Contemporary surgical treatment of primary hyperparathyroidism without intraoperative parathyroid hormone measurement.

INTRODUCTION: Primary hyperparathyroidism (pHPT) is usually the result of a single adenoma that can often be accurately located preoperatively and excised by a focused operation. Intraoperative parathyroid hormone (IOPTH) measurement is used occasionally to detect additional abnormal glands. However, it remains controversial as to whether IOPTH monitoring is necessary. This study presents the results of a large series of focused parathyroidectomy without IOPTH measurement. METHODS: Data from 2003 to 2014 were collected on 180 consecutive patients who underwent surgical treatment for pHPT by a single surgeon. Preoperative ultrasonography and sestamibi imaging was performed routinely, with computed tomography (CT) and/or selective venous sampling in selected cases. The preferred procedure for single gland disease was a focused lateral approach guided by on-table surgeon performed ultrasonography. Frozen section was used selectively and surgical cure was defined as normocalcaemia at the six-month follow-up appointment. RESULTS: Focused surgery was undertaken in 146 patients (81%) and 97% of these cases had concordant results with two imaging modalities. In all cases, an abnormal gland was discovered at the predetermined site. Of the 146 patients, 132 underwent a focused lateral approach (11 of which were converted to a collar incision), 10 required a collar incision and 4 underwent a mini-sternotomy. At 6 months following surgery, 142 patients were normocalcaemic (97% primary cure rate). Three of the four treatment failures had subsequent surgery and are now biochemically cured. There were no complications or cases of persistent hypocalcaemia. CONCLUSIONS: This study provides further evidence that in the presence of concordant preoperative imaging, IOPTH measurement can be safely omitted when performing focused parathyroidectomy for most cases of pHPT.

Acute lower limb ischaemia.

Salvage of the acutely ischaemic lower limb represents a large proportion of the emergency workload for the vascular surgeon. A successful outcome is dependent upon a careful clinical assessment and a prompt multidisciplinary approach to revascularization.

Prospective multicentre study of the natural history of atherosclerotic renal artery stenosis in patients with peripheral vascular disease.

BACKGROUND: Many patients with peripheral vascular disease have coincident renal artery stenosis. The present study characterized the natural history of the condition. METHODS: Some 98 patients (71 men) with more than 50 per cent atherosclerotic renal artery stenosis (unilateral 64, bilateral 34) were recruited prospectively. Measurements of serum creatinine, blood pressure and renal size were recorded at baseline and every 6 months, for a minimum of 2 years. RESULTS: Data were available for 85 patients with a minimum follow-up of 2 years. The mean age was 71 (range 51-87) years. All 52 patients with unilateral renal artery stenosis were managed conservatively (group 1); 21 of the 33 patients with bilateral disease had no intervention (group 2) and the remaining 12 had angioplasty or reconstruction (group 3). The overall mortality rate was 32 per cent at 2 years (27 patients) and this was similar in all three groups. In only three patients was death related directly to renovascular disease; coronary disease accounted for the majority of deaths. All three patients who needed dialysis died within 1 year. In survivors from groups 1 and 3 there was a significant increase in serum creatinine concentration at follow-up. Blood pressure did not increase significantly. CONCLUSION: Patients with renal artery stenosis and peripheral vascular disease had a poor prognosis, but this was not directly attributable to renal failure.

Post-ischaemic organ dysfunction: a review.

OBJECTIVES: The aim of this review is to consider the pathophysiology of ischaemia-reperfusion in organs that may be affected by either its local or remote consequences. Potential therapeutic strategies are also considered. DESIGN: A general discussion of the biochemical (including oxygen free radicals, complement, cytokines) and cellular events (endothelial cells, neutrophils) responsible for the mediation of reperfusion injury is presented, with special consideration of the organ-specific differences affecting the myocardium, central nervous system, gut, liver, kidney and skeletal muscle. Similarly, events which promote remote organ injury are described. CONCLUSIONS: Although it is recognised that prolonged ischaemia results in tissue and organ damage, the concept of reperfusion-induced tissue injury, defined as tissue damage occurring as a direct consequence of revascularisation, is relatively recent. Such events may increase the morbidity and mortality of patients undergoing vascular reconstruction, trauma surgery and transplantation. A clear understanding of the factors responsible for its development is therefore vital if protocols that reduce its impact are to be developed.

Bilaterial renal artery atherosclerosis--the results of surgical treatment.

OBJECTIVES: To assess the outcome of surgical treatment for severe bilateral renal artery stenosis. DESIGN: Non-randomised, prospective, consecutive series. MATERIALS: Twenty-five patients undergoing surgical reconstruction of whom 14 required aortic replacement (aneurysm, n = 7, severe claudication, n = 7). In 22 patients, the principle aim of treatment was preservation or salvage of renal function whilst three patients had intractable hypertension. METHODS: Serum creatinine and blood pressure were measured at the most recent follow-up (minimum 6 months, median 17 months) and compared to preoperative values. RESULTS: Renal function (serum creatinine) improved or stabilised in 16 of 18 patients in whom it was elevated preoperatively (>140 mumol/l; 3 patients on dialysis) whilst one patient with early graft occlusion subsequently required long term dialysis. Blood pressure control was also improved in 14 patients. There were four postoperative deaths (16%) and five patients required re-exploration for postoperative anuria (3) or bleeding (2). CONCLUSIONS: Surgical revascularisation preserves renal function and may improve blood pressure control in patients with advanced multi-system atherosclerosis. The operative morbidity and mortality is significant although historical data suggests that this is less than for similar patients treated medically.

