma that can be life-threatening.
• Diabetic hyperosmolar syndrome: this condition occurs when production of insulin is normal, but it does not work properly. Blood glucose levels may become very high-greater than 600 mg/dL (33 mmol/L). Because insulin is present but not working properly, the body cannot use either glucose or fat for energy. Glucose is then dumped in the urine, causing increased urination. If left untreated, diabetic hyperosmolar syndrome can lead to coma and life-threatening dehydration

MANAGEMENT

Nutritional Therapy

Nutrition, meal planning and weight control are the foundation of diabetes management.

The main objective is to control dietary caloric intake to maintain normal weight. Medical nutrition therapy (MNT), nutritional management of diabetes is complex, a registered dietician who understand dietary management has major responsibilities for designing and teaching aspect of therapeutic plan.

Regular blood sugar monitoring

Regular exercise

Regular diabetes medication or insulin therapy

Alcohol: alcohol and the substances use to make mixed drinks can cause either high or low blood sugar

Stress: the hormones body may produce in response to prolonged stress may prevent insulin from working properly

For women, fluctuations in hormone levels: as hormone levels fluctuate during menstrual cycle, so cans blood sugar level also, particularly in the week before period. Menopause may trigger fluctuations in blood sugar level as well

Pharmacological Management

• Biguanides
• Sulfonylureas
• Meglitinide derivatives
• Alphaglucosidase inhibitors
• Thiazolidinediones (TZDs)
• Glucagon like peptide-1 (GLP-1) agonists
• Dipeptidyl peptidase IV (DPP-4) inhibitors
• Selective sodium-glucose transporter-2 (SGLT-2) inhibitors
• Insulins
• Amylinomimetics
• Bile acid sequestrants
• Dopamine agonists

Insulin Therapy

Some people who have type 2 diabetes need insulin therapy as well. Because normal digestion interferes with insulin taken by mouth, insulin must be injected. Insulin injections involve using a fine needle and syringe or an insulin pen injector – a device that looks like an ink pen, except the cartridge is filled with insulin

Types of insulin are many and include rapid-acting insulin, long-acting insulin and intermediate options. Examples include:

• Insulin lispro (Humalog)
• Insulin aspart (Novolog)
• Insulin glargine (Lantus)
• Insulin detemir (Levemir)
• Insulin isophane (Humulin N, Novolin N)

Life Style and Home Remedies

• Commit to managing your diabetes: Make healthy eating and physical activity part of your daily routine. Establish a relationship with a diabetes educator, and ask your diabetes treatment team for help when you need it
• Wear a tag or bracelet that says you have diabetes. Keep a glucagon kit nearby in case of a low blood sugar emergency and make sure your friends and loved ones know how to use it.
• Schedule a yearly physical exam and regular eye exams
• Keep your immunizations up-to-date. Get a flu shot every year, and get a tetanus booster shot every 10 years
• Take care of your teeth. Diabetes may leave you prone to gum infections. Brush your teeth at least twice a day, floss your teeth once a day, and schedule dental exams at least twice a year
• Pay attention to your feet. Wash your feet daily in lukewarm water. Dry them gently, especially between the toes and moisturize with lotion. Check your feet everyday for blisters, cuts, sores, redness or swelling
• Keep your blood pressure and cholesterol under control
• Quit smoking
• If you drink alcohol, do so responsibly
• Take stress seriously

NURSING MANAGEMENT

Nursing Diagnosis

1. Fluid volume deficit related to osmotic diuresis, gastric loss, excessive diarrhea, nausea and vomiting, limited input

Intervention

• Monitor vital signs, note the presence of orthostatic blood pressure
• Assess breathing and breathe patterns
• Assess temperature, color and moisture
• Assess peripheral pulses, capillary refill, skin turgor and mucous membranes
• Monitor intake output. Record the urine specific gravity
• Measure body weight everyday
• Collaboration fluid therapy as indicated
• Imbalanced nutrition, less than body requirements related to insulin insufficiency.

Intervention

• Measure body weight per day as indicated
• Determine the diet program and diet of patients compared with food that can be spent on the patient
• Auscultation of bowel sounds, record the presence of abdominal pain/abdominal bloating, nausea, vomiting, keep fasting as indicated
• Observation of the signs of hypoglycemia, such as changes in level of consciousness, cold/humid, rapid pulse, hunger and dizziness
• Collaboration in the delivery of insulin, blood sugar tests and diet.
• Risk for infection related to inadequate peripheral defense, changes in circulation and high blood sugar levels

Intervention

• Observation for signs of infection and inflammation such as fever, redness, pus in the wound, purulent sputum, urine color cloudy and foggy
• Increase prevention efforts by performing good handwashing, each contact on all items related to the patient, including his or her own patients
• Maintain aseptic technique in invasive procedures(such as infusion catheter foley, etc)
• Attach catheter/perineal care do well
• Give skin care with regular and earnest. Massage depressed bone area, keep skin dry, dry linen and tight (not wrinkled)
• Position the patient in semifowler position
• Collaboration antibiotics as indicated
• Knowledge deficit: About condition, prognosis and treatment needs related to misinterpretation of information; do not know the source of information

Intervention

• Assess the level of knowledge of the client and family about the disease
• Give an explanation to the client about diseases and conditions now
• Encourage clients and families to pay attention to her diet
• Ask the client and reiterated family of materials that have been given

GLOMERULONEPHRITIS – Etiology, Types, Pathophysiology, Signs and Symptoms, Diagnostic Evaluation and Management

INTRODUCTION

Immunological processes involving the urinary tract predominantly affect the renal glomerulus, the disease process results in glomerulonephritis. It means inflammation of glomeruli, which affects both kidneys equally. It is a type of kidney disease in which the part of kidney (glomeruli) that helps in filter waste and fluids from blood is damaged.

DEFINTION

Glomerulonephritis means inflammation of glomeruli. It is an inflammation of tiny filters of kidney (glomeruli) that helps to remove excess fluid, and waste from bloodstream and pass them into the urine

TYPES

It is of two types acute glomerulonephritis and chronic glomerulonephritis

ACUTE GLOMERULONEPHRITIS

It means active inflammation in glomeruli. Acute glomerulonephritis is most common in children and young adults, but all ages can be affected.

Each kidney is composed of about 1 million filtering screens called glomeruli that remove uremic waste products. The inflammatory process usually begins with the immune system fights off the infection scars tissue forms

There are many diseases that cause an active inflammation within glomeruli. When there is active inflammation occur within the kidney scar tissue may replace normal functional kidney tissue and cause irreversible renal impairment

ETIOLOGY

It is caused when there is problem with immune system or diseases like HIV and lupus that affect immune system. Disorders that attack several organs and can cause glomerulonephritis

It occurs after an infection elsewhere in the body or may develop secondary to systemic disorders

An infection with group A streptococci bacteria

PATHOPHYSIOLOGY

Due to etiological factors, antigen (group A beta hemolytic streptococcus) —- throat infection —- deposition of antigen antibody complex in glomerulus —- increased production of epithelial cells lining the glomerulus —- leukocytes infiltrate the glomerulus —- thickening of the glomerular filtration membrane —- scarring and loss of glomerular filtration membrane —- decreased glomerular filtration rate

SIGNS AND SYMPTOMS

The primary presenting feature of acute glomerulonephritis is hematuria. The urine may be cola, coffee colored because of RBCs and protein plugs

• Proteinuria and elevated (BUN) blood urea and nitrogen and serum creatinine

Other Manifestations

• Oliguria
• Edema fever
• Shortness of breath or dyspnea. Possible flank pain
• Nausea and vomiting
• Abdominal pain
• Back pain, fatigue, weight gain
• Headache, loss of appetite
• Weakness, fatigue
• High blood pressure

DIAGNOSTIC EVALUATION

• History: assess and collect history from patient regarding change in pattern of urination frequency, color or volume

Ask patient for signs and symptoms like headache, nausea, vomiting and loss of appetite

Ask for any history of flank pain

Physical examination: in physical examination assess for adequate intake output

Check vital signs

Monitor weight of patient

Assess patient for edema and any signs and symptoms of infection

• Urinalysis: for the presence of hematuria. A urinalysis may show red blood cells in urine an indicator of damage to the glomeruli. Urinalysis results may also show white blood cells, a common indicator of infection and inflammation and increased protein which results nephron damage.
• Check patient BUN and serum creatinine level. There is an increase in BUN and serum creatinine level
• Needle biopsy: it reveals obstruction of glomerular capillaries from proliferation of endothelial cells. It is a diagnostic test that involves collecting small pieces of tissue, usually through a needle, for examination with a microscope. In this we collect a sample of kidney tissue, to check any unusual deposits, scarring, or infecting organisms that would explain a person’s condition

MANAGEMENT

• Management includes:

Antihypertensive’s to treat high blood pressure and diuretics, they increase the renal blood flow by decreasing renal vascular resistance.

