April E. Mendoza
Anthony G. Charles
Presentation
A 63-year-old man presents to the emergency room complaining of an acute-onset abdominal pain. He described the pain as initially located in the left lower quadrant but now generalized. He has now developed some nausea and vomiting. His last bowel movement was a day prior to presentation. He admits to fever and chills and has been diaphoretic. He denies prior episodes of similar abdominal pain.
His past medical history is significant for non–insulin-dependent diabetes mellitus for over 10 years controlled with an oral hypoglycemic and essential hypertension managed with an angiotensin-converting-enzyme (ACE) inhibitor. His past surgical history is significant for an appendectomy 45 years ago. He has never undergone a screening colonoscopy. He has no known allergies.
His vitals revealed a temperature of 100°F, pulse rate of 120 per minute, respiratory rate of 32, and a blood pressure of 90/53. Physical exam showed an obese man, in acute painful distress. He has no jugular venous distension and his chest exam was unremarkable. Abdominal examination revealed generalized abdominal tenderness with rebound and guarding. The remainder of the exam revealed warm extremities with brisk capillary refill and no evidence of edema. Abdominal radiographic series revealed free air under the diaphragm.
He is diagnosed with a perforated viscous. Exploratory laparotomy confirms perforated sigmoid diverticulitis with extensive abdominal soilage. He undergoes a sigmoid colectomy and Hartman’s procedure. The following morning, he remains mechanically ventilated. His vitals have remained stable; however, he has become oliguric with a urine output of only 20 mL per hour.
Differential Diagnosis
Acute kidney injury (AKI) describes the full spectrum of renal dysfunction that is characterized by the RIFLE criteria. It is based on the extent of injury utilizing the serum creatinine, glomerular filtration rate (GFR), and urine output. The RIFLE criteria consist of five categories of renal dysfunction: Risk, Injury, Failure, Loss, and End-stage renal disease.
The RIFLE Criteria
· Risk—1.5-fold increase in the serum creatinine or GFR decrease by 25% or urine output <0.5 mL/kg/h for 6 hours
· Injury—twofold increase in the serum creatinine or GFR decrease by 50% or urine output <0.5 mL/kg/h for 12 hours
· Failure—threefold increase in the serum creatinine or GFR decrease by 75% or urine output of <0.5 mL/kg/h for 24 hours, or anuria for 12 hours
· Loss—complete loss of kidney function (need for renal replacement therapy [RRT]) for more than 4 weeks
· ESRD—complete loss of kidney function (e.g., need for RRT) for more than 3 months
Postoperative oliguria indicates AKI. Oliguria is defined as urine output <0.5 mL/kg/h in adults or <1.0 mL/kg/h in children weighing <10 kg. Early identification of the etiology can prevent further progression of renal injury. Always consider the possibility of preexisting renal disease in surgical patients, as this carries a higher risk of developing postoperative acute renal failure.
Etiology of AKI is organized into three groups: prerenal, renal, and postrenal. With respect to the patient presented above, we discuss the range of possible causes of his new oliguria.
Prerenal
Hypoperfusion of the kidneys from shock states is the hallmark of prerenal kidney dysfunction. All causes of renal hypoperfusion should be entertained. Hypovolemia and volume depletion should be high on the differential as a cause of this patient’s oliguria owing to third spacing from peritonitis and his emergent abdominal surgery.
Redistributive shock, such as cardiogenic or septic shock, particularly in patients with a longstanding history of diabetes and hypertension may result in poor renal perfusion. Abdominal compartment syndrome with evidence of increased bladder pressures, hypotension, and increased peak inspiratory pressures on the ventilator must also be considered. Persistent hypoperfusion of the kidney may lead to acute tubular necrosis (ATN).
Renal
Renal causes of acute renal dysfunction describe diseases of the renal parenchyma usually ATN. The etiology of ATN is numerous, but potential causes in the surgical patient include ischemia and nephrotoxins such as myoglobin, hemoglobin, contrast media, antibiotics (aminoglycosides, cephalosporins, sulfonamides, vancomycin), and anesthetic agents (methoxy-flurane, enflurane). Other causes are listed in Table 1 and should be considered if the etiopathogenesis of the renal failure remains obscure.
