I.

Acid-Base Imbalance Acid-Base Imbalance: A disruption to the normal acid-base equilibrium in the body. There are four main groups of disorder involving an acid-base imbalance: respiratory acidosis or alkalosis and metabolic acidosis or alkalosis. Obviously the severity of symptoms is determined by the degree of imbalance. It is an abnormality of the human body's normal balance of acids and bases that causes the plasma pH to deviate out of the normal range (7.35 to 7.45).

Pathophysiology Alterations in Acid-Base Balance The terms acidosis and alkalosis describe the clinical conditions that arise as a result of changes in PCO2 and HCO3- concentrations. An alkali represents a combination of one or more alkali metals such as sodium or potassium with a highly basic ion such as a hydroxyl ion (OH-). Sodium bicarbonate (NaHCO3) is the main alkali in the ECF. Although the definitions differ somewhat, the terms alkali and base are often used interchangeably. Thus, the term alkalosis has come to mean the opposite of acidosis. Causes of Types of Acid-Base Imbalance: There are numerous reasons that each of the four processes can occur (detailed in each article). Generally speaking, sources of acid gain include: 1. Retention of carbon dioxide 2. Production of nonvolatile acids from the metabolism of proteins and other organic molecules 3. Loss of bicarbonate in feces or urine 4. Intake of acids or acid precursors Sources of acid loss include: 1. Use of hydrogen ions in the metabolism of various organic anions 2. Loss of acid in the vomitus or urine Signs and Symptoms of Acid-Base Imbalance Hypercapnia - metabolic alkalosis Dilated brain blood vessels - respiratory acidosis Increased pressure inside skull - respiratory acidosis Headache - metabolic alkalosis Confusion - respiratory alkalosis Combativeness - respiratory acidosis Hallucinations - respiratory acidosis Transient psychosis - respiratory acidosis Myoclonic jerks - respiratory acidosis Flapping tremor - respiratory acidosis Stupor - metabolic alkalosis Coma - metabolic acidosis Constricted pupils - respiratory acidosis Reduced tendon reflexes - respiratory acidosis Seizures - metabolic alkalosis Papilledema - respiratory acidosis Breathlessness - respiratory acidosis Cyanosis - respiratory acidosis Pulmonary hypertension - respiratory acidosis Warm skin - respiratory acidosis Nursing Management For Respiratory Alkalosis: Institute safety measures for the patient with vertigo or the unconscious patient. Encourage the anxious patient to verbalize fears Administer sedation as ordered to relax the patient Keep the patient warm and dry

Encourage the patient to take deep, slow breaths or breathe into a brown paper bag (inspire CO2). Monitor vital signs Monitor ABGs, primarily PaCO2; a value less than 35 mmHg indicates too little CO2 (carbonic acid)

For Respiratory Acidosis: Institute safety measures Assist with positioning Monitor I&O and administer fluids as ordered Administer oxygen and medications for order; monitor hourly vital signs and respiratory status (may requires mechanical ventilation) Monitor arterial blood gases (ABGs); pH, PaCO2, HCO3 II. Urinary Tract Infection UTI (Cystitis) Cystitis is an inflammation of the bladder, usually caused by a bacterial infection. It is a common condition, with more than 30% of women experiencing at least one episode in their lifetime. Cystitis occurs when bacteria enter the urethra and travel to the bladder. The bacteria most commonly associated with cystitis are Escherichia coli (E. coli). E. coli is found naturally in the bowel and, in smaller numbers, in the vagina and on the skin between the anus and the vagina (perineum). Women are much more prone to developing cystitis than men. Their shorter urethra allows the bacteria to reach the bladder quickly. In addition, the urethral, vaginal and anal openings are closely located in women, making it easy for bacteria to be transferred. Pathophysiology Infection results from a breakdown in local defense mechanisms in the bladder that allow bacteria to invade the bladder mucosa and multiply. These bacteria can't be readily eliminated by normal micturition.Cystitis is caused by germs, usually bacteria that enter the urethra and then the bladder. These bacteria can lead to infection, most commonly in the bladder. The infection can spread to the kidneys.Most of the time, your body can get rid of these bacteria when you urinate. However, sometimes the bacteria can stick to the wall of the urethra or bladder, or grow so fast that some bacteria stay in the bladder.Women tend to get infections more often than men because their urethra is shorter and closer to the anus. For this reason, women are more likely to get an infection after sexual intercourse or when using a diaphragm for birth control. Menopause also increases the risk for a urinary tract infection. Signs and Symptoms Frequent painful urination - often a burning sensation Urgent need to urinate, even after just urinating Passing only small amounts of urine each time Cloudy, smelly urine or blood in the urine If left untreated, the infection can move from the bladder to the kidneys. Symptoms of a kidney infection include those associated with cystitis as well as fever, chills, back pain, nausea and vomiting. Women with symptoms of a kidney infection should seek immediate medical attention. Diagnostic test The list of diagnostic tests mentioned in various sources as used in the diagnosis of Cystitis includes: Urine tests - to identify any bacteria and test for pus or blood in urine Urine bacterial counts Urography Cystoscopy X-rays Bladder biopsy

Treatment of Cystitis Cystitis is treated with a course of antibiotics. Because the laboratory testing of the urine sample may take several days, the doctor will often prescribe a broad-spectrum antibiotic in the meantime to bring relief from symptoms and to stop any infection progressing. It is important that the complete antibiotic course be taken, even if the symptoms resolve, to prevent the infection recurring. To get relief from symptoms, women can also: drink plenty of fluids reduce their intake of alcohol, tea and coffee as these can all irritate the bladder take urinary alkalinisers (see diagnosis section above) place a hot water bottle, wrapped in a towel, between the legs. This makes the skin around the urethral opening hotter than the urine and so can bring relief when urinating take mild painkillers for pain relief avoid eating foods that can irritate the bladder while infection is present. These include foods with high acid content and amino acids. Nursing Management 1. Monitor: o The bow of the urine to change color, odor and urine patterns o Input and output every 8 hours o The results re urinalis 2. Give analgesics as needed and evaluate its success 3. Consul doctor if: o Previous amber-yellow urine, dark orange, hazy or cloudy o Micturition pattern changes, as an example of heat such as burning during urination, a sense of urgency when urinating o Persistent pain or increasing pain 4. If the frequency becomes a problem, assure access to the bathroom, bedpan under the bed. Instruct the patient to urinate whenever there is a desire. Rational: frequent urination, reduce static urine in the bladder and prevent bacterial growth. UTI (Pyelonephritis) Pyelonephritis is a kidney infection. It is usually bacterial in origin and stems from an infection in another part of the urinary tract, such as the bladder. Pyelonephritis can occur in anyone, although it is more likely to occur in women. Pathophysiology The bacterial infections occur mainly in the renal parenchyma. Most of the diseases causing bacteria belong to the genus Escherichia Coli. The pyelonephritis pathophysiology reveals the presence of various toxins like alpha hemolysin, cytolethal distending toxin, cytotoxic necrotizing factor-1 and secreted auto transporter toxin. Adhesions play an important role in pyelonephritis pathophysiology as there is release of cytokine due LPS shed from a membrane during the process of bacterial lyses. Various physical changes associated with pyelonephritis also include the presentation of high fever and the patient may present a toxic appearance, if there is an underlying problem like sepsis or a perinephric abscess. The pelvic examination will reveal a considerable amount of tenderness in the cervix and uterus would be absent. An abdominal examination shows a suprapubic tenderness that will range from mild to moderate. The bowel sounds will be normoactive and further examination may also reveal CVA (costovertebral angle) tenderness. Causes The most common cause of pyelonephritis is the backward flow (reflux) of infected urine from the bladder to the upper urinary tract. Bacterial infections also may be carried to one or both kidneys through the bloodstream or lymph glands from infection that began in the bladder. Kidney infection sometimes results from urine that becomes stagnant due to obstruction of free urinary flow. A blockage or abnormality of the urinary system, such as those caused by stones, tumors, congenital deformities, or loss of bladder function from nerve disease, increases a person's risk of pyelonephritis. Other risk factors include diabetes mellitus, pregnancy, chronic bladder infections, a history of analgesic abuse, paralysis

from spinal cord injury, or tumors. Catheters, tubes, or surgical procedures may also trigger a kidney infection. The bacteria most likely to cause pyelonephritis are those that normally occur in the feces. Escherichia coli causes about 85% of acute bladder and kidney infections in patients with no obstruction or history of surgical procedures. Klebsiella, Enterobacter, Proteus, or Pseudomonas are other common causes of infection. Once these organisms enter the urinary tract, they cling to the tissues that line the tract and multiply in them. Signs and Symptoms At least half of women have experienced the discomfort with urination caused by a urinary tract infection: painful, urgent, or frequent urination. Pyelonephritis may start with similar symptoms. However, once the infection has spread to the kidney, signs of more severe illness usually result: Back pain or flank pain Fever (usually present) and/or chills Feeling sick (malaise) Nausea and vomiting Confusion (especially in the elderly) Pyelonephritis may cause noticeable changes in the urine, such as: Blood in the urine (hematuria) Cloudy or foul-smelling urine Pain when urinating Increased frequency or urgency of urination Laboratory test In addition to collecting urine samples for urinalysis and urine culture and sensitivity tests, the doctor will take a sample of the patient's blood for a blood cell count. If the patient has pyelonephritis, the urine tests will show the presence of white blood cells, and bacteria in the urine. Bacterial counts of 100,000 organisms or higher per milliliter of urine point to a urinary tract infection. The presence of antibodycoated bacteria (ACB) in the urine sample distinguishes kidney infection from bladder infection, because bacteria in the kidney trigger an antibody response that coats the bacteria. The blood cell count usually indicates a sharp increase in the number of white blood cells. Treatment Treatment of acute pyelonephritis may require hospitalization if the patient is severely ill or has complications. Therapy most often involves a two- to three-week course of antibiotics, with the first few days of treatment given intravenously. The choice of antibiotic is based on laboratory sensitivity studies. The antibiotics used most often include ciprofloxacin (Cipro), ampicillin (Omnipen), or trimethoprimsulfamethoxazole (Bactrim, Septra). Several advances in antibiotic therapy have been made in recent years. In 2003, the U.S. Food and Drug Administration (FDA) approved Cipro extended release tablets (Cipro XR) that could be taken once daily for acute uncomplicated pyelonephritis. A study in Europe also showed that a shorter course than that normally used in the United States could eradicate the bacteria that cause the disease. The primary objective of antimicrobial therapy is the permanent eradication of bacteria from the urinary tract. The early symptoms of pyelonephritis usually disappear within 48 to 72 hours of the start of antibacterial treatment. Repeat urine cultures are done in order to evaluate the effectiveness of the medication. Chronic pyelonephritis may require high doses of antibiotics for as long as six months to clear the infection. Other medications may be given to control fever, nausea, and pain. Patients are encouraged to drink extra fluid to prevent dehydration and increase urine output. Surgery sometimes is necessary if the patient has complications caused by kidney stones or other obstructions, or to eradicate infection. Urine cultures are repeated as part of the follow-up of patients with chronic pyelonephritis. These repeat tests are necessary to evaluate the possibility that the patient's urinary tract is infected with a second organism as well as to assess the patient's response to the antibiotic. Some persons are highly susceptible to reinfection, and a second antibiotic may be necessary to treat the organism. Nursing Management 1. Apply warm moist packs. 2. Provide a warm Sitz bath. 3. Balance rest and activity. 4. Administer analgesic as ordered.

