Daycase hernia surgery: a missed training opportunity.

INTRODUCTION: Traditionally uncomplicated elective hernia operations were performed by surgical trainees; allowing them to develop key competencies and skills transferable to emergency hernia surgery. Daycase surgical units (DCU) are increasingly accommodating operations that traditionally contributed to operating lists in general elective theatres. We aim to assess whether DCU could help improve training in hernia surgery. SUBJECTS AND METHODS: Operative Room Information System (ORMIS) data was collected retrospectively to identify hernia operations performed at a large NHS hospital between January 2007 and 2012. Data collected included operating surgeon(s), procedure performed and procedure time (PT). Hospital coding records were used to collect data related to patient length of stay (LOS), complications, readmissions and deaths within 30 days of procedure. RESULTS: 4668 hernia operations were performed; 3063 in DCU. 91.5% (n = 2803) were open and 8.5% (n = 260) laparoscopic repairs. Trainees assisted in 24.6% (n = 752) and led 7.8% (n = 238) of cases. Overall, the mean PT for consultant led open hernia operations was 37.44 min (95% CI 36.75-38.12) and 43.07 min (95% CI 40.99-45.16) for trainees (p < 0.05). Subgroup analysis of all hernia operations performed showed no significant difference in PT between consultants and trainees when performing open bilateral inguinal, femoral, epigastric, incisional and laparoscopic hernia operations. There were no differences in LOS, readmissions and death rates within 30 days of the operation. CONCLUSIONS: DCU are an underutilised opportunity for trainees to acquire experience of hernia operations. When given the opportunity to lead hernia operations in DCU, trainees have similar PT and complication rates to consultants in many instances. Trainees should be encouraged to assist and lead hernia cases in DCU under adequate supervision to ensure appropriate competency is achieved and high standards are maintained.

Medical therapy for intermittent claudication.

Medical therapy to improve symptoms, stabilise the underlying vascular disease and improve lower limb outcomes is an important and effective adjunct to lifestyle modification and surgical or endovascular interventions in patients with IC. Randomised placebo controlled trials have shown that the phosphodiesterase III inhibitor cilostazol 100mg bid improves pain-free and maximum walking distance, as well as quality of life, in a range of patients with intermittent claudication in whom there is no evidence of tissue necrosis or rest pain. This review summarises the evidence from 8 pivotal trials of cilostazol involving over 2000 patients with intermittent claudication treated for up to 6 months. There is comparatively less evidence to support the use of other treatment modalities for relief of symptoms in intermittent claudication, but there is considerable interest in therapeutic angiogenesis to promote new vessel formation and enhance collateralisation of the lower limb using recombinant growth factor proteins or gene transfer strategies. The rationale for therapeutic angiogenesis is discussed, together with the most recent results from randomised trials in patients with peripheral arterial disease.

Pelviureteric junction disruption as a complication of chemical lumbar sympathectomy.

Chemical lumbar sympathectomy is a commonly performed procedure in vascular surgery and pain management. This case report discusses the management of a patient who suffered pelviureteric junction disruption following phenol injection for ischaemic leg pain despite radiological evidence of correct placement. The authors suspect this is an underreported complication, which could be relevant in obtaining informed consent.

Skeletal muscle ischaemia-reperfusion injury: further characterisation of a rodent model.

BACKGROUND: Postischaemic damage in skeletal muscle may be reflected in changes to microvascular blood flow, vascular permeability, and subsequent tissue viability. Previous preclinical studies have not addressed all these parameters, and have not used periods of ischaemia and reperfusion relevant to the clinical setting. This study aimed to develop an animal model hindlimb ischaemia-reperfusion to simulate acute lower limb ischaemia. METHODS: A rodent model of hindlimb tourniquet-induced ischaemia-reperfusion was employed. Gastrocnemius muscle blood flow (GMBF; radio-labelled microspheres), oedema (GMO; using a wet:dry ratio method) and viability (GMV; histochemistry and computerised planimetry) were quantified. RESULTS: 6 h ischaemia per seresulted in neither muscle oedema nor loss of viability, but these changes were apparent following 4 h reperfusion. Early reperfusion at 10 min demonstrated low reflow, with GMBF improving at 120 min before declining sharply at 240 min. CONCLUSION: Prolonged hindlimb ischaemia followed by reperfusion in this rodent model caused significant reductions in gastrocnemius muscle blood flow, associated with muscle oedema and necrosis. These three parameters have not been previously reported together in the same model. This reproducible model could be used in the evaluation of potential therapeutic intervention strategies aimed at ameliorating skeletal muscle reperfusion injury.

Pro- and anti-inflammatory cytokine release in open versus endovascular repair of abdominal aortic aneurysm.