Provide antibiotics if infection is still present usually penicillin. Helps to reduce infection and prevent further spread of infection

Steroids and other medicines will suppress the immune system. Prednisolone and methylprednisolone is useful and most commonly prescribed drug. It can suppress the inflammatory response in kidney and reduce the permeability of renal blood vessels and reducing the proteinuria

Nutritional Therapy

Dietary protein should be restricted if BUN level is increased

Potassium and sodium should be avoided if edema is present

Dietary protein should be restricted if there is evidence of an increase in nitrogenous wastes

Fluid intake should be restricted

Provide low protein diet to the patient

Provide vegetables, rice, cereals, dried beans, breads

Advise to avoid animal products they are rich source of protein

Eat healthy foods

Get proper rest and sleep

CHRONIC GLOMERULONEPHRITIS – Etiology, Pathophysiology, Signs and Symptoms, Diagnostic Evaluation and Management

Chronic glomerulonephritis is a kidney disorder caused by slow, cumulative damage and scaring of tiny blood filters in the kidneys. These filters known as glomeruli, remove waste products from the blood.

• In  chronic glomerulonephritis, scarring of glomeruli impedes the filtering process, trapping waste products in the blood while allowing red blood cells or protein to escape into the urine, eventually producing the characteristic signs of high blood pressure and swelling in legs and ankles
• The disorder may first come to one’s attention because of high blood pressure. In other, fluid retention or urine may be first signs. Long-term inflammation and scarring of the kidneys may lead to kidney failure in severe cases. Damage may progress without symptoms for months or years by the months or year, by the time symptoms appear, the course of the disorder maybe irreversible

ETIOLOGY

Specific cause is unknown

• Viral infections such as Hepatitis B, C, HIV leads to chronic glomerulonephritis
• Autoimmune disorder such as systemic lupus erythematosus, vasculitis may cause chronic glomerulonephritis
• Acute glomerulonephritis may after a symptom less period of many years, reappear as chronic glomerulonephritis

PATHOPHYSIOLOGY

It is an autoimmune disease caused by the loss of tolerance to self-antigens —- glomeruli have varying degree of hypercellularity and become sclerosed (hardened) —- size of kidney is decreases, and eventually tubular atrophy, chronic interstitial inflammation occur —- kidney’s ability to regulate the internal environment begins to decrease as glomeruli become scarred and resulting in fewer functional nephrons —- results into various symptoms of renal dysfunction that leads to edema, weight loss, irritability, poorly nourished, high blood pressure, nocturia

SIGNS AND SYMPTOMS

Patient with severe disease has no symptoms at all for many years. There condition may be detected when BUN level and serum creatinine level are detected

• Blood or protein in the urine
• Swelling of legs or ankle and other parts of body due to fluid accumulation (edema)
• Shortness of breath due to less blood
• Headache or blood pressure high
• Fatigue, nausea, vomiting, loss of appetite, abdominal pain
• Nocturia (increased need to urinate at night)
• Crackles sound in the lungs, poorly nourished, pale skin color

DIAGNOSTIC EVALUATION

• History: collect any history of acute glomerulonephritis if present

Ask patient for the history of urination changes in patient

Ask for the presence of signs and symptoms

Ask patient for history of abdominal pain, etc

Physical examination: assess patient for edema and swelling, check patient body weight

Monitor patient blood pressure

• Urinalysis and blood tests to know about the elevated level of for the presence of hematuria. A urinalysis may show red blood cells in urine an indicator of damage to the glomeruli. Urinalysis results may also show white blood cells, a common indicator of infection and inflammation and increased protein which results nephron damage
• A blood test to measure protein and creatinine level. Level of creatinine and protein is elevated
• An ultrasound of kidneys maybe performed to evaluate the size of kidneys and any blockages
• CT scan or abdominal ultrasound can be performed to show the damage to the glomeruli
• Renal biopsy maybe performed, under local anesthesia, to extract a small sample of tissue from kidney, to determine the exact cause and the nature of the glomerulonephritis

MANAGEMENT

• Antihypertensive drugs (propranol) maybe prescribed to reduce high blood pressure
• Diuretics (frusemide) may be prescribed to reduce excess fluid retention and increase urine production
• Steroid medications, if immunosuppressive drugs (prednisolone and methyl prednisolone), maybe prescribed for some patients. Prednisolone and methylprednisolone is useful and most commonly prescribed drug. It can suppress the inflammatory response in kidney and reduce the permeability of renal blood vessels and reducing the proteinuria
• In severe cases, where kidney failure occurs, dialysis maybe necessary. Dialysis performs the function of the kidney by removing waste products and excess fluid from the blood when kidney cannot
• A kidney transplant is also an alternative in case of kidney failure. A kidney transplant is a surgical procedure performed to replace a diseases kidney with a healthy kidney from another person

DIET MANAGEMENT

• Provide low salt diet and provide low protein diet, because it reduces the workload on the kidney
• Nuts, dried beans, cereals, vegetables, rice, breads are low in protein
• Limit the amount of animal products
• Take vitamin supplements
• Fluid intake should be restricted
• Provide adequate diet and fruits
• Get proper rest
• Take medication regularly

PREVENTION

• In prevention it can be prevented by limit the salts, fluids, protein
• Control blood pressure, controlling high blood pressure is the most important part of treatment
• Maintain good hygiene practices
• Practicing safe sex helps in preventing the viral infection such as HIV infection and hepatitis which leads to this illness
• Take calcium supplements

NURSING MANAGEMENT

Nursing Assessment

• Observe patient for changes in fluid and electrolyte status and for the signs and symptoms
• Monitor vital signs of patient blood pressure
• Anxiety levels are often extremely high for both the patient and family
• Throughout the course of disease and treatment, the nurse should gives emotional support by providing opportunities for the patient and family to verbalize their concerns, have their questions answered, and explore their options

Nursing Diagnosis

• Ineffective renal tissue perfusion related to damage of glomerular infiltration
• Excess fluid volume related to compromised renal function
• Imbalanced nutrition less than body requirement related to anorexia, nausea, vomiting
• Deficient knowledge regarding condition and treatment
• Activity intolerance related to fatigue, retention of waste products

1. Excess fluid volume related to compromised renal function, decreased urine output, retention of sodium and water

Interventions

• Assess the fluid status of patient
• Check weight daily and record
• Maintain intake output chart
• Monitor vital signs
• Limit fluid intake to the patient
• Explain the rationale for restriction of fluid
• Assist patient to cope up with the discomforts results from fluid restriction
• Provide and encourage oral hygiene, it minimizes the dryness of oral membranes

• Imbalanced nutrition pattern less than body requirements related to anorexia, nausea, vomiting

Interventions

• Assess the nutritional status of the patient
• Monitor weight of patient daily and record it
• Assess the patient nutritional dietary patterns-diet history, food preferences
• Provide patients food preference within dietary restrictions
• Provide low salt and protein diet
• Restrict fluids rich diet to the patient
• Encourage for proper rest
• Provide pleasant surroundings at the meal time

• Deficient knowledge related to disease condition and treatment

Interventions

• Assess the understanding of patient regarding disease condition and treatment
• Provide explanation regarding renal function and consequences of disturbed renal function at the level of patient understanding and guided by patient’s readiness to learn
• Assist patient to identify ways to incorporate changes related to illness and its treatment into lifestyle
• Provide oral and written information as appropriate about: renal function, fluid and dietary restrictions
• Clear all the doubts of the patient
• Provide psychological support to the patient

RESPIRATORY FAILURE – Classification, Etiology, Pathophysiology, Clinical Manifestation, Diagnostic Evaluation and Management

INTRODUCTION

The most important function of the respiratory system is to provide oxygen to the body tissues and remove the carbon dioxide. The body relies primarily on the central nervous system, the pulmonary system, the heart, and the vascular system to accomplish the effective respiration. Respiratory failure develops when one or more of these systems or organs fail to maintain optimal functioning.

