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Provider and Manager of Care: Acute Care Case Study

Admission Summary

R.B., a 69-year old Caucasian male, came to the Emergency Department on January 31st with difficulty urinating and an increased amount of hematuria with painful urination. The patient stated, “I have been noticing for the past few days a decrease in urine output with a lot of blood and clots”. He also complained of pain rating 3/10 to the middle back. The patient continued to state “I have gained so much weight over the past week my rings do not fit”. When asked the amount weight he gained he was unable to inform the health care team. Current weight on admission was 163lbs at 66”. Bilateral edema was noted to the lower extremities with +1 pitting edema. His vital signs on admission were 115/80-67-24-95%RA-98.6. His heart rate was regular and bilateral breath sounds were clear; no respiratory distress was noted

Upon admission, R.B.’s lab results showed highly elevated blood urea nitrogen (BUN) and creatinine (CREA) levels. His red blood cell (RBC), hemoglobin (HgB), and hematocrit (HCT) were decreased. A urinalysis showed positive for nitrite and esterase (indicating a urinary tract infection) with a presence of protein and RBC. The urine had dark red appearance and arterial blood gases (ABGs) showed metabolic acidosis. A Computed tomography (CT) of the abdomen showed a significant impression (see medical management). He was then admitted to the hospital for additional treatment.

Primary Diagnosis and Priority Secondary Diagnosis

The primary medical diagnosis is acute post renal failure (ARF), with a secondary diagnosis of bladder cancer (anaplastic small cell).

Patient History

R.B. has a medical history of benign prostatic hyperplasia (BPH). His surgical history includes cystoscopy with biopsy of the bladder that revealed deeply infiltrative bladder cancer (2009). The patient smoked cigarettes for 20 years and quit 10 years ago.

PATHOPHYSIOLOGY OF THE PRIMARY DIAGNOSIS AND PRIORITY SECONDARY DIAGNOSIS

The pathophysiology of acute renal failure (AFR) is the sudden inability of the kidneys to maintain normal function. This inability affects most of the body’s systems because of the kidney’s important role in maintaining fluid balance, regulating electrolytes, providing constant protection against acid-base imbalances, and controlling blood pressure (Gutierrez & Peterson, 2002). As blood flows through the kidneys, it is filtered, and wastes are removed and sent to the bladder as urine. If kidney function becomes impaired, acute (rapid) or chronic (gradually developing) renal failure may occur. With acute renal failure, kidney function can return to normal if the underlying cause of the failure is discovered and successfully treated (Parmet, 2006).

The etiologies of acute renal failure are generally classified into three major areas: prerenal failure is associated with poor systemic perfusion and decreased renal blood flow to the kidneys. It is the most common cause of renal failure. Prerenal failure can result from severe hypotension or hypovolemia. Cardiac disease or heart failure also can reduce renal blood flow. Decreased blood flow to the kidneys leads to ischemia in the nephrons and prolonged hypoperfusion can lead to tubular necrosis and ARF (Ignatavicius & Workman, 2006).

Intrarenal failure etiology is associated with renal ischemia or toxins. It deals with the failure of the functional components of the kidney that can be damaged directly from nephrotoxic drugs, direct injury, or contrast dye. Actual tissue damage to the kidney caused by inflammatory or immunologic processes or from prolonged hypoperfusion (Ignatavicius & Workman, 2006).

Postrenal failure is the least common renal failure. The etiology is associated with the obstruction of urine flow out of the kidneys. The obstruction results in the backup of urine into the pelvis and functional compartments of the kidneys. This results in damage to the renal structure. Urethral or bladder cancer and renal, ureteral, and bladder stones can obstruct the flow of urine out of the kidneys. Obstruction of the bladder must be bilateral to cause postrenal failure unless only one kidney is functional. BPH or prostate cancer and urethral stricture can impede the flow of urine. Obstruction of the urine collecting system involves anywhere from the calyces to the urethral meatus (Ignatavicius & Workman, 2006).

