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Acute compartment syndrome (ACS) is a syndrome in which local circulation is affected due to increased pressure within the compartment. We previously found in patients with calf fractures, the pressure of fascial compartment could be sharply reduced upon the appearance of tension blisters. Deep fascia, as the important structure for compartment, might play key role in this process. Therefore, the aim of the present study was to examine the differences in gene profile in deep fascia tissue in fracture patients of the calf with or without tension blisters, and to explore the role of fascia in pressure improvement in ACS. Patients with lower leg fracture were enrolled and divided into control group (CON group, n = 10) without tension blister, and tension blister group (TB group, n = 10). Deep fascia tissues were collected and LC-MS/MS label-free quantitative proteomics were performed. Genes involved in fascia structure and fibroblast function were further validated by Western blot. The differentially expressed proteins were found to be mainly enriched in pathways related to protein synthesis and processing, stress fiber assembly, cell-substrate adhesion, leukocyte mediated cytotoxicity, and cellular response to stress. Compared with the CON group, the expression of Peroxidasin homolog (PXDN), which promotes the function of fibroblasts, and Leukocyte differentiation antigen 74 (CD74), which enhances the proliferation of fibroblasts, were significantly upregulated (p all <0.05), while the expression of Matrix metalloproteinase-9 (MMP9), which is involved in collagen hydrolysis, and Neutrophil elastase (ELANE), which is involved in elastin hydrolysis, were significantly reduced in the TB group (p all <0.05), indicating fascia tissue underwent microenvironment reconstruction during ACS. In summary, the ACS accompanied by blisters is associated with the enhanced function and proliferation of fibroblasts and reduced hydrolysis of collagen and elastin. The adaptive alterations in the stiffness and elasticity of the deep fascia might be crucial for pressure release of ACS., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Abstract: Background: Treatment of acute compartment syndrome (ACS)-induced skeletal muscle injury remains a challenge. Previous studies have shown that octanoic acid is a promising treatment for ACS owing to its potential ability to regulate metabolic/epigenetic pathways in ischemic injury. The present study was designed to investigate the efficacy and underlying mechanism of octanoic acid in ACS-induced skeletal muscle injury. Methods: In this study, we established a saline infusion ACS rat model. Subsequently, we assessed the protective effects of sodium octanoate (NaO, sodium salt of octanoic acid) on ACS-induced skeletal muscle injury. Afterward, the level of acetyl-coenzyme A and histone acetylation in the skeletal muscle tissue were quantified. Moreover, we investigated the activation of the AMP-activated protein kinas pathway and the occurrence of mitophagy in the skeletal muscle tissue. Lastly, we scrutinized the expression of proteins associated with mitochondrial dynamics in the skeletal muscle tissue. Results: The administration of NaO attenuated muscle inflammation, alleviating oxidative stress and muscle edema. Moreover, NaO treatment enhanced muscle blood perfusion, leading to the inhibition of apoptosis-related skeletal muscle cell death after ACS. In addition, NaO demonstrated the ability to halt skeletal muscle fibrosis and enhance the functional recovery of muscle post-ACS. Further analysis indicates that NaO treatment increases the acetyl-CoA level in muscle and the process of histone acetylation by acetyl-CoA. Lastly, we found NaO treatment exerts a stimulatory impact on the activation of the AMPK pathway, thus promoting mitophagy and improving mitochondrial dynamics. Conclusion: Our findings indicate that octanoic acid may ameliorate skeletal muscle injury induced by ACS. Its protective effects may be attributed to the promotion of acetyl-CoA synthesis and histone acetylation within the muscular tissue, as well as its activation of the AMPK-related mitophagy pathway., (Copyright © 2024 by the Shock Society.)

Background: Acute compartment syndrome (ACS) is one of the most common complications of musculoskeletal injury, leading to the necrosis and demise of skeletal muscle cells. Our previous study showed that embryonic stem cells-derived mesenchymal stem cells (ESC-MSCs) are novel therapeutics in ACS treatment. As extracellular vesicles (EVs) are rapidly gaining attention as cell-free therapeutics that have advantages over parental stem cells, the therapeutic potential and mechanisms of EVs from ESC-MSCs on ACS need to be explored., Method: In the present study, we examined the protective effects in the experimental ACS rat model and investigated the role of macrophages in mediating these effects. Next, we used transcriptome sequencing to explore the mechanisms by which ESC-MSC-EVs regulate macrophage polarization. Furthermore, miRNA sequencing was performed on ESC-MSC-EVs to identify miRNA candidates associated with macrophage polarization., Results: We found that intravenous administration of ESC-MSC-EVs, given at the time of fasciotomy, significantly promotes the anti-inflammation process, angiogenesis, and functional recovery of muscle in ACS. The beneficial effects were associated with ESC-MSC-EVs affecting macrophage polarization by delivering various miRNAs which regulate NF-κB, JAK/STAT, and PI3K/AKT pathways. Our data further illustrate that ESC-MSC-EVs mainly modulate macrophage polarization via the miR-21/PTEN, miR-320a/PTEN, miR-423/NLRP3, miR-100/mTOR, and miR-26a/TLR3 axes., Conclusion: Together, our results demonstrated the beneficial effects of ESC-MSC-EVs in ACS, wherein the miRNAs present in ESC-MSC-EVs regulate the polarization of macrophages., (© 2023. The Author(s).)

LPIN1 deficiency is an autosomal recessive disease caused by biallelic mutations in LPIN1, where impaired fatty acid metabolism leads to stress in skeletal muscle, resulting in severe rhabdomyolysis, often triggered by fever, exercise, fasting, and anesthesia. It is the second most common cause of severe, recurrent episodes of rhabdomyolysis in early childhood which can result in serious morbidity and mortality. To date, 71 patients have been published in 20 clinical studies in the form of case series. We describe two previously unreported cases, one with a novel LPIN1 mutation that resulted in mortality, and another, to the best of our knowledge, with the first reported compartment syndrome managed with a favorable outcome in this disorder. Recognition of the complications including ventricular arrythmias, acute renal failure and compartment syndrome on the severe end of the spectrum may change the outcome and prognosis of this devastating condition., Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest., (Copyright © 2022. Published by Elsevier B.V.)

