Early assessment of extremity compartment syndrome by biochemical markers in a rat model.

BACKGROUND: This experimental study aimed to define a biochemical marker that will enable early diagnosis of acute compartment syndrome (ACS) of extremities, a mortal condition that occurs due to trauma. METHODS: A total of 15 Wistar rats were included in the study in which saline infusion technique, a clinically compatible ACS model, was applied. After the rats were anesthetized with ketamine-xylazine, the in-compartment pressure of the hind limb was slowly increased with saline delivered through the angiocatheter, and after reaching the target compartment pressure, the pressure level was kept with a rubber tourniquet. The in-compartment pressure level was continuously monitored with a pressure transducer. The rats were divided into three groups. No intervention was applied to the control group (CG) (n = 3). In study group 1 (SG1) (n = 6), ACS was created using the saline infusion technique, keeping the in-compartment pressure between 30 and 40 mmHg for 45 min. In study group 2 (SG2) (n = 6), ACS was created using the saline infusion technique, keeping the in-compartment pressure between 30 and 40 mmHg for 90 min. Fasciotomy was performed on all rats. Tissue samples were obtained for histopathological examination and blood samples for biochemical analysis. RESULTS: Total oxidant status (TOS) (p = 0.004), ischemia-modified albumin (IMA) (p = 0.030), aspartate transferase (AST) (p = 0.003) and neopterin (p = 0.012) levels differed significantly between groups in the early period of muscle ischemia. In fact, TOS levels differed significantly between the groups even in the cellular phase where signs of ischemia were not observed (p = 0.048, p = 0.024). According to histopathological evaluation, there was no significant difference between the groups. DISCUSSION: TOS can be detected in the early reversible stage of ischemia, when the histopathological findings of ACS do not occur.

Open Sciatic Nerve Decompression for Compartment Syndrome after Prolonged Lithotomy Position: A Case Report.

Background: Position-related compressive nerve injury is a frequently reported complication of the lithotomy position. In contrast, compartment syndrome-induced neuropathy after lithotomy with prolonged surgery is rare and prone to misdiagnosis. This case describes the successful open decompression of sciatic neuropathy due to compartment syndrome after a prolonged lithotomy position. Case presentation: A 56-year-old male patient complained of an abnormal sensation in the lower leg and difficulty in dorsiflexion and plantarflexion of the left foot and toes after laparoscopic anterior hepatic sectionectomy for 16 h in a lithotomy position. Physical examination revealed severe pain and paresthesia below the distal left thigh. In manual muscle test grading, dorsiflexion and plantarflexion of the left ankle and toes were classified as grade 1. Computed tomography and magnetic resonance imaging showed ischemic changes in the mid-thigh posterior muscles, and the sciatic nerve was severely swollen at the distal thigh, which was compressed by the proximal edge of the well-leg holder. After debridement of the necrotic tissue and decompression of the sciatic nerve, the pain subsided immediately, and the ankle and toe dorsiflexion motor function improved to grade 4. Conclusions: Most case reports of compressive neuropathy associated with the lithotomy position have been related to conservative treatment. However, if a lesion compressing the nerve is confirmed in an imaging study and the correlation with the patient's symptoms is evident, early surgical intervention can be an effective treatment method to minimize neurological deficits.

Postoperative extremity compartment syndrome in a cancer center: Incidence and risk factors.

OBJECTIVE: Postoperative compartment syndrome is a reported complication with known patient- and treatment-specific risk factors. Cancer patients carry unique risk factors associated with their underlying disease and long, complex procedures. While elevated serum lactate in traumatic and intensive care settings portends higher risk, no laboratory parameter has demonstrated utility in postoperative risk stratification. Postoperative extremity compartment syndrome in the study institution's cancer population was examined and whether intraoperative serum lactate correlates with postoperative compartment syndrome risk was investigated. METHODS: A 1:2 case-control study was performed, which compared cancer patients with postoperative compartment syndrome to those who underwent similar surgical procedures without this complication. Twelve patients were matched to 24 controls by sex, age, surgical procedures, and duration of surgery. Patient and operative variables were analyzed for prognostic significance. RESULTS: The compartment syndrome rate was 0.09% of all cases (n = 13,491); 0.12% of cases ≥ 3 h' duration (n = 9,979), and 0.25% of cases ≥ 5 h (n = 4,811). Compared with controls, the case group had higher median BMI (31.7 kg/m2 vs. 25.4 kg/m2, P = 0.001), and median intraoperative lactate level (4.05 mmol/L vs. 1.5 mmol/L, P = 0.047). CONCLUSION: Our institutional incidence of postoperative compartment syndrome was similar to that of non-oncologic institutions. While many traditional risk factors did not prove to be influential in our patients, elevated median body mass index and intraoperative serum lactate were identified as risk factors for postoperative compartment syndrome in a cancer population.