BACKGROUND: Pro- and anti-inflammatory cytokine release occurs with abdominal aortic aneurysm (AAA) repair although the relative contribution of each is currently poorly understood. Ischaemia-reperfusion injury is thought to play a greater role following open (OR) than endovascular (ER) repair, with resultant greater perioperative morbidity. METHODS: Thirty-two patients undergoing OR (n = 16) and ER (n = 16) of AAA were studied. Systemic venous (SV) blood was taken at induction (baseline), 0 h (last clamp off), 4, 24, 72 and 144 h, and femoral venous (FV) blood (indwelling catheter; lower torso venous effluent) at 0, 4 and 24 h. The cytokines interleukin (IL) 6, IL-8 and IL-10 were measured in these samples. RESULTS: In OR, SV and FV IL-6 increased from baseline to a peak at 24 h (SV 589 pg/ml (P = 0.001 versus baseline) and FV 848 pg/ml (P = 0.05)) before declining at 144 h. In ER, there was a similar pattern but the increase was smaller (24 h: SV 260 pg/ml (P = 0.003 versus baseline) and FV 319 pg/ml (P = 0.06)) at all equivalent timepoints compared with OR. IL-8 peaked earlier (4 h) from baseline in both groups before declining by 144 h, and significant differences between SV and FV were seen only in the OR group. IL-10 levels peaked in both groups at 24 h before declining at 144 h, and there were no significant locosystemic differences between the groups. CONCLUSION: Venous pro-inflammatory cytokine changes (IL-6) are consistent with significantly greater lower-torso reperfusion injury in patients undergoing OR. Smaller responses were seen after ER (IL-6 and IL-8), although both groups showed a similar anti-inflammatory response (IL-10); this pro- and anti-inflammatory imbalance may account for the increased morbidity associated with OR.

Chronic disseminated intravascular coagulopathy cured by abdominal aortic aneurysm repair.

Disseminated intravascular coagulopathy (DIC) may rarely be caused by a previously asymptomatic abdominal aortic aneurysm (AAA). The authors describe a recent case where repair of the AAA provided a complete cure for the patient's bleeding tendency. The multidisciplinary management of this patient is presented, and the evidence for the rare causal role of AAA in DIC is discussed. Coagulation disorders in aneurysm patients are probably under-reported, and warrant careful perioperative assessment.

Do prostaglandins have a salutary role in skeletal muscle ischaemia-reperfusion injury?

OBJECTIVES: the effects of prostaglandins (PG) E1, E2, and the prostacyclin analogue iloprost with and without the addition of free-radical scavengers catalase and superoxide dismutase on gastrocnemius blood flow and oedema were studied in a rodent model of hindlimb ischaemia-reperfusion. METHODS: male Sprague-Dawley rats underwent 6-h hindlimb ischaemia with 4-h reperfusion. Prostaglandins were infused prior to reperfusion and their effects on limb blood flow and oedema examined. RESULTS: control animals exhibited a triphasic pattern of muscle blood flow during reperfusion compared to normal animals. PGE1 did not abolish low reflow at 10 min, relative reperfusion was preserved but reperfusion injury was abolished at 120 min. Muscle blood flow was increased at 240 min compared to controls. Increased limb swelling was also seen. Addition of free-radical scavengers caused the abolition of low reflow. Similar results were seen with iloprost. PGE2 abolished low reflow at 10 min and increased perfusion at 120 min but did not prevent reperfusion injury at 240 min. CONCLUSIONS: PGE1 and iloprost enhance muscle blood flow at 4-h reperfusion, though neither abolishes low reflow; PGE2 improved flow at 10 and 120 min but not after 240 min. This study demonstrates a potentially beneficial role for prostaglandins in improving muscle blood flow in skeletal muscle ischaemia-reperfusion injury.

Serum cortisol binding capacity measured with Concanavalin A-Sepharose in patients with a recent inflammatory response.

It has been suggested that elastase released from activated neutrophils degrades cortisol binding globulin. A novel assay for serum cortisol binding capacity was therefore devised and applied to assess whether such degradation was evident in patients showing a recent inflammatory response as indicated by a raised serum C-reactive protein. In 49 patients with evidence (C-reactive protein > 50 mg/l) of a recent inflammatory response, mean serum cortisol binding capacity (288 nmol/l, S.D. = 82.9) was significantly lower (P < 0.05, t test) than in 48 patients (320 +/- 75.8 nmol/l) whose response was quiescent (C-reactive protein < 6 mg/l) or in 49 healthy controls (335 +/- 72.4 nmol/l). Four patients with septic shock had markedly reduced values (167 +/- 49.9 nmol/l) but low values were not restricted to this condition. It is concluded that a population experiencing a recent inflammatory response exhibits reduced serum cortisol binding capacity but a role for elastase in this process remains to be defined.