R.C. Kester

Percutaneous transluminal angioplasty for intermittent claudication: Evidence on which to base the medicine

OBJECTIVESnThis study aims to assess the impact of PTA on the quality of life (QoL) of claudicants and to analyse which patients and which arterial lesions derive the most benefit.nnnDESIGNnA prospective observational study.nnnMATERIALSnOne hundred and seventeen claudicants undergoing PTA were studied; 35 patients had bilateral disease, whilst 82 had unilateral disease and underwent PTA to a solitary iliac lesion, solitary superficial femoral or a iliac lesion above a diseased superficial femoral artery in 24, 39 and 19 cases, respectively.nnnMETHODSnPatients completed the Short Form 36 (SF36) and EuroQol (EQ) QoL assessment instruments prior to and at 1, 3, 6, and 12 months following intervention. The SF36 produces a QoL profile, whilst the EQ produces two QoL indices.nnnRESULTSnClaudication has a deleterious effect on QoL, especially in patients with multi-segment disease. PTA results in an immediate and lasting improvement in the QoL of claudicants. Unilateral claudicants undergoing PTA to a solitary iliac lesion demonstrate the most marked QoL benefits and 12 months post PTA report a QoL approaching that of an age-matched population. Patients with bilateral claudication undergoing unilateral PTA and unilateral claudicants undergoing PTA to a solitary SFA lesion demonstrate some QoL benefits, but at 12 months post PTA do not approach the QoL scores of an age-matched population. Unilateral claudicants undergoing iliac PTA above a diseased SFA demonstrate minimal QoL changes.nnnCONCLUSIONSnThese results should influence decision making in the management of claudication and it may be possible to prioritise PTA waiting lists to ensure patients with greatest potential benefit are treated with most urgency.

The Hand Arm Vibration Syndrome: A Review

Since its first description over eight decades ago, the hand arm vibration syndrome-- vibration white finger as it was previously known--has become one of the most common prescribed diseases in the industrialized world. This article is intended to provide a broad review of existing evidence and knowledge regarding a disease which, for medicolegal reasons, demands attention from all medical personnel. Detailed discussion is presented regarding: the multifactorial aetiology of the syndrome; suggestions for clinical assessment, laboratory investigations and classification of disease severity; and strategies for the prevention and treatment of the syndrome.

The Aetiology of Raynaud's Phenomenon

The literature on Raynauds phenomenon (RP) describes a complex and confusing picture of abnormalities that has suggested a multifactorial aetiology. Current research suggests that the underlying disorder is related to a local fault at the level of the digital microcirculation. It is likely that many of the biological changes described in RP are secondary manifestations of this primary abnormality. The strong familial relationship of RP suggests a genetic link although this has not yet been characterized. An overactivity of the sympathetic nervous system appears less likely as a candidate for the primary abnormality and dysfunction at the level of the nerve, and vessel wall may be more important. Digital cutaneous neurones show a deficient release of the vasodilatory calcitonin gene related peptide in PR. This may represent a primary fault that is confounded by other factors, which are influenced by cold or emotional triggers. Vasoconstricting substances such as catecholamines, endothelin-1 and 5-hydroxytryptamine, which may all be released in response to cold exposure, could cause digital artery closure and the associated symptoms of RP. In some cases, this would trigger a cascade of neutrophil and platelet activation, which through the release of inflammatory mediators, contribute to the endothelial damage seen with more severe RP. It is hypothesised that disturbance to the intricate functioning of the endothelium, and secondary compensation at local or systemic level, may appear over time. There is, therefore, still a need to differentiate the true aetiological factors from those that are causal associations with Raynauds phenomenon. Progress is slowly being made with better understanding of the intricacies between these factors and the microcirculation. Deepening our comprehension of the ‘normal’ mechanisms that influence microvascular blood flow is necessary to develop a better understanding of the pathophysiology of Raynauds phenomenon.

