Acute tubular necrosis (also called acute tubulointerstitial
nephritis) causes 75% of all cases of AKI. This disorder destroys
the tubular segment of the nephron, causing renal failure and uremia (excess by-products of protein metabolism in the blood). Because acute tubular necrosis is fatal in 40% to 70% of cases, prevention, prompt recognition, and intervention by the critical care nurse are vital. What causes it Acute tubular necrosis may follow two types of kidney injury: Ischemic injury, the most common cause, interrupts blood flow to the kidneys. The longer the blood flow is interrupted, the worse the kidney damage. Nephrotoxic injury usually affects debilitated patients, such as the critically ill and those who have undergone extensive surgery. Blood disruption In ischemic injury, blood flow to the kidneys may be disrupted by: circulatory collapse severe hypotension meet the team Because acute kidney injury affects multiple body systems, a multidisciplinary approach to care is needed, with the critical care nurse coordinating care. Heres how other members of the multidisciplinary team contribute to your patients care: A nephrologist can evaluate and manage the patients kidney function. A respiratory or cardiology specialist may be involved to deal with complications. A nutritional therapist may recommend restrictions or supplements. A physical or occupational therapist may help the patient with energy conservation and rehabilitation. A pharmacist can assist with medication dosing. If a prolonged hospital stay is expected and the patient requires long-term care or home care, social services should be consulted early in the patients care. The patient and his family may benefit from spiritual counseling. Go team! You need to coordinate care for a patient with acute kidney injury trauma hemorrhage dehydration cardiogenic or septic shock surgery anesthetics transfusion reactions. Toxic talk Nephrotoxic injury can result from: ingesting or inhaling toxic chemicals, such as carbon tetrachloride, heavy metals, and methoxyflurane anesthetics a hypersensitivity reaction of the kidneys to such substances as antibiotics and radiographic contrast agents. Cause and effect Some specific causes of acute tubular necrosis and their effects include: a diseased tubular epithelium that allows glomerular filtrate to leak through the membranes and be resorbed into the blood obstructed urine flow from the collection of damaged cells, casts, RBCs, and other cellular debris in the tubules ischemic injury to glomerular epithelial cells, causing cellular collapse and poor glomerular capillary permeability ischemic injury to the vascular endothelium, eventually causing cellular swelling and tubular obstruction. how it happens Deep or shallow lesions may occur in acute tubular necrosis. Lesion lesson With ischemic injury, necrosis creates deep lesions, destroying the tubular epithelium and basement membrane (the delicate layer underlying the epithelium). Ischemic injury causes patches of necrosis in the tubules. Ischemia can also cause lesions in the connective tissue of the kidney. With nephrotoxic injury, necrosis occurs only in the epithelium of the tubules, leaving the basement membrane of the nephrons intact. This type of damage may be reversible. (See A close look at acute tubular necrosis, page 546.) Nephrotoxic injury can result from ingesting or inhaling toxic Toll-taking Toxicity takes a toll on renal structures. Nephrotoxic agents can injure tubular cells by: direct cellular toxic effects coagulation and destruction (lysis) of RBCs oxygen deprivation (hypoxia) crystal formation of solutes. Getting complicated There are several common complications of acute tubular necrosis: Infections (frequently septicemia) complicate up to 70% of all cases and are the leading cause of death. GI hemorrhage, fluid and electrolyte imbalance, and cardiovascular dysfunction may occur during the acute or recovery phase. a close look at acute tubulaS necSosis In acute tubular necrosis caused by ischemia, patches of necrosis occur, usually in the straight portions of the proximal tubules. In areas without lesions, tubules are usually dilated. In acute tubular necrosis caused by nephrotoxicity, the tubules have a more uniform appearance. Neurologic complications are common in elderly patients and occur occasionally in younger patients. Excess blood calcium (hypercalcemia) may occur during the recovery phase. What to look foS Early-stage acute tubular necrosis may be hard to spot because the patients primary disease may obscure the signs and symptoms. The first recognizable sign may be decreased urine output, usually less