Does generalized edema in sepsis increase muscular tissue pressure?

Objective

In sepsis, generalized tissue edema develops as a rule due to fluid management under conditions of systemic capillary leak. Edema formation in a closed and noncompliant anatomic compartment can lead to increased intracompartmental pressure and subsequent tissue damage as seen, for example, in post-ischemic compartment syndrome. We hypothesized that increased intramuscular tissue pressure caused by muscle swelling in a closed fascial space can contribute to skeletal muscle damage in sepsis. The aim of this study was to describe intramuscular pressure changes during massive fluid resuscitation in experimental porcine sepsis.

Material and methods

Seven anesthetised, artificially ventilated and multicatheterized domestic pigs (body weight 29.7 ± 3.9 kg) were randomly subjected to either live E. coli IV infusion to induce sepsis (n = 4) or to a sham procedure (n = 3). Animals were fluid resuscitated with 20 ml/kg per hour Ringer's lactated solution and followed for 24 hours after start of the microbial infusion. Hourly fluid balance and cumulative fluid balance were recorded. Intramuscular pressure was measured every hour using an electronic transducer-tipped catheter system placed into the m. tibialis longus of the right pelvic extremity. For statistical analysis, ANOVA for repeated measures, the Dunnett test and the Mann–Whitney U test were used.

Results

In both groups, positive fluid balance was observed. In septic animals, final cummulative fluid retention was 345 ± 121 ml/kg per 24 hours compared with 149 ± 25 ml/kg per 24 hours in controls (P < 0.00001). Intramuscular pressure increased from initial values (median 10 mmHg, range 6–11 mmHg) gradually in both groups during the experiment to 13 (11–20) mmHg in septic and 16 (15–17) mmHg in controls. Despite lower fluid retention, the intramuscular pressure increased to significantly higher values in the control group (P < 0.01) compared with septic animals. The increase reached statistical significance compared with baseline in hour 5 in controls, and in hour 13 in the septic group. In both groups, the intramuscular pressure never exceeded 20 mmHg, which is clearly below the pressure that is proven to cause skeletal muscle damage in compartment syndrome.

Conclusions

Increased skeletal muscle tissue pressure during fluid retention following crystaloid infusion was observed in both septic and control animals. Tissue pressures did not reach levels proven to promote direct damage to skeletal muscle in any group.

The increase was delayed and significantly lower in septic animals compared with controls despite higher fluid retention in the septic group.