Respiratory failure is a sudden and life-threatening deterioration of the gas exchange functions of the lung and indicates failure of the lungs to provide adequate oxygenation or ventilation for the blood. Acute respiratory failure is defined as the decrease in the arterial oxygen tension to less than 50 mm Hg (hypoxemia) and increase in the arterial carbon dioxide tension, i.e. (hypercapina) to greater than 50 mm Hg, with the arterial pH of less than 7.35. it is a condition in which there is inadequate gas exchange by the respiratory system, with the result that arterial O₂ and CO₂ levels cannot be maintained within their normal ranges.

DEFINITION

• Acute respiratory failure is a condition in which the patient’s breathing apparatus fails in the ability to maintain arterial blood gases within the normal range.
• Ventilatory failure is the inability of the body to sustain respiratory drive or the inability of the chest wall and muscles to mechanically move air in and out of the lungs. The hallmark of ventilator failure is an elevated CO₂ level.
• A sudden inability of the lungs to maintain normal respiratory function. The condition may be caused by an obstruction in the airways or by failure of the lungs to exchange gases in the alveoli.
• Acute respiratory failure is defined as the decrease in the arterial oxygen tension to less than 50 mm Hg (hypoxemia) and increase in the arterial carbon dioxide tension, i.e. (hypercapnia) to greater than 50 mm Hg, with an arterial pH of less than 7.35.

CLASSIFICATION OF RESPIRATORY FAILURE

It is divided into two types:

• Acute respiratory failure
• Chronic respiratory failure

Acute Respiratory Failure

Acute respiratory failure is characterized by hypoxemia (PaO₂ less than 50 mm Hg) and academia (pH less than 7.35). acute respiratory failure occurs rapidly, usually in minutes to hours or days

Types of Acute Respiratory Failure

It is divided into two:

1. Type 1 acute respiratory failure
2. Type 2 acute respiratory failure

• Type 1 acute respiratory failure: Type 1 respiratory failure is defined as hypoxia without hypercapnia and indeed the PaCO₂ may be normal or low. It is typically caused by a ventilation/perfusion (V/Q) mismatch, the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs.
• Type 2 acute respiratory failure: Type 2 respiratory failure is caused by inadequate ventilation, both oxygen and carbon dioxide are affected and buildup of carbon dioxide levels (PaCO₂) that has been generated by the body.

Chronic Respiratory Failure

Chronic respiratory failure is characterized by hypoxemia and hypercapnea with the normal pH (7.35 to 7.45). chronic respiratory failure occurs over a period of months to a year – allows for activation of compensatory mechanism.

Chronic respiratory failure may also be divided into:

• Hypoxemic respiratory failure: when a lung disease causes respiratory failure, gas exchange is reduced because of changes in ventilation (the exchange of air between the lungs and the atmosphere), perfusion (blood flow), or both. Activity of the respiratory muscles is normal. This type of respiratory failure which results from a mismatch between ventilation and perfusion is called hypoxemic respiratory failure. Some of the alveoli get less fresh air than they need for the amount of blood flow, with the net result of a fall in oxygen in the blood. These patients tend to have more difficulty with the transport of oxygen than with removing carbon dioxide. They often overbreathe (hyperventilate) to make up for the low oxygen, and this results in a low CO₂ level in the blood (hypocapnia). Hypocapnia makes the blood more basic or alkaline which is injurious to the cells.
• Hypercapnic respiratory failure: respiratory failure due to a disease of the muscles used for breathing (‘pump or ventilatory apparatus failure’) is called hypercapnic respiratory failure. The lungs of these patients are normal. This type of respiratory failure occurs in patients with neuromuscular diseases, such as myasthenia gravis, stroke, cerebral palsy, poliomyelitis, amylotrophic lateral sclerosis, muscular dystrophy, postoperative situations limiting ability to take deep breaths, and in depressant drug overdoses. Each of these disorders involves a loss or decrease in neuromuscular function, inefficient breathing and limitation to the flow of air into the lungs. Blood oxygen falls and the carbon dioxide increases because fresh air is not brought into the alveoli is needed amounts. In general, mechanical devices that help move the chest wall help these patients.

ETIOLOGY

Brain Disorders

• Stroke: a stroke is sudden loss of brain function resulting from a disruption of blood supply to a part of the brain
• Brain tumors: a brain tumor is a localized intracranial lesion that occupies space within the skull and tends to cause a rise in intracranial pressure
• Depression of respiratory drive with drugs, e.g. narcotic tranquilizer

Chest Wall Dysfunction and Neuromuscular Factor

• Anesthetic blocking agent
• Cervical spinal cord injury
• Neuromuscular disorder
• Neuromuscular blocking agent

Airway Obstruction

• Airway inflammation
• Tumor
• Foreign bodies
• Asthma
• COPD

Interstitial Lung Diseases

• Pneumonia
• Pulmonary tuberculosis
• Pulmonary edema
• Pulmonary fibrosis

Pulmonary Dysfunction

• Asthma
• Emphysema
• Chronic obstructive pulmonary disease
• Pneumonia
• Pneumothorax
• Pulmonary contusion
• Hemothorax
• Acute respiratory distress syndrome (ARDS)

Cardiac Dysfunction

• Pulmonary edema
• Cerebrovascular accident
• Arrhythmia
• Congestive heart failure
• Valve pathology

Other

• Fatigue due to prolonged tachypnea in metabolic acidosis
• Intoxication with drugs (e.g. morphine, benzodiazepines, alcohol) that suppress respiration.

Traumatic Causes

• Direct thoracic injury may result in a number of abnormalities that can lead to respiratory failure
• Direct brain injury can result in loss of respiration

PATHOPHYSIOLOGY

In alveolar ventilation —- nerves and muscles of respiration drive breathing —- failure in alveolar ventilation —- ventilation-perfusion mismatch —- hypercapnia and acidosis during obstructive forms: the residual pressure in the chest impairs inhalation —- increase in workload of breathing —- develops true intrapulmonary shunt —- decreased lung compliance

Mechanism of Pathophysiology

• Respiratory failure can arise from an abnormality in any of the components of the respiratory system, including the airways, alveoli, central nervous system (CNS), peripheral nervous system, respiratory acidosis, and chest wall. Patients who have hypoperfusion secondary to cardiogenic, hypovolemic, or septic shock often present with respiratory failure
• Ventilatory capacity is the maximal spontaneous ventilation that can be maintained without development of respiratory muscle fatigue. Ventilatory demand is the spontaneous minute ventilation that results in a stable PaCO.
• Normally, ventilatory capacity greatly exceeds ventilatory demand. Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both). Ventilatory capacity can be decreased by a disease process involving any of the functional components of the respiratory system and its controller.

