P. A. Grace

Regional hypothermia protects against tourniquet neuropathy

Ischaemic nerve injury has been suggested as the mechanism for post-tourniquet limb paralysis. As hypothermia has been shown to prolong ischaemia time in many tissues, we tested the hypothesis that cold protection would reduce tourniquet induced neural injury. In 16 male Wistar rats a tourniquet was applied to the right hind limb for 3 h. In eight rats both hind limbs were maintained at room temperature (27 degrees C) while the limb temperature was decreased to 4 degrees C by application of cold polyglycol gel packs in the remaining eight animals. Motor nerve conduction velocity (MNCV) and the amplitude of muscle motor units (AMMU) in response to nerve stimulation were measured at 0 h, 1 h and 1 week post-tourniquet release. Application of the tourniquet for 3 h abolished nerve conduction in all animals. Hypothermia resulted in a significant improvement in AMMU (5.8 +/- vs. 0.6 +/- 0.4 mv, p less than 0.05) at 1 h and in MNCV (26.6 +/- 1.6 vs. 8.1 +/- 4.4 ms-1, p less than 0.05) and AMMU (18.5 +/- 2.0 vs. 9.7 +/- 4.5 mv, p less than 0.05) at 1 week. Hypothermia without ischaemia also reduced MNCV (44.2 +/- 9.4 vs. 74.3 +/- 8.9 ms-1, p less than 0.05) and AMMU (28.1 +/- 2.8 vs. 36.3 +/- 8.4 mv, N.S.). These data indicate that hypothermia reduces normal MNCV and protects nerve function during tourniquet ischaemia. These results support the ischaemic hypothesis for post-tourniquet nerve injury. Cold protection may have clinical applications for surgical procedures performed with tourniquet ischaemia.

Are CT infarcts a separate risk factor in patients with transient cerebral ischaemic episodes

CT cerebral infarcts have been reported in a number of studies of patients with transient ischaemic episodes. The hypothesis that these asignomatic infarcts, i.e. without associated clinical neurological deficit reflect the ability of the brain to limit the extent of neuronal damage through its collateral circulation was tested in 50 patients undergoing both CT scanning and cerebral angiography. Out of 50 patients there were 15 patients with a total of 17 infarcts on CT scan. Fourteen of 50 patients had evidence of diminished collateral reserve capacity on cerebral angiography. Ten of these 14 patients (71%) had CT evidence of infarction, in contrast to an incidence of five out of 36 patients (14%) without evidence of diminished collateral reserve. These results indicate that CT infarcts and collateral cerebral circulation must be evaluated as prognostic factors in patients with T.I.A.s.

Biochemical and molecular genetic studies of abdominal aortic aneurysm in an irish population

Abdominal aortic aneurysm (AAA) is a common disease of the elderly exhibiting a complex aetiology. In a survey of 82 Irish aneurysm patients, compared to 79 age- and sex-matched control subjects, we have investigated a number of potential biochemical and molecular genetic markers which are amenable to analysis from blood specimens and which might have predictive value for AAA. No significant differences were observed between patients and control subjects in relation to serum lipids, leucocyte elastase activity or serum alpha 1-antitrypsin concentration. We have used the polymerase chain reaction to screen the patient and control groups in search of disease-associated genetic variation on chromosome 16, particularly in the region of the Cholesteryl Ester Transfer Protein (CETP) gene. Although variation in allele frequencies was detected between patients and controls at the four marker loci studied, no significant gene-disease associations were detected. The absence of gene-disease associations in our study may indicate that the genetic component in the aetiology of AAA in Ireland differs from that in the UK. Alternatively, it may indicate that the high degree of polymorphism at microsatellite loci may make them unsuitable as markers for the study of gene-disease associations in moderately sized populations. We therefore conclude that the biochemical and molecular genetic markers which we have examined are of no predictive value, and that ultrasonography remains the screening modality of choice for abdominal aortic aneurysm.

Aprotinin: The ideal anti-coagulant?

The serine proteinase inhibitor, aprotinin, significantly reduces transfusion requirements during open heart surgery. Whether this benefit is associated with an increased tendency to thrombosis has not been studied. We investigated the effect of aprotinin in an experimental arterial thrombosis model. In 17 male Sprague-Dawley rats, the infrarenal aorta was replaced with 1.0-mm diameter PTFE grafts of varying lengths. The time to graft occlusion, recorded by palpation, Doppler ultrasound and a distal bleeding test, was 20.2 +/- 1.8 min, 35.8 +/- 6.1 min and 43.7 +/- 6.6 min for grafts of 10, 7.5 and 5.0 mm respectively (r = -0.98, p less than 0.05). Following PTFE graft placement 24 Sprague-Dawley rats were given saline (n = 6), aprotinin (n = 6), heparin (n = 6), and heparin + aprotinin (n = 6). The time to occlusion was significantly prolonged in the aprotinin group (71.7 +/- 20.4 min vs. 20.2 +/- 1.8 min, p less than 0.05). The time to thrombosis for heparin + aprotinin and heparin alone was also significantly prolonged (p less than 0.05). Prothrombin times (PT) were 21.9 +/- 3.0 s for control, 29.4 +/- 6.2 s for aprotinin, 40.7 +/- 2.5 s for heparin and 39.9 +/- 14.5 s for heparin + aprotinin (p less than 0.05 vs. control for all values). Bleeding time was not prolonged with aprotinin (3.0 +/- 0.9 min vs. 2.9 +/- 0.7 min). The bleeding time was 18.9 +/- 4.1 min for heparin + aprotinin and 22.5 +/- 2.3 min for heparin alone (p less than 0.05 vs. control for both values).(ABSTRACT TRUNCATED AT 250 WORDS)