a. Urinary Calculi A kidney stone, also known as a renal calculus (from the Latin ren, "kidney" and calculus, "pebble") is a solid concretion or crystal aggregation formed in the kidneys from dietary minerals in the urine. Urinary stones are typically classified by their location in the kidney (nephrolithiasis), ureter (ureterolithiasis), or bladder (cystolithiasis), or by their chemical composition (calcium-containing, struvite, uric acid, or other compounds). About 80% of those with kidney stones are men. Men most commonly experience their first episode between 30 and 40 years of age, while for women the age at first presentation is somewhat later. Pathophysiology Normal urine contains chelating agents, such as citrate, that inhibit the nucleation, growth, and aggregation of calcium-containing crystals. Other endogenous inhibitors include calgranulin (an S-100 calcium binding protein), Tamm-Horsfall protein, glycosaminoglycans, uropontin (a form of osteopontin), nephrocalcin (an acidic glycoprotein), prothrombin F1 peptide, and bikunin (uronic acidrich protein). The biochemical mechanisms of action of these substances have not yet been thoroughly elucidated. However, when these substances fall below their normal proportions, stones can form from an aggregation of crystals. Kidney stones often result from a combination of factors, rather than a single, well-defined cause. Stones are more common in people whose diet is very high in animal protein or who do not consume enough water or calcium. They can result from an underlying metabolic condition, such as distal renal tubular acidosis, Dent's disease, hyperparathyroidism, primary hyperoxaluria or medullary sponge kidney. In fact, studies show about 3% to 20% of people who form kidney stones have medullary sponge kidney. Kidney stones are also more common in people with Crohn's disease. People with recurrent kidney stones are often screened for these disorders. This is typically done with a 24-hour urine collection that is chemically analyzed for deficiencies and excesses that promote stone formation. Causes Dietary factors that increase the risk of stone formation include low fluid intake and high dietary intake of animal protein, sodium, refined sugars, fructose and high fructose corn syrup, oxalate, grapefruit juice, apple juice, and cola drinks. Signs and Symptoms While some kidney stones may not produce symptoms (known as "silent" stones), people who have kidney stones often report the sudden onset of excruciating, cramping pain in their low back and/or side, groin, or abdomen. Changes in body position do not relieve this pain. The abdominal, groin, and/or back pain typically waxes and wanes in severity, characteristic of colicky pain (the pain is sometimes referred to as renal colic). It may be so severe that it is often accompanied by nausea and vomiting. The pain has been described by many as the worst pain of their lives, even worse than the pain of childbirth or broken bones. Kidney stones also characteristically cause blood in the urine. If infection is present in the urinary tract along with the stones, there may be fever and chills. Sometimes, symptoms such as difficulty urinating, urinary urgency, penile pain, or testicular pain may occur due to kidney stones. Diagnostic Exam The diagnosis of kidney stones is suspected when the typical pattern of symptoms is noted and when other possible causes of the abdominal or flank pain are excluded. Imaging tests are usually done to confirm the diagnosis. A helical CT scan without contrast material is the most common test to detect stones or obstruction within the urinary tract. Formerly, an intravenous pyelogram (IVP; an X-ray of the abdomen along with the administration of contrast dye into the bloodstream) was the test most commonly used to detect urinary tract stones, but this test has a greater risk of complications, takes longer, and involves higher radiation exposure than the non-contrasted helical CT scan. Helical CT scans have been shown to be a significantly more effective diagnostic tool than the IVP in the diagnosis of kidney or urinary tract stones. Laboratory Exam microscopic examination of the urine, which may show red blood cells, bacteria, leukocytes, urinary casts and crystals; urine culture to identify any infecting organisms present in the urinary tract and sensitivity to determine the susceptibility of these organisms to specific antibiotics; complete blood count, looking for neutrophilia (increased neutrophil granulocyte count) suggestive of bacterial infection, as seen in the setting of struvite stones;

renal function tests to look for abnormally high blood calcium blood levels (hypercalcemia); 24 hour urine collection to measure total daily urinary volume, magnesium, sodium, uric acid, calcium, citrate, oxalate and phosphate; collection of stones (by urinating through a StoneScreen kidney stone collection cup or a simple tea strainer) is useful. Chemical analysis of collected stones can establish their composition, which in turn can help to guide future preventive and therapeutic management. Medication Ibuprofen Calcium Channel Blockers Nifedipine Tamsulosin Nursing management Administer opioid analgesics (IV or intramuscular) with IV NSAID as prescribed. Encourage and assist patient to assume a position of comfort. Assist patient to ambulate to obtain some pain relief. Monitor pain closely and report promptly increases in severity. Encourage increased uid intake and ambulation. Begin IV uids if patient cannot take adequate oral uids. Monitor total urine output and patterns of voiding. Encourage ambulation as a means of moving the stone through the urinary tract. Strain urine through gauze. Crush any blood clots passed in urine, and inspect sides of urinal and bedpan for clinging stones. Instruct patient to report decreased urine volume, bloody or cloudy urine, fever, and pain. Instruct patient to report any increase in pain. Monitor vital signs for early indications of infection; infections should be treated with the appropriate antibiotic agent before efforts are made to dissolve the stone. b. Urinary Retention Urinary retention is defined as the inability to completely or partially empty the bladder. Suffering from urinary retention means you may be unable to start urination, or if you are able to start, you cant fully empty your bladder. Pathophysiology Normal urine production in an adult is about 1.5-2 L/day. Urine flow depends on 3 factorsa pressure gradient from the glomerulus to the Bowman capsule, peristalsis of the renal pelvis and ureters, and the effects of gravity (ie, hydrostatic pressure). Obstruction of the urinary tract at any level eventually results in elevation of intraluminal ureteral pressure. With prolonged obstruction, ureteral peristalsis is overcome and increased hydrostatic pressures are transmitted directly to the nephron tubules. As pressures in the proximal tubule and Bowman space increase, glomerular filtration rate (GFR) falls. After 12-24 hours of complete obstruction, intratubular pressure decreases to preobstruction levels. If complete obstruction is not relieved, a depressed GFR is maintained by decreases in renal blood flow mediated by thromboxane A2 and angiotensin II (AII). With continued obstruction, renal blood flow progressively falls, resulting in ischemia and incremental nephron loss. Thus, obstructive uropathy may lead to obstructive nephropathy. Several phases of obstructive nephropathy may be seen, including an early hyperemia and a late vasoconstriction followed by regulation of GFR post obstruction. Recovery of GFR depends on the duration and level of obstruction, preobstruction blood flow, and coexisting medical illness or infection. Causes There are two general types of urinary retention: obstructive and non-obstructive. If there is an obstruction (for example, kidney stones), urine cannot flow freely through the urinary track. Nonobstructive causes include a weak bladder muscle and nerve problems that interfere with signals

between the brain and the bladder. If the nerves arent working properly, the brain may not get the message that the bladder is full. Some of the most common causes of non-obstructive urinary retention are: Stroke Vaginal childbirth Pelvic injury or trauma Impaired muscle or nerve function due to medication or anesthesia Accidents that injure the brain or spinal cord Obstructive retention may result from: Cancer Kidney or bladder stones Enlarged prostate (BPH) in men Signs and Symptoms Symptoms of urinary retention may include: Difficulty starting to urinate Difficulty fully emptying the bladder Weak dribble or stream of urine Loss of small amounts of urine during the day Inability to feel when bladder is full Increased abdominal pressure Lack of urge to urinate Strained efforts to push urine out of the bladder Frequent urination Nocturia (waking up more than two times at night to urinate) Diagnosis History and physical examination Urine sample Bladder scan Cytoscopy Xrays and CT scan Prostate Specific Antigen (PSA) Urodynamic Test Medication If retention is due to prostate enlargement, medications to relax the prostate (alpha-blockers) or shrink the tissue (5-alpha reductase inhibitors) may be used. GnRH agonists such as Lupron may also be used, particularly if retention is due to prostate cancer. Nursing Management Facilitate bladder emptying Provide privacy, run water, have the client assume a normal voiding position and provide pain relief. Promote relaxation of the sphincter by providing sitz baths, warm showers, and hot tea to drink Obtain and record strict urinary output every time the client voids. If the client cannot void, perform intermittent catheterization to prevent overdistention of the bladder. Prepare the client for surgical intervention (e.g. dilation of urethra, cystoplasty), if indicated. Provide health education on measure to prevent UTI. c. Neurogenic Bladder This is a dysfunction of the urinary bladder caused by a problem of the nervous system. Types of neurogenic bladder are spastic bladder, reflex bladder, and flaccid bladder. It Neurogenic bladder is impaired bladder function resulting from damage to the nerves that govern the urinary tract. Various nerves converge in the area of the bladder and serve to control the muscles of the

urinary tract, which includes the sphincter muscles that normally form a tight ring around the urethra to hold urine back until it is voluntarily released. A variety of factors can damage these nerves and cause urinary incontinence. In some cases, spontaneous nerve impulses to the bladder trigger spastic unexpected bladder contractions, resulting in accidental voiding of sometimes large amounts of urine. In other types of neurogenic bladder conditions, the bladder may become flaccid and distended and cease to contract fully, resulting in only partial emptying and continual dribbling of small amounts of urine. Rashes may erupt in areas of the skin irritated by urine. Stagnant urine in the bladder also increases the risks of bladder stone formation and urinary tract infections. Such infections, when severe, can lead to life-threatening kidney failure. In some patients, there is a partial loss of anal sphincter control as well Causes and Risk Factors of Neurogenic Bladder Neurogenic bladder can occur at any age, but it is especially common among the elderly. Among the various causes are: Spinal cord injuries resulting in paralysis Other disorders such as syphilis, diabetes mellitus, stroke, ruptured or herniated intervertebral disk Degenerative neurological diseases such as multiple sclerosisand amyotrophic lateral sclerosis Congenital spine abnormalities such as spina bifida Long-term effects of alcoholism In children, a neurogenic bladder may be caused by a birth defect, usually one involving the spinal cord, or it may be acquired as the result of a different problem. Here we look at some of the most common causes of neurogenic bladder: spinal cord trauma central nervous system tumors pelvic tumors spina bifida (myelodysplasia): A birth defect in which the spinal canal does not close completely, exposing the developing spinal cord to injury. Some types of spina bifida are obvious at birth, while others are subtle and only detected by careful inspection of the spine and legs. Spina bifida accounts for 90 percent of cases of neurogenic bladder. What are some risk factors for neurogenic bladder? Risk factors for neurogenic bladder include various birth defects, which adversely affect the spinal cord and function of the bladder, including spina bifida or sacral agenesis and other spinal cord abnormalities. Tumors within the spinal cord or pelvis may also disrupt normal nervous tissue function and place an individual at risk. Traumatic spinal cord injury is also a major risk factor for development of neurogenic bladder. Symptoms of Neurogenic Bladder Symptoms include the following: Urinary incontinence, characterized by either involuntary release of large volumes of urine or continuous dribbling of small amounts. Bed-wetting may occur Frequent urination Persistent urge to urinate despite recent voiding; a constant feeling that the bladder is not completely empty Pain or burning on urination urinary incontinence: Your child may feel the need to urinate frequently and with urgency, as well as experience small urine volume during urination, dribbling urine and loss of sensation of bladder fullness. urinary tract infection: An infection can result from urine being held in the bladder too long. kidney injury: These occur as a result of high pressures caused by urine back-up in the bladder. kidney stones: These may be difficult to diagnose because your child may not be able to feel pain associated with kidney stones if they have spinal cord abnormalities. Symptoms of kidney stones include: o pain

o o

blood in urine fever and chills: This indicates a urinary tract infection caused by an obstructing stone.

Diagnosis of Neurogenic Bladder A thorough patient history is essential to record 24-hour urination patterns, including the actual volume of urine voided, how urgent the feeling is to urinate and any factors that aggravate incontinence. Physical examination will likely include a rectal, genital, and abdominal exam to check for enlargement of the bladder or other abnormalities. A complete neurological examination is also essential. Tests to measure urine output are conducted. To determine whether urine is retained after voiding, the doctor may use an ultrasound-like instrument that estimates the amount left in the bladder or insert a catheter into the bladder. In order to detect whether leakage occurs, a full-bladder stresstest may be necessary. The bladder is filled to capacity via a catheter and the patient is then asked to bend over, cough, or walk. Urine or blood samples may be taken to look for abnormalities including infection and underlying disorders that might be causing or aggravating the condition. When neurogenic bladder is suspected, both the nervous system (including the brain) and the bladder itself are tested. In addition to complete medical history and physical examination, diagnostic procedures may include: Bladder function tests including Urodynamic evaluations, which has two components CMG (Cystometrogram) which measures bladder function, capacity, compliance and voiding and storage pressures. Along with EMG (Electromypography) which measures which help measure urethral sphincter tone and bladder coordination. Radiologic imaging of the of the spine and brain including x-ray and MRI can be used Imaging tests of the bladder and kidneys are performed

Complications Constant urine leakage can cause skin to break down and lead to pressure sores Kidney damage may occur if the bladder becomes too full, causing pressure to build up in the tubes leading to the kidneys and in the kidneys themselves Urinary tract infections Treatment of Neurogenic Bladder Treatment is aimed at enabling the bladder to empty completely and regularly, preventing infection, controlling incontinence, and preserving kidney function. A urinary catheter can be used continuously by patients who have sudden, unexpected bladder contractions. Women usually fare better with such therapy; men are more prone to develop urinary tract infections and complications, including abscess formation. Patients suffering from bladder paralysis can be taught to insert a catheter several times a day to drain the bladder completely and so prevent urine retention that may led to bladder stones and infection. Various medications may help improve bladder muscle control and prevent involuntary muscle contractions. Muscle relaxants, antispasmodics and anticholinergic drugs are also helpful. Bethanechol is the most commonly prescribed drug to help stimulate bladder contractions in patients who retain urine. Surgery may be performed to widen the sphincter to decrease resistance in the bladder outlet and thus maximize bladder emptying Medications may help manage your symptoms. Medicines that make certain nerves more active (bethanechol) Botulinum toxin (Botox) GABA supplements Antiepileptic durgs Newer drugs are also being studied. Exercises to strengthen your pelvic floor muscles (Kegel exercises)