Background: Acute compartment syndrome (ACS), a well-known complication of musculoskeletal injury, results in muscle necrosis and cell death. Embryonic stem cell-derived mesenchymal stem cells (ESC-MSCs) have been shown to be a promising therapy for ACS. However, their effectiveness and potentially protective mechanism remain unknown. The present study was designed to investigate the efficacy and underlying mechanism of ESC-MSCs in ACS-induced skeletal muscle injury., Method: A total of 168 male Sprague-Dawley (SD) rats underwent 2 h of intracompartmental pressure elevation by saline infusion into the anterior compartment of the left hindlimb to establish the ACS model. ESC-MSCs were differentiated from the human embryonic stem cell (ESC) line H9. A dose of 1.2 × 10 6 of ESC-MSCs was intravenously injected during fasciotomy. Post-ACS assessments included skeletal edema index, serum indicators, histological analysis, apoptosis, fibrosis, regeneration, and functional recovery of skeletal muscle. Then, fluorescence microscopy was used to observe the distribution of labeled ESC-MSCs in vivo, and western blotting and immunofluorescence analyses were performed to examine macrophages infiltration in skeletal muscle. Finally, we used liposomal clodronate to deplete macrophages and reassess skeletal muscle injury in response to ESC-MSC therapy., Result: ESC-MSCs significantly reduced systemic inflammatory responses, ACS-induced skeletal muscle edema, and cell apoptosis. In addition, ESC-MSCs inhibited skeletal muscle fibrosis and increased regeneration and functional recovery of skeletal muscle after ACS. The beneficial effects of ESC-MSCs on ACS-induced skeletal muscle injury were accompanied by a decrease in CD86-positive M1 macrophage polarization and an increase in CD206-positive M2 macrophage polarization. After depleting macrophages with liposomal clodronate, the beneficial effects of ESC-MSCs were attenuated., Conclusion: Our findings suggest that embryonic stem cell-derived mesenchymal stem cells infusion could effectively alleviate ACS-induced skeletal muscle injury, in which the beneficial effects were related to the regulation of macrophages polarization., (© 2022. The Author(s).)

Objective: Limb compartment syndrome (CS), a complication of trauma, results in muscle necrosis and cell death; ischemia and inflammation contribute to microvascular dysfunction and parenchymal injury. Carbon monoxide-releasing molecule-3 (CORM-3) has been shown to protect microvascular perfusion and reduce inflammation in animal models of CS. The purpose of the study was to test the effect of CORM-3 in human in vitro CS model, allowing exploration of the mechanism(s) of CO protection and potential development of pharmacologic treatment., Methods: Confluent human vascular endothelial cells (HUVECs) were stimulated for 6 h with serum isolated from patients with CS. Intracellular oxidative stress (production of reactive oxygen species (ROS)) apoptosis, transendothelial resistance (TEER), polymorphonuclear leukocyte (PMN) activation and transmigration across the monolayer in response to the CS stimulus were assessed. All experiments were performed in the presence of CORM-3 (100 μM) or its inactive form, iCORM-3., Results: CS serum induced a significant increase in ROS, apoptosis and endothelial monolayer breakdown; it also increased PMN superoxide production, leukocyte rolling and adhesion/transmigration. CORM-3 completely prevented CS-induced ROS production, apoptosis, PMN adhesion, rolling and transmigration, while improving monolayer integrity., Conclusion: CORM-3 offers potent anti-oxidant and anti-inflammatory effects, and may have a potential application to patients at risk of developing CS., (© 2019 John Wiley & Sons Ltd.)

Background: Type 1 diabetic patients and non-diabetic patients were referred for evaluation for chronic exertional compartment syndrome (CECS) based on clinical examination and complaints of activity-related leg pain in the region of the tibialis anterior muscle. Previous studies using near-infrared spectroscopy (NIRS) showed greater deoxygenation during exercise for CECS patients versus healthy controls; however, this comparison has not been done for diabetic CECS patients., Methods: We used NIRS to test for differences in oxygenation kinetics for Type 1 diabetic patients diagnosed with (CECS-diabetics, n = 9) versus diabetic patients without (CON-diabetics, n = 10) leg anterior chronic exertional compartment syndrome. Comparisons were also made between non-diabetic CECS patients (n = 11) and healthy controls (CON, n = 10). The experimental protocol consisted of thigh arterial cuff occlusion (AO, 1-minute duration), and treadmill running to reproduce symptoms. NIRS variables generated were resting StO2%, and oxygen recovery following AO. Also, during and following treadmill running the magnitude of deoxygenation and oxygen recovery, respectively, were determined., Results: There was no difference in resting StO2% between CECS-diabetics (78.2±12.6%) vs. CON-diabetics (69.1±20.8%), or between CECS (69.3±16.2) vs. CON (75.9±11.2%). However, oxygen recovery following AO was significantly slower for CECS (1.8±0.8%/sec) vs. CON (3.8±1.7%/sec) (P = 0.002); these data were not different between the diabetic groups. StO2% during exercise was lower (greater deoxygenation) for CECS-diabetics (6.3±8.6%) vs. CON-diabetics (40.4±22.0%), and for CECS (11.3±16.8%) vs. CON (34.1±21.2%) (P<0.05 for both). The rate of oxygen recovery post exercise was faster for CECS-diabetics (3.5±2.6%/sec) vs. CON-diabetics (1.4±0.8%/sec) (P = 0.04), and there was a tendency of difference for CECS (3.1±1.4%/sec) vs. CON (1.9±1.3%/sec) (P = 0.05)., Conclusion: The greater deoxygenation during treadmill running for the CECS-diabetics group (vs. CON-diabetics) is in line with previous studies (and with the present study) that compared non-diabetic CECS patients with healthy controls. Our findings could suggest that NIRS may be useful as a diagnostic tool for assessing Type 1 diabetic patients suspected of CECS.

Objective: The aim of this study was to investigate the utility of direct measurement of tissue oxygenation during compartment syndrome (CS) and tourniquet-induced ischemia in a large animal model. We hypothesize that as compartment pressure (CP) rises, circulation within the compartment will decrease resulting in a decreased level of oxygen in the muscle., Methods: This study used a dog model of both CS- and tourniquet-based ischemia. In 15 animals, CS was induced in 1 hind limb with varying degrees of severity using an infusion model. Tourniquet ischemia was induced in the contralateral hind limb for varying durations. The partial pressure of oxygen (PmO2) was continuously monitored using a polarographic oxygen probe in the muscle of both hind limbs. CP was monitored in the CS limb. PmO2 and CP were analyzed after fasciotomy, performed after approximately 7 hours of warm ischemia, or release of tourniquet., Results: With the application of tourniquet ischemia, PmO2 fell from 38.40 to 1.30 mm Hg (P < 0.001) and subsequently rose after release of the tourniquet to 39.81 mm Hg (P < 0.001). Elevated CP induced by infusion was relieved by fasciotomy (52.04-11.37 mm Hg postfasciotomy, P < 0.001). PmO2 readings in the infusion model were significantly higher in pre-CS than during CS (31.77 mm Hg vs. 3.88 mm Hg, P < 0.001) and rebounded after fasciotomy (50.24 mm Hg, P < 0.001), consistent with hyperemic response., Conclusions: Increased CP caused an observable decrease in PmO2 that was reversed by fasciotomy. PmO2 can be directly measured in real time with a polarographic tissue pO2 probe. This study is the first step of evaluating an alternative method for diagnosing acute CS.

