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Kidneys in Crisis: Anesthesia Responses to Oncologic Shock
CASE HISTORY
A 53-year-old male with known intestinal B-cell lymphoma, previously treated with chemotherapy, presented with an acute abdomen characterized by generalized peritonitis, fever, and altered sensorium. CT imaging of the abdomen revealed an ileal perforation with approximately five liters of free ascitic fluid. On arrival his heart rate was 122 beats per minute, blood pressure 86/48 mmHg, and SpO₂ 84% on room air.
Laboratory results showed hemoglobin 8.3 g/dL, serum albumin 2.3 g/dL, phosphorus 5.3 mg/dL, urea 66 mg/dL, creatinine 0.9 mg/dL, C-reactive protein 72 mg/L, and an HbA1c of 10.3%. The surgical plan was emergency exploratory laparotomy for bowel perforation. The anesthetic plan included rapid sequence induction, intraoperative hemodynamic optimization, renal function monitoring, and postoperative ICU care.
RENAL FUNCTION DURING SURGICAL SEPSIS — PATHOPHYSIOLOGICAL BASIS
Several interacting mechanisms contribute to renal dysfunction in this patient. Loss of large volumes of ascitic fluid reduces effective circulating volume, and systemic inflammation with cytokine release (for example tumor necrosis factor-alpha and interleukin-6) produces vasodilation that lowers renal perfusion pressure (calculated as mean arterial pressure minus renal venous pressure), thereby reducing glomerular filtration rate.
At the microvascular level, sepsis causes degradation of the endothelial glycocalyx, increasing capillary permeability and promoting interstitial edema that compromises tubular oxygenation and predisposes to tubular ischemia. Renal autoregulation becomes impaired because of endothelial dysfunction, so the kidney cannot maintain GFR across a range of perfusion pressures.
Elevated intra-abdominal pressure from tense ascites (>12 mmHg) further compresses the renal veins and raises renal interstitial pressure, reducing the transcapillary filtration gradient needed for glomerular filtration. On the molecular level, endotoxin and cytokine signaling (for example IL-1β and IL-6) upregulate inducible nitric oxide synthase (iNOS), increasing nitric oxide production and vasodilation that impairs renal autoregulation (Prowle JR, Bellomo R. Sepsis-associated acute kidney injury. Contrib Nephrol. 2010;165:64–70).
PHARMACOLOGIC TOOLS FOR RENAL PERFUSION
Furosemide (loop diuretic). Furosemide inhibits the Na⁺-K⁺-2Cl⁻ symporter in the thick ascending limb to produce natriuresis and diuresis. Clinically it requires adequate renal perfusion and delivery to the tubular lumen — the drug is albumin-bound and depends on a sufficient filtered load and interstitial osmotic gradients to be effective. In this patient, profound hypoperfusion combined with hypoalbuminemia diminished tubular delivery and the filtered load, which explains why diuresis was inadequate. The mechanistic limitation is inhibition of NKCC2 when the filtered load or interstitial gradient is too low (Chawla LS, et al. Crit Care. 2013;17(5):R207).
Albumin 20%. Exogenous albumin restores oncotic pressure, drawing interstitial fluid back into the intravascular space and improving effective circulating volume. Albumin also protects endothelial glycocalyx and helps preserve capillary integrity by interacting with endothelial receptors (for example gp60 and TIE2), which can stabilize barrier function. In septic patients with hypoalbuminemia, albumin administration can improve responsiveness to vasopressors and diuretics and counteract hemodilution and capillary leak (Wiedermann CJ. Int J Mol Sci. 2021;22(9):4496).
Norepinephrine. As an α₁-adrenergic agonist, norepinephrine induces systemic vasoconstriction to raise systemic vascular resistance and mean arterial pressure, thereby restoring the pressure head across the glomerulus and improving renal perfusion in distributive shock. However, excessive vasoconstriction may compromise renal cortical blood flow. The vasoconstrictive action follows Gq-protein coupled receptor signaling with IP₃-mediated Ca²⁺ release in vascular smooth muscle (Russell JA. Crit Care Med. 2011;39(9):2280–2285).
