A 70-kg male with a 10-day-old crush injury, extensive internal and external degloving, rhabdomyolysis, and sepsis underwent wound debridement under general anesthesia. Despite apparently stable macrocirculatory parameters, he developed severe postoperative oxygen-delivery failure, progressive hypocalcemia after transfusion and albumin therapy, distributive–cytopathic septic shock, and microcirculatory collapse masked by vasopressor support. Serial ABGs revealed rapid transition from compensated physiology to metabolic–mitochondrial failure (lactate 7.7 mmol/L) despite normal SpO₂ and MAP. Thromboelastography normalized following blood products, but tissue perfusion deteriorated. BNP increased to 545 pg/mL with negative troponin and unchanged echocardiography. This case underscores that blood pressure, oxygen saturation, and coagulation normalization cannot be equated with cellular perfusion and metabolic rescue. Lactate kinetics, ionized calcium, and oxygen-delivery physics provide superior physiologic insight for anesthetic decision-making.

Late-phase crush injury complicated by sepsis creates a uniquely hostile landscape for anesthetic management. These patients exhibit simultaneous:

• profound vasoplegia

• disordered venous capacitance

• coagulation–fibrinolysis imbalance

• mitochondrial dysfunction

• microvascular shunting

• transfusion-related biochemical derangements

• calcium–catecholamine uncoupling

Anesthesiologists are often misled by stabilization of MAP and SpO₂, especially in patients supported by norepinephrine and vasopressin. However, macrocirculatory stability provides no assurance of microcirculatory adequacy. Tissue hypoxia and mitochondrial paralysis may progress silently, manifesting only as rising lactate and base deficit.

This case illustrates the principle of hemodynamic incoherence—a state in which blood pressure and organ flow dissociate from capillary perfusion and oxygen utilization.

Preoperative Status

A previously healthy 70-kg male presented 10 days after a major crush injury with internal and external degloving and rhabdomyolysis. He had undergone multiple surgeries elsewhere and arrived with:

• septic physiology

• increasing bilirubin

• hypoalbuminemia

• evolving MODS

• intubated on CPAP

• requiring norepinephrine

Ventilation

• FiO₂: 35%

• PEEP: 5 cmH₂O

• PS: 10 cmH₂O

Hemodynamic Support

• Norepinephrine: 8 mg/50 mL dilution

Preoperative ABG

1. Normal ABG ≠ Normal Physiology

pH normalization reflects buffering, not physiologic health. In sepsis, early maintenance of lactate often precedes abrupt mitochondrial collapse. Ionized calcium was already low, impairing vascular tone and adrenergic signaling.

2. Oxygen Delivery Physics

Calculated CaO₂ ≈ 14.6 mL/100 mL — barely sufficient for a hypermetabolic septic state.

3. Ventilatory Masking

Pressure support temporarily concealed:

• muscular fatigue

• increased CO₂ production

• rising oxygen debt

References

1. West JB. Respiratory physiology: the essentials. 9th ed. Philadelphia: LWW; 2012.

2. Walsh BK, Smallwood CD. Use of noninvasive ventilation. Respir Care. 2017;62:932-950.

3. Marino PL. The ICU Book. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2014.