The carotid stump syndrome

Transient ischaemic attacks (TIAs) following internal carotid artery occlusion are not uncommon. Micro-embolisation from an ipsilateral internal carotid artery stump has been implicated in the pathogenesis of such TIAs. We report six patients who had persistent TIAs in association with an occluded ipsilateral internal carotid artery and a carotid stump. Four patients who underwent surgery and stump exclusion remain asymptomatic at 2 years while of two patients who were treated with antiplatelet therapy, one remains asymptomatic and one died from a cerebro-vascular accident.

Spinal Cord Perfusion Pressure in Dogs after Control of Proximal Aortic Hypertension during Thoracic Aortic Cross-clamping with Esmolol or Sodium Nitroprusside

Background:Spinal cord perfusion pressure may be reduced when sodium nitroprusside is used to control proximal aortic hypertension during thoracic aortic clamping. The effect of esmolol infusion on spinal cord perfusion pressure during thoracic aortic clamping is unknown. This study compares spinal cord perfusion pressure following control of proximal hypertension with either sodium nitroprusside or esmolol during thoracic aortic clamping. Methods:The thoracic aorta was cross-clamped for 30 min in 18 dogs anesthetized with halothane. A control group (n = 6) received no treatment of proximal hypertension during cross-clamping. In two other groups, proximal arterial pressure was controlled (100 mmHg) by infusion of either sodium nitroprusside (n = 6) or esmolol (n = 6). Brachial and femoral arterial pressures, spinal cord perfusion pressure, pulmonary artery occlusion, central venous pressures, and cardiac output were monitored. Neurologic assessment was performed 24 h following surgery. Results:Femoral arterial pressure was lower with nitroprusside (14 ± 3 mmHg) compared to esmolol (24 ± 4 mmHg) after 15 min of aortic cross-clamping. Cerebrosplnal fluid pressure Increased during aortic cross-clamping in the sodium nitroprusside group (from 7 ± 5 to 16 ± 6 mmHg) but not in esmolol or control groups. Spinal cord perfusion pressure was lower with nitroprusside at 15 min of aortic cross-clamping (2 ± 4 mmHg) compared to control (15 ± 7 mmHg) and esmolol groups (17 ± 11 mmHg). Esmolol Infusion reduced cardiac output and increased ventricular filling pressures compared to control and nitroprusside groups. Conclusions:Esmolol was associated with greater spinal cord perfusion pressure, but adverse hemodynamic effects, when compared with nitroprusside during thoracic aortic cross-damping. When only surviving dogs (4 control, 5 esmolol, 6 nitroprusside) are considered, the Incidence of neurologic deficit was greater in nitroprusside-treated dogs than in either control or esmolol-treated dogs. No difference in outcome was present when all dogs are considered.

Pararectus Retroperitoneal Radical Nephrectomy

We describe a new pararectus retroperitoneal approach to the kidney, which allows easy identification and occlusion of the renal vessels before mobilization of the kidney. This approach potentially reduces morbidity, hospital stay and cost. The technique has been used in 4 cases of radical nephrectomy for tumor and in 1 for pyonephrosis.

How much heparin? A simple in vitro test

A simple in vitro test to calculate the dose of heparin required to achieve optimal in vivo anticoagulation during surgery has been assessed in 15 patients who subsequently underwent vascular surgery. Heparin was added to four aliquots of patients blood in vitro to give five solutions with heparin concentrations ranging from 0-0.8 units/ml of plasma. The activated partial thromboblastic times (APTT) of each of these samples was then measured and the natural log (ln) of the APTT calculated. The natural log of the APTT in vitro was then plotted against the in vitro heparin concentration. From this linear correlation the concentration of heparin required to achieve an APTT 2.5 times the normal in vitro (Hc) for the 15 different patients was calculated and ranged from 0.4-0.75 units/ml (median 0.47). Based on an estimate of the plasma volume (PV), the bolus dose of heparin given intravenously to each patient to produce an equivalent anticoagulant response in vivo was calculated (Hc x PB). Heparin boli administered ranged from 1000-2000 units (median 1500). The mean in vivo APTT achieved was 77% of the predicted value (range 62%-123%). Such an estimation of an in vivo response, by means of an in vitro test, should help to more accurately predict the effects of heparin in vivo and individualise anticoagulation dosage.