Papillary Necrosis Treatment & Management
- Author: Christopher Powell, MD; Chief Editor: Bradley Fields Schwartz, DO, FACS more...
Because ischemia is such a prominent underlying factor in the development of renal papillary necrosis, promptly resuscitate patients and treat their hypoxia, if present. In addition, patients with acute disease may require broad-spectrum intravenous antibiotics, hydration, glycemic control, and urinary alkalinization. Cessation of analgesic abuse stabilizes and may improve renal function.
In patients without acute ureteral obstruction, treat the infectious and metabolic complications of renal papillary necrosis by replacing insensible losses, maintaining hydration, alkalinizing the urine, and administering antibiotics directed toward the pathogen (as revealed by culture or Gram stain and by observing for the development of obstruction or sepsis). Patients with hematuria significant enough to cause an acute drop in their hematocrit level may require blood transfusions. Patients with sickle cell disease may require exchange transfusions, and patients with diabetes who have acute infectious complications and refractory hyperglycemia may require insulin therapy. Basically, ameliorate the ischemia with hydration and alkalinization, treat the underlying cause of the renal papillary necrosis (eg, maintain normal glycemic state), and institute targeted antibiotic therapy.
Patients with renal papillary necrosis may require diagnostic and therapeutic urologic intervention. The urologist is responsible for evaluating any obstruction, hematuria, overwhelming infection, and associated malignancies and for preventing recurrences of these sequelae.
Acute obstruction with concomitant urinary tract infection is a urologic emergency that requires immediate percutaneous nephrostomy to relieve the obstruction, ureteral stent placement, or endoscopic retrieval of the obstructing sloughed papillae. Endoscopic retrieval is not recommended unless the offending papillae are crowning or extruding from the ureteral orifice; even then, the procedure is challenging. Retrograde pyelography and ureteroscopy are useful diagnostic tools, but consider these only when the patient is afebrile and after intravenous administration of antibiotics. Otherwise, a ureteral stent would suffice, delaying retrograde instrumentation until the patient is afebrile.
The recommended treatment is to drain the dilated collecting system either endoscopically or percutaneously. In patients with severe disease who are febrile and have smoldering sepsis, percutaneous nephrostomy is preferred because it does not require general anesthesia and carries a smaller risk of pyelovenous reflux and worsening sepsis. Cystoscopy and ureteral stent placement allow cystoscopic surveillance of the bladder, which is necessary if hematuria is the presenting symptom. However, in a patient with hydronephrosis, high fever, leukocytosis, and overt sepsis, the preferred treatment is to percutaneously drain the kidney. Perform diagnostic cystoscopy and RPGs (if necessary) later, when the patient's situation is not so dire.
Nephrectomy may be life-saving in patients with overwhelming infection (ie, emphysematous pyelonephritis). Consider that papillary necrosis is primarily a bilateral disease, and these patients must be informed that this may result in progressive renal failure and possible dialysis dependency in the future.
In selected patients, ureteroscopic investigation of a ureteral filling defect may be warranted. A basket catheter can be introduced through the ureteroscope to extract the offending sloughed papilla. This is performed only in afebrile patients, after broad-spectrum intravenous antibiotics have been administered.
Patients who present with hematuria, even if all the diagnostic interventions indicate papillary necrosis, require a full urologic workup for their hematuria. A thorough evaluation of the urinary tract, as outlined in Lab Studies, limits the differential diagnoses of hematuria, excluding other possible causes. Attribute the hematuria to papillary necrosis only after performing the studies listed in Lab Studies and deeming the results negative.
Keep in mind that, if the patient's system is acutely obstructed with possible pyonephrosis, retrograde studies such as RPG and ureteroscopy are contraindicated because they are likely to cause or exacerbate sepsis from pyelovenous reflux of purulent material from the lower urinary tract. If this clinical scenario occurs, decompress the system with either a double-J ureteral stent or, preferably, a nephrostomy tube. Send any urine or pus obtained from these procedures for microscopic analysis, Gram stain, and culture. After proper decompression, administer systemic antibiotics with empiric coverage until the Gram stain and culture results are received. Once the patient responds systemically, with stable hemodynamics, no fever, no acidosis, and no leukocytosis, the urologist can proceed with the diagnostic workup.
If the infection rages and the patient does not improve despite supportive measures and proper antibiotic coverage, a nephrectomy may be life-saving. However, remember that the disease is usually bilateral.
Surgery may be indicated for associated anatomic anomalies that predispose patients to urinary stasis and recurrent urinary tract infections. Treatable conditions include calculi, ureteropelvic junction obstruction, vesicoureteral reflux, ureteral strictures, and ureteroceles.
If transitional cell carcinoma of the collecting system is identified, thoroughly evaluate the patient for metastatic disease. If metastases are not found, the proper treatment for presumed invasive transitional cell carcinoma of the upper urinary tract is radical nephroureterectomy, removing the entire transmural ureter and a cuff of bladder mucosa. Recently, some physicians are resecting and staging tumors endoscopically and are treating selected patients more conservatively (ie, surveillance, if the tumor does not invade the muscle layer). Nevertheless, nephroureterectomy remains the criterion standard.