TABLE 1. Renal Etiologies of Acute Kidney Injury
Postrenal
Postrenal causes of renal dysfunction can usually be quickly identified by physical examination. Removing or replacing the urinary catheter can usually diagnose an enlarged prostate or a clogged catheter. Physical examination can identify a full bladder, or a bladder scan can be used in the case of obese patients. Direct ureteral injury has an incidence of 1% to 2% during abdominal surgery. Injury ranges from ligation, transection, devascularization, and partial laceration of the ureter. Though rare, usually bilateral ureteral injury will present with significant acute renal dysfunction.
Presentation Continued
The patient is extubated the following morning and is awake, but confused. Physical examination reveals normal heart and chest sounds. His abdomen is mildly distended and generalized edema is present. He denies pain except for tenderness at the incision site on palpation. His central venous pressure (CVP) ranges from 4 to 6 cm H2O. His current blood pressure recordings have been between 100 to 110 mm Hg systolic and 50 to 80 mm Hg diastolic. Review of the chart shows a preoperative creatinine of 1.5 mg/dL with a postoperative creatinine now at 3.2 mg/dL.
Workup
The initial diagnostic evaluation for acute renal dysfunction should start with a review of the patient’s history and a physical examination. Adjunctive invasive monitoring, urinary catheterization, trends in urine and serum chemistry (sodium, potassium, urea, and creatinine), urine microscopy, and ancillary tests such as bladder and renal ultrasonography have an additional role in identifying and categorizing the cause of renal dysfunction and subsequent renal failure.
Examination
Assessing the neurologic function, perfusion status, and signs of volume overload gives the clinician a better idea of the cause, severity, and progression of renal dysfunction. This patient has some signs of volume overload as evidenced by peripheral edema, which could be caused from cardiac or renal failure. Indeed, cardiac failure could be the cause of the renal failure. His abdomen is mildly distended, but not tense to suggest abdominal compartment syndrome. Neither rectal nor stomal exam reveals melena, frank blood, or evidence of prostate enlargement.
The bladder is not palpable. His catheter was flushed to ensure no obvious obstruction in the tubing (Table 2).
TABLE 2. Physical Exam and Possible Indications of’AKI
Laboratory and Ancillary Testing
In all surgical patients, it is imperative to initially consider prerenal causes of renal failure. If the patient’s CVP is low, with associated hypotension and tachycardia, a fluid challenge test may be a useful to determine the cause, particularly if the patient responds by increasing urine output. With new-onset oliguria, the clinician should also be prompted to obtain urine electrolytes, as well as a urinary analysis (UA) (Table 3).
TABLE 3. Common Urinary Analysis Findings and Possible Indications
aRBC: red blood cell
The addition of urine electrolytes especially urinary sodium and creatinine is imperative. If renal failure exists, this test can demonstrate whether the origin is prerenal or renal; the two most common causes in the acute setting. These values allow the clinician to calculate fractional excretion of sodium (FeNA).
In many situations, calculating the fractional excretion of urea or FeUrea may be more appropriate and accurate. It is well described that the use of diuretics, such as furosemide and bumetanide, can falsely elevate the excretion of sodium. Liver cirrhosis and other medical problems also affect the excretion of sodium. Urea and nitrogen byproducts remain relatively constant and should be considered in these circumstances (Table 4).
TABLE 4. Key lab findings of Pre-renal and Renal causes of AKI
FeNa = Una × Pcr/Pna × Ucr multiply by 100
FeUrea = Uurea × Pcr/Purea × Ucr multiply 100
Cardiac dysfunction remains a potential cause of oliguria. In this patient, an EKG, cardiac enzymes, echocardiography, chest radiograph, and serum chemistry panel should also be considered. Invasive monitoring can complement exam findings and give a better idea of volume status. These tests may correlate physical exam findings.
Renal ultrasonography can be useful if the initial workup cannot help guide the diagnosis. This is a quick, noninvasive method to evaluate obstructive causes of renal failure and can also identify signs chronic disease.
Invasive Tests
Invasive tests that contribute to management of renal failure include central venous and arterial monitoring, and/or pulse contour continuous cardiac output (PiCCO). Renal biopsy should rarely be warranted in the acute setting. It is reserved for when all tests and workup have remained unrevealing and the condition continues without improvement. It is also useful for the evaluation of acute glomerulonephritis/vasculitis or isolated hematuria with proteinuria.