Thoracoabdominal compartment syndrome complicating right-sided diaphragmatic eventration with co-existent unilateral renal agenesis

Diaphragmatic eventration (DE) associated with intestinal malrotation and renal agenesis is a rare entity. The authors report a case of a 69-year-old man who had symptoms of heart failure. He had a previous imaging diagnosis of right diaphragmatic eventration and dilated cardiomyopathy. He died on the second day after the hospital admission and had a post mortem examination that confirmed complete right diaphragmatic eventration, intestinal malrotation, left renal agenesis, dilated cardiomyopathy, and anteriorly rotated right kidney and had findings suggestive of a thoracoabdominal compartment syndrome. Thoracoabdominal compartment syndrome is described as transmission of abdominal pressure through a defective diaphragm causing compression of the hemithorax viscera and mediastinal shift with a hemodynamic alteration. The association of these anomalies is rare, and the possibility of this finding in a patient with eventration should always be considered.

Acute compartment syndrome in the limb.

Compartment syndrome of the limb is a true orthopaedic emergency that warrants prompt evaluation and treatment. Acute compartment syndrome of the limb is not uncommon and has the potential to cause devastating morbidity and mortality. Failure to provide urgent surgical intervention once established can lead to irreversible tissue damage within hours of onset. Compartment syndrome can occur across all limbs, the buttocks and even the abdomen, but this article focuses solely on the diagnosis of acute compartment syndrome of the limb. Acute compartment syndrome can have a wide range of causes, with trauma representing approximately 70% of cases.

Compartmental Strabismus.

Recent reports confirm innervational compartments of select rectus extraocular muscles as well as the superior oblique.1 Histopathological and orbital imaging studies demonstrate well defined compartmental innervation of the horizontal rectus muscles with less differentiation in the vertical rectus muscles. Acquired vertical misalignment not associated with cyclovertical muscle dysfunction has been associated with horizontal rectus muscle compartment dysfunction. Pattern and other forms of strabismus have been associated with segmental or compartmental abnormal innervation of the extraocular muscles. Taking advantage of segmental function and innervation, selective weakening and strengthening procedures have been used to treat patients with incomitant near/distance disparities, incomitant vertical and torsional strabismus, and patients with A- and V-pattern strabismus.

Releasing Burn-Induced Compartment Syndrome by Enzymatic Escharotomy-Debridement: A Case Study.

Burn-induced compartment syndrome represents a serious and acute condition in deep circumferential burns of the extremities which, if left untreated, can cause severe complications. The surgical escharotomy that releases the high subdermal pressure is the therapeutic treatment of choice for burn-induced compartment syndrome. Guidelines for escharotomy indications and timing include pressure greater than 30 mm Hg and 6 Ps (Pain, Pallor, Paresthesia, Paralysis, Pulseless, and Poikilothermia). Nevertheless, despite the need for an early as possible pressure release, escharotomy is often delayed when a capable surgeon is not available, or if the indication is not completely clear to justify potential risks associated with surgical escharotomy. Early treatment of circumferential burns of the extremities with a Bromelain-based enzymatic agent NexoBrid® may represent a less traumatic and invasive procedure to reduce intra-compartmental pressure, replacing surgical escharotomy. This case study of 23 patients describes the variation of compartmental pressure in patients with circumferential burns of the extremities treated with NexoBrid® enzymatic escharotomy-debridement. All the patients were treated with NexoBrid® within 2 to 22 hours post-injury in our Burn Intensive Care Center. The excessive pressure recorded before treatment returned to normal below 30 mm Hg and an approximately 60% reduction of the compartmental pressure was observed in most cases within 1 hour from NXB application. On NexoBrid® removal after 4 hours complete debridement-escharotomy of the burns was achieved. Enzymatic escharotomy-debridement appears to be a useful and safe method to reduce postburn compartmental pressure. Additional randomized, well-controlled powered studies are needed to further support these results.