Give the patient intravenous hydration and withhold food for 8 hours. Obtain informed consent; the patient must be aware that ureteroscopy and ureteral stent placement are possibilities.
Ensure that the patient has medical clearance to undergo a procedure that requires general anesthesia.
Common complications after any instrumentation of the ureter include infection, extravasation and urinoma formation, bleeding, ureteral stricture, and urosepsis due to pyelovenous backflow. Persistent postoperative fever or failure to thrive may be harbingers of the complications listed above.
Ensure that patients clearly understand that, if they require an indwelling ureteral stent, these devices are associated with a host of unique complications.
Proper follow-up includes a visit with a general practitioner to prevent further exacerbations and to manage any associated conditions. Follow-up may include a referral to specialists, as deemed necessary by the primary care doctor.
Stopping analgesic intake and controlling blood pressure help to preserve renal function, and preventing symptomatic urinary infections with long-term, low-dose medical therapy reduces the morbidity associated with renal papillary necrosis. If analgesic use is indispensable to certain patients, instruct them to hydrate accordingly. Reports indicate that adequate hydration may help prevent lesions in persons who must take analgesics long-term.
Physicians may find prophylactic antibiotics useful for treating patients with obstructed urinary tracts who are not surgical candidates. Patients who receive urinary tract intervention require follow-up evaluations with a urologist, particularly if they require further treatment. In any case, hematuria in these patients requires a complete evaluation by the urologist.
Necrotic papillae represent a fertile environment for the deposition of both infectious organisms and lithogenic sediment. This necrotic deposition can lead to the development of florid pyelonephritis, perirenal abscesses, and sepsis. Calculous formation compounds the necrosis because certain bacteria thrive within the calculi. Calculi can also propagate, which may lead to further obstruction, increased pyelovenous pressure, and worsened ischemia.
Always consider sloughed papillae as a cause of ureteral obstruction in the differential diagnoses of flank pain, colic, and hematuria, especially when no calculi are visible and particularly in patients with diabetes.
The development of transitional cell carcinoma of the renal pelvis or calyces is a serious complication, particularly in patients with papillary necrosis associated with analgesic abuse.
Outcome and Prognosis
The prognosis of renal papillary necrosis depends on the etiology of the ischemic insult, the number of associated pathologic factors, the dispersal of the necrosis, the involvement of one or both kidneys, and the overall health of the patient. Elderly debilitated patients with multiple medical problems have a poor prognosis, as do patients with overwhelming sepsis and multiple comorbidities. The prognosis is generally worse in patients with diabetes, specifically those who are not compliant and who are prone to severe episodes of hyperglycemia because of the systemic nature of their disease.
Considering the synergistic nature of its predisposing factors, papillary necrosis may be avoided by controlling chronic diseases such as sickle cell disease, diabetes, and cirrhosis. Patients with such conditions should be careful to avoid excessive use of analgesics that are known to be associated with papillary necrosis. Patients who use such analgesics should be screened for signs and symptoms of urinary tract infections and/or urinary obstruction and treated accordingly. When papillary necrosis arises unexpectedly (ie, in a patient with sepsis), the treatment focus should be to prevent urinary tract infections (eg, by avoiding unnecessary use of indwelling catheters), to maintain adequate hydration and homeostasis, to avoid analgesics and other nephrotoxic medications, and to maintain tight glycemic control in patients with diabetes.
Future and Controversies
Significant contributions aimed at improving the prevention, diagnosis, and treatment of renal papillary necrosis include preliminary studies by Falkenberg et al, who are investigating monoclonal antibodies that may provide direct diagnostic access to the renal papilla and may allow for early detection of papillary damage. Monoclonal antibodies specific for papillary antigens have been used to detect these antigens in urine following toxic insults to the kidney. Further work has been performed by Price et al in which renal papillary antigen 1 (RPA-1) has been demonstrated to be an excellent marker of renal papillary necrosis that can be used to detect this toxicity in preclinical safety testing.
Studies by Garber et al have revealed that the angiotensin-converting enzyme (ACE) inhibitor enalapril has a protective and therapeutic effect in rats with bromoethylamine-induced renal papillary necrosis, which is characterized by marked interstitial fibrosis, impressive decreases in the glomerular filtration rate, and albuminuria. Histologic examination of rats treated with enalapril reveals a 67-88% decrease in renal papillary necrosis. These studies also demonstrate renoprotective effects of enalapril, including a significant improvement in the glomerular filtration rate and elimination of albuminuria.
A report from Abe et al described the treatment of renal papillary necrosis in a patient with diabetes. Prostaglandin E1 was infused intravenously at a dose of 40 mg/d for 14 days. This attempt at improving renal circulation increased both creatinine clearance and renal plasma flow, with a concomitant decrease in proteinuria. Vasodilatory agents such as prostaglandin E1 may improve renal circulation and hemodynamics and should be considered as possible therapy for renal papillary necrosis, particularly in patients with diabetes.
Finally, although they are a reasonable course of preventive treatment, prophylactic antibiotics are by no means standard treatment in patients with renal papillary necrosis. The utility of antibiotics requires further study. More importantly, prevention of nosocomial urinary tract infection should take precedence. If indwelling catheters are necessary or if the patient has risk factors for urinary stasis or frank obstruction, prophylactic antibiotics may prove useful.
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