Vasopressin. Acting on V1 receptors, vasopressin causes splanchnic vasoconstriction and helps preserve renal and cerebral perfusion. It can be particularly useful in vasoplegia refractory to catecholamines, reducing catecholamine requirements and remaining effective in acidotic or adrenergically unresponsive states. Its downstream signaling activates phospholipase C and the IP₃/DAG pathway, producing Ca²⁺-mediated vasoconstriction and bypassing downregulated adrenergic receptors in sepsis (Gordon AC, et al. Am J Respir Crit Care Med. 2010;182(5):576–583).
CRRT DECISIONS IN SEPSIS AND AKI
Clinical triggers observed in this case that supported renal replacement therapy included oliguria (<0.3 mL/kg/hr), lactate 3.0 mmol/L, metabolic acidosis (HCO₃⁻ 17.7 mmol/L with pH 7.35), and evolving volume overload after administration of five liters of crystalloids with minimal urine output and increasing ventilator demands. Pathophysiological considerations included risk of worsening tubular injury, progressive fluid overload causing impaired oxygenation, and accumulation of inflammatory mediators.
Continuous renal replacement therapy (CRRT) offers several advantages in this context. Continuous, slow fluid removal minimizes intravascular volume shifts and avoids the hypotension that can occur with intermittent hemodialysis. CRRT removes uremic toxins, assists in acid-base control, and can help clear inflammatory mediators and lactate while providing time for tubular recovery. At the cellular level, controlled fluid removal limits ischemia–reperfusion injury and may reduce neutrophil extracellular trap burden in acute kidney injury (Mehta RL, et al. Am J Kidney Dis. 2001;38(2):383–409).
CASE TIMELINE AND INTEGRATED REFLECTION
The clinical course progressed as follows. On postoperative day (POD) 0 urine output was about 200 mL, norepinephrine requirement increased, and vasopressin was started. CRRT was initiated because of fluid overload and acidosis, with an initial lactate of about 3.0 mmol/L and pH approximately 7.35. By POD 1 urine output improved to 625 mL and norepinephrine requirement decreased, with continuation of CRRT. On POD 2 urine output rose to 2.16 L and vasopressors were weaned, allowing CRRT discontinuation as renal recovery ensued. By POD 3 urine output was adequate, the patient was off renal replacement, pH normalized to 7.48, lactate decreased to 1.1 mmol/L, and extubation followed a successful spontaneous breathing trial.
KEY TAKEAWAYS AND PRACTICAL POINTS
Urine output is a perfusion-dependent marker rather than a pure measure of intrinsic renal function; it reflects renal blood flow and systemic hemodynamics. Loop diuretics such as furosemide should not be administered reflexively; their effectiveness depends on sufficient renal perfusion and, in hypoalbuminemic states, adequate drug delivery to the tubular lumen. Exogenous albumin can support endothelial function, restore oncotic pressure, and improve response to diuretics and vasopressors in selected patients. Norepinephrine is the first-line agent to restore perfusion pressure in septic vasoplegia, while vasopressin serves as a valuable adjunct in catecholamine-refractory hypotension. Early CRRT is a supportive therapy to manage fluid overload, correct acid–base disturbances, and clear inflammatory mediators; it is not a failure but a bridge to recovery when used appropriately. Finally, dynamic bedside tools — IVC ultrasound, serial lactate trends, and arterial blood gas analysis — are essential to guide intraoperative and ICU fluid and renal management.
REFERENCES
Prowle JR, Bellomo R. Sepsis-associated acute kidney injury: macrohemodynamic and microhemodynamic alterations. Contrib Nephrol. 2010;165:64–70.
Chawla LS, et al. Development and standardization of a furosemide stress test. Crit Care. 2013;17(5):R207.
Wiedermann CJ. Hypoalbuminemia as surrogate and culprit of infections. Int J Mol Sci. 2021;22(9):4496.
Russell JA. Vasopressin and norepinephrine in septic shock. Crit Care Med. 2011;39(9):2280–2285.
Gordon AC, et al. The effects of vasopressin on acute kidney injury in septic shock. Am J Respir Crit Care Med. 2010;182(5):576–583.
Mehta RL, et al. Renal replacement therapy in acute renal failure: an update. Am J Kidney Dis. 2001;38(2):383–409.