Ischaemia reperfusion (I/R) injury refers to tissue damage caused when blood supply returns to the tissue after a period of ischaemia. Matrix metalloproteinases (MMPs), neutrophil gelatinase-associated lipocalin (NGAL) and cytokines are biomarkers involved in several vascular complications. The aim of this study was to evaluate the role of MMPs, NGAL and inflammatory cytokines in I/R syndrome. We conducted an open label, multicentric, parallel group study, between January 2010 and December 2013. Patients with acute limb ischaemia were enrolled in this study and were divided into two groups: (i) those subjected to fasciotomy and (ii) those not subjected to fasciotomy, according to the onset of compartment syndrome. Plasma and tissue values of MMPs and NGAL as well as plasma cytokines were evaluated. MMPs, NGAL and cytokine levels were higher in patients with compartment syndrome. Biomarkers evaluated in this study may be used in the future as predictors of I/R injury severity and its possible evolution towards post-reperfusion syndrome., (© 2014 Medicalhelplines.com Inc and John Wiley & Sons Ltd.)

Background: The use of wavelengths of the near-infrared region by near-infrared spectroscopy (NIRS) has been studied for several applications in vascular disease. This systematic review aims to explore the clinical relevance of monitoring muscle tissue oxygenation in vascular disease with NIRS., Methods: A systematic search in PubMed, EMBASE, CINAHL and Cochrane databases was performed to identify clinical NIRS studies, published until April 2015, involving muscle tissue oxygenation in vascular disease., Results: After screening 183 manuscripts, 38 studies (n=2010) were included. Studies concerned peripheral arterial disease (PAD) (twelve studies, n=848), compartment syndrome of lower extremities (seven studies, n=205), deep vein thrombosis (DVT) (six studies, n=429), buttock and lower extremity ischaemia in abdominal aortic aneurysm repair (six studies, n=139), free flap failure (five studies, n=354), and spinal cord ischaemia in thoracoabdominal aortic aneurysm repair (two studies, n=35). Nine studies compared NIRS with gold standards and provided cut-off values. Four studies regarding chronic compartment syndrome and DVT determined higher sensitivity (78%-97%) than specificity (56%-76%). Two studies regarding PAD and buttock claudication determined higher specificity (87%-95%) than sensitivity (33%-88%). Three studies regarding free flap failure determined sensitivity and specificity of 100%., Conclusion: We found sufficient evidence to use NIRS in clinical setting for assessment of chronic compartment syndrome of lower extremities, and as surveillance tool for detection of free flap failure. So far, clinical relevance of routine use of NIRS in other vascular applications is less clear. Cut-off values to discriminate are not yet unanimous and better validation has to be awaited for., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Crush injuries represent a spectrum of injury to body parts as result of trauma. Presentations vary from minor contusions to limb-threatening damage. Typically, the injury involves multiple tissues, from skin and subcutaneous, to muscle and tendons, to bone and joints. In their most severe presentations, predictable complications--including osteomyelitis, non-union of fractures, amputations and failed flaps--occur in approximately 50 percent of the cases with standard of practice surgical and medical interventions. Skeletal muscle-compartment syndrome (SMCS) is another consequence of trauma, but in this situation the target tissues are muscles and nerve. Edema and/or bleeding within the confines of the fascial envelope can increase the pressure within the skeletal muscle-compartment. When the tissue fluid pressure within the compartment exceeds the capillary perfusion pressure to the muscles and nerves in the compartment, these tissues are rendered ischemic and manifest the signs and symptoms of SMCS. The SMCS, especially in its incipient stages before a fasciotomy is required, is a therapeutic challenge since no means to arrest its progression exist other than hyperbaric oxygen (HBO2). Unfortunately, HBO2 is woefully neglected as an adjunct for managing crush injury and SMCS. Strong arguments exist for its use based on evidenced-based information and how HBO2 mitigates the pathology of these conditions.

While intracompartmental pressure monitoring is a widely used diagnostic tool to measure intracompartmental pressures in the setting of compartment syndrome, its invasive nature has prompted the development of noninvasive techniques, such as near-infrared spectrometry. We prospectively assessed the association between tissue oxygen saturation measured by near-infrared spectrometry and compartment pressure measured by intracompartmental pressure monitoring in a cohort of patients with compartment syndrome of the lower extremity. We hypothesized that tissue oxygen saturation measured by near-infrared spectrometry would negatively correlate with intracompartmental pressures. Tissue oxygen saturation was determined for all 4 compartments of the lower extremity in 7 patients using near-infrared spectrometry. All patients subsequently underwent lower-extremity fasciotomies. Mechanism of injury, compartment pressures, blood pressure, near-infrared spectrometry measurement of tissue oxygen saturation, and characteristics of the muscle at the time of fasciotomy were recorded. The strength of the correlations between tissue oxygen saturation and absolute and relative compartment pressures was estimated based on mixed linear (growth) models with repeated observations nested within patients. Our analyses demonstrated no significant relationship between tissue oxygen saturation measured by near-infrared spectrometry and the absolute or relative compartment pressures. This suggests that compartment tissue oxygen saturation measurements by near-infrared spectrometry do not correlate with the diagnosis of compartment syndrome, and that near-infrared spectrometry would not serve as a reliable diagnostic tool., (Copyright 2011, SLACK Incorporated.)

Background: The aim was to investigate whether or not glutamine, an antioxidant effective amino acid, improves the reperfusion-induced oxidative injury of abdominal hypertension., Methods: Wistar Albino rats were used. Group 1: Abdominal compartment syndrome alone: With the rats under anesthesia, intraabdominal pressure was obtained. Three days later, the rats were sacrificed, and intestine, lung and liver samples were removed for determination of tissue malondialdehyde (MDA) and glutathione (GSH) levels as oxidative injury parameters and of myeloperoxidase (MPO) activity as an inflammatory parameter. Trunk blood was analyzed for the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Group 2: Abdominal compartment syndrome and glutamine: intragastric glutamine was given for seven days before and three days following establishment of the abdominal compartment syndrome model. The same examination procedure was then performed. Group 3: Glutamine administration alone. Group 4: Control group., Results: Intraabdominal pressure significantly increased the intestine, lung and liver MDA levels and MPO activities in comparison to the control group. Glutamine was associated with decreased MDA levels and MPO activities and increased GSH levels., Conclusion: Glutamine appears to have protective effects against reperfusion-induced oxidative damage via its anti-inflammatory and antioxidant effect.

Objectives: This study investigated the effects of intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) on gut barrier function in critically ill surgical patients., Methods: A prospective observational cohort study on patients with severe acute pancreatitis or abdominal sepsis admitted to an intensive care or high-dependency unit. Intra-abdominal pressure (IAP) and plasma levels of immunoglobulin G (IgG) and IgM antiendotoxin core antibodies (EndoCAb) and procalcitonin (ProCT) were measured serially., Results: Among 32 recruited patients, 24 (75%) and 8 patients (25%) developed IAH and ACS, respectively. The state of ACS was associated with significant reductions in plasma IgG EndoCAb (P = 0.015) and IgM EndoCAb (P = 0.016) and higher concentrations of plasma ProCT (P = 0.056) compared with absence of ACS. Resolution of IAH and ACS was associated with significant recovery of plasma IgG EndoCAb (P = 0.003 and P = 0.009, respectively) and IgM EndoCAb (P = 0.002 and P = 0.003, respectively) and reduction in plasma ProCT concentration (P = 0.049 and P = 0.019, respectively). Negative correlations were observed between IAP and plasma IgG EndoCAb (P = 0.003) and IgM EndoCAb (P = 0.002)., Conclusions: Intra-abdominal hypertension and ACS are associated with significantly higher endotoxin exposure and ProCT concentrations, suggestive of gut barrier dysfunction. Resolution of IAH and ACS is associated with evidence for recovery of gut barrier function.