Keeping a diary of when you urinate, the amount you urinated, and if you leaked urine. This may help you learn when you should empty your bladder and when it may be best to be near a bathroom. Learn to recognize the symptoms of urinary infections (UTIs), such as burning when you urinate, fever, low back pain on one side, and a more frequent need to urinate. Cranberry tablets are used to prevent UTIs. Some people may need to use a urinary catheter. This is a thin tube that is inserted into your bladder: You may need a catheter to be in place all the time (indwelling catheter) You may need a catheter to be placed in your bladder 4 to 6 times a day to keep your bladder from becoming too full (intermittent catheterization) Sometimes surgery is needed. Surgeries for neurogenic bladder include: Artificial sphincter Electrical device implanted near the bladder nerves, to stimulate the bladder muscles Sling surgery Creation of an opening (stoma) in which urine flows into a special pouch (this is called urinary diversion)

d. URINARY INCONTINENCE Urinary incontinence is the loss of bladder control. This means that you can't always control when you urinate. Urinary incontinence can range from leaking a small amount of urine (such as when coughing or laughing) to having very strong urges to urinate that are difficult to control. PATHOPHYSIOLOGY Micturition requires coordination of several physiological processes. Somatic and autonomic nerves carry bladder volume input to the spinal cord, and motor output innervating the detrusor, sphincter, and bladder musculature is adjusted accordingly. The cerebral cortex exerts a predominantly inhibitory influence, whereas the brainstem facilitates urination by coordinating urethral sphincter relaxation and detrusor muscle contraction. As the bladder fills, sympathetic tone contributes to closure of the bladder neck and relaxation of the dome of the bladder and inhibits parasympathetic tone. At the same time, somatic innervation maintains tone in the pelvic floor musculature as well as the striated periurethral muscles. When urination occurs, sympathetic and somatic tones in the bladder and periurethral muscles diminish, resulting in decreased urethral resistance. Cholinergic parasympathetic tone increases, resulting in bladder contraction. Urine flow results when bladder pressure exceeds urethral resistance. Normal bladder capacity is 300-500 mL, and the first urge to void generally occurs between bladder volumes of 150 and 300 mL. Incontinence occurs when micturition physiology, functional toileting ability, or both have been disrupted. The underlying pathology varies among the different types of incontinence (ie, stress, urge, mixed, reflex, overflow, and functional incontinence). Stress incontinence pathophysiology During episodes of stress incontinence, an increase in intra-abdominal pressure (eg, from laughing, sneezing, coughing, climbing stairs) raises pressure within the bladder to the point where it exceeds the urethras resistance to urinary flow. Leakage ceases when bladder pressure again falls below urethral pressure. The major cause of stress incontinence is urethral hypermobility due to impaired support from pelvic floor. A less common cause is an intrinsic sphincter deficiency, usually secondary to pelvic surgeries. In either case, urethral sphincter function is impaired, resulting in urine loss at lower than usual abdominal pressures. In women with stress urinary incontinence, either or both mechanisms may be present, although some authors hold that stress incontinence does not develop in patients with poor pelvic support unless intrinsic sphincter deficiency is also present. Urethral hypermobility Urethral hypermobility is related to impaired neuromuscular functioning of the pelvic floor coupled with injury, both remote and ongoing, to the connective tissue supports of the urethra and bladder neck.

When this occurs, the proximal urethra and the bladder neck descend to rotate away and out of the pelvis at times of increased intra-abdominal pressure. Because the bladder neck and proximal urethra move out of the pelvis, more pressure is transmitted to the bladder. During this process, the posterior wall of the urethra shears off the anterior urethral wall to open the bladder neck when intrinsic sphincter deficiency is present. In women without urethral hypermobility, the urethra is stabilized during stress by three interrelated mechanisms. One mechanism is reflex, or voluntary, closure of the pelvic floor. Contraction of the levator ani complex elevates the proximal urethra and bladder neck, tightens intact connective tissue supports, and elevates the perineal body, which may serve as a urethral backstop. Some hypothesize that under normal circumstances, any increase in intra-abdominal pressure is transmitted equally to the bladder and proximal urethra. This is likely due to the retropubic location of the proximal and mid urethra within the sphere of intra-abdominal pressure. At rest, the urethra has a higher intrinsic pressure than the bladder. This pressure gradient relationship is preserved if acute increases in intra-abdominal pressure are transmitted equally to both organs. Intrinsic sphincter deficiency Intrinsic sphincter deficiency is a condition in which the urethral sphincter is unable to coapt and generate enough resting urethral closing pressure to retain urine in the bladder. The anatomic support of the urethra may be normal.

Occult stress incontinence Stress incontinence on prolapse reduction (previously termed latent stress incontinence) is a term used to describe stress incontinence observed only after reduction of pelvic prolapse. Some believe that kinking of the urethra caused by the prolapse itself provides for at least part of the continence mechanism. Urge incontinence pathophysiology Urge incontinence is involuntary urine loss associated with a feeling of urgency. The corresponding urodynamic term is detrusor overactivity, which is the observation of involuntary detrusor contractions during filling cystometry. These contractions may be voluntary or spontaneous and may or may not cause symptoms of urgency and/or urgency incontinence. However, a study using a quality of life assessment of women with incontinence showed that women with urge incontinence from detrusor overactivity consistently had a worse quality of life than did women with other urodynamic diagnoses. Urge incontinence may be a result of detrusor myopathy, neuropathy, or a combination of both. When the identifiable cause is unknown, it is termed idiopathic urge incontinence. When a definable causative neuropathic disorder exists, the coexisting urinary incontinence disorder is termed neurogenic detrusor overactivity. Symptoms of overactive bladder or urge incontinence in the absence of neurologic causes are known as detrusor instability. The term overactive bladder describes a syndrome of urinary urgency, usually accompanied by frequency and nocturia, with or without urgency urinary incontinence, in the absence of urinary tract infection or other obvious pathology. Mixed incontinence pathophysiology Mixed incontinence is urinary incontinence resulting from a combination of stress and urge incontinence. Approximately 40-60% of females with incontinence have this combination. Although it is generally defined as detrusor overactivity and impaired urethral function, the actual pathophysiology of mixed urinary incontinence is still being investigated. While generally thought of as separate etiologies for incontinence, some indirect evidence may link these disorders in some instances. In mixed incontinence, the bladder outlet is weak and the detrusor is overactive. A classic example of mixed incontinence is a patient with meningomyelocele and an incompetent bladder neck with a hyperreflexic detrusor; however, a combination of urethral hypermobility and detrusor instability is a more common scenario. Mixed incontinence is a common finding in older patients with urinary incontinence disorders. Often, stress incontinence symptoms precede urge incontinence symptoms in these individuals. Urgency without actual urge-related urine loss also is a common complaint of patients with stress incontinence. Reflex incontinence pathophysiology

Reflex incontinence is due to neurologic impairment of the central nervous system. Common neurologic disorders associated with reflex incontinence include stroke,Parkinson disease, and brain tumors. Reflex incontinence also occurs in patients with spinal cord injuries and multiple sclerosis. When patients with suprapontine or suprasacral spinal cord lesions present with symptoms of urge incontinence, this is known as detrusor hyperreflexia. Spinal cord injuries interrupt the sacral reflex arc from the suprasacral spinal cord, cerebral cortex, and higher centers. These pathways are crucial for voluntary and involuntary inhibition. In the initial phase of spinal cord injury, the bladder is areflexic and overflow incontinence results. Later, detrusor hyperreflexia usually is found upon urodynamic evaluation. Overflow incontinence pathophysiology The major contributing factor to overflow incontinence is incomplete bladder emptying secondary to impaired detrusor contractility or bladder outlet obstruction. Impaired detrusor contractility is typically neurogenic in nature; causes include diabetes mellitus, lumbosacral nerve disease from tumors, meningomyelocele, MS, prolapsed intravertebral disks, and high spinal cord injuries. Less common causes of overflow incontinence include AIDS, genital herpes affecting the perineal area, and neurosyphilis. Functional incontinence Functional incontinence is seen in patients with normal voiding systems but who have difficulty reaching the toilet because of physical or psychological impediments. In some cases, the cause is transient or reversible. In others, a permanent problem can be identified. The etiology of the incontinence may be iatrogenic, environmental, situational, or disease related. The following common mnemonic, DIAPPERS, is helpful in remembering the functional contributors to incontinence : D - Delirium I - Infection, urinary A - Atrophic urethritis or vaginitis P - Pharmacologic agents P - Psychiatric illness E - Endocrine disorders R - Reduced mobility or dexterity S - Stool impaction Continuous incontinence This severe type of incontinence is characterized by constant or near constant leakage with no symptoms other than wetness. Generally, this represents a significant breech in the storage capabilities of the bladder or urethra. Urogenital fistulas are a classic example. Pediatric urinary incontinence Pediatric incontinence disorders are classified according to cause. Primary incontinence disorders generally are due to congenital structural disorders, including ectopic ureter, exstrophy, epispadias, and patent urachus. Secondary structural causes can result from obstruction from urethral valves, congenital urethral strictures, and large ectopic ureteroceles. In addition, trauma can result in secondary structural incontinence. Neurogenic lesions make up the next category of pediatric incontinence disorders. These include spinal dysraphism, tethered spinal cord, and spinal cord tumors. Nocturnal enuresis is the most common pediatric incontinence disorder. For discussion of this topic, see Enuresis. Etiology Even in an individual patient, urinary incontinence may have multiple etiologies, with varying degrees of contribution to the overall disorder. Structural and functional disorders involving the bladder, urethra, ureters, and surrounding connective tissue can contribute. In addition, a disorder of the spinal cord or central nervous system (CNS) may be the major etiologic factor in some cases. Medical comorbidities also can be important. Finally, some cases of urinary incontinence may be pharmacologically induced. The most common cause of stress incontinence in women is urethral hypermobility secondary to poor anatomic pelvic support. Women may lose this pelvic support with postmenopausal estrogen loss, childbirth, surgery, or certain disease states that affect tissue strength. A less common cause of stress incontinence is intrinsic sphincter deficiency, which can result from the aging process, pelvic trauma, surgery (eg, hysterectomy, urethropexy, pubovaginal sling), or neurologic dysfunction.

The most common cause of intrinsic sphincter deficiency in men is radical prostatectomy for prostate cancer or transurethral resection of the prostate for benign prostatic hyperplasia. A less common cause of intrinsic sphincter deficiency is trauma to the bladder neck or prostate, resulting from pelvic fracturedue to high-impact deceleration injuries. Contributing factors with aging-related urinary incontinence include a weakening of connective tissue, genitourinary atrophy due to hypoestrogenism, increased incidence of contributing medical disorders, increased nocturnal diuresis, and impairments in mobility and cognitive functioning. Other factors that may increase the risk of developing incontinence include obesity, straining at stool as a child or young adult, heavy manual labor, chronic obstructive pulmonary disease, and smoking. In many cases of incontinence that are due to detrusor overactivity, the problem is idiopathic in nature. Less frequent causes of urinary incontinence include complications of urologic procedures or pelvic radiation therapy. In the pediatric population, it includes enuresis and congenital abnormalities of the genitourinary system. What causes Urinary Incontinence? Below are a list of conditions and diseases that contribute and/or cause urinary incontinence:

urinary tract or vaginal infections effects of medications constipation weakness of certain muscles in the pelvis blocked urethra due to an enlarged prostate Diseases and disorders involving the nervous system muscles (e.g., multiple sclerosis, Parkinsons disease, spinal cord injury and stroke). some types of surgery diabetes delirium dehydration pregnancy and childbirth overactive bladder weakness of the muscles holding the bladder in place weakness of the sphincter muscles surrounding the urethra birth defects enlarged prostate spinal cord injuries Multiple factors have been found to be associated with urinary incontinence, yet the leading culprits of incontinence have been neurologic disease, prostatic disease, and obstetric factors. Studies have found that pregnancy, mode of delivery and parity (the number of children a woman has had) are all factors that can increase the risk of incontinence. Women who delivered babies (via cesarean section or vaginal delivery) have much higher rates of stress incontinence than women who never delivered a baby. Women who developed incontinence during pregnancy or shortly after delivery have higher risk of sustained incontinence than those who did not. Increased parity (having more babies) also increases the risk. Age is also known to be a factor. As the human body ages, muscle loss and weakness occur and the urinary tract is not spared. Menopausal women can also suffer from urine loss as a result of decreased estrogen levels. Interestingly, replacement estrogen has not been found to help the symptoms. Many medications have been associated with urinary incontinence. These include: diuretics, estrogen, benzodiazepines, tranquilizers, antidepressants, hypnotics, and laxatives. Poor overall general health has