CLINICAL MANIFESTATIONS

• Paroxysmal nocturnal dyspnea
• Orthopnea
• Pulmonary edema
• Confusion and reduced consciousness may occur
• Neurological features may include restlessness, anxiety, confusion, seizures or coma
• Tachycardia and cardiac arrhythmias
• Cyanosis
• Polycythemia
• Cor pulmonale
• Pulmonary hypertension
• Right ventricular failure
• Hepatomegaly
• Peripheral edema

DIAGNOSTIC EVALUATION

• Arterial blood gas analysis: confirmation of the diagnosis
• Renal function tests and LFTs: may provide clues to the etiology or identify complications associated with respiratory failure. Abnormalities in electrolytes such as potassium, magnesium and phosphate may aggravate respiratory failure and other organ dysfunctions
• Serum creatine kinase and troponin I: to help exclude recent myocardial infarction. Elevated creatine kinase may also indicate myositis
• Thyroid function test: hypothyroidism may cause chronic hypercapnic respiratory failure
• Spirometry: to evaluate lung capacity
• Echocardiography: if a cardiac cause of acute respiratory failure is suspected
• Pulmonary function tests are useful in the evaluation of chronic respiratory failure
• ECG: to evaluate a cardiovascular cause, it may also detect dysrhythmias resulting from severe hypoxemia or acidosis.
• Right heart catheterization: should be considered if there is uncertainty about cardiac function, adequacy of volume replacement, and systemic oxygen delivery
• Pulmonary capillary wedge pressure may be helpful in distinguishing cardiogenic from noncardiogenic edema

MANAGEMENT

Management of acute respiratory failure is dependent upon the cause and its severity. The principle of management of acute respiratory failure is the following:

• Treat the cause
• Maintain a patient airway
• Provide adequate ventilation
• Provide optimum oxygen
• Carry out chest physiotherapy

The main goal of treating of respiratory failure is to get oxygen to lungs and organs and remove the carbon dioxide from the body

The promoting effective airway clearance effective gas exchange

Preventive complication of immobility

Monitoring and documenting indication of altered tissue perfusion

Promoting comfort

Correction of hypoxemia

Correction of hypercapnia

Airway an another goal is to treat the underlying cause of the condition

Administration of Oxygen

Nasal prongs, nasal catheters, or face masks are commonly used to administer oxygen to the spontaneously breathing patient

The actual fraction of inspired oxygen depends upon:

• Flow rate of oxygen
• Degree of mouth breathing
• Patency of nasal passage
• Inspection of insertion of nasal catheter

Positive End Expiratory Pressure (PEEP)

• Used with mechanical ventilation
• Increases interthoracic pressure
• Keeps the alveoli open
• Decreases shunting
• Improves gas exchange

Management of Upper Airway Obstruction

As soon as upper airway obstruction is diagnosed, measures must be taken to correct it.

• The mouth is opened to see if tongue has fallen back or if there are secretions, blood clot or any particles obstructing the airway
• Extension of the head is the simplest way of relieving upper airway obstruction by the tongue falling back
• If simple extension of the head is not adequate to clear the airway, the mandible should be forced forward
• Maneuver is designed to put further tension on the musculature that supports the tongue. It is best executed by standing behind the patient
• If maneuver is not adequate and partial airway obstruction still exists, then oral airway may have to be inserted or end tracheal intubation be done
• If assisted ventilation is required, a resuscitator bag and mask are used initially prior to intubation and mechanical ventilation

Medical Management

Medical management includes:

• Antibiotics for pneumonia infection
• Bronchodilators: reduce bronchospasm, COPD
• Diuretics for pulmonary edema
• Chest physical therapy and the hydration to mobilize secretions
• Maintain fluid and electrolytes and avoid fluid overload
• Intubation and mechanical ventilation

COMPLICATIONS

• Oxygen toxicity if prolonged high FIO₂ required
• Barotrauma may occur from excessive intra-alveolar pressure
• Ventilator-associated pneumonia
• Infection to the lower respiratory tract due to intubation
• Dental or vocal cord trauma
• Gastric complications: distension from air entering the GI tract, stress ulcers from hyperacidity and inadequate nutrition
• Other complications include deep venous thromboembolism, skin breakdown, malnutrition, stress and anxiety

NURSING MANAGEMENT

Nursing Assessment

• Note the changes suggesting increased work of breathing or pulmonary edema
• Assess breathing sound
• Assess sign of hypoxemia and hypercapnea
• Analyze the ABG and compare the previous values
• Determine hemodynamic status and compare it with previous value

Nursing Diagnosis

• Impaired gas exchange related to inadequate respiratory center activity or chest wall movement, airway obstruction, or fluid in lung
• Ineffective airway clearance related to increased or tenacious secretion
• Acute pain related to inflammatory process and dyspnea
• Anxiety related to pain, dyspnea and serious conditions

Nursing Intervention

• Improve gas exchange:

Administer oxygen to maintain PaO₂ of 60 mm Hg, using devices that provide increased oxygen concentration

Monitor fluid balance by intake and output measurement, urine-specific gravity, daily weight measurement

Provide measures to prevent atelectasis and promote chest extension and secretion clearance as per advice, spirometer

Elevated head level to 30 degrees

Monitor adequacy of alveolar ventilation by frequent measurement of respiratory system

Administer antibiotic, cardiac medication and diuretics as prescribed by doctor

• Maintain airway clearance:

Administer medication to increase alveolar function

Perform chest physiotherapy to remove mucus

Administer IV fluids

Suction patient as needed to assist with removal of secretions

• Relieving pain:

Watch patient for sign of discomfort and pain

Position the head elevated

Give prescribed morphine and monitor for pain-relieving sign

• Reducing anxiety:

Correct dyspnea and relieve from physical discomfort

Speak calm and slowly

Explain diagnostic procedure

REHABILITATION OF DISASTER VICTIMS – Challenges of Rehabilitation, Kinds of Reactions and Psychosocial Interventions

In the post-disaster period, along with relief, rehabilitation and the care of physical health and injuries, mental health issues need to be given importance. Apart from material and logistic help, the suffering human beings will require human interventions.

CHALLENGES OF REHABILITATION

• Ensuring that people living in the relief camps have access to regular food supplies, additional set of clothes, sanitation drinking water, public health intervention immunization, preventive health care, heat and rain proof shelters, child care and education facilities and support.
• Ensuring access to basic entitlements in terms of their compensation, government schemes and credit institutions so that they can rebuild their homes and livelihood back to the same levels as before the disaster.
• Ensuring livelihood reintegration
• Ensuring legal right and social justice to the disaster victims including filing of FIRs, investigation and contesting cases in the court
• Providing psychosocial counseling and support for dealing with loss, betrayal and anger.
• Community based rehabilitation for widows orphans, elderly, children and physically disabled
• Actively rebuilding a culture of communal harmony and trust

KINDS OF REACTIONS SHOWN BY DISASTER VICTIMS

• Physical impact: stomach aches, diarrhea, headaches, and body aches, physical impairments (limbs, sight, voice, hearing), injuries, fever, cough, cold, miscarriage etc.
• Emotional reactions: anger, betrayal, irritability, revenge-seeking, fear, anxiety, depression, withdrawal, grief, addiction to pan masala, cigarette, beedi, drug abuse (flask back, numbness, depression)
• Socioeconomic impact: loss of trust between communities, lack of privacy, single parent families, widows, orphan state with loss of both parents, discontinuity in educational plans (e.g. loss of employment, homelessness migration, disorganization of life routines, material loss).

PSYCHOSOCIAL INTERVENTIONS

Principles

• Ventilation
• Empathy
• Active listening
• Social support
• Externalization of interest
• Lifestyle choice
• Relaxation and recreation
• Spirituality
• Health care
• Work with individuals (willing to talk immediately unwilling to talk)

For people who are willing to talk immediately

Listen attentively

Do not interrupt

Acknowledge that you understand the pain and distress by learning forward

Look into the eyes

Console them by patting on the shoulders or touching or holding their hand as they cry

Respect the silence during interaction; do not try to fill it in by talking

Keep reminding them I am with you. It is good you are trying to release your distress by crying. It will make you feel better

Do not ask them to stop crying

For those unwilling to talk (angry, or remain mute and silent)

Do not get anxious or feel rejected, remain calm

Maintain regular contact and greet them

Maintain interaction

Acknowledge that you understand they are not to blame

Tell them you will return the next day or in a couple of days

Tell them you are not upset or angry because he or she did not talk

Once the person starts talking, maintain a conversation using the following queries like how you are and how are your other family members, what can individuals do to recover?