Background: To avoid ischemic necrosis, compartment syndrome is a surgical emergency treated with decompression once identified. A potentially lethal, oxidant-driven reperfusion injury occurs after decompression. N-acetylcysteine is an antioxidant with the potential to attenuate the reperfusion injury., Questions/purposes: We asked whether N-acetylcysteine could preserve striated muscle contractility and modify neutrophil infiltration and activation after simulated compartment syndrome release., Materials and Methods: Fifty-seven rats were randomized to control, simulated compartment syndrome, and simulated compartment syndrome plus N-acetylcysteine groups. We isolated the rodent cremaster muscle on its neurovascular pedicle and placed it in a pressure chamber. Chamber pressure was elevated above critical closing pressure for 3 hours to simulate compartment syndrome. Experiments were concluded at three times: 1 hour, 24 hours, and 7 days after decompression of compartment syndrome. We assessed twitch and tetanic contractile function and tissue myeloperoxidase activity. Ten additional rats were randomized to control and N-acetylcysteine administration after which neutrophil respiratory burst activity was assessed., Results: The simulated compartment syndrome decreased muscle contractility and increased muscle tissue myeloperoxidase activity compared with controls. Treatment with N-acetylcysteine preserved twitch and tetanic contractility. N-acetylcysteine did not alter neutrophil infiltration (myeloperoxidase activity) acutely but did reduce infiltration at 24 hours, even when given after decompression. N-acetylcysteine reduced neutrophil respiratory burst activity., Conclusion: N-acetylcysteine administration before or after simulated compartment syndrome preserved striated muscle contractility, apparently by attenuating neutrophil activation and the resultant oxidant injury., Clinical Relevance: Our data suggest a potential role for N-acetylcysteine in the attenuation of muscle injury after release of compartment syndrome and possibly in the prophylaxis of compartment syndrome.

Background: Clinicians have postulated that decreased atmospheric pressure during air evacuation exacerbates muscle edema and necrosis in injured limbs. The present study investigated whether the mild hypobaric, hypoxic conditions of simulated flight during muscle reperfusion worsened muscle edema and muscle injury in an established animal model., Methods: Twenty male Sprague-Dawley rats underwent tourniquet-induced hind limb ischemia for 2h. After removal of the tourniquet, rats were divided into two groups (n=10/group), and exposed to either (1) hypobaric, hypoxic conditions (HB) of 522 mm Hg (simulating 10,000 feet, the upper limit of normal aircraft cabin pressure), or (2) normobaric, normoxic conditions (NB) of 760 mm Hg (sea level), for 6h. Muscle wet weight, muscle dry:wet weight ratios, viability, and routine histology were measured on the gastrocnemius and tibialis anterior muscles. Blood samples were analyzed for percentage hematocrit, leukocyte count, and coagulation status., Results: Ischemia resulted in significant edema in both groups (P<0.05). Normobaric normoxia caused greater edema in the gastrocnemius compared with hypobaric hypoxia; the tibialis anterior was not significantly different between groups. The decrease in body weight for NB and HB was 3.4+/-1.4 and 10.7+/-1.2g, respectively (P<0.05). Hematocrit was 44.7+/-0.5 and 42.6+/-0.6 (P<0.05)., Conclusions: The hypobaric, hypoxic conditions of simulated medical air evacuation were not associated with increased muscle edema following 2h of ischemic injury. This suggests that other factors, such as resuscitation, may be the cause of muscle edema in flight-evacuated patients., (Published by Elsevier Inc.)

Objective: To investigate of the value of monitoring of saturation of blood oxygen of the injured extremity on prevention of osteofascial compartmental syndrome., Methods: Twenty patients of osteofascial compartmental syndrome included 13 male and 7 female with an average age of 32 years ranging from 13 to 60. There were 13 cases of tibial and fibual fractures, 3 cases of tibial plateau fractures, 4 cases of femoral shaft fractures. SpO2 on the end of injured extremities were dynamic monitored and osteofascial compartmental pressure was measured by modified Whiteside method. The data of two group were compared., Results: Among 20 cases, it's negative correlation between the data of pulse blood oxygen saturation and osteofascial compartmental pressure., Conclusion: The method of dynamic monitor extremity SpO2 can reflect indirectly the ischemia in muscle and nerve and report the early diagnosis and management of osteofascial compartmental syndrome.

Background: The purpose of this study was to study the impact of intra-abdominal hypertension (IAH) on the intestine., Materials and Methods: One hundred and twenty Sprague-Daley rats were divided into four groups. In the ACS group, the intra-abdominal pressure (IAP) was increased to 20 mmHg. In the ACS/DE group, increased IAP was followed by decompression. In the control1 and control2 groups, the IAP remained unchanged. Malondialdehyde (MDA), myeloperoxidase (MPO), glutathione (GSH) and glutathione peroxidase (GSH-Px) enzymes of the intestine were measured. Additionally, ileal tissues were obtained for histopathological examinations and apoptosis detection. Liver, spleen and mesenteric lymph nodes were obtained for microbiological analysis., Results: In the presence of IAH, MDA and MPO were increased, while GSH and GSH-Px were decreased. Microbiological analysis suggested bacterial translocation across the gut. Morphological examinations indicated that the Chiu's score and apoptotic index in the ACS/DE group were the highest in the four groups., Conclusions: Oxidative stress plays an important role in the intestinal damage and bacterial translocation in abdominal compartment syndrome. Additionally, the influence of oxygen free radicals occurs mainly during the period of reperfusion rather than during the IAH period.

Study Design: Case report of a patient who presented with compartment syndrome with acute renal failure after surgery for lumbar disc prolapse in knee-chest position., Objective: To describe an unusual complication of compartment syndrome in lower limb with acute renal failure following discectomy in knee-chest position., Summary of Background Data: Compartment syndrome and acute renal failure following lumbar discectomy in knee-chest position has been described in only 2 cases previously., Methods: Case report and review of literature., Result: Subsequent to prolonged surgery in knee-chest position this patient developed compartment syndrome with acute renal failure. Immediate fasciotomy was done, resulting in good recovery., Conclusion: Spine surgeon performing discectomy in knee-chest position should be aware of such an unusual complication in the postoperative period, especially if the surgery gets prolonged. Time and position should be monitored carefully to avoid such a serious complication. Early diagnosis and urgent intervention in the form of fasciotomy is required for good results.