been associated with incontinence. Specifically, diabetes, stroke, high blood pressure, smoking history, Parkinson's, back problems, obesity, Alzheimer's, and pulmonary disease have all been associated with incontinence. Incontinence may be sudden and go away after a short period of time. Or, it may continue long-term. Causes of sudden or temporary incontinence include: Bedrest -- for example, when recovering from surgery Certain medications (such as diuretics, antidepressants, tranquilizers, some cough and cold remedies, and antihistamines for allergies) Mental confusion Pregnancy Prostate infection or inflammation Stool impaction from severe constipation, which causes pressure on the bladder Urinary tract infection or inflammation Weight gain Causes that may be more long-term: Alzheimer's disease Bladder cancer Bladder spasms Depression Large prostate in men Nervous system conditions, such as multiple sclerosis or stroke Nerve or muscle damage after radiation treatment to the pelvis Pelvic prolapse in women -- falling or sliding of the bladder, urethra, or rectum into the vagina, which may be caused by pregnancy and delivery Problems with the urinary tract Spinal cord injuries Weakness of the sphincter, the circle-shaped muscles that open and close the bladder (this can be caused by prostate surgery in men, or surgery to the vagina in women) What are the different types of urinary incontinence? Stress urinary incontinence: Stress incontinence is leakage that occurs when there is an increase in abdominal pressure caused by physical activities like coughing, laughing, sneezing, lifting, straining, getting out of a chair or bending over. The major risk factor for stress incontinence is damage to pelvic muscles that may occur during pregnancy and childbirth. Stress incontinence is when urine leaks because of sudden pressure on your lower stomach muscles, such as when you cough, laugh, lift something or exercise. Stress incontinence usually occurs when the pelvic muscles are weakened, for example by childbirth or surgery. Stress incontinence is common in women. Urge urinary incontinence: Also referred to as "overactive bladder," this type of incontinence is usually accompanied by a sudden, strong urge to urinate and an inability to get to the toilet in time. Frequently, some patients with urge incontinence may leak urine with no warning. Risk factors for urge incontinence include aging, obstruction of urine flow, inconsistent emptying of the bladder and a diet high in bladder irritants (such as coffee, tea, colas, chocolate and acidic fruit juices). This occurs when the need to urinate comes on very suddenly, often before you can get to a toilet. Your body may only give you a warning of a few seconds to minutes before you urinate. Urge incontinence is most common in the elderly and may be a sign of a urinary tract infection or an overactive bladder. Mixed urinary incontinence: Mixed incontinence is a combination of urge and stress incontinence.

Overflow urinary incontinence: Overflow incontinence occurs when the bladder does not empty properly and the amount of urine produced exceeds the capacity of the bladder. It is characterized by frequent urination and dribbling. Poor bladder emptying occurs if there is an obstruction to flow or if the bladder muscle cannot contract effectively. Overflow incontinence This type of incontinence is the uncontrollable leakage of small amounts of urine. It's caused by an overfilled bladder. You may feel like you can't empty your bladder all the way and you may strain when urinating. This often occurs in men and can be caused by something blocking the urinary flow, such as an enlarged prostate gland or tumor. Diabetes or certain medicines may also cause the problem. Functional incontinence This type occurs when you have normal urine control but have trouble getting to the bathroom in time. You may not be able to get to the bathroom because of arthritis or other diseases that make it hard to move around. Diagnosis A thorough physical examination looking for correctable causes of leakage, including impacted stool, constipation, prostate disease and prolapse or hernias, will be conducted. Usually a urinalysis and cough stress test will be performed at the first evaluation. If findings suggest further evaluation is necessary, tests such as cystoscopy or urodynamics may be recommended. Cystoscopy is performed by placing a small scope or camera through the urethra and into the bladder. Urodynamics is an outpatient test that is done with a tiny tube in the bladder inserted through the urethra and often with a second small tube in the rectum. The bladder is filled and the patient is asked to void while pressure measurements are recorded. How is Urinary Incontinence Treated? Treatment for incontinence depends not only on the type of incontinence a person has but also the gender of the patient. What are the treatment options for stress incontinence in women? In most cases of incontinence, conservative or minimally-invasive management is the first line of treatment. This may include fluid management, bladder training or pelvic floor exercises. However, when the symptoms are more severe, when conservative measures are not helpful or are unsatisfactory the next best treatment option is surgery. Behavioral Modification: Mild to moderate stress incontinence in the female is initially treated with behavior modification. Decreasing the volume of fluid ingested as well as eliminating caffeine and other bladder irritants can help significantly. Pelvic Floor Muscle Training: Strengthening or Kegel exercises can fortify the pelvic floor and sphincter muscles and improve urinary control. These exercises include repeated contractions of isolated muscles several times a day. Sometimes techniques including biofeedback, electrical stimulation of the pelvic muscles, and weighted vaginal cones can be helpful in teaching the patient how to isolate these muscles. Periurethral Injections: One of the surgical treatments for this condition, used in both males and females, is urethral injections of bulking agents to assist the closing of the urethral mucosa. The injections are done under local anesthesia with the use of a cystoscope and a small needle.

Sub urethral Sling Procedures: The most common and most popular surgery for stress incontinence is the sling procedure. Today, most of these procedures are being called by the names TVT or TOT. In this operation, a narrow strip of material is used either from: cadaveric tissue (from a cadaver), autologous tissue (from your own body), or soft mesh (synthetic material). It is applied under the urethra to provide a hammock of support and improve urethral closure. Retropubic Colposuspension: Another option is abdominal surgery in which the vaginal tissues or periurethral tissues are affixed to the pubic bone. The long-term results are positive, but the surgery requires longer recuperation time and is generally only used when other abdominal surgeries are also required. This procedure can also be performed laparoscopically Bladder Neck Needle Suspension: A long needle is used in these procedures to thread sutures from the vagina to the abdominal wall. The suture incorporates paraurethral tissue at the level of the bladder neck. These procedures were found to be less effective than open retropubic suspensions and slings and as a result are rarely done today. Anterior Vaginal Repair: Sutures are placed in the periurethral tissue and fascia in order to elevate and support the bladder neck. This procedure has also fallen out of favor for inferior long-term outcomes compared to open retropubic suspensions and slings. What additional treatment options are available for stress incontinence in men? Men should also initially be managed with behavioral modifications and pelvic floor exercises. Periurethral injections can be used in men as well. If these measures fail, surgical options are available, which are different from those performed in women. Male Sling: In male patients with stress incontinence, an alternative is to perform a urethral compression procedure, called a male sling. This is done with the use of a segment of cadaveric tissue or soft mesh to compress the urethra against the pubic bone. It is placed through an incision in the perineum (the area between the scrotum and the rectum). Artificial Urinary Sphincter: The most effective treatment for male incontinence is implantation of an artificial urinary sphincter. This device is made from silicone and has three components that are implanted into the patient. The cuff is the portion that provides circular compression of the urethra and therefore prevents leakage of urine from occurring. This is placed around the urethra after an incision is made in the perineum. What are the treatment options for urge incontinence? For urge incontinence there are also multiple treatment options available. The first step is behavior modifications including drinking less fluid, avoiding caffeine, alcohol and spicy foods, not drinking at bedtime, and timed voiding. Exercising the pelvic muscle (Kegel exercises) can also help. It is important to keep a log on the frequency of urination, number of accidents, the amount of fluid lost, the fluid intake and the number of pads used. This helps the urologist tailor treatment to your specific needs. Medications: The mainstay of treatment for overactive bladder and urge incontinence is medication. This consists of use of bladder relaxants that prevent the bladder from contracting without the patient's

intention. The most common side effect of the medication is dryness of the mouth, constipation or changes in vision. Sometimes, reduction of medication takes care of the side effects. Combinations of medications can also be used in some situations. Neuromodulation: Other alternatives can be considered in patients who fail to respond to behavior modification and/or medication. A new and exciting technology is the use of a bladder pacemaker to control bladder function. TREATMENT OPTIONS FOR OVERFLOW INCONTINENCE The treatment for overflow incontinence is complete empting of the bladder. When the bladder is allowed to cycle properly with filling and emptying on a regular basis urine loss is usually prevented. Patients with neurologic conditions, diabetic bladder, or patients with obstruction secondary to prostate disease or organ prolapse can develop this type of incontinence. Overflow incontinence due to obstruction should be treated with medication or surgery to remove the blockage. This may include resection of prostatic tissue or urethral stricture or repair of pelvic organ prolapse. If no blockage is found, the best treatment is to instruct the patient to perform self-catheterization a few times a day. By emptying the bladder regularly, the incontinence often disappears. Treatment depends on what's causing the problem and what type of incontinence you have. If your urinary incontinence is caused by a medical problem, the incontinence will go away when the problem is treated. Kegel exercises and bladder training help some types of incontinence through strengthening the pelvic muscles. Medicine and surgery are other options. What are Kegel exercises? Stress incontinence can be treated with special exercises, called Kegel exercises (see the box below). These exercises help strengthen the muscles that control the bladder. They can be done anywhere, any time. Although designed for women, the Kegel exercises can also help men. It may take 3 to 6 months to see an improvement. Kegel exercises To locate the right muscles, try stopping or slowing your urine flow without using your stomach, leg or buttock muscles. When you're able to slow or stop the stream of urine, you've located the right muscles. Squeeze your muscles. Hold for a count of 10. Relax for a count of 10. Repeat this 10 to 20 times, 3 times a day. You may need to start slower, perhaps squeezing and relaxing your muscles for 4 seconds each and doing this 10 times, 2 times a day. Work your way up from there. What is bladder training? Bladder training is a way of learning to manage urinary incontinence. It is generally used for stress incontinence, urge incontinence or a combination of the 2 types (mixed incontinence). Some bladder training techniques are explained in Bladder Training for Urinary Incontinence. e. Benign prostatic hyperplasia (BPH) Benign prostatic hyperplasia (BPH), benign enlargement of the prostate (BEP), adenofibromyomatous hyperplasia and incorrectly referred to benign prostatic hypertrophy, is an increase in size of the prostate. PATHOPHYSIOLOGY The prostate gland undergoes two growth spurts: once during adolescence and the other around the age of 50. Though the prostate continues to grow during most of a man's life, the enlargement does not usually cause problems until late in life. About 75 percent of men over the age of 50 and 90 percent of men in their 70s and 80s have had some symptoms of BPH. The benign growth occurs when old cells do not die (as they once did) while new cells continue to grow. This accumulation of cells thickens the prostate, which can narrow the urethra, resulting in urination problems. BPH involves hyperplasia (an increase in the number of cells) rather than hypertrophy (a growth in the size of individual cells), but the two terms are often used interchangeably, even amongst urologists.] t

involves hyperplasia of prostatic stromal and epithelial cells, resulting in the formation of large, fairly discrete nodules in the periurethral region of the prostate. When sufficiently large, the nodules compress the urethral canal to cause partial, or sometimes virtually complete, obstruction of the urethra, which interferes with the normal flow of urine. It leads to symptoms of urinary hesitancy, frequent urination, dysuria (painful urination), increased risk of urinary tract infections, and urinary retention. Although prostate specific antigen levels may be elevated in these patients because of increased organ volume and inflammation due to urinary tract infections, BPH does not lead to cancer or increase the risk of cancer. Causes and Risk Factors of Benign Prostatic Hyperplasia The cause of BPH is not well understood. No definite information on risk factors for the condition exists. For centuries, it has been known that BPH occurs mainly in older men and that it doesn't develop in men whose testes were removed before puberty. For this reason, some researchers believe that factors related to aging and the testes may spur the development of BPH. As the urethra is squeezed more tightly by the enlarged prostate, the bladder may not be able to completely empty. Rarely, this blockage may cause repeated urinary tract infections and start the process of bladder or kidney damage. It may also cause acuteurinary retention (a sudden inability to urinate ) which requires a visit to the emergency room. The cause of BPH is not well understood, but researchers theorize that BPH could be caused by: the aging process testosterone levels - As men age, the amount of activetestosterone in the blood decreases, leaving a higher proportion of estrogen. Dihydrotestosterone (DHT) - DHT is a substance derived from testosterone in the prostate, which may help control its growth. Most animals lose their ability to produce DHT as they age, however, some research indicates that with a drop in blood testosterone level, older men continue to produce and accumulate high levels of DHT in the prostate. cell "instructions" - Some researchers suggest that BPH may develop as a result of "instructions" given to cells early in life. According to this theory, BPH occurs because cells in one section of the gland follow these instructions and "reawaken" later in life. Symptoms of Benign Prostatic Hyperplasia Less than half of all men with BPH have symptoms of the disease, which include: Dribbling at the end of urinating Inability to urinate (urinary retention) Incomplete emptying of your bladder Incontinence Needing to urinate two or more times per night Pain with urination or bloody urine (these may indicate infection) Slowed or delayed start of the urinary stream Straining to urinate Strong and sudden urge to urinate Weak urine stream A hesitant, interrupted, or weak stream Urgency and leaking or dribbling More frequent urination, especially at night The obstructive (problems with urethra and urination) symptoms of BPH are: difficulty initiating a urine stream a hesitant, interrupted and weak stream urgency and leaking or dribbling blood in the urine As the urethra becomes narrower, the bladder wall becomes thicker and the bladder itself becomes smaller, causing: more frequent urination

