The very high ratio of RBF to kidney weight allows the kidney to efficiently preserve PV after injury and hemorrhage (Table 59-1).3,10 Renal vasoconstriction at the efferent arteriole permits a rise in renal vascular resistance (RVR) from a normal 5000–8000 dyne s/cm5 with a concomitant decrease in RBF from 1250 to 800 mL/min while maintaining a normal GFR (Fig. 59-2). This phenomenon of maintained GFR despite a reduction in RBF is known as autoregulation (Fig. 59-2). Excretion of metabolites is thus maintained, while 400 mL of blood/min is redirected to core areas. Both experimental and clinical studies show that autoregulation allows GFR to be maintained while RBF is decreased to 70% of normal.2,3,11 The filtration fraction (GFR/ERPF) under such circumstances increases from a normal of 20% to as high as 40%.3,11 More severe hypovolemia causes vasoconstriction at both the afferent and efferent arterioles, thus leading to a reduction in GFR (Table 59-1). The mechanism for the rise in RVR is multifactorial due primarily to the renal perfusion of peripherally generated catecholamines that, in turn, activates the JGA to stimulate intrarenal renin release. This stimulates the renin-angiotensin-aldosterone system (RAAS) which not only promotes sodium reabsorption but may also increase RVR.7,12,13 When the RVR increases above 14,000 dyne s/cm5, the RBF falls below 500 mL/min, thereby allowing over 700 mL/min to be redirected to core organs. When hypovolemia causes hypotension below 70 mm Hg, GFR ceases and essentially all RBF is redirected to the systemic circuit (Table 59-1). This causes renal ischemia and potentiates ARF.
TABLE 59-1Graded Renal Response to Acute Hypovolemia ||Download (.pdf) TABLE 59-1 Graded Renal Response to Acute Hypovolemia
|Severity of hemorrhage ||Volume deficit (mL) ||Blood pressure (torr) ||Renal plasma flow (mL/min) ||Filtration rate (mL/min) ||Sodium clearance (mL/min) ||Osmolar clearance (mL/min) ||Urine output (mL/min) ||Renal vascular resistance (dyne s/cm5) |
|Normal ||5000 ||120/80 ||650 ||125 ||1.5 ||2.0 ||1.0 || 6000 |
|Class I || 700 ||120/80 ||520 ||115 ||1.3 ||2.0 ||0.9 || 5500 |
|Class II ||1200 ||115/80 ||260 || 60 ||0.7 ||1.3 ||0.3 || 8000 |
|Class III ||1600 || 90/70 || 85 || 10 ||0.1 ||0.1 ||0.1 ||10,000 |
|Class IV ||2000 || 60/40 || 10 ||2 ||0 ||0 ||0 ||12,000 |
Mild to moderate hemorrhage causes efferent arteriolar vasoconstriction resulting in reduced RBF (520 mL/min) while maintaining GFR (125 mL/min). This is known as autoregulation that redirects blood flow to the systemic circuit without compromising filtration and excretion.
During hypoperfusion, the kidney conserves salt and water due to decreased GFR, increased ADH, and increased renin release with aldosterone generation.3,13 When PV and CO are restored, the renal vasoconstriction subsides—first at the preglomerular afferent arteriole and later at the postglomerular efferent arteriole. The increase in RVR, however, may persist for many hours and even days in patients with a severe hemorrhagic shock.3,13,19
The Kidney During Operation After Injury
During operation, the kidney exerts the same autoregulatory response to a PV deficit as described above. The major difference reflects the altered humoral response brought about by general anesthesia, especially in the marginally volemic patient in whom systemic vasoconstriction was maintaining a blood pressure prior to induction. This was first described by Ladd during the Korean conflict.12 Civilian studies have shown the same phenomenon.2,3 The sudden reduction in protective vasoconstriction plus continued bleeding from injured organs precipitates a marked reduction in PV and CO causing hypotension, increased RVR, and decreased RBF with an abrupt reduction in CI flow; the consequent fall in GFR causes oliguria or anuria, which may persist as ARF after operation.2,12
The prime objective during operation is to correct the depleted PV and ineffective CO while hemostasis is obtained. When hemostasis has been achieved and the blood pressure has been restored, oliguria often persists. Osmotic or loop diuretics, such as mannitol or furosemide, have been advocated in this setting on the assumption that induced diuresis increases RBF, GFR, and urine output, and prevents ARF.2,14 Most studies, however, show that diuresis in this setting provides no renal protection.16,17 Loop diuresis in combination with low-dose dopamine, likewise, affords no renal protection during major surgery.17 Induced diuresis causes a further decrease in effective PV, thus making the likelihood of ARF greater.18 Furthermore, induced diuresis interferes with one of the crucial monitors of effective postoperative PV replacement, namely, uninduced urine output rates.