Objective: To investigate whether microdialysis is capable of assessing metabolic derangements during intra-abdominal hypertension (IAH), and whether monitoring of the rectus abdominis muscle (RAM) by microdialysis represents a reliable approach in the early detection of organ dysfunctions in abdominal compartment syndrome (ACS)., Design: Prospective, randomized, controlled animal study., Setting: University animal research facility., Subjects: Fifteen isoflurane-anesthetized and mechanically ventilated Sprague-Dawley rats., Interventions: IAH of 20 mmHg was induced for 3 h and followed by decompression and reperfusion for another 3-h period (n = 10). Five sham-operated animals served as controls. Microdialysis was performed in the anterior gastric wall, liver, kidney, and RAM. The anterior cervical muscles served as distant reference. Glucose, lactate, pyruvate, and glycerol was analyzed throughout the 6-h experiment., Measurements and Main Results: Prolonged IAH induced significant cardiopulmonary dysfunction and persistent abdominal organ injury. Microdialysis revealed a significant increase of lactate/pyruvate and glycerol in kidney, intestine and liver, indicating ischemia, energy failure, and cell membrane damage. In addition, at 3 h IAH glucose was significantly decreased in all organs studied. The distant reference did not show any alteration of lactate/pyruvate, glycerol, and glucose over the entire 6-h observation period. In contrast to the other organs, microdialysis of the RAM showed an early and more pronounced increase of lactate, lactate/pyruvate and glycerol already at 1 h IAH. It is noteworthy that lactate, glycerol, and glucose did not completely recover upon decompression of IAH., Conclusions: Our data suggest that continuous microdialysis in the RAM may represent a promising tool for early detecting IAH-induced metabolic derangements.

Most of the existing reports on abdominal compartment syndrome (ACS) deal with pathophysiology, focusing on its clinical picture and course, and knowledge of the histopathological features of ACS is very poor. Since the heart, kidneys and lungs are the organs primarily targeted for injury in multi-organ failure, we investigated the expression of TNFalpha and apoptosis in tissue specimens of the heart. This retrospective study was conducted at the Department of Forensic Pathology, University of Foggia. A retrospective review of records extending over a period of 4 years, from 1 April 2001 to 31 March 2005, was carried out and all cases subjected to medico-legal autopsy during this period, whose detailed history and case records were available, were the subjects of our study. Over a 4-year period, on 848 cases subjected to medico-legal autopsy, three cases qualified for inclusion into the study. The immunohistochemical study revealed an intensive positive result for TNFalpha in heart specimens. The TUNEL assay was positive in heart specimens too. The presented study can contribute to elucidate the pathophysiology of fatal ACS and also define efficient markers for future therapeutic approaches suggesting anti-TNFalpha strategies may be useful in the management of ACS.

Objective: Goal-directed nutritional support is essential to improving morbidity and mortality. Open abdominal decompression is similarly crucial to the successful treatment of intra-abdominal hypertension and abdominal compartment syndrome. The open abdomen, however, places the patient at risk for potentially significant fluid, electrolyte, and presumably protein losses from the exposed viscera. Although nutritional protein assessments are frequently utilized to measure urinary nitrogen, these calculations do not consider the loss of protein from the open abdomen. We hypothesize that accurate assessment of nitrogen balance in the patient requiring an open abdomen must include either a measurement or estimation of abdominal fluid nitrogen loss., Design: Prospective, observational cohort study., Setting: Adult surgical/trauma intensive care unit of a level I trauma center., Patients: Surgical/trauma patients requiring laparotomy., Interventions: Serial 24-hr collections of urine and abdominal fluid protein were performed to characterize abdominal fluid protein loss and evaluate the clinical effect of accounting for abdominal fluid nitrogen as part of nitrogen balance calculations., Measurements and Main Results: Nitrogen intake correlates with urinary nitrogen loss but not with abdominal fluid nitrogen loss. Abdominal fluid nitrogen loss is significant and remains relatively stable in the early postoperative period. Nutritional calculations that fail to account for abdominal fluid nitrogen loss significantly overestimate actual nitrogen balance by an average of 3.5 g/24 hrs., Conclusions: The open abdomen represents a significant source of protein/nitrogen loss in the critically ill. Failure to account for this loss in nutritional calculations may lead to underfeeding and inadequate nutritional support with a direct effect on patient outcome. Although direct measurement of abdominal fluid protein loss may be optimal, an estimate of 2 g of nitrogen per liter of abdominal fluid output should be included in the nitrogen balance calculations of any patient with an open abdomen.

Background: Intra-abdominal hypertension leads to visceral organ hypoperfusion, and subsequent decompression may cause ischemia-reperfusion, releasing toxic metabolites. This study focuses on the effect of intra-abdominal hypertension on hepatic antioxidant store and the susceptibility of hepatocytes to oxidant injury., Methods: Sprague-Dawley rats (150-180 g) were acclimatized to an environment for 3 days and then divided into two groups according to challenge based on intra-abdominal pressure (0 and 30 cm H2O for control and experimental groups, respectively). After a 90-minute challenge, the rats underwent immediate laparotomy for decompression; after a further 30 minutes, one fragment of liver from the lingual lobe (>0.1 g) was excised to measure glutathione (GSH) in vivo before portal vein perfusion. After hepatocyte isolation (viability rate > 85%), the cell density was set at 1 x 10/mL for each well. The samples were cultured in an incubator for 12 hours, after which varying concentrations of t-butyl hydroperoxide (TBHP) (0.0, 0.5, 1.0, and 2.0 mmol/L) were added into the wells. After another 5-hour incubation, the total store of intracellular GSH in vitro (GSHVT) and the hepatocyte survival rates were measured for different groups of TBHP challenge using GSH assay and MTT kits., Results: The control and experimental groups consisted of 10 and 8 rats, respectively, that successfully completed the entire experimental procedure. Compared with the control group, the in vivo GSH store was significantly reduced after the intra-abdominal pressure challenge (mean +/- SE, 968.1 +/- 63.5 vs. 1,581.0 +/- 115.3 nmol/g of protein; p = 0.001). After the hepatocyte isolation, the GSHVT stores at various TBHP concentrations in the experimental rats were also similarly and significantly decreased relative to the control animals (894.4 +/- 56.4, 804.2 +/- 118.4, 586.9 +/- 86.6, and 410.2 +/- 87.4 nmol/g of protein vs. 1,282.2 +/- 112.0, 1,156.6 +/- 91.0, 995.2 +/- 92.7, and 866.8 +/- 62.4 nmol/g of protein for TBHPs of 0.0, 0.5, 1.0, and 2.0 mmol/L, respectively; all p < 0.05). Moreover, from photocytometry, the hepatocyte survival rates were significantly reduced for the experimental rats compared with the control animals after challenge with various TBHP concentrations (survival was 100%, 91.1%, 81.3%, and 72.8% vs. 100%, 99.2%, 95.0%, and 88.2%, respectively, for TBHPs of 0.0, 0.5, 1.0, and 2.0 mmol/L; p < 0.05 for the last two)., Conclusion: This animal study demonstrated that intra-abdominal hypertension and subsequent decompression deplete the total in vivo GSH store in rat livers, probably via the mechanism of ischemia-reperfusion injury, and the GSHVT after hepatocyte isolation, which makes the isolated hepatocytes of rats more susceptible to oxidant challenge.