Patients with postrenal failure may have renal manifestations that include oliguria (decreased urine output) or intermittent anuria (no urine output), and increase urine specific gravity. Cardiac manifestations include hypertension, tachycardia, and jugular vein distention and EKG changes: tall T waves. Respiratory manifestations include shortness of breath, orthopnea, rales or crackles, pulmonary edema, and friction rub. Gastrointestinal manifestations include anorexia, nausea, vomiting, and flank pain. Neurological manifestations include lethargy, headache, tremors, and confusion. General manifestations are generalized edema and weight gain (Ignatavicius & Workman, 2006).

The pathophysiology of bladder cancer is often used to describe urothelial cancers, a malignant type of tumor. Urothelium is the lining found in the kidney, renal pelvis, ureters, urinary bladder, and urethra. Most urothelial cancers occur in the bladder. The growth of urothelium cells is well controlled, ensuring that only the right number of cells is always present in the excretion system. Normal cell replication is needed to repair or replace tissue. In bladder cancer, an altered growth of urothelium cells invades the surrounding tissue. These extra cells grow together to form masses called tumors. These tumors can cause obstructions with urination resulting in the back up of urine into the kidneys. This is the primary cause of post ARF. Once the cancer spreads beyond the cell layer, they are highly invasive and metastatic. If untreated, the tumor continues to invade surrounding tissues and spreads to distant sites, ultimately leading to death (Ignatavicius & Workman, 2006).

The greatest known etiology for bladder cancer is tobacco use. Also, exposure to certain toxins used in hairdressing, rubber, paint, electric cable, and textile industries increase the risk of bladder cancer. Other risks include Schistosoma haematobium (a parasite) infection, excessive use of drugs containing phenacetin, and long-term use of cyclophosphamide. This cancer is most common after 60 years of age (Ignatavicius & Workman, 2006).

Hematuria is the most common sign/symptom associated with bladder cancer. Other physical manifestations include dysuria, frequency, and urgency (American Cancer Society, n.d.). Also, changes in the color and the amount of urine may occur with bladder cancer. Patients may complain of abdominal discomfort and tenderness with noted bladder distention (Ignatavicius & Workman, 2006).

The large tumor in the bladder resulted in the obstruction of urine to leave the bladder causing post ARF. The inability to void urine resulted in the urine to back up into the kidneys resulting in damage. The clinical picture of R.B.’s complaints of lower back pain, difficulty with urination, decreased urine output, increase in weight gain, and hematuria show a relationship of post ARF with bladder cancer.

ACTUAL OR POTENTIAL IMPACT OF RELEVANT MEDICAL/SURGICAL HISTORY ON THE PRIMARY DIAGNOSIS AND PRIORITY SECONDARY DIAGNOSIS

R.B.’s history of BPH has a potential impact to the primary diagnosis of post ARF. BPH is an enlargement of the prostate gland and as the prostate continues to enlarge over time, it obstructs the urethra. Symptoms of BPH include reduced or interrupted urinary flow, inability to empty the bladder, and increased frequency of urination (Gutierrez & Peterson, 2002). BPH can lead to secondary obstructions causing further episodes of post ARF.

BPH could have a potential impact on bladder cancer by chronic bladder irritation. BPH causes urinary retention that irritates the urinary tract system. However, there is a potential impact with urinary infections, kidney and bladder stones. Bladder irritation has been linked with bladder cancer, but does not necessarily cause bladder cancer (American Cancer Society, n.d.).

R.B.’s history of smoking has a potential impact to post ARF in that smoking can irritate the urinary tract system. This irritation in the ureters could lead to scar tissue resulting in the reflux of urine into the kidneys leading to post ARF. Tobacco use for 20 years is an actual impact between the secondary diagnosis of bladder cancer. Smokers are more than twice as likely to get bladder cancer as nonsmokers. Smoking causes about half the deaths from bladder cancer among men. The chemicals from tobacco smoke damage the cells that line the inside of the bladder resulting in cellular changes increasing the risk of bladder cancer (American Cancer Society, n.d.).