Postoperative non-traumatic compartment syndrome (PNCS) in gynecologic surgery.

PURPOSE: The postoperative non-traumatic compartment syndrome (PNCS) is a rare, but serious postoperative complication. Etiology, risk factors and clinical manifestation of PNCS are not well characterized since data in gynecologic and obstetric patients are limited. METHODS: We performed a retrospective monocentric study of patients who underwent surgery for gynecologic or obstetrics conditions and identified five cases of PNCS, which were analyzed and compared to a control cohort in regard of incidence, clinical presentation, risk factors and clinical outcome. RESULTS: Five cases of PNCS were identified among 19.432 patients treated between 2008 and 2019 with an incidence rate of 0.026%. The clinical examination was shown to be unreliable, lacking sensitivity in most clinical signs. Young age, obesity and long operation time were risk factors for the development of a PNCS. Fasciotomy for the treatment of a PNCS should not be delayed, since permanent function loss may occur early. CONCLUSION: A low threshold of clinical suspicion might be prudent to identify PNCS following gynecologic surgery. In the presence of the described risk factors, any suspicion of a PNCS should be evaluated further and if necessary treated with fasciotomy urgently.

An atypical presentation of leiomyosarcoma causing extremity compartment syndrome of the crural region in a Dutch Warmblood mare: a case report.

A 12-year-old Warmblood mare was presented with an acute onset left hindlimb lameness associated with generalised soft tissue swelling of the entire limb and medial saphenous vein (MSV) thrombophlebitis. A presumptive diagnosis of extremity compartment syndrome (ECS) was made. Due to the clinical deterioration, emergency fasciotomy of the crural fascia and biopsy was performed. Histological and immunohistochemical examination of the samples confirmed a diagnosis of leiomyosarcoma likely originating from the tunica media of the MSV. This report is the first to describe an unique combination of ECS and thrombophlebitis associated with a leiomyosarcoma in a horse.

Risk factors for death and amputation in acute leg compartment syndrome.

INTRODUCTION: The primary objective of this study is to determine whether time from injury to fasciotomy is associated with increased risk for death or limb amputation in patients with acute leg compartment syndrome. The secondary objective of this study is to identify other risk factors for death or limb amputation in patients with acute leg compartment syndrome. METHODS: In an institutional review board approved retrospective study, we identified 546 patients with acute compartment syndrome of 558 legs treated with fasciotomies from January 2000 to June 2015 at two Level I trauma centers. Our primary outcome measures were death and limb amputation during inpatient hospital admission. Electronic medical records were analyzed for patient-related factors and treatment-related factors. Bivariate analyses were used to screen for variables associated with our primary outcome measures, and explanatory variables with a p value below 0.05 were included in our multivariable logistic regression analyses. RESULTS: In-hospital death occurred in 6.6% and in-hospital limb amputation occurred in 9.5% of acute leg compartment syndrome patients. Neither death nor limb amputation was found to be associated with time from injury to fasciotomy. Multivariable logistic regression analyses showed that older age (p = 0.03), higher modified Charlson Comorbidity Index (p = 0.009), higher potassium (p = 0.02), lower hemoglobin (p = 0.002), and higher lactate (p < 0.001) were associated with death, and diabetes mellitus (p = 0.05), no compartment pressure measurement (p = 0.009), higher PTT (p = 0.03), and lower albumin (p = 0.01) were associated with limb amputation. CONCLUSIONS: Time to fasciotomy is not found to be associated with death or limb amputation in acute leg compartment syndrome. Death and limb amputation are associated with patient-related factors and injury severity. LEVEL OF EVIDENCE: Level III Prognostic.

Pressure related injuries: A burning issue?