The purpose of this study was to investigate whether an intra-abdominal pressure (IAP) of 30 mmHg lasting 24 h in a porcine model will lead to a condition comparable with the abdominal compartment syndrome (ACS) in humans. We examined 12 intubated and anesthetized domestic pigs with a mean body weight of 52.5 +/- 4.9 kg. Using a CO2 pneumoperitoneum, the IAP was increased to 30 mmHg (study group, n = 6) for an investigation period of 24 h. In the control group, the IAP remained unchanged. Investigated parameters were cardiac output (CO), peak inspiratory pressure (PIP), urine output (UO), as well as serum alanine aminotransferase (ALT), lactate, lipase, and alkaline phosphatase (AP). Additionally, histopathological examinations were performed. In the study group, CO was significantly reduced compared with the control group. All animals of this group became anuric and their PIP exceeded 40 cm H2O. Furthermore, ALT, AP, lipase, and lactate were significantly increased. Histopathologically, high-grade atelectasis in the lower lobes of the lung together with medium grade liver necrosis, medium grade proximal tubular epithelial necrosis, and medium grade mucosal bowel damage were observed. In this porcine model, an intra-abdominal pressure of 30 mmHg led to a condition comparable with the ACS. Because function or integrity of additional organ systems was impaired, an IAP of 30 mmHg has to be considered a predisposition for the multi-organ dysfunction syndrome in this porcine model.

Background/purpose: Abdominal compartment syndrome (ACS) may complicate abdominal closure in patients with abdominal wall defects, abdominal trauma, intraperitoneal bleeding, and infection. Increased intraabdominal pressure (IAP) leads to respiratory compromise, organ hypoperfusion, and a high mortality rate. This study evaluates the efficacy of continuous direct monitoring of IAP and gastric tissue pH in detecting impending ACS., Methods: Ten mongrel puppies weighing 2.8 to 6.4 kg underwent general endotracheal anesthesia, placement of an intraabdominal inflatable balloon to simulate ACS and a Swan-Ganz catheter to measure direct IAP. A gastric tonometer, nasogastric tube, foley catheter, and arterial catheter also were inserted. Half-hourly inflation's of the intraabdominal balloon were used to simulate the development of ACS. Direct intraabdominal (IAP), gastric (GP), bladder (BP), and peak airway pressures (PAP) were measured. Gastric tonometry fluid and arterial blood gas levels were obtained during inflation, and the gastric tissue pH level was calculated. Data were statistically analyzed using Pearson's correlation coefficients., Results: Baseline pressures were 2 to 5 cm H(2)O in the stomach and bladder catheters, 1 to 3 mm Hg in the intraabdominal catheter, and correlated with a gastric tissue pH level of 7.4. Significantly high correlation coefficients (cc) were observed between IAP versus BP (cc, 0.77; P <.002). IAP versus GP (cc, 0.79; P <.002) and IAP versus PAP (c, 0.83; P <.0004). A high negative correlation coefficient was noted between gastric pH and IAP (cc, 0.61; P <.026). The pH level dropped to 7.0 with BP and GP of 20 cm H(2)O and IAP of 10 mm Hg, to 6.8 at 30 cm H(2)O and 20 mm Hg, and 6.5 at 40 cm H(2)O and 30 mm Hg, respectively. However, correlation coefficients between gastric tissue pH and BP, GP, or PAP were not significant., Conclusions: These data suggest that continuous direct intraabdominal pressure monitoring is a simple and effective method that correlates well with indirect bladder or gastric pressure measurement. Changes in gastric tissue pH in association with increased intraabdominal pressure may be an early indicator of impending abdominal compartment syndrome. These observations indicate that these techniques may be more sensitive than current methods of indirect measurement, which may be associated with delayed recognition of ACS.

Objective: Abdominal compartment syndrome (ACS) has multiple well-described etiologies, but almost no attention has focused on ACS in the absence of abdominal injury. This study describes a secondary ACS that occurs after severe hemorrhagic shock with no evidence of abdominal injury., Methods: The trauma registry at a Level I trauma center was reviewed for a 13-month period beginning July 1, 1997., Results: During the study period, there were 46 of 1,216 intensive care unit admissions (4%) who required laparotomy and mesh closure of the abdominal wall because of visceral edema. In that subgroup, six patients (13% of mesh closures, 0.5% intensive care unit admissions) had hemorrhagic shock (5/1, blunt/penetrating trauma) but no evidence of intra-abdominal injury. Associated extremity compartment syndrome developed in two of six (33%). Overall mortality was four of six (67%), secondary to sepsis (n = 3), and head injury (n = 1). Time from admission to decompression averaged 3 hours in survivors and 25 hours in nonsurvivors (overall average = 18+/-9 hours). Resuscitation volume before abdominal decompression averaged 19+/-5 liters of crystalloid and 29+/-10 units of packed red blood cells. Bladder pressure averaged 33+/- 3 mm Hg. Decompression significantly improved peak inspiratory pressure (p < 0.003) and base deficit (p < 0.003)., Conclusion: ACS can occur with no abdominal injury; The incidence of secondary ACS was 0.5% in this cohort trauma intensive care unit patients, so it probably occurs more frequently than is currently appreciated. Because survivors were decompressed 20 hours before nonsurvivors, early recognition might improve outcomes. On the basis of these observations, we recommend that bladder pressures should be routinely checked and acted on appropriately when resuscitation volumes approach 10 liters of crystalloid or 10 units of packed red cells.

Background: The diagnosis of compartmental syndrome (CS) may be delayed because current monitoring techniques are invasive and intermittent and the compartment pressure (CP) that predicts ischemia is variable. Fiber-optic devices using near-infrared (NIR) wavelength reflection can determine the redox state of light-absorbing molecules and have been used to monitor venous hemoglobin saturation to detect ischemia during low-flow states. The purpose of this study was to determine if NIR spectroscopy can provide continuous, transcutaneous, noninvasive monitoring for muscle ischemia in an animal model of CS., Methods: Nine swine were anesthetized and a 20-mm NIR probe was placed over the anterolateral compartment of the hind leg to provide continuous determination of muscle oxyhemoglobin level. Needles were inserted into the compartment to measure CP. A nerve stimulator was placed over the peroneal nerve to induce dorsiflexion twitch. Albumin was infused into the muscle to incrementally increase CP until there was complete loss of dorsiflexion, then after 20 minutes fasciotomy was performed., Results: All animals lost dorsiflexion at CP of 43+/-14 mm Hg. There was a significant inverse correlation between CP and oxyhemoglobin level (r = -0.78; p < 0.001) and a correlation between oxyhemoglobin and perfusion pressure (mean arterial pressure minus CP) (r = 0.66; p < 0.001). Redox state was a more consistent predictor of twitch loss than perfusion pressure., Conclusion: Muscle oxyhemoglobin level measured by NIR spectroscopy strongly reflected CP, perfusion pressure, and loss of dorsiflexion twitch. Currently available portable NIR devices may provide the benefit of continuous, noninvasive monitoring for CS. Further studies to determine the role of this technology in the detection of compartmental syndrome are warranted.