Intraoperative protection of the kidney in a hypovolemic, hypotensive patient must be directed toward obtaining hemostasis and improving the cardiovascular status by PV expansion with crystalloid solution, blood, and blood products. Inotropic support should be added when PV expansion causes an elevated central pressure despite persistent hypotension and oliguria. Resuscitation in his setting is best accomplished by a balanced electrolyte solution rather than 0.9% saline which may contribute to ARF by the resultant hyperchloremia and acidosis.18 Experimental and clinical studies show that a temporary delay in reestablishing urine flow after mean arterial pressure (MAP) is restored results from a prolonged rise in RVR after hypovolemia is corrected.7,10 Renal vasodilation, experimentally, can reverse this lagging oliguria, but such therapy is difficult and hazardous in humans.10 Based on clinical observations, many patients in whom the MAP has been restored are still PV and IFS depleted, resulting in a marked increase in both total peripheral resistance (TPR) and RVR. The persistent elevation in RVR is likely due to the prior ischemic insult and not perfusion by catecholamines in stable patients; measurements of renin and arginine vasopressin (AVP) at this time have been normal (C. E. Lucas and I. K. Rosenberg, Surgical renal study unit, unpublished data). Thus, pharmacologic intervention with angiotensin-converting enzyme blockade or nitrous oxide would likely be ineffective.13 Since both peripheral and renal vasoconstriction can lead to a doubling of total resistance, the CO may be reduced by 50% of normal despite a normal MAP. Thus, the PV may be only 1500 mL after the MAP rises to normal. Assuming that concomitant oliguria reflects this vasoconstriction and PV depletion, the rapid infusion of 1 or 2 L of balanced electrolyte solution plus whole blood, if indicated, will restore RBF, GFR, and urine output. This approach protects renal function in the early postoperative period. The few patients who are unresponsive to this regimen may be treated by a loop diuretic, such as furosemide (40 mg), which typically produces a dramatic diuresis. Such patients, however, must be monitored closely since even small dosages of a loop diuretic may induce excessive diuresis, leading to subsequent hypovolemia and hypotension.16,17
Early Postoperative Juxtamedullary Washout and Polyuria
An interesting, but potentially hazardous, renal response to shock in injured patients is a transient period of polyuria during or immediately after operation (Fig. 59-3).19 This polyuria is not excessive, seldom exceeding 250 mL/30 min, and usually abates by 5 hours following operation (Table 59-2). This phenomenon tends to occur in patients who have had a major hemorrhagic shock insult requiring more than 15 blood transfusions prior to successful hemostasis.19 On arrival to the SICU, the blood pressure and pulse normalize while the urine output exceeds 3 mL/min (ie, 180 mL/h) at the expense of effective PV. The urine sodium concentration exceeds 40 mEq/L and the fractional excretion of sodium (FENa) or CNa exceeds 3%. Therapy for this syndrome should be by maintenance of effective PV as judged by vital signs until the polyuric phase subsides, usually by 2–5 hours after operation.19
Following restoration of PV during and shortly following operation, a renal concentrating defect may exist whereby a patient may have a low-normal MAP (84 torr) with a markedly reduced GFR (35 mL/min) while excreting a large urine volume (8.2 mL/min; 500 mL/h). This concentrating defect is likely due to inner medullary washout of osmoles, thus impairing reabsorption of sodium and water in response to aldosterone and AVH. This phenomenon seldom lasts more than 5 hours following conclusion of operation.