The relationship between the primary diagnosis of post ARF and secondary diagnosis of bladder cancer involves the reflux of urine. Urine can irritate the bladder and ureters causing inflammation and scar tissue to form. R.B.’s history of BPH and smoking could lead to further irritation and scar tissue to form increasing the risk of post ARF.

MEDICAL MANAGEMENT: ARF

The primary goal of post ARF is to prevent further renal damage and support the kidneys as they heal. Recommended textbook medical interventions for post ARF includes dietary/activity interventions and lab/diagnostic testing. The proper medical management can reverse the damages caused to the kidneys.

Diet restrictions consist of a high-calorie, low-protein diet with restrictions in sodium and potassium intake. The amount of fluid permitted is generally calculated to equal the urine volume plus 500 mL. Restrictions to activity include bed rest to reduce the further breakdown of protein. These restrictions are necessary in post ARF to prevent further complication to the kidneys (Ignatavicius & Workman, 2006).

There are several changes in laboratory values in the patient with post ARF. Expect to see rising BUN, CREA, and abnormal electrolytes values. Patients with ARF, however, do not have the anemia associated with chronic renal failure unless there is hemorrhagic blood loss. However, uremic hemolysis can develop and may be the cause of anemia in the early phase of ARF. Urinalysis in AFR show concentrated specific gravity and presence of urine sediment and hemoglobin. In postrenal failure urine, sodium levels and specific gravity may be near normal (Ignatavicius & Workman, 2006).

Diagnostic testing for post ARF includes abdomen x-rays to show possible obstructions such as stones in the renal pelvis, ureters, or bladder. Computed tomography (CT) scans without contrast dye can identify obstructions or tumors. Ultrasonography is used to determine kidney size and the patency of the ureters. Renal biopsy may be performed if the cause of ARF is uncertain or immunologic disease is suspected (Ignatavicius & Workman, 2006).

On admission, dietary and activity interventions for R.B. included a 40-gram low-protein diet and a high calorie intake of 3000. Sodium restriction of 3-grams and potassium restriction of 60 mEq with a strict fluid restriction of 1500 mL/day was implemented. Actual medical managements implemented for R.B included daily lab draws. On admission to the ER a complete blood count (CBC) showed decreased levels of hemoglobin (HgB) 7.0 (n= 14-18), red blood cells (RBC) 2.86 (n=4.7-6.1), and hematocrit (HCT) 26.3% (n=42%-52%). Renal function tests revealed highly elevated BUN of 83 (n=10-20) and CREA level at 6.8 (n=0.6-1.2). Atrial blood gases (ABGs) were drawn and reflected metabolic acidosis with a pH of 7.33 (n = 7.35 –7.45), PaCO2 of 35 (n = 45 –35), and HCO3 of 20 (n = 22-26). (No further ABGs were drawn). Electrolyte panel reflected elevated sodium (Na) level of 158 (n=136-145) and potassium (K) level of 5.6 (n=3.5-5.0). A urinalysis show positive for a urinary tract infection (n=negative). The presence of protein (n=absent), RBC (n=absent), and dark red appearance (n=yellow/clear). Upon discharge, the patient’s lab values reflected normal ranges in the CBC, BUN/CREA, and K and Na levels. A negative urinalysis was also obtained with yellow/clear urine.

Diagnostic tests for R.B. included an abdominal CT that revealed evidence of bilateral hydronephrosis with bilateral ureters obstructed distally. Also, a large tumor was noted in the bladder. Upon discharge, R.B. was scheduled to follow up with an urologist and oncologist for further outpatient treatment for bladder cancer.