Work with Families

• Share their experience of loss as a family
• Contact relatives to mobilize support and facilitate recovery
• Participate in rituals like prayers, keeping the dead persons photographs
• Make time for recreation
• Resume normal activities of the pre-disaster days with the family
• Try and do things together as a writ and support one another
• Be together as a family member. Do not send women and children and the aged too far off places for the sake of safety
• Restart activities that are special to your family like having meals together, praying, playing games, etc
• Keep touching and comforting your parents, children, spouse and the aged in your family
• Keep in constant touch with the family member who is hospitalized

Work with the Community

• Group mourning
• Group meetings
• Supporting group initiatives
• Cultural aspects
• Rally
• Group participation for rebuilding efforts
• Sensitization process

Rehabilitation of Special Groups

1. Aged people can be helped by

• Keeping them with their near and dear ones
• Visiting them regularly and spending time with them
• Touching them and allowing them to cry
• Re-establishing their daily routines
• Making them feel responsible by giving them some work to carry out which is not too difficult
• Getting them involved in relief work by requesting for their suggestion and advice, etc.
• Keeping them informed of positive news
• Attending to their medical ailments
• Organizing small group prayer meetings

Disabled People

• Removing them to places of safety
• Keeping them informed what is happening
• Getting them involved in activities
• Integrate them in group discussions
• Attend to their specific needs (wheel chairs, hearing aids)
• Helping them overcome their feeling of insecurity
• Taking cognizance of the fact that mentally challenged people, especially the women and children are vulnerable to sexual abuse and help them

Women

• Help them to be with their families
• Keep informing them what is happening
• Involve them in activities
• Involving them in relief and rehabilitation activities
• Initiating self-help formation
• Involve them in recreation
• Making them to spend time with young widows or people who have lost their children and supporting them

Children

• Letting him/her to be close to adults who are loved and familiar
• Re-establishing some sort of a routine for them like eating, sleeping, going for programs
• Actions like touching, hugging, reassuring them verbally
• Allowing them to take about the event
• Encourage them to play
• Involve them in activities like painting and drawing, where then can express their emotions
• Organize story telling sessions, singing, songs and games
• Praising coping behavior
• Provide referral if required
• Spending time on their studies once they return to school

Policies Related to Emergency and Disaster Management

This policy aims at:

• Promoting a culture of prevention, preparedness and resilience at all levels through knowledge, innovation and education
• Encouraging mitigation measures based on technology, traditional wisdom and environmental sustainability
• Mainstreaming disaster management into the developmental planning process
• Establishing institutional and technological frameworks to create an enabling regulatory environment and a compliance regime
• Ensuring efficient mechanism for identification, assessment and monitoring of disaster risks
• Developing contemporary forecasting and early warning systems backed by responsive and fail-safe communication with information technology support
• Ensuring efficient response and relief with a caring approach towards the needs of the vulnerable sections of the society
• Undertaking reconstruction as an opportunity to build disaster resilient structures and habitat for ensuring safer living and
• Promoting a productive and protective partnership with the media for disaster management

Policy Statement

To develop and implement an integrated action plan that will create an effective disaster management system at local, national and international levels.

Focus Areas and Strategies for Intervention

• Making disaster risk reduction a development priority:

To incorporate disaster risk principles in the development agenda and other country programme

To enhance institutional capacity in disaster risk reduction

To develop national platforms for disaster risk reduction

• Improving early warning systems:

To monitor continuously the hazard and vulnerability threats

To develop standard risk and monitoring instruments

Do a risk and hazard mapping

To foster an understanding of disaster management mechanisms through dissemination of information and advocacy

• Addressing priority development concerns to reduce underlying risk factors:

To integrate disaster risk reduction in poverty reduction strategy paper

To address sources of vulnerability especially outbreak of diseases and pests (HIV/AIDS, Avian Flu, locusts, etc)

To sensitize both local and traditional authorities with a view to understanding disaster prevention as a development challenge

Mainstream gender and youth policies in the development agenda

• Effective disaster response through disaster preparedness:

To promote contingency planning in all government departments and all other sectors to ensure alignment of national, local and district disaster management plans

To review and periodically rehearse national preparedness and contingency plans for major hazards

To ensure that operational capacity exists within disaster management systems to enhance community resilience

Policy Implementation Agencies and Structures

The policy will adopt various approaches to ensure that risk reduction in particular and disaster management in general is a national and local priority with strong involvement of local actors, the victims of disaster and institutional basis for implementation

Agencies

• NGOs
• Civil Society Organizations
• Government Agencies
• UN Agencies
• Private Sector

Functions

• Identify, assess and monitor disaster risks and enhance early warning systems
• Use indigenous knowledge, innovation, practices and education to build a culture a safety and resilience at all levels
• Strengthen disaster preparedness for effective response at all levels
• Creation of Disaster Prevention Volunteer Corps at local and national levels to be fully trained and equipped to identify, assess and monitor disaster events

Operational Mechanism

This policy will be implemented through the following strategic actions:

• Sensitization programmes and advocacy on disaster prevention
• Mainstreaming disaster prevention and management in school curricula and development programmes
• Factor disaster scenarios into economic planning and programmes
• Capacity building and information sharing
• Monitoring and Evaluation

EMERGENCY CONDITIONS – Shock (Etiology, Pathophysiology, Signs and Symptoms, Diagnostic Evaluation and Management)

SHOCK

Clinical syndrome characterized by decreased tissue perfusion and impaired cellular metabolism resulting in an imbalance between the supply and demand for oxygen and nutrients

ETIOLOGY AND PATHOPHYSIOLOGY

• Cardiogenic shock occurs when either systolic or diastolic dysfunction of the pumping action of the heart results in compromised cardiac output (CO).

Precipitating causes of cardiogenic shock include myocardial infarction (MI), cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary hypertension, cardiac tamponade, and myocardial depression from metabolic problems.

Hemodynamic profile will demonstrate an increase in the pulmonary artery wedge pressure (PAWP) and pulmonary vascular resistance

SIGNS AND SYMPTOMS

Tachycardia, hypotension, a narrowed pulse pressure, tachypnea, pulmonary congestion, cyanosis, pallor, cool and clammy skin, decreased capillary refill time, anxiety, confusion, and agitation.

• Hypovolemic shock occurs when there is a loss of intravascular fluid volume

Absolute hypovolemia results when fluid is lost through hemorrhage, gastrointestinal (GI) loss (e.g. vomiting, diarrhea), fistula drainage, diabetes insipidus, hyperglycemia, or diuresis.

Relative hypovolemia results when fluid volume moves out of the vascular space into extravascular space (e.g., interstitial or intracavitary space) and this is called third spacing

The physiologic consequences of hypovolemia include a decrease in venous return, preload, stroke volume and CO resulting in decreased tissue perfusion and impaired cellular metabolism.

Clinical manifestations depend on the extent of injury or insult, age and general state of health and may include anxiety, an increase in heart rate, CO, and respiratory rate and depth, and a decrease in stroke volume, PAWP, and urine output.

• Neurogenic shock is a hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above an last up to 6 weeks, or in response to spinal anesthesia.

Immediate reaction causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permeability resulting in fluid leaks from the vascular space into the interstitial space

Clinical manifestations can include anxiety, confusion, dizziness, chest pain, incontinence, swelling of the lips and tongue, wheezing, stridor, flushing, pruritus, urticaria and angioedema.

• Septic shock is the presence of sepsis with hypotension despite fluid resuscitation along with the presence of tissue perfusion abnormalities

In severe sepsis and septic shock, the initiated body response to an antigen is exaggerated resulting in an increase in inflammation and coagulation, and a decrease in fibrinolysis

Endotoxins from the microorganisms cell wall stimulate the release of cytokines and other proinflammatory mediators that act through secondary mediators such as platelet-activating factor.

Clinical presentation for sepsis is complex. Patients will usually experience a hyperdynamic state characterized by increased CO. Persistence  of a high CO beyond 24 hours is ominous and often associated with hypotension and multiple organ dysfunction syndrome (MODS). Initially patients will hyperventilate as a compensatory mechanism, resulting in respiratory alkalosis followed by respiratory acidosis and respiratory failure. Other clinical signs include alteration in neurologic status, decreased urine output, and GI dysfunction.

