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Orthopaedic Proceedings
Vol. 93-B, Issue SUPP_III | Pages 280 - 280
1 Jul 2011
Lawendy A McGarr G Phillips J Sanders DW Bihari A Badhwar A
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Purpose: Severe compartment syndrome is associated with renal failure, end organ damage, and systemic inflammatory response syndrome (SIRS). Intravital videomicroscopy (IVVM) is a useful tool to study capillary perfusion and inflammation in end organs such as the liver and lungs. In this study, the systemic effect of hindlimb compartment syndrome was studied using hepatic IVVM. The purpose was to measure the effect of increased hindlimb intracompartmental pressure on hepatocyte viability, inflammation, and blood flow in a rodent model.

Method: Ten Wistar rats were randomised into control (C) and Compartment Syndrome (CS) groups. Animals were anaesthetized with 5 % isoflurane. Mean arterial pressure was monitored using a carotid artery catheter. Elevated intracompartmental pressure (EICP) was induced by saline infusion into the anterior compartment of the hind limb and maintained for 2 hours between 30–40mmHg in the CS group. Two hours following fasciotomy, the liver was analyzed using IVVM to quantify capillary perfusion as a measure of microvascular dysfunction. The numbers of adherent and rolling leukocytes in venules and sinusoids were quantified to measure the inflammatory response. Irreversible hepatocyte injury was measured using a fluorescent vital dye which labels the nuclei of severely injured cells.

Results: Hepatocellular injury was significantly higher in the CS group (325±103 PI labeled cells/10-1 mm2) compared to controls (30±12 PI labeled cells/10-1 mm2)(p=0.0087). The number of adherent venular white blood cells (WBC) was significantly higher for the CS group (5±2/hpf) than controls (0.2±0.2)(p=0.0099). Volumetric blood flow was not significantly different between CS and controls.

Conclusion: After only 2 hours of compartment syndrome in this animal model, the number of activated white blood cells increased 25-fold and liver cellular injury increased 10-fold compared to controls. Marked systemic inflammation and hepatocellular damage was detected in response to isolated limb compartment syndrome. Compartment syndrome is a low-flow ischemia/reperfusion injury with a profound inflammatory response. Further research into the severe end-organ damage associated with compartment syndrome is required.


The Bone & Joint Journal
Vol. 98-B, Issue 8 | Pages 1132 - 1137
1 Aug 2016
Lawendy A Bihari A Sanders DW Badhwar A Cepinskas G

Aims

Compartment syndrome results from increased intra-compartmental pressure (ICP) causing local tissue ischaemia and cell death, but the systemic effects are not well described. We hypothesised that compartment syndrome would have a profound effect not only on the affected limb, but also on remote organs.

Methods

Using a rat model of compartment syndrome, its systemic effects on the viability of hepatocytes and on inflammation and circulation were directly visualised using intravital video microscopy.


The Bone & Joint Journal
Vol. 102-B, Issue 5 | Pages 627 - 631
1 May 2020
Mahon J Ahern DP Evans SR McDonnell J Butler JS

Aims

The timing of surgical fixation in spinal fractures is a contentious topic. Existing literature suggests that early stabilization leads to reduced morbidity, improved neurological outcomes, and shorter hospital stay. However, the quality of evidence is low and equivocal with regard to the safety of early fixation in the severely injured patient. This paper compares complication profiles between spinal fractures treated with early fixation and those treated with late fixation.

Methods

All patients transferred to a national tertiary spinal referral centre for primary surgical fixation of unstable spinal injuries without preoperative neurological deficit between 1 July 2016 and 20 October 2017 were eligible for inclusion. Data were collected retrospectively. Patients were divided into early and late cohorts based on timing from initial trauma to first spinal operation. Early fixation was defined as within 72 hours, and late fixation beyond 72 hours.