Code Red: Stabilizing a Sepsis Storm from the Anesthesia Frontline

Ink & Air

Clinical Background

A 51-year-old male with type 2 diabetes mellitus and a recent Frey’s procedure for chronic pancreatitis was admitted to the ICU with a liver abscess, which was drained via pigtail catheter. His course was complicated by septic shock and multiorgan dysfunction syndrome (MODS). He required vasopressor support, ventilator assistance, and had evidence of renal, hematologic, and metabolic dysfunction.

Septic Shock and Vasopressor Dependency

Sepsis in this patient is driven by a cytokine storm involving interleukin-1, interleukin-6, and tumor necrosis factor-alpha, along with bacterial endotoxin release from Gram-negative organisms. Lipopolysaccharide binds to Toll-like receptor 4 on macrophages, activating inducible nitric oxide synthase and leading to excessive nitric oxide production. This results in systemic vasodilation, reduced systemic vascular resistance, and distributive shock. Endothelial dysfunction further promotes capillary leak, causing third spacing and relative hypovolemia.

Norepinephrine at 26.6 mcg/min (approximately 0.38 mcg/kg/min for a 70 kg patient) acts predominantly on alpha-1 receptors to induce vasoconstriction, raising systemic vascular resistance and restoring mean arterial pressure. Its modest beta-1 activity increases heart rate and contractility, which may impose additional strain in patients with concentric left ventricular hypertrophy.

During anesthesia, norepinephrine must be continued to prevent intraoperative hypotension. Hemodynamically stable induction agents such as etomidate or ketamine are preferred over vasodilatory agents like propofol.

Left Ventricular Hypertrophy and Volume Status

The patient demonstrates concentric left ventricular hypertrophy, most likely due to chronic hypertension and diabetes-related remodeling. This structural change impairs diastolic relaxation, elevates left ventricular end-diastolic pressure, and predisposes to pulmonary venous congestion and edema. Reduced compliance makes the ventricle sensitive to tachycardia and volume loading.

IVC diameter of 19 mm with poor collapsibility, together with a central venous pressure of 14 mmHg, suggests volume overload and elevated right atrial pressure. Hypoalbuminemia at 2.1 g/dL worsens interstitial fluid accumulation due to reduced oncotic pressure.

For anesthesia, fluid boluses should be avoided as they exacerbate pulmonary edema. Advanced monitoring, such as transesophageal echocardiography, can provide intraoperative guidance for volume management and right ventricular function.

Perfusion and Oxygen Delivery

The patient’s lactate of 8.6 mmol/L indicates profound tissue hypoperfusion and mitochondrial dysfunction. Sepsis impairs cellular oxidative phosphorylation, forcing reliance on anaerobic glycolysis and generating lactic acidosis. Persistent elevation reflects microcirculatory shunting, where blood bypasses capillaries despite adequate macro-hemodynamics.

Arterial blood gases show metabolic acidosis with pH 7.22, bicarbonate 11.7 mmol/L, and base excess of –15. This state increases the risk of arrhythmias and reduces vasopressor responsiveness.

During anesthesia, oxygen delivery should be optimized by maintaining hemoglobin, ensuring MAP ≥65 mmHg, and closely monitoring oxygenation through pulse oximetry and ventilation via capnography.

Norepinephrine Use Versus Fluid Restriction

Norepinephrine is necessary to counteract vasoplegia and ensure organ perfusion. In this patient with preserved systolic function, hypotension is largely driven by systemic vasodilation rather than poor cardiac contractility. Moderate-dose norepinephrine effectively addresses this physiology.

However, fluid overload is evident, with a positive balance of 2.4 L, elevated CVP, and non-collapsing IVC. In the setting of diastolic dysfunction, further fluid administration would worsen pulmonary edema and impair oxygenation. Capillary leak from sepsis and low oncotic pressure from hypoalbuminemia further aggravate third spacing. For this reason, vasopressors rather than fluids are the mainstay of support. Goal-directed fluid therapy with dynamic indices is preferable, and albumin may be considered in select cases for oncotic support.

Management Plan

Respiratory Support

Lung-protective ventilation remains essential, with tidal volumes around 6 mL/kg of ideal body weight, plateau pressures kept below 30 cmH₂O, and PEEP set between 8 and 12 cmH₂O according to ARDSnet protocols. Oxygen saturation should be maintained at 92–96% while minimizing FiO₂ exposure to reduce oxygen toxicity. Sedation should be titrated to allow spontaneous breathing trials when feasible.

For anesthesia, ventilator settings must be preserved during procedures such as catheter checks. Agents like low-dose propofol or dexmedetomidine provide sedation without significant respiratory depression.

Hemodynamic Optimization

The goal is to maintain MAP ≥65 mmHg while avoiding fluid overload. Norepinephrine should be titrated carefully, with vasopressin considered as an adjunct if escalating doses are required. Albumin may be used to support oncotic pressure, but only under guided monitoring.

In patients with persistent tachycardia after shock resolution, esmolol infusion may reduce myocardial oxygen consumption and improve diastolic filling, particularly in the presence of LVH. Intraoperative monitoring with arterial lines is mandatory.

Renal Support

Acute kidney injury is evident, with low urine output and rising creatinine. Management includes avoidance of nephrotoxic drugs, close electrolyte monitoring, and initiation of continuous renal replacement therapy if anuria, refractory hyperkalemia, severe acidosis, or fluid overload occurs. Continuous modalities such as CVVHDF are preferred in hemodynamically unstable patients.

Metabolic and Acid-Base Management

Correction of lactic acidosis centers on restoring tissue perfusion rather than bicarbonate supplementation, which should be reserved for severe acidosis with pH <7.15 and hemodynamic instability. Optimization of oxygen delivery through adequate hemoglobin levels and perfusion pressure is the key intervention.

Hematologic and Coagulation Support

Severe thrombocytopenia (platelets 15,000/µL) requires careful transfusion strategy. Platelets should be given if counts fall below 10,000/µL prophylactically, or below 20,000/µL in the presence of active bleeding or before invasive procedures. Monitoring for disseminated intravascular coagulation with fibrinogen, D-dimer, and coagulation studies is essential. Regional anesthesia is contraindicated unless platelet counts are corrected.

Infectious Disease Management

The source of sepsis is a polymicrobial liver abscess. Drainage has been achieved with a pigtail catheter, which must be checked for patency daily. Antibiotic therapy with piperacillin-tazobactam and metronidazole is appropriate initial coverage, but escalation to meropenem should be considered if resistant Gram-negative organisms are suspected. Antifungal therapy with fluconazole may be warranted in high-risk ICU patients. Antibiotics should be de-escalated once culture results are available.

Summary

This patient represents a prototypical case of septic shock complicated by multiorgan dysfunction in the postoperative setting of chronic pancreatitis surgery. He is vasopressor-dependent due to distributive shock, fluid-intolerant because of LVH and sepsis-related capillary leak, and at risk of worsening pulmonary edema with additional fluid loading. Management centers on norepinephrine, strict fluid restriction, lung-protective ventilation, renal support, correction of metabolic derangements, and close hemodynamic monitoring. Source control of infection with pigtail drainage and appropriate antibiotics is paramount.

For anesthesia, the key priorities are to maintain vasopressor support, avoid excessive fluid administration, use hemodynamically stable sedative agents, and prepare for rapid intervention in case of deterioration.