bladder irritability a sudden strong urge to urinate, especially at night urge incontinence - (occurs when bladder muscles are too active. People with urge incontinence lose urine as soon as they feel a strong desire to go to the bathroom.) Due to the location of the prostate, BPH causes a number of urinary symptoms. The prostate is located just below where the bladder empties into the urethra (which is a thin tube that carries urine from the bladder, through the penis, to outside the body). As the prostate enlarges, it impinges the flow of urine through the urethra. Frequency - urinating much more often than normal. Urgency - having a sensation that you need to urinate immediately. Nocturia - getting up to urinate multiple times during the night. Hesitancy - difficulty starting the urine stream DIAGNOSTIC EXAMS Urine flow rate Post-void residual urine test to see how much urine is left in your bladder after urination Pressure flow studies to measure the pressure in the bladder as you urinate Urinalysis to check for blood or infection Urine culture to check for infection Prostate-specific antigen (PSA) blood test to screen for prostate cancer Cystoscopy prostate specific antigen (PSA), a blood test to screen for prostate cancer urinary cytology, a urine test to screen for bladder cancer a measurement of post-void residual volume (PVR), the amount of urine left in the bladder after urinating

uroflowmetry, or urine flow study, a measure of how fast urine flows when a man urinates cystoscopy, a direct look in the urethra and/or bladder using a small flexible scope urodynamic pressure-flow study that tests the pressures inside the bladder during urination ultrasound of the kidney or the prostate Additionally, a physical exam will be performed, including a digital rectal exam (DRE). This procedure involves the doctor inserting a latex-gloved finger into the rectum and feeling the prostate for any lumps or hard spots (that may indicate prostate cancer) and checking the size of the prostate to diagnose BPH. If there is a suspicion of prostate cancer, your doctor may recommend a biopsy with rectal ultrasound. Medical Treatment of BPH

There are two forms of medical treatment for BPH: a series of drugs called alpha blockers relaxes the muscles within the prostate and bladder neck, allowing the flow of urine to improve; a second family of medication, 5-alpha reductase inhibitors, will cause some large prostates to shrink and thereby improve flow , although the action is slow and maximum response may take 6-12 months to achieve. The herbal saw palmetto is a biologic 5-alpha reductase inhibitor.

There

are four drugs

in

the

alpha

blocker

family:

terazocin/Hytrin, Side effects for

doxasacine/Cardura , tamulosin/Flomax and

alfuzacin/Uroxatrol.

all four may include dizziness, decreased erections and retrograde ejaculations, (dry orgasms).

Finasteride/Proscar and dutasteride/Avodart are the 5-alpha reductase inhibitors available and will slowly shrink prostates. The herbal, saw palmetto works in a similar fashion, but as an herbal is less wellcontrolled

5-alpha reductase inhibitors artificially lowers PSA, the prostate cancer blood test. Surgical Treatment of BPH There are three forms of surgical treatment for BPH: TURP/PVP Laser, minimally invasive procedures and open surgery

TURP or transurethral resection of the prostate, (known euphemistically as "roto-rooter"), remains the gold standard for treatment of significant BPH. A specialized telescope, called a resectoscope, is inserted under anesthesia, into the urethra, and the overgrown prostate tissue is cut away from the inside using electric current.

The new (2003) high power Laserscope, PVP Green Light laser is very similar to a TURP, but by using laser there is virtually no bleeding and patients frequently go home the same day, most without a catheter

Minimally invasive procedures include a family of procedures that destroy islands of tissuee within the prostate using different forms of energy: laser, microwave, radio-frequency waves, or ultrasound.

A newer minimally invasive procedure,Thermodilation or Prolieve combines TUMT with balloon dilation of the prostate, an older technology that afforded a rapid but short lived improvement in voiding.

Cryotherapy or freezing is another minimally invasive procedure for obstructive BPH. Similar to the heat induced treatments, an iceball is formed within the prostate, and the destroyed tissues slowly sloughs.

Open surgery for BPH is relatively rare but is sometimes needed for very large prostate glands. The procedure requires a hospital stay. Results are usually good an seen shortly after surgery. Complications include, bleeding, infection, scarring, retrograde ejaculation, incontinence and occasionally, impotence among others

Nursing Management of BPH Relieve retention by inserting an indwelling foley catherter ( need physicians order for catheterization) which is left in place for 2-4 weeks to let the bladder recover from injury due to over distention. Catheter should not be forced . If the nurse cannot insert it, the urologist should be notified. After insertion, observe the client for hourly output, hematuria and shock( which may be caused by the sudden increased flow of urine due to the inability of the kidneys to reabsorb water and electrolytes) Encourage fluids unless contraindicated to decrease the risk of urinary tract infections. Intake should be 30ml/kg/day. Discourage clients from taking medications that contain alpha adrenergic agonists e.g cold medications. They can cause a man with BPH to have urinary retention.

III. Kidney Disorders a. Glomerulonephritis Glomerulonephritis (gloe-mer-u-lo-nuh-FRY-tis) is inflammation of the tiny filters in your kidneys (glomeruli). Glomeruli remove excess fluid, electrolytes and waste from your bloodstream and pass them into your urine. Also called glomerular disease, glomerulonephritis can be acute a sudden attack of inflammation or chronic coming on gradually. If glomerulonephritis occurs on its own, it's known as primary glomerulonephritis. If another disease, such as lupus or diabetes, is the cause, it's called secondary glomerulonephritis. If severe or prolonged, the inflammation associated with glomerulonephritis can damage your kidneys. PATHOPHYSIOLOGY Most human glomerulonephritides are triggered by immune-mediated injury exhibiting both humoral and cellular components. The cellular immune response contributes to the infiltration of glomeruli by circulating mononuclear inflammatory cells (lymphocytes and macrophages) and crescent formation in the absence of antibody deposition. This mechanism plays a primary role in some types of GN such as minimal change nephrotic syndrome or focal glomerulosclerosis and antineutrophil cytoplasmic antibodies-positive GN. Some evidence also supports a role for T cells and platelets in glomerular pathology. The humoral immune response leads to immune deposit formation and complement activation in glomeruli. Antibodies can be deposited within the glomerulus when circulating antibodies react with intrinsic autoantigens (antiglomerular basement membrane disease), or with extrinsic antigens that have been trapped within the glomerulus (post-infectious GN), or by trapping of immune complexes that have formed in the systemic circulation (cryoglobulinaemia). Injury usually occurs as a consequence of the activation and release of a variety of inflammatory mediators (complement activation, cytokines, growth factors, and vasoactive agents) that initiate a complex interplay of events that ultimately result in the structural and functional characteristics of immune glomerular disease. A variety of non-immunological metabolic, haemodynamic, and toxic stresses can also induce glomerular injury. These include hyperglycaemia (diabetic nephropathy), lysosomal enzyme defects, and high intraglomerular pressure (systemic hypertension and overload of functioning nephrons following loss of other nephrons due to other causes). A few glomerular diseases are due to hereditary defects resulting in deformity of the glomerular basement membrane (e.g., type IV collagen). Causes A variety of conditions can cause glomerulonephritis, ranging from infections that affect your kidneys to diseases that affect your whole body, including your kidneys. Sometimes the cause is unknown. Here are some examples of conditions that can lead to inflammation of the kidneys' glomeruli: Infections

Post-streptococcal glomerulonephritis. Glomerulonephritis may develop a week or two after recovery from a strep throat infection or, rarely, a skin infection (impetigo). An overproduction of antibodies stimulated by the infection may eventually settle in the glomeruli, causing inflammation. Symptoms usually include swelling, reduced urine output and blood in the urine. Bacterial endocarditis. Bacteria can occasionally spread through your bloodstream and lodge in your heart, causing an infection of one or more of your heart valves. Those at greatest risk are people with a heart defect, such as a damaged or artificial heart valve. .

Viral infections. Among the viral infections that may trigger glomerulonephritis are the human immunodeficiency virus (HIV), which causes AIDS, and the hepatitis B and hepatitis C viruses. Immune diseases

Lupus. A chronic inflammatory disease, lupus can affect many parts of your body, including your skin, joints, kidneys, blood cells, heart and lungs. Goodpasture's syndrome. A rare immunological lung disorder that may mimic pneumonia, Goodpasture's syndrome causes bleeding (hemorrhage) into your lungs as well as glomerulonephritis. IgA nephropathy. Characterized by recurrent episodes of blood in the urine, this primary glomerular disease results from deposits of immunoglobulin A (IgA) in the glomeruli Vasculitis

Polyarteritis. This form of vasculitis affects small and medium blood vessels in many parts of your body, such as your heart, kidneys and intestines. Wegener's granulomatosis. This form of vasculitis affects small and medium blood vessels in your lungs, upper airways and kidneys. Conditions that are likely to cause scarring of the glomeruli

High blood pressure. Damage to your kidneys and their ability to perform their normal functions can occur as a result of high blood pressure. Glomerulonephritis can also cause high blood pressure because it reduces kidney function.

Diabetic kidney disease. Diabetic kidney disease (diabetic nephropathy) can affect anyone with diabetes. Diabetic nephropathy usually takes years to develop. Good control of blood sugar levels and blood pressure may prevent or slow kidney damage.

Focal segmental glomerulosclerosis. Characterized by scattered scarring of some of the glomeruli, this condition may result from another disease or occur for no known reason. Chronic glomerulonephritis sometimes develops after a bout of acute glomerulonephritis. In some people there's no history of kidney disease, so the first indication of chronic glomerulonephritis is chronic kidney failure. Infrequently, chronic glomerulonephritis runs in families. One inherited form, Alport syndrome, may also involve hearing or vision impairment. What are the signs and symptoms of glomerulonephritis? A symptom is something the patient feels or reports, while a sign is something other people, including the doctor may detect. For example, a headache may be a symptom while a rash may be a sign. Some patients may not show any clear symptoms. The type of signs and symptoms will usually depend on whether it is the acute or chronic form, and its cause. For some people, their first indication that something is not right is when the results of a urine or blood sample test come back.

Urine - if the glomeruli are damaged there will be a small amount of blood and/or protein in the urine, which may be visible or will show up in a urine test. If symptoms are more severe the individual's urine will turn visibly red - sometimes it may be Cocacola colored. If the urine is cloudy or frothy it means that excess protein is present (proterinuria). A healthy adult urinates between 1 to 1.5 liters per day. People with severe glomerulonephritis may spend two or three days without being able to urinate; and when they do, there may be blood and/or protein in the urine.

Kidney damage - in the initial stage the inflammation of the kidneys may not be evident. Symptoms may suddenly appear, or come on about three weeks after infection. Patients with glomerulonephritis caused by kidney damage may have the following signs or symptoms: o An elevated body temperature (typically about 38C, 100.4F) o Breathing difficulties

Edema (swelling), especially in the hands, face, feet, ankles or abdomen o Loss of appetite o Nausea o Pallor o Vision problems o Vomiting Hypertension (high blood pressure) Fatigue Kidney pain - although pain in the kidneys is possible, it is unusual. When pain is felt, it is usually in the upper back, behind the ribs. Sometimes the pain may be intense. Kidney pain might be a symptom of kidney stones or a kidney infection, instead of glomerulonephritis.

Risk Factors

Post-streptococcal glomerulonephritis - strep infections of the throat and impetigo (a skin infection) may cause glomerulonephritis. Impetigo is a much less common cause than throat infection. As treatment for most streptococcal infections improve, this cause is becoming much less common. TB (tuberculosis) - glomerulonephritis can develop as a complication of tuberculosis. Syphilis - glomerulonephritis can develop as a complication of syphilis. Injecting illegal drugs - people who inject illegal drugs are at a much higher risk of developing glomerulonephritis. Bacterial endocarditis - this is an infection in at least one of the heart valves. Patients with a heart defect have a higher risk of developing bacterial endocarditis and eventually glomerulonephritis. Some viral infections - people infected with the HIV, hepatitis B and C viruses are more likely to develop glomerulonephritis compared to others. Lupus - this is a chronic inflammatory condition caused by an autoimmune disease (the body's immune system attacks itself, its own tissues). People with lupus are more likely to develop compared to people without it. Goodpasture's syndrome - this is also an autoimmune disease which causes lung and kidney disease. The patient may bleed in the lungs and develop glomerulonephritis. IgA nephropathy - immunoglobulin A (IgA) deposits appear in the glomeruli, eventually causing glomerulonephritis. Polyarteritis - this is an autoimmune disease in which the arteries become inflamed (arteritis). As the arteries are involved it can affect any organ in the body, including the kidneys. Wegener's granulomatosis - a rare kind of inflammation of the small arteries and veins (vasculitis) that typically involves the vessels that supply lung, sinus and kidney tissue.