INTRODUCTION: To the majority of health care professionals, burns present as a challenging and potentially distracting diagnosis. Because of their perceived complexity, they often eclipse other medical problems which can often be life threatening. Pressure related injuries, in rare instances can mimic and be mistaken for full thickness burns. Long lies may cause pressure necrosis of decubitus areas and compartment syndrome of vulnerable areas. Compartment syndrome, is a surgical emergency requiring prompt diagnosis and intervention. It may be missed in the context of a long lie after a collapse and maybe detrimental to patients' prognosis. METHODS: We reviewed cases referred to our Burns unit in the last four months to find cases of pressure related injuries referred as burn wounds. Furthermore, we also performed a literature search to find any similar cases to ours. RESULTS: Two cases, with acute pressure related injuries from long lies had been mistaken for burn wounds, were referred to our unit in the last four months. In one case a missed compartment syndrome resulted in a below elbow amputation. CONCLUSION: Pattern analysis and recognition are very important diagnostic tools in medicine. Detailed history taking and examination cannot be emphasised enough. Training both emergency departments and plastic surgeons in recognising long lie related injuries will decrease possible associated dangers such as missing a compartment syndrome.

Carbon monoxide-releasing molecule-3 (CORM-3) offers protection in an in vitro model of compartment syndrome.

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.

An Acute Paraspinal Compartment Syndrome: Anatomic Description of the Compartment and Surgical Technique.

An acute paraspinal compartment syndrome (CS) is a rare condition and is only described in a few case reports. In our spine surgery department, a 16-year-old boy with severe low back pain due to a lumbar paraspinal CS. was treated with a paraspinal fasciotomy. After this case, we performed a cadaver study to determinate the compartment. The objective of this paper is to give a description of the anatomic lumbar paraspinal compartment and our surgical technique, a transmuscular paraspinal approach described by Wiltse and colleagues. The lumbar CS is most often seen in the lateral compartment where the erector spinae muscle, subdivided into the iliocostalis and the longissimus, is encased within a clear fascia. Lumbar paraspinal CS is a rare complication but should always be recognized. A thorough knowledge of the anatomy helps you to understand the clinical signs and start a correct treatment.

Suspected Compartment Syndrome, Consumptive Thrombocytopenia, and Anemia Secondary to a Ruptured Arterial Aneurysm or Pseudoaneurysm Following Multiple Stifle Surgeries.

A 12 yr old male neutered beagle was presented on transfer to the intensive care unit with severe anemia, thrombocytopenia, and bruising detected 1 day after undergoing tibial plateau leveling osteotomy surgery. The patient had undergone extra-capsular stifle stabilization surgery 14 wk prior to treat ligament disease in the same knee. Laboratory testing and treatment for anemia, presumptive immune-mediated thrombocytopenia, and possible hemostatic disorder was initiated. A persistent anemia, progressive thrombocytopenia, and the development of a firm swelling and neurologic impairment in the limb raised concerns for compartment syndrome (CS). A musculoskeletal ultrasound revealed a large aneurysm in the caudal thigh surrounded by abnormal muscle tissue. The patient underwent amputation of the limb and recovered without further complication. Pathology findings were consistent with the development of femoral CS secondary to a ruptured peripheral arterial aneurysm or a pseudoaneurysm. A consumptive thrombocytopenia and regenerative anemia were attributed to periodic or progressive thrombosis of the vessel and regional hemorrhage. Postoperative CS can develop in combination with peripheral arterial aneurysm or pseudoaneurysm, and screening for vascular abnormalities as well as CS should be considered in complicated recovery from orthopedic surgery with compatible clinical signs including progressive soft tissue swelling, persistent anemia, and thrombocytopenia.

Correlation Between IL-20 and De Quervain's Disease Severity.

De Quervain's disease is a stenosing tenosynovitis of the first dorsal compartment of the wrist. Histopathological studies have reported that the thickening of the first dorsal retinaculum is characterized by degeneration rather than inflammation. However, significant infiltration of mast cells and macrophages was noted in a torn tendon study, which suggested that innate immune pathways are part of the mechanism that mediates early tendinopathy. Recently, Interleukin-20 (IL-20) has been reported to provoke potent inflammation and regulate angiogenesis and chemotaxis, which are important for the pathogenesis of inflammatory diseases. The main purpose of our study was to investigate the correlation between IL-20 and tumor necrosis factor (TNF-α) and clarify the potential predictor of tendinopathy progression. Hematoxylin and eosin (H & E) and immunohistochemistry (IHC) staining were used to score and analyze the clinical outcome. TNF-α, IL-20 and related inflammation cytokines were examined. Moreover, the tenocytes were cultured with a stimulator and were used to examine inflammatory cytokine secretions. A real-time polymerase chain reaction (Real-time PCR) was used to detect the gene expression profile. The IHC data showed that TNF-α is up-regulated in grade III de Quervain's. The analysis data showed that IL-20 is positively correlated with TNF-α and disease severity. The real-time PCR showed that the inflammation stimulator enhanced the expression of IL-20 mRNA expression. Inflammation cytokines such as TNF-alpha, transforming growth factor-ß (TGF-ß) and IL-1 have been used as predictors of de Quervain's; IL-20 is a new predictor based on this study. In the future, IL-20 expression's involvement in the molecular mechanism of the severity of de Quervain's should be further investigated.