Measuring intracompartmental pressure is a well-accepted method in evaluating a compartment syndrome, which may occur after limb ischaemia followed by reperfusion. As a compartment syndrome is paralleled by a decreased microcirculation it should be possible also to evaluate a compartment syndrome by measuring intramuscular partial oxygen tension (PO2). In this study, anaesthetized rats (spontaneous breathing via tracheotomy) were subjected to infrarenal ligation of the aorta. A pressure catheter was placed subfascial in the crural muscle group of one hind limb, whereas the contralateral side was prepared with a PO2 catheter. Besides a sham operated group, three experimental groups were subjected to either 2, 4 or 6 h of ischaemia followed by 4 h of reperfusion. One further group was also subjected to 4 h of ischaemia and 4 h of reperfusion but received a fasciotomy at the time of reperfusion. Compartment pressure and intramuscular PO2 were recorded every 15 min. For histological examination muscle specimens were obtained after each experiment. Two hours of ischaemia followed by 4 h of reperfusion did not result in any morphological changes and also in no significant change in compartment pressure during both phases, whereas PO2 significantly dropped during ischaemia (from 19.0 mmHg to 3.0-5.0 mmHg) and returned to normal during reperfusion. In prolonged ischaemia (4 h) morphologically a severe interstitial oedema was evident, compartment pressure increased during reperfusion (from 2.0 mmHg to 8.8 mmHg) and PO2 dropped during ischaemia to 3.0 mmHg and did not return to normal during reperfusion (10.5 mmHg versus 19.0 mmHg normal). In the case of 6 h ischaemia, partial necrosis and no interstitial oedema was found morphologically. There was no significant change in compartment pressure throughout the study, and PO2 remained significantly decreased even during reperfusion (2.0-3.0 mmHg). Normal compartment pressure could mislead to false negative interpretation of microcirculatory disorders preceding or following compartment syndrome, whereas PO2 clearly identifies the microcirculatory state of the muscle. Thus, intramuscular PO2 monitoring presents a valuable method in evaluating compartment syndrome, especially where there are suspected clinical signs and risk of ischaemia but normal compartment pressure.

Surgery in the lithotomy position can provoke ischaemic lesions in the lower leg. We assessed lower leg oxygen saturation using near-infrared spectroscopy (NIRS) in 42 patients undergoing urinary tract surgery. Lower leg perfusion pressure was calculated as the difference of mean arterial pressure to pressure in an air bag supporting the lower leg and the hydrostatic pressure difference from the level of the lower leg to the heart. During elevation of the lower leg for 25 (3-65) min (median and range), mean arterial pressure decreased from 100 (73-125) to 77 (53-112) mmHg and the lower leg perfusion pressure dropped from 103 (80-122) to 21 (-6-65) mmHg, corresponding to a reduction in oxygen saturation of the medial gastrocnemius muscle from 68% (40-100%) to 58% (20-96%) (P < 0.01). The results demonstrate significant desaturation of the calf muscles during surgery in the lithomy position.

Variations in the levels of muscle hemoglobin and of myoglobin oxygen saturation can be detected non-invasively with near-infrared spectroscopy. This technique could be applied to the diagnosis of chronic compartment syndrome, in which invasive testing has shown increased intramuscular pressure associated with ischemia and pain during exercise. We simulated chronic compartment syndrome in ten healthy subjects (seven men and three women) by applying external compression, through a wide inflatable cuff, to increase the intramuscular pressure in the anterior compartment of the leg. The tissue oxygenation of the tibialis anterior muscle was measured with near-infrared spectroscopy during gradual inflation of the cuff to a pressure of forty millimeters of mercury (5.33 kilopascals) during fourteen minutes of cyclic isokinetic dorsiflexion and plantar flexion of the ankle. The subjects exercised with and without external compression. The data on tissue oxygenation for each subject then were normalized to a scale of 100 per cent (the baseline value, or the value at rest) to 0 per cent (the physiological minimum, or the level of oxygenation achieved by exercise to exhaustion during arterial occlusion of the lower extremity). With external compression, tissue oxygenation declined at a rate of 1.4 +/- 0.3 per cent per minute (mean and standard error) during exercise. After an initial decrease at the onset, tissue oxygenation did not decline during exercise without compression. The recovery of tissue oxygenation after exercise was twice as slow with compression (2.5 +/- 0.6 minutes) than it was without the use of compression (1.3 +/- 0.2 minutes).

Currently, the definitive diagnosis of chronic compartment syndrome is based on invasive measurements of intracompartmental pressure. We measured the intramuscular pressure and the relative oxygenation in the anterior compartment of the leg in eighteen patients who were suspected of having chronic compartment syndrome as well as in ten control subjects before, during, and after exercise. Chronic compartment syndrome was considered to be present if the intramuscular pressure was at least fifteen millimeters of mercury (2.00 kilopascals) before exercise, at least thirty millimeters of mercury (4.00 kilopascals) one minute after exercise, or at least twenty millimeters of mercury (2.67 kilopascals) five minutes after exercise. Changes in relative oxygenation were measured with use of the non-invasive method of near-infrared spectroscopy. In all patients and subjects, there was rapid relative deoxygenation after the initiation of exercise, the level of oxygenation remained relatively stable during continued exercise, and there was reoxygenation to a level that exceeded the pre-exercise resting level after the cessation of exercise. During exercise, maximum relative deoxygenation in the patients who had chronic compartment syndrome (mean relative deoxygenation [and standard error], -290 +/- 39 millivolts) was significantly greater than that in the patients who did not have chronic compartment syndrome (-190 +/- 10 millivolts) and that in the control subjects (-179 +/- 14 millivolts) (p < 0.05 for both comparisons). In addition, the interval between the cessation of exercise and the recovery of the pre-exercise resting level of oxygenation was significantly longer for the patients who had chronic compartment syndrome (184 +/- 54 seconds) than for the patients who did not have chronic compartment syndrome (39 +/- 19 seconds) and the control subjects (33 +/- 10 seconds) (p < 0.05 for both comparisons).

Isolated intact quiescent myocytes from the adult rat were used as a model system for investigating the determinants of contracture induced by metabolic deprivation. The model simulated the pattern of contracture and ATP decline seen in the intact heart during ischemia. Three new insights into the contracture process were gained: (1) in the quiescent cell system, the rate of onset of contracture was independent of external Ca2+, supporting the view that the Ca2+ dependence of the rate of onset in the whole heart is related to beat-dependent substrate utilization; (2) the second phase of ATP decline was paralleled by a decline in the percentage of cells which had not undergone contracture, suggesting that-in any cell-contracture is immediately preceded by a total loss of ATP; and (3) oligomycin delayed the onset of contracture by 55 +/- 12%, suggesting that mitochondrial ATPase activity is a significant drain on energy resources in the quiescent ischemic heart.