NURSING MANAGEMENT: ARF

Recommended textbook interventions for post ARF include daily weighing and assessing weight changes. Excessive fluid accumulation can result in weight gain. The nurse management includes assessing and monitoring lab values when ordered and reporting significant values to the physician. Proper recording and monitoring of fluid intake and urine output every shift. Assess location and extent of edema if present on the patient; evaluating mucous membranes and skin turgor for signs of dehydration every shift. Checking and recording of vital signs, particularly blood pressure for elevations every four hours. Teaching the patient about dietary restrictions of sodium, protein, and potassium. Educating the patient the pathophysiology and sign/symptoms of post ARF (Ignatavicius & Workman, 2006).

R.B.’s physical assessment showed blood pressure ranges of 127/85 – 115/80, heart rate 61-89, and temperature 98.6-98 degrees. RB appeared well nourished and of appropriate weight with no physical impairments. RB had a significant weight gain prior to admission with pitting edema in the lower extremities that was noted throughout admission. The patient’s weight ranged between 163-169 pounds throughout admission.

RB’s vital signs were assessed every six hours while his intake and output was monitored and recorded every shift. Urinary output from admission to Feburary 10th was <475mL/day with an intake of 1800-2000mL/day. Surgery for bilateral nephrotomy tubes was schedule for February 9th (see surgical management). The bilateral nephrostomy bags were emptied and recorded as needed. The nephrostomy tubes were irrigated with five mL of normal saline every shift to remain patent. Lab values were monitored with daily lab draws and daily reports of elevated BUN/CREA were informed to the physician. Mucous membranes and skin turgor for signs of dehydration were monitored every shift

R.B. was taught about the signs and symptoms of ARF, and when to contact the doctor. He was educated on the importance of keeping a record of his daily weight and intake/urinary output. He was instructed to continue a low protein, sodium, potassium diet at home. He was educated on how to care for the nephrostomy tubes/bags. Before discharge, he verbalized/demonstrated understanding of the teachings implemented.

PHARMACOLOGICAL MANAGEMENT: ARF

The textbook recommends the fluid challenges and diuretics such as Lasix to promote renal blood flow. If oliguric renal failure is diagnosed, the fluid challenges and diuretics are discontinued. Low-dose dopamine may be given to enhance renal blood flow and to increase blood pressure. Calcium channel blockers may be used to treat ARF resulting from nephrotoxic acute tubular necrosis (ATN). These drugs prevent the influx of calcium into the kidney cells, maintain kidney cell integrity, and improve the glomerularalr filtration rate (GFR) by improving renal blood flow (Ignatavicius & Workman, 2006).

Actual pharmacological interventions for RB included Lasix, a loop diuretic to increase urinary output. Lasix40mg IV push was given after the bilateral nephrostomy tubes procedure for three days then was changed to 80mg tablets twice daily. Lasix (with nephrostomy tubes) improved drainage output to 1800-2000mL/day. Ciprofloxacin 400mg IV, a broad-spectrum anti-infective, was given every 12hr x 3 days to correct the urinary tract infection. A repeated urinalysis was negative for nitrite and esterase.

SURGICAL MANAGEMENT: ARF

The recommended textbook surgical intervention for post ARF involves the primary goal of removing the obstruction. Depending on the cause of the obstruction determines to procedure to be performed. For example, BPH is corrected by a transurethral resection of the prostate (TURP). It involves the surgeon inserting a resectoscope (an instrument similar to a cystoscope, but with a cutting and cauterizing loop) into the urethra. The enlarged portion of the prostate gland is the resected in small pieces. This alleviates the obstructed urethra and restores the flow of urine. Kidney stones unable to pass through the urinary tract result in the surgical management procedure of lithotripsy. This procedure breaks the stone using sound, laser, or dry shock waves to break up the stone allow the normal flow of urine to take place. Stents may be used for ureters that have become obstructed by tumors; this method ensures the drainage of urine. Certain stents such as a double J stent are placed in the proximal end of the kidney down the ureter to the bladder for patency. This stops the reflux of urine into the kidneys (Ignatavicius & Workman, 2006).