STAGES OF SHOCK

• Compensatory Stage

Decrease in circulating blood volume

Sympathetic nervous system stimulated, release catecholamines (epinephrine and norepinephrine), bronchodilation and increased cardiac output occurs. To maintain blood pressure; increase heart rate and contractility increases in peripheral vasoconstriction due to stimulation of beta adrenergic fibers (cause vasoconstriction of blood vessels of skin and abdominal viscera) and increase in heart rate and contractility.

Renin-angiotensin release of aldosterone-reabsorb H₂O and sodium. Get fluid shift from interstitial to capillaries due to decrease in hydrostatic pressure in capillaries

Shunting blood from the lungs-ventilation-perfusion mismatch

Circulation maintained, but only sustained short time without harm to tissues

• Progressive Stage

Altered capillary permeability (3^rd spacing)

In the lungs: alveolar or pulmonary edema, ARDS, increased pulmonary artery pressures

Cardiac output decreases and coronary perfusion is decreased. Decreased myocardial perfusion-arrhythmias and myocardial ischemia

Kidneys: elevated BUN and creatinine

Metabolic acidosis, anaerobic metabolism and kidneys cannot excrete acids and reabsorb bicarbonate

GI-ischemia causes ulcers and GI bleed

Liver: cannot eliminate waste products, elevated ammonia and lactate, bilirubin (jaundice) bacteria released in bloodstream

Hematologic: disseminated intravascular coagulopathy (DIC)

• Refractory Stage

Anaerobic metabolism starts. Lactic acid build-up

Increased capillary blood leak, worsens hypotension and tachycardia, also get cerebral ischemia

Get profound hypotension and hypoxemia

Cellular death leads, tissue, death, vital organs fail and death occurs (lungs, liver and kidneys result in accumulation of waste products. One organ failure leads to another.

Recovery unlikely

DIAGNOSTIC EVALUATION

• Blood: RBC, hemoglobin and hematocrit
• Arterial Blood Gases: respiratory alkalosis and metabolic acidosis
• Electrolyte (Na level increased early, decreased later if hypotonic fluid given) K decrease later increase K with cellular breakdown and renal failure
• BUN and creatinine increased, specific gravity increased then fixed at 1.010
• Blood cultures: identify causative organism in septic shock
• Cardiac enzymes: diagnosis of cardiogenic shock
• Glucose: increased early then decreased
• DIC screen: fibrinogen level, platelet count, PTT and PT, thrombin time
• Lactic acid: increased
• Liver enzymes: ALT, AST and GGT increased

MANAGEMENT

• General management strategies for a patient in shock begin with ensuring that the patient has a patient airway and oxygen delivery is optimized. The cornerstone of therapy for septic, hypovolemic and anaphylactic shock is volume expansion with the administration of the appropriate fluid
• It is generally accepted that isotonic crystalloids, such as normal saline, are used in the initial resuscitation of shock. If the patient does not respond to 2 to 3 L of  crystalloids, blood administration and central venous monitoring maybe instituted
• The primary goal of drug therapy for shock is the correction of decreased tissue perfusion

Sympathomimetic drugs cause peripheral vasoconstriction and are referred to as vasopressor drugs (e.g. epinephrine and norepinephrine)

The goals of vasopressor therapy are to achieve and maintain a mean arterial pressure (MAP) of 60 to 65 mm Hg and the use of these drugs is reserved for patients unresponsive to other therapies

The goal of vasodilator therapy, as in vasopressor therapy, is to maintain Mean arterial pressure at 60 mm Hg or greater

Vasodilator agents most often used are nitroglycerin (in cardiogenic shock) and nitroprusside)

COLLABORATIVE CARE

Cardiogenic Shock

• Overall goal is to restore blood flow to the myocardium by restoring the balance between oxygen supply and demand
• Definitive measures include thrombolytic therapy, angioplasty with stenting, emergency revascularization and valve replacement
• Care involves hemodynamic monitoring, drug therapy (e.g. diuretics to reduce preload), and use of circulatory assist devices (e.g. intra-aortic balloon pump, ventricular assist device)

Hypovolemic Shock

• The underlying principles of managing patients with hypovolemic shock focus on stopping the loss of fluid and restoring the circulating volume
• Fluid replacement is calculated using a 3:1 rule (3 ml of isotonic crystalloid for every 1 ml of estimated blood loss)

Septic Shock

• Patients in septic shock require large amounts of fluid replacement, sometimes as much as 6 to 10 L of isotonic crystalloids and 2 to 4 L of colloids, to restore perfusion
• Vasopressor drug therapy maybe added and vasopressin maybe given to patient’s refractory to vasopressor therapy
• Intravenous corticosteroids are recommended for patients who require vasopressor therapy, despite fluid resuscitation, to maintain adequate BP
• Antibiotics are early component of therapy and are started after obtaining cultures
• Drotrecogin alpha, a recombinant form of activated protein C, has demonstrated promise in treating patients with severe sepsis.
• Glucose levels should be maintained at less than 150 mg/dl
• Stress ulcer prophylaxis with histamine (H2)-receptor blockers and deep vein thrombosis prophylaxis with low dose unfractionated heparin or low molecular weight heparin are recommended

Neurogenic Shock

• Treatment of neuogenic shock is dependent on the tissue

In spinal cord injury, general measures to promote spinal stability are initially used

Definitive treatment of the hypotension and bradycardia involves the use of vasopressor and atropine respectively

Fluids are administered cautiously as the cause of the hypotension is generally not related to fluid loss

The patient is monitored for hypothermia

Anaphylactic Shock

• Epinephrine is the drug of choice to treat anaphylactic shock
• Diphenhydramine is administered to block the massive release of histamine
• Maintaining a patent airway is critical and the use of nebulization with bronchodilators is highly effective
• Endotracheal intubation or cricothyroidotomy maybe necessary
• Aggressive fluid replacement, predominantly with colloids, is necessary
• Intravenous corticosteroids maybe helpful in anaphylactic shock if significant hypotension persists after 1 to 2 hours of aggressive therapy

NURSING MANAGEMENT

• Acute Intervention

The role of the nurse in shock involves

Monitoring the patient’s ongoing physical and emotional status to detect subtle changes in the patient’s condition

Planning and implementing nursing interventions and therapy

Evaluating the patient’s response to therapy

Providing emotional support to the patient and family and

Collaborating with other members of the health team when warranted by the patient’s condition

NURSING CARE

• Neurologic status, including orientation and level of consciousness, should be assessed every hour or more often.
• Heart rate, rhythm, BP, central venous pressure and PA pressures including continuous cardiac output should be assessed at least every 15 minutes.
• The patient’s ECG should be continuously monitored to detect dysrhythmias that may result from the cardiovascular and metabolic derangements associated with shock. Heart sounds should be assessed for the presence of an S3 and S4 sound or new murmurs. The presence of an S3 sound in an adult usually indicated heart failure.
• The respiratory status of the patient in shock must be frequently assessed to ensure adequate oxygenation, detect complications early and provide data regarding the patient’s acid base status.
• Pulse oximetry is used to continuously monitor oxygen saturation.
• Arterial blood gases (ABGs) provide definitive information on ventilation and oxygenation status, and acid base balance.
• Most patients in shock will be intubated and on mechanical ventilation.
• Hourly urine output measurements assess the adequacy of renal perfusion and a urine output of less than 0.5 ml/kg/hour may indicate inadequate kidney perfusion.
• BUN and serum creatinine values are also used to assess renal function.
• Tympanic or pulmonary arterial temperatures should be obtained hourly if temperature is elevated or subnormal, otherwise every 4 hours.
• Capillary refill should be assessed and skin monitored for temperature, pallor, flushing, cyanosis and diaphoresis
• Bowel sounds should be auscultated at least every 4 hours and abdominal distention should be assessed
• If a nasogastric tube is inserted, drainage should be checked for occult blood as should stools
• Oral care for the patient in shock is essential and passive range of motion should be performed three or four times per day
• Anxiety, fear and pain may aggravate respiratory distress and increase the release of catecholamines
• The nurse should talk to the patient, even if the patient is intubated, sedated and paralyzed or appears comatose. If the intubated patient is capable of writing, a pencil and paper should be provided.

