Case Summary

A 29-year-old male presented with a right foot degloving injury, right subclavian artery thrombosis, brachial plexus avulsion, and a right hip fracture. He underwent orthopedic fixation, subclavian artery thrombectomy, and brachial plexus exploration.

Perioperative lactate monitoring revealed a preoperative lactate of 1.4 mmol/L, which rose to 3.5 mmol/L after revascularization. On postoperative day one, lactate remained at 3.5 mmol/L, and by postoperative day two it decreased to 0.7 mmol/L. Perfusion was maintained with a pulse pressure variation (PPV) of less than 15% and stable hemodynamics. Management included intravenous fluids, norepinephrine, mannitol 100 mL, thiamine, and sodium bicarbonate.

Why This Topic Matters to Anesthesiologists

Anesthesiologists frequently encounter metabolic and perfusion disturbances in trauma and vascular surgery. Reperfusion lactic acidosis is an important perioperative phenomenon that, if unrecognized, can contribute to multiorgan dysfunction. Prompt recognition and intervention can improve survival, reduce intensive care unit stay, and prevent complications. A molecular-level understanding of reperfusion injury and knowledge of pharmacologic strategies enable anesthesiologists to deliver precise and targeted therapy.

Perioperative Monitoring of Right Limb Vascularity

Accurate assessment of limb perfusion was critical following revascularization. Continuous pulse oximetry on the right hand provided real-time waveforms reflecting distal flow. Doppler assessment intraoperatively confirmed arterial patency and re-established circulation. Temperature and capillary refill time were compared with the contralateral limb as indirect markers of perfusion. The presence of bright red surgical field bleeding further confirmed tissue reperfusion. Serial lactate monitoring was used as a systemic indicator of perfusion recovery.

References

Awad S, Varadhan KK, Ljungqvist O, Lobo DN. A meta-analysis of the utility of pulse oximetry waveform for detecting peripheral perfusion. Crit Care Med. 2010;38(2):701–706.

Gelinas J, Dharmarajan K, Rajaram R, et al. Utility of serial lactate measurements in vascular surgery. J Vasc Surg.2013;57(6):1569–1574.

Pathophysiology of Reperfusion Lactic Acidosis

During the ischemic phase, absence of oxygen forces cells to shift to anaerobic glycolysis, resulting in increased lactate production. ATP depletion disrupts ion gradients maintained by Na⁺/K⁺ ATPase, leading to cell edema and necrosis. Hydrogen ion accumulation produces intracellular acidosis.

In the reperfusion phase, reintroduction of oxygen causes a burst of reactive oxygen species and oxidative stress. Capillary integrity is compromised, causing vascular leak and tissue edema. Washout of ischemic metabolites releases lactate, potassium, and myoglobin into systemic circulation. Oxygen delivery and cellular oxygen utilization remain transiently mismatched, perpetuating lactate elevation.

Additional contributors include catecholamine surges—both endogenous and from vasopressor therapy—which enhance β₂-mediated glycolysis. Stress-induced hypermetabolism elevates lactate through non-hypoxic mechanisms, while reduced hepatic clearance during hypoperfusion prolongs systemic lactate accumulation.

References

Eltzschig HK, Eckle T. Ischemia and reperfusion: cellular mechanisms of tissue injury. Anesthesiology. 2011;114(5):971–984.

Levy B, Gibot S, Franck P, et al. Relation between muscle Na⁺/K⁺ ATPase activity and lactate accumulation during shock states. Intensive Care Med. 2005;31(5):698–703.

Garcia-Alvarez M, Marik P, Bellomo R. Sepsis-associated hyperlactatemia. Crit Care. 2014;18(5):503.

Sodium Bicarbonate in Lactic Acidosis

Sodium bicarbonate therapy is indicated when pH falls below 7.1, bicarbonate is less than 10 mEq/L, hypotension is refractory to vasopressors, or when severe acidosis produces myocardial depression and arrhythmias.

The buffering mechanism involves binding of hydrogen ions, which raises extracellular pH, restores intracellular enzyme function such as pyruvate dehydrogenase and ATPase activity, improves the efficacy of catecholamines, and reduces pulmonary vasoconstriction and myocardial depression.

An initial bolus of 1–2 mEq/kg of 8.4% sodium bicarbonate is typically given over 10–20 minutes. Repeat dosing is guided by arterial blood gases, avoiding overcorrection. In cases of persistent acidosis, bicarbonate may be given as an infusion in dextrose or sterile water.

References

Kraut JA, Madias NE. Lactic acidosis. N Engl J Med. 2014;371(24):2309–2319.

Stacpoole PW. Lactic acidosis: relationship to the pathogenesis and therapy of shock. Crit Care Med. 1996;24(6):948–956.

Kim HJ, Son YK, An WS. Effect of sodium bicarbonate administration on mortality in patients with lactic acidosis: a retrospective analysis. PLoS One. 2013;8(6):e65283.

Supportive Therapy

Mannitol was administered as an osmotic diuretic to promote renal excretion of lactate and potassium, reducing metabolic burden. Thiamine was provided as a cofactor for pyruvate dehydrogenase, facilitating the conversion of pyruvate into the TCA cycle rather than lactate. Norepinephrine was titrated to maintain mean arterial pressure above 65 mmHg, supporting organ perfusion with minimal additional lactate production. Fluid therapy was guided by pulse pressure variation below 15%, avoiding both hypoperfusion and fluid overload. Serial arterial blood gases and lactate levels were measured every 4–6 hours to guide therapy and ensure resolution of metabolic derangements.

References

Oud L. Thiamine treatment of lactic acidosis: a review. Ann Intensive Care. 2022;12(1):5.

Cakirca M, Erdem A, Erdem D. The effect of mannitol on acute renal failure and lactic acidosis in rhabdomyolysis. Am J Emerg Med. 2016;34(6):1180.e3–1180.e5.

Dünser MW, Hasibeder WR. Sympathetic overstimulation during critical illness: adverse effects of adrenergic stress. J Intensive Care Med. 2009;24(5):293–316.

Anesthetic Considerations

Key intraoperative strategies included maintaining adequate perfusion by keeping mean arterial pressure above 65 mmHg, ensuring normothermia, and avoiding hypovolemia. Drugs known to increase lactate production, particularly β-agonists, were minimized where feasible. Deep sedation and, when indicated, neuromuscular blockade reduced endogenous catecholamine surges and the associated lactate generation. Multimodal analgesia was employed to attenuate the surgical stress response and sympathetic activation.

References

Butterworth J, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 6th ed. McGraw-Hill Education; 2018.

Myburgh JA, Mythen MG. Resuscitation fluids. N Engl J Med. 2013;369(13):1243–1251.

Levy B, Sadoune LO, Gelot AM, et al. Evolution of lactate metabolism in critically ill patients: a retrospective analysis. Crit Care. 2008;12(6):R186.

Conclusion

Reperfusion lactic acidosis following subclavian artery thrombectomy reflects a complex interplay of ischemia-reperfusion biochemistry, oxidative stress, and systemic metabolic derangements. Anesthesiologists play a central role in recognizing perfusion abnormalities, monitoring acid-base balance, and implementing targeted therapies. Sodium bicarbonate can serve as a temporizing intervention in critically acidotic patients while definitive measures are undertaken. This case emphasizes the importance of vigilant monitoring, timely pharmacological support, and precise hemodynamic management to optimize patient outcomes in complex vascular trauma.