Unlabelled: Skeletal-muscle necrosis was evaluated in previously pressurized canine compartments using technetium-99m stannous pyrophosphate and classic histological criteria. Intracompartmental necrosis was quantitated in the anterolateral muscle compartment of each dog by uptake of 99mTc stannous pyrophosphate using the contralateral anterolateral compartment as an internal control. Representative specimens of muscle were sampled in experimental and control legs of each dog and were analyzed by qualitative histological techniques. Muscle necrosis was assessed in compartments forty-eight hours after pressurization to levels of ten to 120 millimeters of mercury for eight hours in thirty-seven dogs. In another dog, neither anterolateral compartment was pressurized so that both compartments acted as control muscle. The results in these experiments identify a threshold pressure level (thirty millimeters of mercury) and duration (eight hours) at which significant muscle necrosis occurs at normal blood pressure. Our findings imply that a quantitative relationship exists between incorporation of 99mTc stannous pyrophosphate and the level of intracompartmental pressure. This uptake technique, however, is not suitable for diagnosing compartment syndrome in patients with a threatened compartment syndrome. We suggest that intracompartmental pressure measurements by the wick-catheter technique, in conjunction with clinical findings, offer the best means for diagnosing compartment syndrome., Clinical Relevance: Significant muscle necrosis associated with an impending compartment syndrome occurs at a threshold intracompartmental pressure of thirty millimeters of mercury after eight hours. Since time variables are often unknown in suspected compartment syndromes, fasciotomy is recommended when intracompartmental pressure exceeds thirty millimeters of mercury in a patient with normal blood pressure. The use of this threshold pressure level as an indication for fasciotomy requires a device for measuring intracompartmental pressure such as the wick catheter.

The muscle proteins of rabbits with the compartment syndrome caused by tourniquet were studied by SDS-polyacrylamide gel electrophoresis and the compartment pressure post-ischemia was measured. The post-ischemic pressure in the anterior compartment increased more than that in the deep-posterior compartment. The phoretic patterns of structural and soluble proteins changed after ischemia, and their degeneration appeared to depend on the degree of pressure increase. In ischemic contracture, the patterns of myosin light chains of type 1 fibers changed to those of type 2 fibers. This indicated the possibility of fiber type transformation from type 1 to type 2 in ischemic contracture.

In an experimental ischemic compartment syndrome in dogs, phosphorus (31P) nuclear magnetic resonance (NMR) spectroscopy was used to determine the tissue pressure threshold at which resting skeletal muscle begins to use anaerobic energy sources due to insufficient cellular oxygen delivery. The interactive effects of systemic perfusion pressure and moderate muscle trauma on this anaerobic threshold were also evaluated. The severity of cell injury produced by various degrees of compartment pressurization over an eight-hour period was concomitantly studied using muscle biopsy and electron microscopy. Clinical correlation of a preliminary patient series studied using 31P-NMR demonstrated that the threshold for cellular metabolic derangement in skeletal muscle subjected to increased tissue pressure was more closely associated with the difference between mean arterial blood pressure (MABP) and compartment pressure than with the absolute compartment pressure alone. The difference is termed MABP-compartment pressure, or delta P. The lowest delta P at which a normal cellular metabolic state can be maintained is approximately 30 mmHg in normal muscle and 40 mmHg in moderately traumatized muscle. It is imperative to interpret compartment pressure measurements in light of the degree of soft tissue trauma sustained and the patient's blood pressure, as well as the clinical signs and symptoms.

Because it is postulated that compartment syndrome developing secondary to an acute arterial occlusion may be due to reperfusion injury, oxygen-derived free radicals have been implicated in its genesis. To assess the possible beneficial effect of free radical scavengers in this setting, we used a previously established in vivo canine model of compartment syndrome to compare four groups: group I, no treatment; group II, prophylactic fasciotomy; group III, intravenous albumin conjugated superoxide dismutase (SOD); group IV, intravenous mannitol (hydroxyl radical scavenger). Both hind limbs were completely devascularized at the popliteal level except for an isolated pedicle to the anterior compartment. The right limb served as the nonischemic control, whereas the left underwent 8 hours of ischemia followed by reperfusion. Continuous monitoring of transfascial oxygen tension (tfPO2) demonstrated severe ischemia during occlusion (tfPO2 5.7 +/- 5.1 mm Hg) and restoration of blood flow with reperfusion (mean tfPO2 50 to 60 mm Hg). Measurements of compartment pressure were significantly higher after reperfusion in groups I, III, and IV when compared with those of group II (p less than 0.001, groups I and II; p less than 0.01, group IV). Extent of muscle necrosis assessed by technetium pyrophosphate scanning and expressed as a ratio of left to right legs was as follows: group I, 8.9 +/- 5.0; group II, 2.6 +/- 0.5; group III, 2.8 +/- 0.8; group IV, 1.8 +/- 0.6. Muscle contraction studies 16 hours after reperfusion indicated abnormal findings in all but group II. In conclusion, administration of free radical scavengers did not preserve normal neuromuscular function despite a significant reduction in muscle damage.(ABSTRACT TRUNCATED AT 250 WORDS)

In this study, the tolerance of skeletal muscle to tourniquet application (ischemia) and to acute compartment syndrome (ischemia and pressure) was compared. In five animals, the cuff of a pneumatic tourniquet was inflated to 350 millimeters of mercury at the level of the thigh for three hours. In five other animals, an acute experimental compartment syndrome was created in one anterolateral compartment by autologous plasma infusion. The compartment pressure (measured by wick catheter) was maintained at a level equal to the mean arterial pressure for three hours. At three hours, reperfusion was established in both groups, either by tourniquet release or by decompressive fasciotomy and epimysiotomy. During both the ischemic period and a two-hour recovery period immediately thereafter, the mean intracellular pH and high-energy phosphate profile (levels of adenosine triphosphate and phosphocreatine) of the muscles of the anterolateral compartment were monitored non-invasively by phosphorus nuclear magnetic-resonance spectroscopy. Muscle biopsies were done the following day to take specimens for electron microscopic analysis of ultrastructural cellular degeneration. During ischemia, the cellular levels of phosphocreatine decreased at an identical rate in both groups. In contrast, the levels of adenosine triphosphate diminished rapidly in the animals with the compartment syndrome, but remained unchanged in the tourniquet group. Ischemic muscle acidosis was more severe in dogs with the compartment syndrome. In the tourniquet group, the phosphocreatine, adenosine triphosphate, and pH were all normal within fifteen minutes after release of the tourniquet, but these values remained depressed even two hours after fasciotomy in the group with compartment syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this study was to quantitate the intracellular high-energy phosphate compounds during 6 hours of tissue ischemia in the anterior tibial compartment of beagles subjected to an induced traumatized compartment syndrome. The goal of this work was to provide clinicians with objective criteria to augment clinical judgment regarding surgical intervention in the impending compartment syndrome. A beagle model was utilized in which the Delta pressure (difference between the mean arterial pressure and compartment pressure) could be controlled. The model, in conjunction with 31P-magnetic resonance spectroscopy (MRS), allowed a measure of high-energy phosphate compounds and pH in the compartment at various Delta pressures. The extent of ischemic metabolic insult in the compartment was then quantitated. Our data suggest the following: 1) lower Delta pressures result in a proportionally greater drop in the intracellular phosphocreatine ratio and pH; 2) at lower Delta pressures, there is proportionally greater decline in the percentage recovery post-fasciotomy; 3) blood pressure is extremely important and periods of hypotension may result in increased muscle damage at lower compartment pressures.