The following conditions may cause scarring of the glomeruli: Hypertension (high blood pressure) - hypertension can damage the kidneys and subsequently their normal functioning. Glomerulonephritis itself can cause hypertension because kidney function is undermined - the kidneys play a vital role in regulating our blood pressure. Diabetic nephropathy (diabetic kidney disease) - any patient with diabetes has the potential to develop diabetic nephropathy. Kidney damage may be prevented, or at least significantly slowed down with good diabetes control. Focal segmental glomerulosclerosis - segmental collapse of glomerular capillaries (small vessels). There may be scattered scarring of some of the glomeruli. Acute glomerulonephritis - an attack of acute glomerulonephritis may develop into chronic (long-term) glomerulonephritis. If the patient has no history of kidney disease, the first indication of chronic glomerulonephritis will be chronic kidney failure. Genetic factors - there is a certain type of glomerulonephritis that runs in families. However, most people with glomerulonephritis do not have a family member who has/had the condition. Long-term medications - some medications, if taken over the long-term, may increase a patient's likelihood of developing glomerulonephritis. Examples include: NSAIDs (non-steroidal anti-inflammatory drugs), such as ibuprofen and aspirin.

Gold injections, for the treatment of rheumatoid arthritis. Lithium, for the treatment of depression. Penicillamine, for the treatment of arthritis. Hodgkin's disease - this is a type of cancer which can result in glomeruli being damaged. Sickle cell disease - a genetic blood disease in which there is an abnormal form of hemoglobin.

Diagnosis of glomerulonephritis It is not uncommon for a patient to have no signs and symptoms and find out he/she has glomerulonephritis after a check-up or tests linked to hypertension, or fatigue - or during routine antenatal check-ups. Urine test - if the doctor suspects possible glomerulonephritis a urine test may be ordered to check for blood or protein.

Blood test - levels of antigens and antibodies in the blood may help doctors in their diagnosis. Throat swab - some cells from the back of the patient's throat are taken and sent to the lab. Renal function tests - patients who have kidney disease may have to undergo further tests to find out whether they have glomerulonephritis. Renal function tests are a range of tests, including blood and urine samples which are checked for certain substances released by the kidneys. This is also called a kidney function test. Blood levels of sodium, chloride, potassium and urea will be checked. The tests may also tell the doctor whether the patient is producing less urine that usual. Kidney biopsy - patients with chronic glomerulonephritis may need to have a small sample of kidney tissue removed for testing to find out how serious the condition is. The doctor extracts tissue samples using a small needle. The patient will normally receive a local anesthetic. A kidney biopsy has a small risk of bleeding. Imaging tests - if the doctor finds evidence of damage, diagnostic studies may be ordered so that the kidneys can be visualized. This may include a kidney X-ray, anultrasound scan, or a CT (computerized tomography) scan. What are the treatment options for glomerulonephritis? The type of treatment the patient receives will depend on whether he/she has acute (sudden) or chronic (long-term, gradual progression) glomerulonephritis, what the underlying cause is, and how severe the signs and symptoms are. Glomerulonephritis cases which follow a strep infection usually resolve themselves without treatment. Diet and fluid intake - the patient will likely be advised to reduce fluid intake and refrain from consuming alcoholic drinks or those with a high salt or potassium content. The patient may be referred to a dietician who will give advice on potassium and salt intake, among other things. Blood chemistry will need to be checked regularly to make sure levels of potassium, sodium, and chloride are right. Hypertension - in order to treat the hypertension and halt or slow down kidney function decline, the doctor may prescribe diuretics, Angiotensin-converting enzyme (ACE) inhibitors, and Angiotensin-converting enzyme (ACE) inhibitors, which help to relax the blood vessels, reducing the workload of the heart. Hypertension can cause further kidney decline and other health problems and needs to be controlled.

The following medications may also be prescribed to treat possible underlying causes: Bacterial infections - a targeted antibiotic. Lupus or vasculitis - corticosteroids and immunosuppressants. IgA - possibly fish oil supplements.

Goodpasture's syndrome - plasmapheresis is a procedure designed to reduce blood plasma levels without depleting the body of its blood cells. Antibodies are removed and donated plasma replaces the depleted plasma. Acute glomerulonephritis and kidney failure - temporary dialysis can help control hypertension and remove surplus fluid. If kidney transplant is not possible, usually because the patient's poor health would not withstand the procedure, dialysis becomes the only available therapy. Kidney dialysis is when a machine is utilized to do the kidney's job of filtering out waste products from the body.

What are the possible complications of glomerulonephritis? Hypertension (high blood pressure) This is a common complication because our kidneys play a key role in blood pressure regulation. Untreated hypertension can lead to serious health problems, including heart failure and pulmonary edema. Other organs Although the kidneys are usually the only organs affected, the body's immune system can damage other parts of the body. Kidney disease or kidney failure The kidneys can become so damaged that they fail completely if the condition is left untreated. Loss of function of the filtering part of the nephron may result in accumulation of waste products if this happens rapidly the patient can develop acute kidney failure and will need emergency dialysis. If the kidneys gradually lose function and continue to do so the patient will develop chronic (long-term) kidney failure. When the kidneys function at under 10% of their normal capacity the patient is in what is known as end-stage kidney disease, and will require regular dialysis or a kidney transplant to stay alive. Prevention Most forms of glomerulonephritis are not preventable. However, the following may help prevent complications of the disease itself or potential underlying causes: Make sure you get immediate treatment for a strep infection that causes a sore throat or impetigo. Take steps to prevent yourself from becoming infected by bacteria and viruses, such as HIV, which may raise your risk. If you have diabetes make sure you adhere to your treatment plan. Keep your blood pressure under control. Although keeping fit, getting at least 7 hours good sleep every night, and eating a well balanced diet high in fruit and vegetables has not been clinically proven to lower glomerulonephritis risk, it will lower your risk of developing an infection complication. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. NURSING MANAGEMENT Provide best rest during the acute phase. Perform passive range of motion exercises for the patient on bed rest. Allow the patient to resume normal activities gradually as symptoms subside. Consult the dietician about a diet high in calories and low in protein, sodium, potassium, and fluids. Protect the debilitated patient against secondary infection by providing good nutrition and hygienic technique and preventing contact with infected people. Check the patients vital signs and electrolyte values. Monitor intake and output and daily weight. Report peripheral edema or the formation of ascites. Explain to the patient taking diuretics that he may experience orthostatic hypotension and dizziness when he changes positions quickly. Provide emotional support for the patient and his family. If the patient is scheduled for dialysis, explain the procedure fully.

b. Nephrotic syndrome Nephrotic syndrome is a group of symptoms that include protein in the urine, low blood protein levels, high cholesterol levels, high triglyceride levels, and swelling. A kidney disease with proteinuria, hypoalbuminemia, and edema. Nephrotic-range proteinuria is 3 grams per day or more. On a single spot urine collection, it is 2 g of protein per gram of urine creatinine. Pathophysiology Nephrotic syndrome results from damage to the kidneys glomeruli, the tiny blood vessels that filter waste and excess water from the blood and send them to the bladder as urine. Damage to the glomeruli from diabetes, or even prolonged hypertension causes the membrane to become porous, so that small proteins such as albumin pass through the kidneys into urine. As protein continues to be excreted, serum albumin is decreased, which in turn decreases the serum osmotic pressure. Capillary hydrostatic fluid pressure becomes greater than capillary osmotic pressure, which results in generalized edema. As fluid is lost into the tissues, the plasma volume decreases, stimulating secretion of aldosterone to retain sodium. This additional water also passes out of the capillaries into the tissue leading to even greater edema. Causes Nephrotic syndrome is usually caused by damage to the clusters of tiny blood vessels (glomeruli) of your kidneys. The glomeruli filter your blood as it passes through your kidneys, separating things your body needs from those it doesn't. Healthy glomeruli keep blood protein (mainly albumin) which is needed to maintain the right amount of fluid in your body from seeping into your urine. When damaged, glomeruli allow too much blood protein to leave your body, leading to nephrotic syndrome. Many

possible

causes

Many diseases and conditions can cause glomerular damage and lead to nephrotic syndrome, including: Minimal change disease. The most common cause of nephrotic syndrome in children, this disorder results in abnormal kidney function, but when the kidney tissue is examined under a microscope, it appears normal or nearly normal. The cause of the abnormal function typically can't be determined.

Focal segmental glomerulosclerosis. Characterized by scattered scarring of some of the glomeruli, this condition may result from another disease or a genetic defect or occur for no known reason. Membranous nephropathy. This kidney disorder is the result of thickening membranes within the glomeruli. The exact cause of the thickening isn't known, but it's sometimes associated with other medical conditions, such as hepatitis B, malaria, lupus and cancer.

Diabetic kidney disease. Diabetes can lead to kidney damage (diabetic nephropathy) that affects the glomeruli. Systemic lupus erythematosus. This chronic inflammatory disease can lead to serious kidney damage. Amyloidosis. This disorder occurs when substances called amyloid proteins accumulate in your organs. Amyloid buildup often affects the kidneys, damaging their filtering system. Blood clot in a kidney vein. Renal vein thrombosis, which occurs when a blood clot blocks a vein connected to the kidney, can cause nephrotic syndrome. Heart failure. Some forms of heart failure, such as constrictive pericarditis and severe right heart failure, can cause nephrotic syndrome. SYMPTOMS Oedema (fluid retention) is a main symptom Oedema occurs when fluid leaks out of blood vessels into the body tissues. This causes swelling and puffiness of the affected tissues. The swelling is usually painless, but the swollen tissues may feel tight.

With children, the face is often affected first and the face becomes puffy. With adults, the ankles often become swollen at first (as gravity helps fluid to pool in the lower legs). As oedema becomes worse, the calves, then the thighs may become swollen. In severe cases, the oedema can become extensive. Fluid may accumulate in the lower back, the arms, in the abdominal cavity (ascites) or in the chest between the lungs and the chest wall (pleural effusion). Ascites can cause abdominal pain and discomfort due to distension. Pleural effusions may cause chest pain and breathlessness. The main reason why fluid leaks out from the blood vessels and into the body's tissues with nephrotic syndrome is because of a low level of protein in the blood. As protein is lost from the body in the urine, the body makes more protein in the liver which passes into the bloodstream. However, in time the amount made by the liver cannot keep up with the amount lost by the leaky kidneys, and so the blood level of protein goes down. If the blood level of protein is low then fluid tends to leak out of the blood vessels into the body tissues. (Protein and other chemicals in the blood exert an osmotic pressure which tends to pull fluid into the blood vessels. If the concentration of protein reduces, the osmotic pressure reduces, and fluid leaks out.) Note: nephrotic syndrome is just one cause of oedema. There are other causes of oedema. For example, heart failure is the most common cause of oedema, especially in older people. Other symptoms that may develop include: Your urine may appear frothy. Tiredness, lethargy and a poor appetite. Diarrhoea and/or vomiting (especially in children). If the nephrotic syndrome persists for a long time then you may develop wasting of your muscles, and your nails may become white (called leukonychia). Depending on the cause of the nephrotic syndrome, you may also have other symptoms. For example, if you have nephrotic syndrome as a complication of rheumatoid arthritis you may have a range of other symptoms caused by the arthritis. Some conditions of the kidney can cause high blood pressure and/or kidney failure. Assessment/Clinical Manifestations/Signs and Symptoms Major manifestations is edema (usually periorbital in dependent areas *sacrum, ankles and hands] and ascites) Malaise, headache, irritability and fatigue Foamy urine Anorexia, abdominal discomfort Laboratory and diagnostic study findings Proteinuria (exceeding 3 to 3.5 g/day) Microscopic hematuria Needle biopsy of the kidney for histologic examination to confirm diagnosis Treatments and drugs Treatment for nephrotic syndrome involves treating any underlying medical condition that may be causing your nephrotic syndrome. Your doctor may also recommend medications that may help control your signs and symptoms or treat complications of nephrotic syndrome. Medications may include:

Blood pressure medications. Drugs called angiotensin-converting enzyme inhibitors reduce blood pressure and also reduce the amount of protein released in urine. Medications in this category include

benazepril (Lotensin), captopril (Capoten) and enalapril (Vasotec). Another group of drugs that works in a similar way is called angiotensin II receptor blockers and includes losartan (Cozaar) and valsartan (Diovan).