Presentation Continued
His urine output has continually decreased now with a total of 50 cc of urine in 24 hours, although he has received several liters of fluid. He is 15 L positive and now has crackles bilaterally on chest exam with increasing extremity edema. His CVP is elevated at 15. Cardiac enzymes and BNP (brain natriuretic peptide) are within normal limits, and he has had no EKG changes consistent with evolving heart disease. His creatinine has climbed to 6 mg/dL from his baseline of 1.5 mg/dL. His BUN (blood urea nitrogen) is approaching 70 mg/dL, and his ABG (arterial blood gas) reveals a pH of 7.25. A UA shows epithelial cell casts. RRT is now considered the next best step in his management.
Diagnosis and Treatment
The patient is diagnosed with acute renal failure secondary to ATN. Underresuscitation in the face of sepsis, emergent surgery and third spacing likely resulted in renal dysfunction and ischemic injury that further evolved into ATN. Underlying renal insufficiency made him especially susceptible to this injury.
Early identification and supportive measures are the only treatment options. It is important to reduce further injury and stop any potentially nephrotoxins. Once supportive measures prove futile and renal dysfunction continues, RRT should be initiated.
Indications for RRT are seen in Table 5.
TABLE 5. Indications for Renal Replacement Therapy
Clinical Approach to Acute Renal Dysfunction
Adequate perioperative resuscitation is crucial for preventing renal dysfunction. Invasive monitoring may prove a helpful adjunct in surgical patients with AKI. It is well known that the mortality is increased in this subset of critically ill patients.
Key clinical components.
1. Ensure proper perioperative resuscitation, minimize exposure to nephrotoxins, monitor fluid balance.
2. Examine the patient.
3. Employ the trends in serum and urine chemistry to help confirm the diagnosis and guide therapeutic endpoints.
4. Consider adjunctive monitoring such as echocardiogram prior to invasive monitoring.
5. Consider the need for RRT if patient meets criteria.
Figure 1 describes the initial workup and management of patients with clinical findings consistent with AKI.
FIGURE 1 • Diagnostic workup and evaluation of a patient with Oliguria.
Pitfalls in management include
1. Failure to examine the patient and review preexisting comorbidities
2. Indiscriminate use of diuretics in the face of hypotension and underresuscitation
3. Prolonged use of diuretics when patient meets criteria for dialysis
4. Ignoring respiratory status in acute renal failure
5. Misinterpreting information gathered from invasive monitoring
Case Conclusion
The patient was started on RRT. His preexisting comorbidities made him susceptible to acute renal dysfunction and ultimately renal loss when his clinical course was complicated by hypotension and sepsis. The patient required dialysis for 6 weeks and eventually regained renal function. His favorable outcome is likely a result of proper resuscitation and the appropriate use of RRT.
TAKE HOME POINTS
· Use baseline chemistries to assess renal function.
· Ensure adequate perioperative resuscitation.
· Surgical patients must be assumed to have a prerenal cause until proven otherwise.
· All types of redistributive shock are also prerenal causes of AKI and failure.
· Be cognizant of comorbidities.
· Avoid nephrotoxic medications-aminoglycosides, IV contrast, etc.
· Diuretics may be utilized only after correction of shock.
· Use of diuretics does not alter the course of renal failure.
· Consider RRT when patient meets criteria.
· Renal failure is associated with increased mortality in surgical patients.
SUGGESTED READINGS
Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure-definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004;8:204–212.
Diskin CJ, Stokes TJ, Dansby LM, et al. The comparative benefits of the fractional excretion of urea and sodium in various azotemic oliguric states. Nephron Clin Pract. 2010;114:145–150.
Madaio MP. Renal biopsy. Kidney Int. 1990;38:529.
Mullin RJ. Acute renal failure. In: Cameron JL, ed. Current Surgical Therapy. Philadelphia, PA: Mosby, 2008;1200–1206.
Stafford RE, Cairns BA, Meyer AA. Renal failure. In: Souba WW, Fink MP, Jurkouch GS, et al., eds. ACS Surgery: Principles and Practice. New York, NY: WebMD professional publishing, 2006;1408–1412.