CEREBROVASCULAR ACCIDENT (STROKE) – Etiology, Risk Factors, Signs and Symptoms, Diagnostic Evaluation and Management

• A cerebrovascular accident is also called a CVA, brain attack, or stroke. It occurs when blood flow to a part of the brain is suddenly stopped and oxygen cannot get to that part. This lack of oxygen may damage or kill the brain cells. Death of a part of the brain may lead to loss of certain body functions controlled by that affected part and it last longer than 24 hours
• A transient ischemic attack (TIA) – also called a mini stroke, is a brief episode of symptoms similar to those have in a stroke. A transient ischemic attack is caused by a temporary decrease in blood supply to part of brain. It last less than five minutes.

ETIOLOGY AND TYPES

1. Ischemic Stoke

Any ischemic stroke occurs when a blood clot blocks a blood vessel, preventing blood and oxygen from getting to a part of the brain. When a clot forms somewhere else in the body and gets lodged in a brain blood vessel, it is called an embolic stroke. When the clot forms in the brain blood vessel, it is called a thrombotic stroke.

• Hemorrhagic Stroke
• A hemorrhagic stroke occurs when a blood vessel ruptures, or hemorrhages, which then prevents blood from getting to part of the brain. The hemorrhage may occur in a blood vessel in the brain, or in the membrane that surrounds the brain. It maybe of the following types:
• Intracerebral hemorrhage: in an intracerebral hemorrhage, a blood vessel in the brain bursts and spills into the surrounding brain tissue, damaging brain cells. Brain cells beyond the leak are deprived of blood and damaged. High blood pressure, trauma, vascular malformations, use of blood-thinning medications and other conditions may cause intracerebral hemorrhage
• Subarachnoid hemorrhage: in a subarachnoid hemorrhage, an artery on or near the surface of brain bursts and spills into the space between the surface of brain and skull. This bleeding is often signaled by a sudden, severe headache. A subarachnoid hemorrhage is commonly caused by the rupture of an aneurysm, a small sack-shaped or berry-shaped outpouching on an artery in the brain.

RISK FACTORS

• High blood pressure
• Cigarette smoking or exposure to second hand smoke
• High cholesterol level
• Diabetes
• Overweight or obese
• Physical inactivity
• Obstructive sleep apnea
• Cardiovascular disease, including heart failure, heart defects, heart infection or abnormal heart rhythm
• Use of some birth control pills or hormone therapies that include estrogen
• Heavy drinking
• Use of drugs such as cocaine and methamphetamines
• Having regular checkups after being diagnosed with preeclampsia
• Personal or family history of stroke, heart attack or TIA
• Being age 55 or older
• Race-Black has higher risk of stroke than people of other races
• Gender-stroke is more common in women than men, and more deaths from stroke occur in women

PATHOPHYSIOLOGY

1. Due to thrombosis or embolism, some neurons die because of lack of oxygen and nutrients —- infarction of the cerebral vessels known as stroke —- tissue injury triggers an inflammatory response which increases intracranial pressure —- the injury disrupts metabolism leading to changes in ionic transport, localized acidosis, and free radical formation —- calcium, sodium and water accumulate in the injured cells and excitatory neurotransmitters are released —- continued cell cellular injury and swelling both occurs resulting to further cell damage —– Brain Death

• Impaired cerebral tissue perfusion (hemorrhagic) —- infarction of the cerebral vessels known as stroke —- space-occupying blood clots put more pressure on the brain tissues —- the regulatory mechanisms of the brain attempt to maintain equilibrium by increasing BP and ICP —- the ruptured cerebral vessels may constrict to limit blood loss however; this vasospam will result to further ischemia and necrosis of brain tissues —- Brain Death 

SIGNS AND SYMPTOMS  

• Difficulty walking
• Dizziness
• Loss of balance and coordination
• Difficulty speaking or understanding others who are speaking
• Numbness or paralysis in the face, leg, or arm, most likely on just one side of the body
• Blurred or darkened vision
• A sudden headache, especially when accompanied by nausea, vomiting, or dizziness

DIAGNOSTIC EVALUATION

• Physical examination
• Personal and family history of heart disease, TIA or stroke
• Blood tests: to evaluate the clotting time, bleeding time, etc
• Computerized tomography scan: brain imaging plays a key role in determining a stroke and what type of stroke maybe experiencing. A CT scan uses a series of X-rays to create a detailed image of brain. A CT scan can show a brain hemorrhage, tumors, strokes and other conditions. A dye is injected into blood vessels to view blood vessels to view blood vessels in neck and brain in greater detail
• Magnetic resonance imaging: an MRI uses powerful radio waves and magnets to create a detailed view of brain. An MRI can detect brain tissue damaged by an ischemic stroke and brain hemorrhages
• Carotid ultrasound: in this test, sound waves create detailed images of the inside of the carotid arteries in neck. This test shows buildup of fatty deposits (plaques) and blood flow in carotid arteries
• Cerebral angiogram: in this test, a thin, flexible tube (catheter) is inserted through a small incision, usually in groin, and guides it through major arteries and into carotid or vertebral artery. A dye is injected into blood vessels to make them visible under X-ray imaging. This procedure gives a detailed view of arteries in brain and neck
• Echocardiogram: this imaging technique uses sound waves to create a picture of heart. It can help to find the source of blood clots

MANAGEMENT

Prevention

There are many risk factors for having a stroke. Correspondingly, there are many measures that can be taken to help prevent them. These preventive measures are similar to the actions that you would take to help prevent heart disease, and include the following:

• Maintain normal blood pressure
• Limit saturated fat and cholesterol intake
• Refrain from smoking and drink alcohol in moderation
• Control diabetes
• Maintain a healthy weight
• Get regular exercise
• Eat a diet rich in vegetables and fruits

Medical Management

• Aspirin, an antithrombotic drug, is an immediate treatment after an ischemic stroke to reduce the likelihood of having another stroke. Aspirin prevents blood clots from forming.
• Other blood-thinning drugs, such as heparin, warfarin, or aspirin in combination with extended release dipyridamole may also be used, but these are not usually used in the emergency room setting.
• Intravenous injection of tissue plasminogen activator (TPA): some people who are having an ischemic stroke can benefit from an injection of a recombinant tissue plasminogen activator (TPA), also called alteplase, usually given through a vein in the arm. This potent clot-busting drug needs to be given within 4.5 hours after stroke symptoms begin if it is given into the vein. This drug restores blood flow by dissolving the blood clot causing stroke
• Carotid endarterectomy: in the carotid endarterectomy, a surgeon removes fatty deposits (plaques) from carotid arteries. In this procedure, a small incision along the front of neck, opens carotid artery, and removes fatty deposits that block the carotid artery.
• Angioplasty and stents: in an angioplasty, a surgeon inserts a catheter with a mesh tube and balloon on the tip into an artery in groin and guides it to the blocked carotid artery in neck. Surgeon inflates the balloon in the narrowed artery and inserts a mesh tube into the opening to keep artery from becoming narrowed after the procedure.
• Surgical clipping: a surgeon places a tiny clamp at the base of the aneurysm, to stop blood flow to it. This can keep the aneurysm from bursting
• Coiling (endovascular embolization): in this procedure, a surgeon inserts a catheter into an artery in groin and guides it to brain using X-ray imaging. Then guides tiny detachable coils into the aneurysm (aneurysm coiling). The coils fill the aneurysm, which blocks blood flow into the aneurysm and causes the blood to clot