TABLE 59-2Impaired Concentration During and Shortly After Operation ||Download (.pdf) TABLE 59-2 Impaired Concentration During and Shortly After Operation
| ||MAP (torr) ||ERPF (mL/min) ||GFR (mL/min) ||U/O (mL/min) ||CNa (mL/min) ||Cosm (mL/min) ||CH2O (mL/min) |
|Operation || 84 ||— || 35 ||8.5 ||5.9 ||8.1 || 0.4 |
|Postoperative (5 h) ||100 ||260 || 90 ||3.9 ||4.3 ||6.0 ||–2.0 |
|Postoperative (15 h) || 98 ||— ||110 ||1.6 ||1.8 ||3.1 ||–1.5 |
The mechanism for early postoperative polyuria is unclear but likely is due to an inner medullary (CIII) washout of osmoles. During shock, the primary reduction in RBF occurs in the outer cortex (CI) with less reduction in juxtamedullary (CII) flow; this is referred to as cortical to medullary shunting.2,3 Since the juxtamedullary nephrons have loops of Henle that affect interstitial medullary (CIII) tonicity, a relative increase in RBF to these nephrons may cause a “washout” of osmoles. This disrupts the countercurrent regulatory system and precludes effective sodium and water reabsorption from the collecting ducts when outer cortical flow is first reestablished.19
Increased osmotic diuresis with polyuria may also be due to the overutilization of solutions containing 5% dextrose. Marked hyperglycemia (500–1000 mg/100 mL) and hyperosmolemia (310–320 mOs/L) have occurred in patients resuscitated exclusively with crystalloid solutions containing 5% dextrose. This hazard is circumvented by limiting the amount of 5% dextrose in crystalloid solution to 2000 mL after which a nonglucose balanced electrolyte solution is infused along with whole blood and blood products as needed.2,19
Postoperative Oliguria During Extravascular Fluid Sequestration Phase
Following operative control of bleeding after severe hemorrhagic shock, there are major shifts in sodium, water, and protein from the plasma into the IFS. This causes reduced PV, MAP, CO, RBF, GFR, and urine output. This phase of extravascular fluid sequestration lasts about 36 hours in patients who have received an average of 15 RBC transfusions prior to operative control of bleeding.20 Part of the IFS expansion includes intrapulmonary sequestration resulting in respiratory insufficiency.20 Successful therapy mandates a careful balance to maintain perfusion and protect the kidney while not overloading the pulmonary circulation (Fig. 59-4).
Following an operation requiring 23 RBC units and 9 L crystalloid solution, this patient became oliguric (1 hour) and was treated with low-dose furosemide causing prompt diuresis and hypotension. Fluid bolus restored pressure (2 hours) and inotropes were added for rising central pressures (steroid use was part of a prospective randomized trial). Low-dose dopamine was added at 7 hours and this improved perfusion pressure. Furosemide at hour 9 reproduced prompt diuresis and hypotension treated with additional fluid bolus through hour 10. Clearly, loop diuresis during the fluid update phase is hazardous. The patient made a full recovery.
When the intravenous infusion rate is decreased because of increased weight gain and IFS sequestration, the MAP falls, causing a fall in RBF and potential ARF. Mesenteric leukotrienes which colocalize with 5-lipoxygenase activating protein and may contribute to ARF after hemorrhagic shock; mesenteric lymph diversion of the 5-lipoxygenase ameliorates the subsequent kidney insult in a rodent hemorrhagic shock model.21 This typically occurs during the initial 12 hours after operation and causes decreased ERPF, GFR, UO, CNa, and COsm. During this period of obligatory IFS expansion, the patient may need many liters of balanced electrolyte solution to maintain kidney perfusion. Inotropes and ventilator support are often needed.21 Restoring PV, hemoglobin level, coagulation status, and normal MAP enables the kidney to maintain GFR and urine output even though RBF may be reduced. CNa and COsm during this period reflect the underlying renal circulatory status and are decreased when RBF is lowered but return to normal when the effective circulatory volume is restored; CH2O is negative at this time.11 Excess crystalloid resuscitation, especially, during the latter portion of the fluid uptake phase is detrimental causing acute lung injury, cardiac compromise, and, even, the abdominal compartment syndrome. Restricting crystalloids, however, will not prevent IFS expansion but will lead to PV depletion with reduced perfusion with the need for inotropic support and vasopressors. This sequence promotes ARF which, in the fluid sequestration phase, usually results in death.2,20,22 A therapeutic balance is required.
The technique used to provide ventilatory support during the fluid uptake phase may also affect kidney function.23,24 High tidal volumes (>10 mL/kg body weight), with or without high positive end-expiratory pressure (PEEP > 10 cm H2O) may improve oxygen tension by reducing atelectasis but compromise oxygen delivery reducing CO.23 This reduces MAP, CO, ERPF, CNa, COsm, and urine output.24 The renal response is mediated through sinoaortic baroreceptors and renal vein pressure.25,26 The SICU team must adjust ventilatory settings with renal function in mind.