than 400 mL/24 hours. Difficult to detect Acute tubular necrosis is difficult to detect in its early stages, so look closely at members of high-risk populations, such as elderly patients or those with diabetes, and be alert for subtle signs and symptoms during your nursing assessments. Other signs and symptoms depend on the severity of systemic involvement and may include: bleeding abnormalities vomiting of blood dry skin and mucous membranes lethargy confusion agitation edema fluid and electrolyte imbalances muscle weakness with hyperkalemia cardiac arrhythmias. Mortality can be as high as 70%, depending on complications from underlying diseases. The patient with a nonoliguric form of acute tubular necrosis has a better prognosis. What tests tell you Acute tubular necrosis is difficult to diagnose except in advanced stages. The following tests are commonly performed: Urinalysis shows dilute urine, low osmolality, high sodium levels, and urine sediment containing RBCs and casts. Blood studies reveal high BUN and serum creatinine levels, low serum protein levels, anemia, platelet adherence defects, metabolic acidosis, and hyperkalemia. ECG may show arrhythmias from electrolyte imbalances and, with hyperkalemia, a widening QRS complex, disappearing P waves, and tall, peaked T waves. Acute tubular necrosis is difficult to detect in its early stages, so look closely at patients who are members of high-risk groups, such as elderly how its tSeated The patient with acute tubular necrosis requires vigorous supportive measures during the acute phase until normal kidney function is restored. Therapy may include: diuretics and fluids to flush tubules of cellular casts and debris and to replace lost fluids (initially) emergency I.V. infusion of 50% glucose, regular insulin, and sodium bicarbonate in case of hyperkalemia sodium polystyrene sulfonates given by mouth or by enema to reduce potassium levels calcium channel blockers and prostaglandins, which may aid in treating nephrotoxic acute tubular necrosis. Furthermore Treatment for the patient with acute tubular necrosis may also include: daily replacement of projected and calculated fluid losses transfusion of packed RBCs for anemia non-nephrotoxic antibiotics for infection hemodialysis or peritoneal dialysis to prevent severe fluid and electrolyte imbalance and uremia. What to do Take steps to maintain the patients fluid balance. Accurately record intake and output, including wound drainage, NG tube output, and hemodialysis or peritoneal dialysis balances. Weigh the patient daily. Assist with insertion of a central venous or PA catheter to monitor fluid status. Monitor hemodynamic parameters as indicated. Watch the patient for fluid overload, a common complication when infusing large fluid volumes. Monitor Hb levels and HCT, and administer blood products, as needed. Use fresh packed cells instead of whole blood to prevent fluid overload and heart failure. Maintain electrolyte balance. Monitor laboratory results and report imbalances. Monitor the patients vital signs, oxygen saturation, cardiac rhythm, and cardiopulmonary status. Treat hypotension immediately to avoid renal ischemia. Monitor vital signs closely. Fever and chills may signal the onset of an infection, which is the leading cause of death in acute tubular necrosis. (See Temperature regulation in elderly patients.) Check for potassium content in prescribed drugs (for example, potassium penicillin). Provide dietary restriction of foods All this talk about vigorous treatment has tired me out! Watch out for fluid overload! Its a common complication when infusing large fluid containing sodium and potassium, such as bananas, orange juice, and baked potatoes. Provide adequate calories and essential amino acids while restricting protein intake to maintain an anabolic state. Total parenteral nutrition may be indicated for a critically ill and debilitated or catabolic patient. Use sterile technique, especially when handling catheters, because the critically ill or debilitated patient is vulnerable to infection. Administer sodium bicarbonate, as ordered, for acidosis or assist with dialysis in severe cases. Provide the patient with reassurance and emotional support. Encourage him and his family to verbalize their concerns. Fully explain each procedure. To prevent acute tubular necrosis, make sure the patient is well hydrated before surgery or after X-rays requiring use of a contrast medium. Administer mannitol, as ordered, to the high-risk critically ill patient before and during these procedures. Administer nephrotoxic drugs cautiously and avoid using contrast dyes in the high-risk patient.