Water pills. Water pills (diuretics) help control swelling by increasing your kidneys' fluid output. Diuretic medications include furosemide (Lasix) or spironolactone (Aldactone). Cholesterol-reducing medications. Medications called statins can help lower cholesterol levels. Statins include atorvastatin (Lipitor), fluvastatin (Lescol), lovastatin (Altoprev, Mevacor), pravastatin (Pravachol), rosuvastatin (Crestor) and simvastatin (Zocor).

Blood thinners. Medications called anticoagulants help decrease your blood's ability to clot and reduce your risk of developing blood clots. Anticoagulants include heparin or warfarin (Coumadin). Immune-system-suppressing medications. Medications to control the immune system, such as corticosteroids, may decrease the inflammation that accompanies certain kidney disorders, such as membranous nephropathy. Medical Management Objective of management is to preserve renal function. Bed rest for a few days to promote diuresis and reduce edema. Diet with high biologic protein (0.8 g/kg/day) to replenish urinary losses Low sodium, low saturated fat, liberal potassium Pharmacologic therapy Diuretics for severe edema, in combination with angiotensin-converting enzyme (ACE) inhibitors Adrenocorticosteroids to reduce proteinuria Antineoplastic agents (Cytoxan) or immunosuppressive agents Nursing Management In the early stages, nursing management is similar to that of acute glomerulonephritis As the disease worsens, management is similar to that of chronic renal failure Monitor intake and output; note signs of low plasma volume and impaired circulation with prerenal acute renal failure Instruct patient receiving steroids or cyclosporine regarding medication and signs and symptoms that must be reported to the physician Instruct patient in selecting a high-protein diet while restricting cholesterol and fat intake c. Renal Failure Renal failure is a serious medical condition affecting the kidneys. When a person suffers from renal failure, their kidneys are not functioning properly or no longer work at all. Renal failure can be a progressive disease or a temporary one depending on the cause and available treatment options. The kidneys are glands that are located in the abdominal region just above the pelvis on either side of the body. When functioning normally, the kidneys separate and filter excess water and waste from the blood stream. The kidneys are responsible for producing urine, which is used to flush away the toxins. The kidneys also maintain a healthy balance of fluids and electrolytes, or salt compounds, in the body. In renal failure the kidneys undergo cellular death and are unable to filter wastes, produce urine and maintain fluid balances. This dysfunction causes a build up of toxins in the body which can affect the blood, brain and heart, as well as other complications. Renal failure is very serious and even deadly if left untreated. Signs and Symptoms

Symptoms can vary from person to person. Someone in early stage kidney disease may not feel sick or notice symptoms as they occur. When kidneys fail to filter properly, waste accumulates in the blood and the body, a condition called azotemia. Very low levels of azotaemia may produce few, if any, symptoms. If the disease progresses, symptoms become noticeable (if the failure is of sufficient degree to cause symptoms). Renal failure accompanied by noticeable symptoms is termed uraemia. Symptoms of kidney failure include:

High levels of urea in the blood, which can result in:

Vomiting and/or diarrhea, which may lead to dehydration Nausea Weight loss Nocturnal urination More frequent urination, or in greater amounts than usual, with pale urine Less frequent urination, or in smaller amounts than usual, with dark coloured urine Blood in the urine Pressure, or difficulty urinating Unusual amounts of urination, usually in large quantities A build up of phosphates in the blood that diseased kidneys cannot filter out may cause: o Itching o Bone damage o Nonunion in broken bones o Muscle cramps (caused by low levels of calcium which can be associated with hyperphosphatemia) A build up of potassium in the blood that diseased kidneys cannot filter out (called hyperkalemia) may cause: o Abnormal heart rhythms [6] o Muscle paralysis Failure of kidneys to remove excess fluid may cause: o Swelling of the legs, ankles, feet, face and/or hands o Shortness of breath due to extra fluid on the lungs (may also be caused by anemia) Polycystic kidney disease, which causes large, fluid-filled cysts on the kidneys and sometimes the liver, can cause: o Pain in the back or side Healthy kidneys produce the hormone erythropoietin which stimulates the bone marrow to make oxygen-carrying red blood cells. As the kidneys fail, they produce less erythropoietin, resulting in decreased production of red blood cells to replace the natural breakdown of old red blood cells. As a result, the blood carries less hemoglobin, a condition known as anemia. This can result in: o Feeling tired and/or weak o Memory problems o Difficulty concentrating o Dizziness o Low blood pressure Proteins are usually too big to pass through the kidneys, but they can pass through when the glomeruli are damaged. This does not cause symptoms until extensive kidney damage has occurred,[7] after which symptoms include: o Foamy or bubbly urine o Swelling in the hands, feet, abdomen, or face Other symptoms include: o Appetite loss, a bad taste in the mouth o Difficulty sleeping o Darkening of the skin o Excess protein in the blood o With high dose penicillin, renal failure patients may experience seizures
o o o o o o o o o

There are two types of renal failure: 1. Acute renal failure occurs suddenly and is usually initiated by underlying causes, for example dehydration, infection, serious injury to the kidney or the chronic use of over the counter pain medications like Tylenol (acetaminophen) or Advil (ibuprofen). Acute renal failure is often reversible with no lasting damage. Causes Acute kidney failure usually occurs when the blood supply to the kidneys is suddenly interrupted or when the kidneys become overloaded with toxins. Causes of acute failure include accidents, injuries, or complications from surgeries in which the kidneys are deprived of normal blood flow for extended periods of time. Heart-bypass surgery is an example of one such procedure. Drug overdoses, accidental or from chemical overloads of drugs such as antibiotics or chemotherapy, may also cause the onset of acute kidney failure. Unlike chronic kidney disease, however, the kidneys can often recover from acute failure, allowing the patient to resume a normal life. People suffering from acute failure require supportive treatment until their kidneys recover function, and they often remain at increased risk of developing future kidney failure.[9] Among the accidental causes of renal failure is the crush syndrome, when large amounts of toxins are suddenly released in the blood circulation after a long compressed limb is suddenly relieved from the pressure obstructing the blood flow through its tissues, causing ischemia. The resulting overload can lead to the clogging and the destruction of the kidneys. It is a reperfusion injury that appears after the release of the crushing pressure. The mechanism is believed to be the release into the bloodstream of muscle breakdown products notably myoglobin, potassium, and phosphorus that are the products of rhabdomyolysis (the breakdown of skeletal muscle damaged by ischemic conditions). The specific action on the kidneys is not fully understood, but may be due in part to nephrotoxic metabolites of myoglobin. Management 1. Management: Volume Status 1. Normal Volume Status 1. Limit Fluid Intake to Urine Output + 300-500 ml/day 2. Limit Sodium Intake to 2 grams per day 2. Volume Overloaded 1. Limit Fluid intake to less than Urine Output 2. Limit Sodium Intake to less than 2 grams per day 3. Consider Loop Diuretic 4. Consider Dialysis 3. Volume Depleted 1. First: Restore Volume with Isotonic saline 2. Next: Limit Intake to Urine Output + 300-500 ml/day 3. Limit sodium intake to 2 grams per day 2. Management: Potassium 1. Hyperkalemia 1. Look for potassium source 2. Eliminate parenteral potassium 3. Reduce Dietary Potassium intake <50 meq per day 4. Consider potassium binding resin (Kayexalate) 5. Aggressive management if Serum Potassium >6 mEq/L 1. See Hyperkalemia 2. Consider Dialysis 2. Normokalemia 1. Limit Potassium intake to 50 meq per day 3. Management: Acid-Base Status 1. Acidemia 1. Look for cause of acidosis (See Arterial Blood Gas) 2. Reduce protein intake to 0.6 g/kg/day 3. Aggressive management if pH <7.2 or bicarbonate <15 1. Consider oral bicarbonate or 2. Consider isotonic IV bicarbonate 3. Consider Dialysis 2. Normal pH

1. Limit protein intake to 0.8 g/kg/day 4. Nutritional Intake 1. Maintain 30-50 KCal/Kg/day 5. Management: Uremia 1. Absent 1. Limit protein intake to 0.9 g/kg/day 2. Present 1. Reduce protein to 0.6 g/kg/day 2. Check for Gastrointestinal Bleeding 3. See Dialysis indications below 6. Management: Dialysis Indications 1. Blood Urea Nitrogen >100 mg/dl 2. Serum Creatinine >10 3. Uremic Signs (e.g. Pericarditis, Encephalopathy) 4. Significant bleeding 5. Refractory severe Metabolic Acidosis (pH <7.20) 6. Refractory severe Hyperkalemia (potassium >6.0) 7. Volume Overload 7. Management: Medications 1. Assess medications for toxicity 1. Check drug levels 2. Adjust dosages for Renal Function 2. Stop Nephrotoxic Drugs 1. NSAIDs 2. ACE Inhibitors 3. Aminoglycosides 4. Avoid repeating Radiocontrast Material 5. Avoid high dose Diuretics in critically ill patients 1. Avoid Diuretics in relatively resistant patients 2. Associated with higher mortality 3. Discourages prior strategy to overcome oliguria 4. Mehta (2002) JAMA 288:2547-53 6. Dopamine does not drop ARF risk in critically ill 1. Kellum (2001) Crit Care Med 29:1526-31

2. Chronic renal failure is more serious than acute renal failure because symptoms may not appear until the kidneys are extremely damaged. Chronic renal failure can be caused by other long term diseases, such as diabetes and high blood pressure. Chronic renal failure can worsen over time, especially when the problem has gone undiagnosed and treatment is delayed. Causes CKD has numerous causes. The most common is diabetes mellitus. The second most common is long-standing, uncontrolled hypertension, or high blood pressure. Polycystic kidney disease is another well-known cause of CKD. The majority of people afflicted with polycystic kidney disease have a family history of the disease. Other genetic illnesses affect kidney function, as well. Overuse of common drugs such as aspirin, ibuprofen, and acetaminophen (paracetamol) can also cause chronic kidney damage.[10] Some infectious diseases, such as hantavirus, can attack the kidneys, causing kidney failure. Management Goal of management are to retain kidney function and maintain homeostasis for as long as possible. All factors that contribute to ESRD and those that are reversible (e.g. obstruction) are identified and treated. Complications can be prevented or delayed by administering prescribed antihypertensives, cardiovascular agents, anticonvulsants, erythropoietin (Epogen), iron supplements, phosphatebinding agents (antacids), and calcium supplements. Dietary intervention is needed, with careful regulation of protein intake, fluid intake to balance fluid losses, and sodium intake and with some restrictions of potassium.

Adequate intake of calories and vitamins is ensured. Calories are supplied with carbohydrates and fats to prevent wasting. Protein is restricted; protein must be of high biologic value (dairy products, eggs, meats) Vitamin supplementation Fluid allowance is 500 to 600 mL of fluid or more than the 24-hour urine output

3. Renal dialysis Renal dialysis is a medical process that becomes necessary when the normal functions of the kidneys become compromised by kidney failure. The kidneys help keep the body and its blood healthy by removing harmful wastes from the blood. Renal dialysis involves filtering the blood of excess fluid, minerals, and waste when the kidneys can no longer do so on their own. Typically, patients with less than 85% kidney function will be recommended for renal dialysis, though the actual level of kidney function for recommendation may vary from patient to patient. Renal dialysis is typically takes place in one of two ways. Either the patient regularly attends a dialysis center or the patient receives dialysis at home. Either way, renal dialysis requires the use of a special machine that pumps blood out of the body, where it undergoes filtration, and then returns it to the body. Patients who receive renal dialysis because of chronic kidney failure will typically have a permanent port surgically installed for ease of access because regular dialysis is necessary. However dialysis can also be performed on a single or limited treatment basis if it becomes necessary due to an acute illness that effects the kidneys. In essence, renal dialysis is a way to artificially replicate some of the necessary functions of the kidneys. For patients with chronic kidney failure, dialysis is the only way to filter out toxins that would otherwise impact the body and eventually cause death. Once a patient with chronic kidney failure begins renal dialysis they typically do not stop unless they receive a kidney transplant. Nursing Management Provide conservative therapy, as indicated. Maintain strict fluid control; daily fluid intake should equal 500 ml (insensible loss) plus the amount of the previous 24 hours urine output; daily weight; and strict intake and output Encourage intake of high biologic value protein foods such as eggs, dairy products, and meats (causes positive nitrogen balance needed for growth and healing) Encourage high-calorie, low-protein, low-sodium, and low-potassium snacks between meals. Encourage alternating activity with rest. Encourage independence as much as possible. Assess the client and familys response to chronic illness. Encourage therapeutic conversations to help cope with chronic illness. Provide symptomatic treatment. Be prepared to identify and treat complications, which include hyperkalemia, pericarditis, pericardial effusion, pericardial tamponade, hypertension, anemia, and bone disease. Administer prescribed medication, which may include ion exchange resin, alkalizing agents, antibiotics, erythropoeitin, folic acid supplements, iron supplements, phosphate-binding agents, calcium supplements, histamine receptor antagonists, and proton-pump inhibitors. Prepare the client for peritoneal dialysis, if indicated. Assist with the procedure as instructed, maintaining septic technique and monitoring for signs and symptoms of peritonitis. (rigid, boardlike abdomen, fever, cloudy peritoneal fluid) Prepare the client for and assist with hemodialysis, if indicated. Provide proper shunt care, and assess for possible complications. (bleeding due to heparinization, hypovolemia, hypotension due to excessive water removal, dialysis disequilibrium syndrome (headache, confusion, and seizures) due to rapid removal of urea from plasma.) Prepare the client for kidney transplantation, if indicated. Provide postoperative care for any client who has undergone major surgery with special attention to catheter patency and adequacy, intake and output, fluid replacement, and protection from infection. Monitor for signs and symptoms of complications such as: 1)Graft rejection (fever, elevated white blood cell count, electrolyte abnormalities, abnormal renogram) 2)Infection stemming from immunosuppressive therapy (sepsis pneumonia, wound infection, and urinary tract infection) IV. Care of Burn Patients BURNS

