Chapter 37
Nursing Care of Patients With Disorders of the Urinary System
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Etiology AKI is often classified as prerenal, intrarenal, or postrenal. These categories relate to the causes leading to the injury. Each category is associated with the location of the cause in the kidney. Understanding the cause can point to the direc- tion of treatment plans helpful to the patient. PRERENAL INJURY. Prerenal (before the kidney) injury, the most common cause of AKI, occurs when a decrease or interruption of blood supply to the kidneys impairs filtration. This may be due to decreased blood pressure from dehydra- tion, surgery, blood loss, shock, or trauma to or blockage in the arteries that carry blood to the kidneys. Use of NSAIDs and cyclooxygenase-2 (COX) inhibitors can also lead to prerenal injury. They impair the autoregulatory responses of the kidney by blocking prostaglandin, necessary for renal perfusion. Prerenal injury is diagnosed by evaluating possible causes. To determine if dehydration is the cause, an IV fluid chal- lenge can be given. With increased IV fluid, more blood vol- ume flows to the kidneys, which increases urine output and waste product filtering. An arteriogram of the renal arteries determines if the blood supply to the kidneys is decreased or blocked; angioplasty may then be used to open the blockage. INTRARENAL INJURY. Intrarenal (inside the kidney) injury occurs with damage to the nephrons inside the kidney. The most common causes are ischemia, toxins, and reduced blood flow that lead to acute tubular necrosis (tubular cells die). Other causes are infections leading to glomerulonephritis, trauma to the kidney, exposure to nephrotoxins , reactions to contrast agents or medications (causing acute interstitial nephritis), and severe muscle injury, which releases sub- stances that harm the kidneys. A number of substances can be toxic to the kidneys (nephrotoxic) when they enter the body (Table 37.5). Kidney damage is most likely to occur when these substances enter the body in high concentrations or when pre-existing kidney damage is present for some other reason. Many commonly administered medications can be nephrotoxic. For example, aminoglycosides are nephrotoxic antibiotics; when they are administered, peaks and troughs of the drugs are carefully monitored to avoid toxic levels. POSTRENAL INJURY. Postrenal (after the kidney) injury is associated with an obstruction that blocks the flow of urine out of the body. Only 5% of AKIs are classified as postre- nal. The blood supply to the kidneys and nephron function may be normal, but urine cannot drain out of the kidney. This results in the backup of urine and impaired nephron function. Common causes are kidney stones, tumors of the ureters or bladder, and an enlarged prostate that blocks the flow of urine. Surgical intervention may be needed to correct the problem.
• Chemicals, such as arsenic, carbon tetrachloride, lead, and mercuric chloride • NSAIDs such as aspirin, ibuprofen, and naproxen, which can be harmful to the kidneys Protective Measures Including the Following • Before administering nephrotoxic contrast media or med- ications, check serum GFR and serum creatinine levels and report abnormalities to the HCP. • With contrast media tests, ensure patients are not dehy- drated. For at-risk patients (decreased GFR with or without diabetes or comorbidities), hydrate with IV fluids before and after the test. Avoid NSAIDs. • Ensure peak/trough levels of nephrotoxic medications are monitored per institutional policy. INITIATING PHASE. In this onset phase, an event occurs that causes AKI. It begins at the time of renal injury and lasts until the occurrence of symptoms. This phase lasts for hours to days. OLIGURIC PHASE. In the oliguric phase, less than 400 mL of urine is produced in 24 hours. Fifty percent of those with AKI experience this phase, which occurs from 24 hours to 7 days after the initial phase and can last 2 weeks to sev- eral months. Renal function recovery decreases as the phase continues. In the oliguric phase, fluid is retained, electrolytes become imbalanced, and waste products are not excreted as urine out- put decreases. Signs of fluid volume overload occur. Serum potassium rises while sodium is lost in the urine, creating normal or low serum sodium level. The longer the phase lasts, the more symptoms increase, including metabolic acidosis from reduced hydrogen ion excretion and sodium bicarbon- ate levels, increased phosphate and decreased calcium levels, abnormal blood cells (RBCs, WBCs, platelets), neurologic effects such as confusion, seizures, and coma, and effects on all body systems as is seen in CKD (discussed later). DIURETIC PHASE. As the kidneys begin to excrete waste prod- ucts again, 1 to 3 L/day of urine is produced. Osmotic diure- sis occurs from the elevated waste products (urea), which the body is attempting to eliminate. The kidneys are not yet able to concentrate urine, so dehydration and hypotension are a concern. It is important to monitor for hypovolemia, hypona- tremia, hypokalemia, and hypotension in this phase. Serum BUN and serum creatinine levels are high until the end of this phase. This phase may last 1 to 3 weeks. RECOVERY PHASE. In this final phase, recovery begins as the GFR rises. Serum waste product levels (BUN, creati- nine) decrease greatly within the first 2 weeks of this phase. This phase can last up to a year. Those who recover usually do so without complications. Older adults are more at risk for reduced recovery of renal function. In those who do not recover their renal function, CKD occurs.
• WORD • BUILDING • nephrotoxin: nephro—kidney + toxin—poison
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