VASCULAR REVIEW: The aetiology of Raynaud's phenomenon

Abstract The literature on Raynauds phenomenon (RP) describes a complex and confusing picture of abnormalities that has suggested a multifactorial aetiology. Current research suggests that the underlying disorder is related to a local fault at the level of the digital microcirculation. It is likely that many of the biological changes described in RP are secondary manifestations of this primary abnormality. The strong familial relationship of RP suggests a genetic link although this has not yet been characterized. An overactivity of the sympathetic nervous system appears less likely as a candidate for the primary abnormality and dysfunction at the level of the nerve, and vessel wall may be more important. Digital cutaneous neurones show a deficient release of the vasodilatory calcitonin gene related peptide in PR. This may represent a primary fault that is confounded by other factors, which are influenced by cold or emotional triggers. Vasoconstricting substances such as catecholamines, endothelin-1 and 5-hydroxytryptamine, which may all be released in response to cold exposure, could cause digital artery closure and the associated symptoms of RP. In some cases, this would trigger a cascade of neutrophil and platelet activation, which through the release of inflammatory mediators, contribute to the endothelial damage seen with more severe RP. It is hypothesised that disturbance to the intricate functioning of the endothelium, and secondary compensation at local or systemic level, may appear over time. There is, therefore, still a need to differentiate the true aetiological factors from those that are causal associations with Raynauds phenomenon. Progress is slowly being made with better understanding of the intricacies between these factors and the microcirculation. Deepening our comprehension of the `normal mechanisms that influence microvascular blood flow is necessary to develop a better understanding of the pathophysiology of Raynauds phenomenon.

Exercise-induced Neutrophil Activation in Claudicants: a Physiological or Pathological Response to Exhaustive Exercise?

OBJECTIVESnTo assess the effect of exhaustive exercise on neutrophil activation and degranulation in claudicants and controls. We investigated the hypothesis that neutrophil activation and degranulation are normal responses to exhaustive exercise in healthy patients.nnnDESIGNnThis was a controlled experimental two-group study.nnnMATERIALSnExercise was performed using a fixed workload treadmill test. Neutrophil activation was assessed by flow cytometry of whole blood labelled with anti-CD11b mouse IgG, and neutrophil degranulation in terms of plasma elastase measured by enzyme-linked immunosorbent assay.nnnMETHODSnTwenty-eight claudicants with stage 1 chronic leg ischaemia, and 22 healthy controls were recruited. Blood and urine samples were collected before and after treadmill exercise. Claudicants exercised to their maximum walking distance, and controls at a higher fatigue workload for a maximum of 20 min.nnnRESULTSnExercise produced a brief but significant neutrophilia in both groups. Neutrophil CD11b expression increased significantly after exercise only in the claudicants, and was associated with a significant rise in plasma neutrophil elastase. These indices remained unchanged in the control group at all time points despite exercise at a fatigue level.nnnCONCLUSIONnThe inflammatory response associated with exercise in claudicants is not simply a physiological response to exhaustive exercise.

An Introduction to Quality of Life Analysis: The New Outcome Measure in Vascular Surgery

any population sample or illness group, and thus are applicable to a wide range of health problems. The majority of generic instruments reflect the WHO definition of health by assessing the theoretically or empirically distinct aspects of health, commonly termed domains or dimensions. Domains frequently measured by generic instruments include: physical functioning (mobility, self care), emotion or mood (anxiety, depression, vitality), social functioning (social activities, contact and isolation), role performance (work, housework), pain, and other commonly performed daily activities, e.g. sleep and sexual functioning. These generic instruments can be further subdivided into those which provide a single global score or health index and those which provide a number of domain scores or health profile. Some instruments provide both. The main advantage of a single index is that it can be incorporated into quality adjusted life year (QALY) calculations and can thus be used in cost effectiveness/utility analyses. This broad approach to QL analysis facilitates comparisons between different disease groups and different centres; however, responsiveness may suffer.

How effective is acute normovolaemic haemodilution in femoro-distal bypass surgery?

BACKGROUNDnRecent guidelines have emphasised the use of autologous blood in the surgical setting. The aim of this study was to analyse the efficacy and efficiency of acute normovolaemic haemodilution (ANH) as a blood conservation intervention in patients undergoing elective femoro-distal surgery for critical limb ischaemia.nnnMETHODSnForty patients were studied prospectively. The volume of the blood collected was derived as follows: Blood volume removed = patients blood volume (initial haematocrit - final haematocrit/average haematocrit) where final haematocrit is 30% and patients blood volume is 70 and 65 ml/kg for a man and a woman, respectively.nnnRESULTSnTwenty-five patients were suitable for ANH and 15 patients were excluded because of poor ventricular function, anaemia or renal disease. Nine of the 25 patients (44%) had <500ml of surgical blood loss and would have avoided homologous blood transfusion (HBT). Four of the patients lost >2000ml of blood and could not avoid HBT through ANH. Twelve patients had moderate blood loss (950-1400 ml), with eight of these patients requiring transfusion. Four patients avoided exposure to homologous blood.nnnCONCLUSIONnANH is in evolution and as a single blood conservation intervention, contributes only modestly to blood conservation.