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By RENNY CHACKOCASE HISTORY
A 53-year-old male with known intestinal B-cell lymphoma, previously treated with chemotherapy, presented with an acute abdomen characterized by generalized peritonitis, fever, and altered sensorium. CT imaging of the abdomen revealed an ileal perforation with approximately five liters of free ascitic fluid. On arrival his heart rate was 122 beats per minute, blood pressure 86/48 mmHg, and SpO₂ 84% on room air.
Laboratory results showed hemoglobin 8.3 g/dL, serum albumin 2.3 g/dL, phosphorus 5.3 mg/dL, urea 66 mg/dL, creatinine 0.9 mg/dL, C-reactive protein 72 mg/L, and an HbA1c of 10.3%. The surgical plan was emergency exploratory laparotomy for bowel perforation. The anesthetic plan included rapid sequence induction, intraoperative hemodynamic optimization, renal function monitoring, and postoperative ICU care.
RENAL FUNCTION DURING SURGICAL SEPSIS — PATHOPHYSIOLOGICAL BASIS
Several interacting mechanisms contribute to renal dysfunction in this patient. Loss of large volumes of ascitic fluid reduces effective circulating volume, and systemic inflammation with cytokine release (for example tumor necrosis factor-alpha and interleukin-6) produces vasodilation that lowers renal perfusion pressure (calculated as mean arterial pressure minus renal venous pressure), thereby reducing glomerular filtration rate.
At the microvascular level, sepsis causes degradation of the endothelial glycocalyx, increasing capillary permeability and promoting interstitial edema that compromises tubular oxygenation and predisposes to tubular ischemia. Renal autoregulation becomes impaired because of endothelial dysfunction, so the kidney cannot maintain GFR across a range of perfusion pressures.
Elevated intra-abdominal pressure from tense ascites (>12 mmHg) further compresses the renal veins and raises renal interstitial pressure, reducing the transcapillary filtration gradient needed for glomerular filtration. On the molecular level, endotoxin and cytokine signaling (for example IL-1β and IL-6) upregulate inducible nitric oxide synthase (iNOS), increasing nitric oxide production and vasodilation that impairs renal autoregulation (Prowle JR, Bellomo R. Sepsis-associated acute kidney injury. Contrib Nephrol. 2010;165:64–70).
PHARMACOLOGIC TOOLS FOR RENAL PERFUSION
Furosemide (loop diuretic). Furosemide inhibits the Na⁺-K⁺-2Cl⁻ symporter in the thick ascending limb to produce natriuresis and diuresis. Clinically it requires adequate renal perfusion and delivery to the tubular lumen — the drug is albumin-bound and depends on a sufficient filtered load and interstitial osmotic gradients to be effective. In this patient, profound hypoperfusion combined with hypoalbuminemia diminished tubular delivery and the filtered load, which explains why diuresis was inadequate. The mechanistic limitation is inhibition of NKCC2 when the filtered load or interstitial gradient is too low (Chawla LS, et al. Crit Care. 2013;17(5):R207).
Albumin 20%. Exogenous albumin restores oncotic pressure, drawing interstitial fluid back into the intravascular space and improving effective circulating volume. Albumin also protects endothelial glycocalyx and helps preserve capillary integrity by interacting with endothelial receptors (for example gp60 and TIE2), which can stabilize barrier function. In septic patients with hypoalbuminemia, albumin administration can improve responsiveness to vasopressors and diuretics and counteract hemodilution and capillary leak (Wiedermann CJ. Int J Mol Sci. 2021;22(9):4496).
Norepinephrine. As an α₁-adrenergic agonist, norepinephrine induces systemic vasoconstriction to raise systemic vascular resistance and mean arterial pressure, thereby restoring the pressure head across the glomerulus and improving renal perfusion in distributive shock. However, excessive vasoconstriction may compromise renal cortical blood flow. The vasoconstrictive action follows Gq-protein coupled receptor signaling with IP₃-mediated Ca²⁺ release in vascular smooth muscle (Russell JA. Crit Care Med. 2011;39(9):2280–2285).