Are caused by a transfer of energy from the heat source of the body. Heat can be transferred through conduction or electromagnetic radiation. Categories of Burns 1. Thermal burns - are caused by exposure to or contact with flames, hot liquids, semi liquid (steam), semisolid or hot object ( residential fire, explosive, automobile accident, scald injury, ignition). 2. Chemical burns- caused by tissue contact with strong acids, alkali, organic compounds (household cleaning object). 3. Electrical burns caused by heat that is generated by electrical energy as it passes through the body (faulty wiring, high voltage power lines struck by lightning). 4. Radiation least common and rare caused by exposure to radioactive source ( use of ionizing radiation in industry, therapeutic radiation source of medicine, sunburn due to exposure to ultraviolet rays). CLASSIFICATION ACCORDING TO BURN DEPTH 1. Superficial burn (1st degree) Burn affects the entire epidermis only. The skin appears pink and red. There is local pain and edema, blister absent for 24 hours. No treatment is needed, heals in 3-7 days e.g. sunburn 2. Partial thickness burn (2nd degree) Both epidermis and the dermis are affected. Large thick walled blisters develop often covering the burn area. The underlying area usually appears wet and shiny. The wound is painful, appears red with exudates, blanching of the area is followed by capillary refill, hair follicle appears intact. Usually heals in 21-28 days. 3. Full thickness burn (3rd degree) Burn bothe the dermis and the epidermis and the underlying structures such as the subcutaneous tissue, muscles and bone. The color is deep red, white or black, or brown. The burned area is dry, hard leathery appearance due to loss of epidermal elasticity. Painless due to destruction of the nervous fibers. Hair follicles and sweat glands are destroyed. CLASSIFICATION ACCORDING TO BURN SIZE 1. Rule Of Mine rule as of applicable to adults only. The body is divided into areas, each of which represents 9% (multiples of nine) of the total BSA, but is not accurate in infants and children. 2. Lund and Browner Method based on the work of Berknow, which modifies the percentage for bony segments according to age. Ex. Head and neck area of the child has a larger area or segment of the body surface area than adult. This is more accurate than the rule of nine. PATHOPHYSIOLOGY OF BURN Pathophysiology Of Burn A. Emergent Phase ( Initial Phase) Fluid shift and edema formation occurs within 24 hours to 48 hours post burn, then fluid mobilization occurs approximately 48 to 72 hours. Phase is characterized by fluid loss, edema formation, and continues until fluid mobilization and dieresis occurs. B. Intermediate (Acute Phase) Begins when dieresis is complete. Clients response to shifts from initial response to repair of damage tissue . Wound healing begins and wound coverage is initiaited. Phase end when all areas of the burns is healed and grafted. II. The initial effect of burn is dilatation of capillaries and small blood vessels in the area, plasma seeps into surrounding tissue producing blisters and edema

III. The increase in capillary permeability and histamine release from the injured cells precipitate in the increase on fluid volume. This is the primary importance in the first 24 hours to 36 hours post burn. Plasma to interstitial fluid shift occurs, as the capillary walls become more permeable to water, sodium ,and plasma proteins. Colloidal osmotic pressure decreases with an increase loss of proteins from the vascular spaces. Hemoconcentration occurs as a result of fluid shift out of the vascular spaces. IV. Electrolyte Shift Sodium is initially shifted to the interstitial spaces and remain there until edema subsides or diereses occurs. Injured cells or hemolyzed cells release potassium into the extracellular spaces. As diuresis begins, serum potassium may be markedly elevated but as diuresis continous potassium moves back into the cell causing severe decrease in the serum potassium levels. With adequate fluid replacement the integrity of the capillary membrane is restored , fluid shifts and edema subsides. Nursing Diagnosis 1. Fluid volume deficit (FVD) related to increase capillary permeability. 2. Ineffective gas exchange r/t carbon monoxide poisoning (smoke inhalation, upper airway obstruction) 3. Increased risk for altered body temperature r/t loss of skin to microcirculation and open wound. 4. Altered nutrition less than body requirements r/t nutritional requirement secondary to the altered GIT function. Nursing Interventions Curative: A. On The Scene (first Aid) 1. Extinguish flames from clothes on fire by dropping and rolling the patient on the floor, smother the flame with blanket, rug or coat. Avoid standing because the victim breathes flame and smoke. Avoid running because this fans the flames. 2. Soak burned area with cold water briefly. 3. Remove jewelry to prevent constriction secondary to rapidly developing edema. 4. Cover wound with the sterile dressing or clean cloth to minimize bacterial contamination and decrease pain from air current 5. Avoid ointments or salivas. 6. If chemical burn, (corrosive), iirrigate immediately with running water. B. Airway, Breathing, and Circulation Breathing must be assessed for patients airway through oropharyngeal suctioning following the administration of 100% oxygen. If there is edema in the airway, do endotracheal intubation for hyperinflation with ambubag. Circulatory system can be assessed. C. Prevention Of Shock 1. IV therapy to prevent shock NPO, keep sidelying position (vomits because of paralytic ileus resulting from stress of injury. 2. If IV care is very delayed and the patient is conscious, give per orem fluid prescribed as follows: 1 liter of water, add I tsp. salt (3grams) + NaHCO3 (1.5grams) Nursing Intervention during the Intermediate Phase Curative :

1. Maintain oxygen and patent airway. Pulmonary care such as turning, deep breathing and suctioning. Proper positioning for optimal chest expansion. 2. Explain fluid and electrolyte balance a. Assess vital signs, during output and CVP b. Daily weight and I & O c. Assess for hyperand hypovolemia d. Assess for level of consciousness (LOC) e. Elevate the affected extremity to decrease edema 3. Maintain normal body temperature a. Acetaminophen for fever b. Hypothermia blanket for fever 4. Improving Nutritional Status Following thermal injuries, the patients nutritional requirements are dramatically increased. But in the early post burn period: a. Patient is unable to take nutrients per orem because the GIT responses to injury. b. Gastric dilatation and ileus occur manifested by distended abdomen, nausea and vomiting. c. Prevent aspiration during feeding per NGT. d. Administer Histamine blocker/order severely burned client are prone to duodenal ulcer because of hypersecretion of gastric acid and erosion of gastric mucosa in response to stress or burn (Curlings ulcer) 5. Wound Care Includes cleaning and debridement, application of topical antimicrobial, dressing, gauze, biologic biosynthetic material may be used. a. Wound cleaning is by total immersion hydrotherapy bedside baths, walk in bath tub or a whirlpool bath may be used. Tap water saline or iodine diluted or antiseptic solution may be used. Hydrotherapy provides an excellent medium for exercising the extremeties and exercising the entire body. This is limited to 20-30 minute to prevent chilling. Wound dressing is changed 20 minutes after the administration of an analgesic. b. Topical antimicrobial therapy- does not sterilize the burn but simply reduces the number of bacteria. Silver sulfadiazine (Silvaderine) compare with Mafenide Acetate and other antimicrobial agents, it is more effective in controlling infection, causes no pain on an application and does not disturb acid-base balance, electrolyte or renal function, and does not stain. Silver sulfadiazine Cerium Nitrate effective in gram-negative bacteria Silver Nitrate Solution (0.5% aqueous solution) prevents eschar contamination, bacteriostatic. Other topical agents Povidone iodine ointment 10% and Betadine solution effective against a wide variety of gram negative and positive organisms, as Gentamicin sulfate and Nitrofurazone (Furacin) Preventive: 1. Prevention of Infection a. Maintain aseptic technique for wound care and for any invasive procedures like IV insertion, urinary catheterization and suctioning. b. Report signs of septicemia and promptly intervene c. Tube drainage and draining containers should be changed regularly. d. Meticulous handwashing prior to each patient contact Rehabilitative The goal is for the patient to gain independence through achievement of maximal functional recovery.

a. Promote wound healing diet high in protein, calories, minerals and vitamins b. Prevent or minimize deformities and hypertrophic scarring through physical therapy patient is free from contractures with full extremity flexion and extension. c. Increase strength and function and provide emotional support and education d. Psychological as well as emotional rehabilitation. General Analysis (For patients with alteration in urinary elimination) 1. Safe, effective care environment a. High risk for infection b. Knowledge deficit 2. Physiological integrity a. Pain b. High risk for fluid volume deficit c. Functional incontinence 3. Psychosocial integrity a. Ineffective individual coping b. Altered patterns of sexuality c. Anxiety 4. Health promotion/maintenance a. Impaired adjustment b. Altered health maintenance c. Knowledge deficit General Nursing Planning, Implementation, and Evaluation Goal 1 : Client will be free from infection Implementation 1. Collect necessary urine specimen for culture and sensitivity 2. Teach women properly perineal hygiene 3. Use and teach client good handwashing technique 4. Use strict sterile technique during catheterization procedures 5. Provide daily foley catheter care using proper techniques. 6. Administer antibiotic as ordered for 10-14 days. 7. Increase fluid intake to 3000-5000 ml/day, if not contraindicated by renal or cardiovascular status. 8. Acidify urine through acid-ash diet (e.g. meats, eggs, cheese, fish, fowl, whole grains, plums,prunes) or by administration of methanamine bippurate (Hiprex) or Vit. C if compatible with antibiotic therapy. 9. Teach good oral hygiene techniques. 10. Teach client with chronic kidney infection signs and symptoms of upper respiratory infections (URIs) and importance of seeking early treatment; screen client from staff or significant others with URIs, teach client to avoid exposure to persons with infections (streptococcal infections can lead to glumerulonephritis). 11. Monitor level of potential nephrotoxic agents (i.e. gentamicin, tetracycline, tobramycin) 12. Teach client potentially nephrotoxic agents.

Evaluation Clients is free from dysuria, frequency, fever, and other signs of infection; states procedure for proper perineal hygiene, takes medication as prescribed, has I&O of at least 3000-5000/day; lists signs

and symptoms of URI and need for early treatment, states potentially nephrotoxic agents to avoid in the future. Goal 2 : Client will be free from discomfort Implementation 1. Administer sitz bath to decrease urethral burning. 2. Administer phenazopyridine hydrochloride (pyridium) or a urinary antispasmodics if ordered. 3. Apply hot water bottle or heating pad suprapubic region. Evaluation Client is free from pain discomfort reports no burning with urination. Goal 3 : Clients normal urinary function will be maintained. Implementation 1. Measure urine output accurately 2. Collect urine specimens for routine urinalysis. 3. Encourage adequate fluid intake. 4. Observe for early signs of renal failure. Evaluation Clients urine output remains equal to greater than 30ml/hr, client remains free from symptoms of renal failure. Goal 4 : Client and significant others will receive emotional support Implementation 1. Provide encouragement when client becomes frustrated with treatment and progression of illness. 2. Explain cause of disease and treatment to client and significant others to (SO) as necessary. 3. Allow client and significant others to express fears, feelings and questions. 4. Encourage discussion of diagnosis and ways to cope with problems (e.g. group session for families). 5. Prepare client for possibility of hemodialysis or peritoneal dialysis. 6. Refer to social service or pastoral care as needed. Evaluation Clients and SO state necessity of treatment show increasing acceptance of diagnosis and treatment work through feelings and fears, discuss altered body image; and have plans to alter lifestyle.

NCM 103-A Research

Submitted by: Kerwin Ian S. Mempin Submitted to: Mrs. Teresita Ong