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Skeletal muscle necrosis is quantified using technetium-99m stannous pyrophosphate (99mTc-PYP) in pressurized muscle compartments after severe blood loss. Six dogs (15 to 20 kg) were anesthetized by pentobarbital sodium (25 mg/kg IV) and hemorrhaged to a hypotensive state. Left hind-leg muscle compartments were pressurized to a level of 20 mm Hg for 6 hours by infusing autologous plasma. Intracompartmental pressure was continuously monitored by the wick catheter. The right leg served as a control. Forty-eight hours following pressurization, 5 mCi of 99mTc-PYP were injected IV, and 3 hours later each dog was sacrificed and pressurized and control muscles were resected simultaneously, weighed, and counted for 99mTc-PYP uptake. Significant uptake appeared in muscle compartments pressurized for 6 hours at 20 mm Hg, indicating that 20 mm Hg in a hypotensive state produces a degree of necrosis as great as that produced by 40 to 50 mm Hg in a normotensive state. We conclude that an acute compartment syndrome occurs in a hypotensive individual at an intramuscular pressure level considerably less than the threshold pressure level in an individual with normal blood pressure.

The effect of a colloid (dextran-70) infusion on increased microvascular fluid and protein flux after thermal injury was compared with that seen with a crystalloid infusion. Lymph flow (QL) and lymph/phasma (L/P) protein content were used to monitor microvascular fluid flux and protein permeability in the lung and in burned and nonburned soft tissues, namely, skin and subcutaneous tissue, for 72 h in 13 sheep given a 30% TBS full-thickness burn. Vascular pressures were maintained constant with dextran in saline or lactated Ringer's. Mean fluid requirements for dextran were one-half that for crystalloid during the 24-h resuscitation period. However, plasma proteins decreased by 50% with dextran compared to 30% with crystalloid. An increase of 2-2.5 fold in QL was seen during resuscitation in the lung and nonburned soft tissue with crystalloid while the L/P protein ratio decreased, indicating no change in protein permeability. This QL response was prevented during dextran infusion. A rebound increase in soft tissue QL occurred after discontinuation of dextran, probably as a result of the severe residual hypoproteinemia. Burn QL and L/P were markedly increased during the entire 72-h period, indicating increased permeability. Dextran infusion accentuated the QL response in the burn microcirculation. We conclude that dextran decreases edema in nonburned tissue, but appears to increase the protein loss from burn tissue.