Vasopressin. Acting on V1 receptors, vasopressin causes splanchnic vasoconstriction and helps preserve renal and cerebral perfusion. It can be particularly useful in vasoplegia refractory to catecholamines, reducing catecholamine requirements and remaining effective in acidotic or adrenergically unresponsive states. Its downstream signaling activates phospholipase C and the IP₃/DAG pathway, producing Ca²⁺-mediated vasoconstriction and bypassing downregulated adrenergic receptors in sepsis (Gordon AC, et al. Am J Respir Crit Care Med. 2010;182(5):576–583).
CRRT DECISIONS IN SEPSIS AND AKI
Clinical triggers observed in this case that supported renal replacement therapy included oliguria (<0.3 mL/kg/hr), lactate 3.0 mmol/L, metabolic acidosis (HCO₃⁻ 17.7 mmol/L with pH 7.35), and evolving volume overload after administration of five liters of crystalloids with minimal urine output and increasing ventilator demands. Pathophysiological considerations included risk of worsening tubular injury, progressive fluid overload causing impaired oxygenation, and accumulation of inflammatory mediators.
Continuous renal replacement therapy (CRRT) offers several advantages in this context. Continuous, slow fluid removal minimizes intravascular volume shifts and avoids the hypotension that can occur with intermittent hemodialysis. CRRT removes uremic toxins, assists in acid-base control, and can help clear inflammatory mediators and lactate while providing time for tubular recovery. At the cellular level, controlled fluid removal limits ischemia–reperfusion injury and may reduce neutrophil extracellular trap burden in acute kidney injury (Mehta RL, et al. Am J Kidney Dis. 2001;38(2):383–409).
CASE TIMELINE AND INTEGRATED REFLECTION
The clinical course progressed as follows. On postoperative day (POD) 0 urine output was about 200 mL, norepinephrine requirement increased, and vasopressin was started. CRRT was initiated because of fluid overload and acidosis, with an initial lactate of about 3.0 mmol/L and pH approximately 7.35. By POD 1 urine output improved to 625 mL and norepinephrine requirement decreased, with continuation of CRRT. On POD 2 urine output rose to 2.16 L and vasopressors were weaned, allowing CRRT discontinuation as renal recovery ensued. By POD 3 urine output was adequate, the patient was off renal replacement, pH normalized to 7.48, lactate decreased to 1.1 mmol/L, and extubation followed a successful spontaneous breathing trial.
KEY TAKEAWAYS AND PRACTICAL POINTS
Urine output is a perfusion-dependent marker rather than a pure measure of intrinsic renal function; it reflects renal blood flow and systemic hemodynamics. Loop diuretics such as furosemide should not be administered reflexively; their effectiveness depends on sufficient renal perfusion and, in hypoalbuminemic states, adequate drug delivery to the tubular lumen. Exogenous albumin can support endothelial function, restore oncotic pressure, and improve response to diuretics and vasopressors in selected patients. Norepinephrine is the first-line agent to restore perfusion pressure in septic vasoplegia, while vasopressin serves as a valuable adjunct in catecholamine-refractory hypotension. Early CRRT is a supportive therapy to manage fluid overload, correct acid–base disturbances, and clear inflammatory mediators; it is not a failure but a bridge to recovery when used appropriately. Finally, dynamic bedside tools — IVC ultrasound, serial lactate trends, and arterial blood gas analysis — are essential to guide intraoperative and ICU fluid and renal management.
REFERENCES
Prowle JR, Bellomo R. Sepsis-associated acute kidney injury: macrohemodynamic and microhemodynamic alterations. Contrib Nephrol. 2010;165:64–70.
Chawla LS, et al. Development and standardization of a furosemide stress test. Crit Care. 2013;17(5):R207.
Wiedermann CJ. Hypoalbuminemia as surrogate and culprit of infections. Int J Mol Sci. 2021;22(9):4496.
Russell JA. Vasopressin and norepinephrine in septic shock. Crit Care Med. 2011;39(9):2280–2285.
Gordon AC, et al. The effects of vasopressin on acute kidney injury in septic shock. Am J Respir Crit Care Med. 2010;182(5):576–583.
Mehta RL, et al. Renal replacement therapy in acute renal failure: an update. Am J Kidney Dis. 2001;38(2):383–409.