Chapter 37
- Renal Function Monitoring
- Solomon Aronson
Renal dysfunction remains a serious complication during the perioperative
period in critically ill patients undergoing major surgery.[1]
[2]
[3]
[4]
[5]
[6]
[7]
The onset of acute perioperative renal failure portends a poor prognosis from the
loss of renal function with consequent volume and solute overload and from associated
life-threatening complications, including sepsis, respiratory failure, gastrointestinal
hemorrhage, and central nervous system dysfunction. Acute renal failure (ARF) requiring
dialysis develops in 1% to 7% of patients after cardiac or major vascular surgery
and is strongly associated with morbidity and mortality[8]
[9]
[10]
[11]
(see Chapter 50
and Chapter
52
). The mortality rate of ARF was 91% during World War II, 68% in Korea,
and 67% in Vietnam. Today, depending on associated comorbidities, postoperative
renal failure is responsible for up to 60% mortality in the postoperative period.
ARF in the presence of no other comorbidities has about a 10% to 40% mortality rate,
whereas ARF in the intensive care unit setting carries a 50% to 80% mortality rate.
[12]
Perioperative renal failure accounts for one
half of all patients requiring acute dialysis.[12]
Perhaps one reason for the persistently frequent incidence of perioperative renal
failure is a shift in medical populations to older and more critically ill patients
undergoing increasingly higher-risk procedures. The persistently frequent incidence
of perioperative renal failure observed may also result from our inability to adequately
monitor renal function changes and to predict the onset of ARF in the operative and
critical care setting.
An understanding of how to interpret information derived from
monitoring presumes an understanding of terms used to describe the observations made.
In the case of renal function monitoring, these assumptions may not always be warranted.
Perioperative renal failure, for example, has been
defined clinically as the need for postoperative dialysis or, in some cases, as a
postoperative serum creatinine level exceeding a predetermined preoperative value
(e.g., an increase of 0.5 mg/dL or of 50% or more). In one review,[13]
no two studies of 26 defined ARF the same way. The overall reported frequency of
ARF among all patients admitted to the hospital is 1%[14]
and may increase to 2% to 5%[4]
[15]
during hospitalization; however, there is no universally accepted standard for detecting
renal insufficiency or failure. Reporting on the cause, incidence, and management
of renal dysfunction also varies greatly because of wide variations in the definition
of terms used to describe degrees of renal dysfunction in the literature. It is
not surprising therefore that an estimated 5% of the general population has renal
disease (however defined) that is severe enough to adversely affect surgical outcome.
[16]
Several mechanisms involving a renal tubule, a tubulointerstitial
process, and a reduction in filtering capacity of the glomerulus have been implicated
in renal dysfunction. Prerenal causes are responsible for most cases of perioperative
ARF. Since World War II, it has become clear that ARF can result from decreased
renal blood flow from myriad causes ( Table
37-1
). Prerenal azotemia accounts for 70% of general community-acquired
ARF[14]
[15]
and
for
TABLE 37-1 -- Causes of renal hypoperfusion associated with acute renal failure
Intravascular Volume Depletion |
Major trauma, burns, crush syndrome |
Fever |
Hemorrhage |
Diuretic use |
Pancreatitis, vomiting, diarrhea, peritonitis, dehydration, NPO
status, bowel preparations |
Decreased Cardiac Output |
Congestive heart failure or low output syndrome |
Pulmonary hypertension, massive pulmonary embolism |
Positive pressure mechanical ventilation |
Increased Renal/Systemic Vascular Resistance
Ratio |
Renal vasoconstriction |
α-Adrenergic agonists |
Hypercalcemia, amphotericin |
Cyclosporine |
System vasodilation |
Afterload reduction |
Antihypertensive medications |
Anaphylactic shock |
Anesthesia sepsis |
Renovascular Obstruction |
Renal artery: atherosclerosis, embolism, thrombosis, dissecting
aneurysm, vasculitis |
Renal vein: thrombosis, compression |
Glomerular and Small-Vessel Obstruction |
Glomerulonephritis |
Vasculitis |
Toxemia of pregnancy |
Hemolytic uremic syndrome |
Disseminated intravascular coagulation |
Malignant hypertension |
Radiation injury |
Increased Blood Viscosity |
Macroglobulinemia |
Polycythemia |
Interference with Renal Autoregulation |
Prostaglandin inhibitors in presence of congestive heart failure
(CHF), nephritic syndrome, cirrhosis, hypovolemia |
Angiotensin-converting enzyme inhibition in presence of renal
artery stenosis or CHF |
more than 90% of perioperative ARF.[13]
[17]
Typically, an early compensatory phase of normal renal adaptation (e.g., pre-prerenal
failure) progresses to become decompensatory as prerenal failure ensues.[18]
ARF may be characterized as an abrupt decline in renal function at this transitional
stage. Depending on preexisting reserve capacity, this stage may persist for hours
to days. At this point, the key decline in renal function is sufficient to result
in retention of nitrogenous end products of metabolism and cessation of fluid and
electrolyte homeostasis. These events are not reversible by modifying nonrenal factors
and are difficult to predict. Prerenal azotemia and tubular ischemic injury represent
extreme examples of the same problem (i.e., insufficient renal blood flow). When
describing prerenal azotemia progressing to renal failure, the terms acute
tubular necrosis, vasomotor nephropathy,
and ischemic tubular injury are often used interchangeably
in the literature.
Although most causes of ischemic renal failure are reversible,
after a critical point of prolonged severe ischemia, necrosis may be irreversible.
[19]
In patients with inadequate renal blood flow,
this irreversible injury is commonly caused by the added risk of drugs that alter
the intrarenal distribution of blood flow by abnormal hemodynamics or by preexisting
disease[20]
(see Chapter
52
, Chapter 54
,
and Chapter 56
). These predisposing
variables, as well as the onset and pathogenesis of perioperative renal failure,
are often difficult to determine because direct assessment of renal hemodynamics
and renal tubular function is typically not possible. Renal function must often
be indirectly assessed. An understanding of normal renal physiology and of the pathophysiology
of ARF is critical. Because perioperative treatment strategies depend on differentiating
normal from abnormal renal function, understanding the limitations of commonly used
renal function monitoring techniques is also important.
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