Role of neutrophil-endothelial adhesion in skeletal muscle reperfusion injury.

During postischaemic revascularization neutrophil-endothelial adhesion in the skeletal muscle microcirculation, promoted by the neutrophil adhesion molecule Mac-1, may impair muscle blood flow and release oxygen free radicals and proteolytic enzymes which causes further tissue injury. This study has assessed the effect of an anti-Mac-1 monoclonal antibody on the severity of skeletal muscle injury in a rat model of 6-h hindlimb ischaemia and 4-h reperfusion. In control animals a sustained impairment of muscle perfusion was associated with neutrophil sequestration, muscle infarction and muscle oedema (P < 0.001 versus normal rats). In contrast, intravenous administration of anti-Mac-1 monoclonal antibody before revascularization prevented neutrophil recruitment, reduced muscle necrosis and improved postischaemic muscle perfusion at 120 and 240 min (not significantly different from normal), thus confirming that neutrophils are important cellular mediators of skeletal muscle reperfusion injury. Monoclonal antibodies targeting neutrophil adhesion molecules may, therefore, have a role in the prevention of this complication of limb revascularization.

Role of neutrophil depletion and elastase inhibition in modifying skeletal muscle reperfusion injury.

This study investigated the effect of neutrophil depletion and neutrophil elastase inhibition on the severity of skeletal muscle reperfusion injury. In a rodent model, indices (experimental/normal limb) of gastrocnemius muscle viability (histochemical staining), oedema (wet:dry weight ratio) and myeloperoxidase content (neutrophil recruitment) were assessed in normal (no ischaemia), ischaemic (6-h unilateral hindlimb ischaemia), control (6-h ischaemia and 4-h reperfusion), neutrophil-depleted rats (given antineutrophil serum) and rats receiving the neutrophil elastase inhibitor Elafin. Neutrophil recruitment muscle infarction and oedema did not occur in normal limbs, or in those subjected to ischaemia without reperfusion. In contrast increased muscle myeloperoxidase levels (P < 0.001), muscle infarction (P < 0.01) and oedema (P < 0.001) all occurred in the reperfused limbs of control animals compared with those of normal and ischaemic rats. Antineutrophil serum and Elafin both reduced neutrophil recruitment during reperfusion (P < 0.001 and P < 0.01 respectively) and muscle viability was preserved. Reperfusion oedema still occurred however, suggesting that altered endothelial permeability is mediated by factors other than neutrophils.

Role of thromboxane A2 in muscle injury following ischaemia.

The effect of a thromboxane A2 receptor antagonist (GR32191) on gastrocnemius muscle blood flow, oedema and viability was assessed in a rodent model of 6-h unilateral hindlimb ischaemia and 4-h reperfusion, and the results compared with those in control and normal groups, and in animals undergoing 6-h ischaemia alone. Control animals demonstrated reduced muscle blood flow throughout reperfusion (at 10 min, P < 0.01 versus normal, P not significant versus ischaemia; at 120 min, P < 0.05 versus normal and ischaemia; at 240 min, P < 0.01 versus normal, P not significant versus ischaemia), and the development of muscle oedema (P < 0.01 versus normal and ischaemia) and muscle necrosis (P < 0.01 versus normal and ischaemia). In contrast, the thromboxane A2 receptor antagonist enhanced muscle blood flow (at 10 min, P < 0.01 versus control; at 120 min, P < 0.05 versus control; at 240 min, P < 0.01 versus control) and preserved muscle viability (P < 0.01 versus control; P not significant versus normal and ischaemia). These results indicate that thromboxane A2 is an important mediator of skeletal muscle reperfusion injury and suggest that administration of a thromboxane A2 receptor antagonist may improve limb salvage rates after surgery for acute ischaemia.

Neutrophils and the endothelium in post-ischemic alterations in skeletal muscle blood flow.

Thromboxane A2, leukotriene B4, and NE are all released from ischemic muscle during reperfusion. Thromboxane A2 levels peaked at 10 min and this potent vasoconstrictor may be responsible for low reflow. Neutrophil elastase levels did not rise until 240 min of reperfusion, following that of leukotriene B4 at 120 min, indicating that neutrophil recruitment and activation is a relatively late event following revascularization. In conclusion, it would appear that endothelial factors have a significant role in the vasomotor changes that account for low reflow. Equally altered neutrophil function almost certainly contributes to the final development of reperfusion injury.

Skeletal muscle reperfusion injury: pathophysiology and clinical considerations.

Skeletal muscle reperfusion injury following revascularization of an acutely ischaemic limb undoubtedly contributes to the morbidity and mortality of this surgical emergency. This article reviews the experimental evidence which has defined the biochemical events responsible for the pathogenesis of this injury, with particular emphasis on the roles played by free radicals, neutrophils and products of lipid peroxidation. Finally, the clinical relevance of both the local and systemic effects of the injury is considered, together with suggestions for potential therapeutic strategies based on the results of laboratory work.

Life-threatening stridor presenting in a patient with rheumatoid involvement of the larynx.

A case of a female patient with extensive rheumatoid arthritis who presented to the Accident and Emergency Department with life-threatening stridor is described. Although clinical involvement of the larynx is found in over a third of patients with severe rheumatoid arthritis, acute airways obstruction is fortunately a very rare complication. Stridor is probably precipitated in the acute situation in such patients as a result of upper respiratory tract infection.