NURSING MANAGEMENT

Nursing Diagnosis

1. Ineffective cerebral tissue perfusion related to interruption of blood flow

Interventions

• Determine factors related to individual situation, cause for coma, decreased cerebral perfusion and potential for increased ICP
• Monitor and document neurological status frequently and compare with baseline
• Monitor vital signs, i.e. hypertension/hypotension, compare BP readings in both arms, heart rate and rhythm, auscultate for murmurs, respirations, noting patterns and rhythm, e.g. periods of apnea after hypervenitilation, Cheyne-Stokes respiration.
• Evaluate pupils, noting size, shape, equality, light reactivity
• Document changes in vision, e.g., reports of blurred vision, alternations in visual field and perception
• Assess higher functions, including speech, if patient is alert
• Position with head slightly elevated and in neutral position
• Maintain bedrest, provide quiet environment, and restrict visitors as indicated. Provide rest periods between care activities, limit duration of procedures
• Prevent straining at stool, holding breath
• Assess for nuchal rigidity, twitching, increased restlessness, irritability, onset of seizure activity
• Administer supplemental oxygen as indicated
• Administer medications as indicated: alteplase, anticoagulants, e.g., warfarin sodium, low-molecular weight heparin, antiplatelet agents, aspirin, dipyridamole, ticlopidine. Antihypertensives, peripheral vasodilators, e.g., cyclandelate, papaverine, isoxsuprine, steroids, e.g., dexamethasone
• Prepare for surgery, as appropriate, e.g., endarterectomy, microvascular bypass, cerebral angioplasty
• Monitor laboratory studies as indicated, e.g., prothrombin time (PT), activated partial thromboplastin time (aptt) time, dilantin level

• Impaired physical mobility related to neuromuscular abnormality

• Assess functional ability of impairment initially and on a regular basis
• Change positions at least every 2 hour (supine, sidelying) and possibly more often if placed on affected side.
• Position in prone position once or twice a day if patient can tolerate
• Prop extremities in functional position, use footboard during the period of flaccid paralysis. Maintain neutral position of head.
• Use arm sling when patient is in upright position, as indicated.
• Evaluate use and need for positional aids and splints during spastic paralysis, place pillow under axillae to abduct arm, elevate arm and hand
• Observe affected side for color, edema, or other signs of compromised circulation
• Inspect skin regularly, particularly over bony prominences. Gently massage any reddened areas and provide aids such as sheepskin pads as necessary
• Begin active/passive range of motion exercise to all extremities
• Assist to develop sitting balance (e.g. raise head of bed, assist to sit on edge of bed, having patient sue the strong arm to support body weight and strong leg to move affected leg, increase sitting time) and standing balance (e.g. put flat walking shoes on patient, support patient’s lower back with hands while positioning own knees outside patient’s knees, assist in using parallel bars/walkers).
• Get patient up in chair as soon as vital signs are stable, except following cerebral hemorrhage
• Pad chair seat with foam or water-filled cushion, and assist patient to shift weight at frequent intervals
• Provide egg-crate mattress, water-bed, flotation device, or specialized beds (e.g. kinetic), as indicated

• Disturbed sensory perceptions related to disturbed sensory reception and neuromuscular dysfunction

Interventions

• Observe behavioral responses e.g., hostility, crying, inappropriate affect, agitation, hallucination
• Eliminate extraneous noise and stimuli as necessary
• Speak in calm, quiet voice, using short sentences. Maintain eye contact
• Reorient patient frequently to environment, staff, and procedures
• Evaluate for visual deficits. Note loss of visual field, changes in depth perception (horizontal/vertical planes), and presence of diplopia
• Approach patient from visually intact side. Leave light on, position objects to take advantage of intact visual fields. Patch affected eye if indicated
• Assess sensory awareness, e.g. differentiation of hot/cold, dull/sharp, position of body parts/muscle, joint sense
• Stimulate sense of touch; e.g. give patient objects to touch, grasp
• Protect from temperature extremes, assess environment for hazards. Recommend testing warm water with unaffected hand

• Ineffective coping related to situational crisis and cognitive perceptual changes

Interventions

• Assess extent of altered perception and related degree of disability. Determine functional independence measure score
• Identify meaning of the loss, dysfunction and change to patient. Note ability to understand events, provide realistic appraisal of situation
• Determine outside stressors, e.g. family, work, social, future nursing/healthcare needs
• Encourage patient to express feelings, including hostility or anger, denial, depression sense of disconnectedness
• Note whether patient refers to affected side as ‘it’ or denies affected side and says it is ‘dead’
• Identify previous methods of dealing with life problems. Determine presence and quality of support systems
• Emphasize small gains either in recovery of function or independence
• Support behaviors and efforts such as increased interest, participation in rehabilitation activities
• Monitor for sleep disturbance, increased difficulty concentrating and statements of inability to cope, lethargy, and withdrawal
• Refer for neuropsychological evaluation and/or counseling if indicated

• Self-care deficit related to neuromuscular impairment and decreases strength and endurance

Interventions

• Assess abilities and level of deficit (0-4 scale) for performing ADLs
• Avoid doing things for patient that patient can do for self, but provide assistance as necessary
• Be aware of impulsive behavior and actions suggestive of impaired judgment
• Maintain a supportive, firm attitude. Allow patient sufficient time to accomplish task.
• Provide positive feedback for efforts and accomplishments
• Create plan for visual deficits that are present, e.g. place food and utensils on the tray related to patient’s unaffected side, situate the bed so that patient’s unaffected side is facing the room with the affected side to the wall, position furniture against wall and out of travel path
• Provide self-help devices, e.g. button/zipper hook, knife-fork combinations, long-handled brushes, extensions for picking things up from floor, toilet riser, leg bag for catheter, shower chair
• Assist and encourage good grooming and makeup habits
• Encourage family member to allow patient to do as much as possible for self
• Assess patient’s ability to communicate the need to void and ability to use urinal, bedpan. Take patient to the bathroom at frequent and periodic intervals for voiding if appropriate
• Identify previous bowel habits and re-establish normal regimen. Increase bulk in diet, encourage fluid intake, increased activity

• Risk for impaired swallowing related to neuromuscular dysfunction

Intervention

• Review individual pathology and ability to swallow, noting extend of paralysis, clarity of speech, facial, tongue involvement, ability to protect airway and episodes of coughing or choking, presence of adventitious breath sounds, amount and character of oral secretions
• Have suction equipment available at bedside, especially during early feeding efforts
• Promote effective swallowing, e.g. schedule activities, medications to provide a minimum of 30 min rest before eating, provide pleasant environment free of distractions, assist patient with head control and support, and position based on specific dysfunction
• Place patient in upright position during and after feeding as appropriate
• Provide oral care based on individual need prior to meal
• Season food with herbs, spices, lemon juice, etc. according to patient’s preference, within dietary restrictions
• Place food of appropriate consistency in unaffected side of mouth
• Touch parts of the cheek with tongue blade and apply ice to weak tongue
• Feed slowly, allowing 30-45 min for meals
• Offer solid foods and liquids at different times
• Maintain upright position for 45-60 min after eating
• Maintain accurate intake output, record calorie count
• Encourage participation in exercise
• Administer IV fluids and or tube feedings
• Coordinate multidisciplinary approach to develop treatment plan that meets individual needs

• Knowledge deficit related to lack of exposure and cognitive limitation

Interventions

• Evaluate type and degree of sensory-perceptual involvement
• Include family in discussions and teaching
• Discuss specific pathology and individual potentials
• Identify signs and symptoms requiring further follow-up, e.g. changes or decline in visual, motor, sensory function, alternation in mentation or behavioral responses, severe headache
• Review current restrictions or limitations and discuss planned resumption of activities (including sexual relations)
• Provide written instructions and schedules for activity, medication, important facts
• Encourage patient to refer to lists communication or notes instead of depending on memory
• Discuss plans for meeting self-care needs
• Refer to discharge planner, home care supervisor, visiting nurse
• Suggest patient reduce or limit environmental stimuli, especially during cognitive activities
• Recommend patient seek assistance in problem-solving process and validate decisions, as indicated
• Review importance of balanced diet, low in cholesterol and sodium if indicated. Discuss role of vitamins and other supplements
• Refer to reinforce importance of follow-up care by rehabilitation team, e.g. physical, occupational, speech, vocational therapists.