Transient Orbital Compartment Syndrome Caused by Spontaneous Lamina Papyracea Dehiscence.

Orbital compartment syndrome typically occurs due to trauma or burns. Here we discuss a case of spontaneous lamina papyracea dehiscence associated with transient orbital compartment syndrome. A previously healthy woman presented to the Emergency Department complaining of unilateral eye pain after nose blowing. The patient did not have any pupillary or extra-ocular movement abnormalities; however, she did have mildly decreased visual acuity in the affected eye. Intraocular pressure was found to be elevated and a subsequent CT scan showed orbital emphysema with spontaneous dehiscence of the lamina papyracea. The intraocular pressure decreased within hours, and ultimately, she required no intervention. [Full article available at http://rimed.org/rimedicaljournal-2018-02.asp].

Systemic Administration of Carbon Monoxide-Releasing Molecule-3 Protects the Skeletal Muscle in Porcine Model of Compartment Syndrome.

OBJECTIVES: Acute limb compartment syndrome, a complication of musculoskeletal trauma, results in muscle necrosis and cell death. Carbon monoxide, liberated from the carbon monoxide-releasing molecule-3, has been shown protective in a rat model of compartment syndrome. The purpose of this study was to test the effect of carbon monoxide-releasing molecule-3 in a preclinical large animal model of compartment syndrome, with the ultimate goal of developing a pharmacologic adjunct treatment for compartment syndrome. DESIGN: Animal research study. SETTING: Basic research laboratory in a hospital setting. SUBJECTS: Male Yorkshire-Landrace pigs (50-60 kg). INTERVENTIONS: Pigs underwent 6 hours of intracompartmental pressure elevation by infusing fluid into the anterior compartment of the right hind limb. Carbon monoxide-releasing molecule-3 was administered systemically (2 mg/kg, IV) at fasciotomy, followed by 3-hour reperfusion. MEASUREMENTS AND MAIN RESULTS: Muscle perfusion, inflammation, injury, and apoptosis were assessed in the skeletal muscle. Systemic leukocyte activation was assessed during compartment syndrome and reperfusion. Elevation of hind limb intracompartmental pressure resulted in significant microvascular perfusion deficits (44% ± 1% continuously perfused capillaries in compartment syndrome vs 76% ± 4% in sham; p < 0.001), increased tissue injury (ethidium bromide/bisbenzimide of 0.31 ± 0.07 in compartment syndrome vs 0.17 ± 0.03 in sham; p < 0.05), apoptosis (fluorescence in vivo/bisbenzimide of 0.26 ± 0.06 in compartment syndrome vs 0.13 ± 0.03 in sham; p < 0.05), and systemic leukocyte activation (14.7 relative luminescence units/10 polymorphonuclear leukocytes in compartment syndrome vs 1.0 ± 0.1 in baseline; p < 0.001). Systemic application of carbon monoxide-releasing molecule-3 at fasciotomy increased the number of continuously perfused capillaries (68% ± 3%; p < 0.001), diminished tissue injury (ethidium bromide/bisbenzimide of 0.13 ± 0.04; p < 0.05), apoptosis (fluorescence in vivo/bisbenzimide of 0.12 ± 0.03; p < 0.05), and blocked systemic leukocyte activation (3.9 ± 0.3 relative luminescence unit/10 polymorphonuclear leukocytes; p < 0.001). CONCLUSIONS: Administration of carbon monoxide-releasing molecule-3 at fasciotomy offered protection against compartment syndrome-induced microvascular perfusion deficit, tissue injury, and systemic leukocyte activation. The data suggest the potential therapeutic application of carbon monoxide-releasing molecule-3 to patients at risk of developing compartment syndrome.