On February 5th, R.B.’s actual surgical management included a TURP with fulguration and evacuation of clots. A fulguration is the destruction of living tissue with an electric spark. This was done to resolve the urinary obstructions. At that time, a cystoscopy (visual examination of the bladder) was done to look for abnormalities. A tumor was noted and biopsied resulting in the diagnosis of anaplastic small cell bladder cancer.

Urinary output did not return after the TURP was performed related to the bladder cancer. On February 9th, a bilateral nephrostomy tube procedure with bilateral double J-stents was done to drain urine. This was to restore kidney function and prevent further damage to the kidneys. Bilateral nephrostomy involves creating an opening into the kidney to maintain temporary or permanent urinary drainage. At discharge, the nephrostomy tubes were left in place to allow the flow of urine. Intake and urine output difference were <500mL.

PROVIDER AND MANAGER ROLE: NURISNG CARE PLAN

Priority Nursing Diagnosis

“P” Impaired urinary Elimination

“R” Decrease in urine output related to bladder obstruction

“C” 1. Infrequent urination (voiding less then every 6 hours).

2. Inability to urinate.

3. Dysuria.

Priority Patient Goal

The patient will demonstrate increase in urine output by discharge as evidence by:

Urination every 6 hours with no post voiding residual volume.

Void clear/yellow urine >150cc per void.

State and absence in pain with urination.

Three Priority Nursing Interventions

The nurse will monitor/report/record bladder scan volumes after voiding to assess post residual volumes.

Assess/encourage urinary elimination every two hours, noting pain.

Educate patient to monitor urine output with each void including color/consistence.

Evaluation of Progress toward Patient Goal

The goal of impaired urinary elimination was not met. R.B. continued to have infrequent urination, moderate hematuria, and dysuria. A TURP procedure was performed to allow the flow of urine and was unsuccessful. Further treatment included bilateral nephrostomy tubes. R.B. was discharged with nephrostomy tubes and continued being unable to void. Appointments were scheduled with an oncologist and urologist upon discharge for further treatment.

PROVIDER AND MANAGER ROLE

Provider of Care Role

As provider of care, I selected priority-nursing diagnoses based on analysis of assessment data in caring for R.B. I collaborated with the patient, family, and health team members to meet the client’s needs. I identified significant information with lab values and patient findings and notified the appropriate physician. I developed teaching plans based on R.B.’s learning abilities so he could be discharged with nephrostomy tubes. I administered Lasix and ciprofloxacin with minimal supervision and implemented physician orders with supervision of my preceptor.

Member of the Discipline and the Role of the Multi-Disciplinary Team

The multidisciplinary team that cared for R.B. included pharmacy supplying the correct dose of each medication. The charting secretary inputted orders correctly into the computer. The dietician consulted with the patient to ensure that his nutritional needs and restrictions related to ARF were met. Housekeeping kept the room clean and presentably. The physicians had the responsibility of determining medications/treatments for R.B.’s diagnosis. As the RN, I was responsible for assessing the patient and implementing the plan of care.

Manager of Care Role

As a Manager of Care, I establish priority of care based on my patient’s condition. I demonstrated this by looking at labs, doctors’ orders, and receiving morning report. I also made sure that any issues or concerns regarding my patient’s condition were addressed properly. Abnormal assessments were dealt with accordingly by communicating with the physicians. As an RN, I delegated to the nursing aid to provide morning care while I worked with the LPN to administer oral medications on time.

Growth in the Manager of Care Role

I have learned that to better understand the diagnosis of a patient; I need to focus on their past medical history to see a clearer patient picture. The importance of the labs, procedures, medications, and doctors’ orders need to be followed to ensure the best health for the patient. Communicating with RNs during shift change and members of the health care team allows for accurate/safe medical care.

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