Leaking abdominal aortic aneurysm presenting as an inguinal mass.

Two patients with leaking abdominal aortic aneurysm (AAA) presenting as a tender inguinal mass are reported. Unusual presentations such as this often cause delays in definitive surgery which result in increased morbidity and mortality. It follows that the diagnosis of a leaking AAA should be considered in all patients with a tender pulsatile abdominal mass regardless of the presentation.

Cryofibrinogenaemia and acute gangrene in systemic sclerosis.

A 49 year old man with systemic sclerosis developed ischaemia of his extremities with massive peripheral gangrene. High levels of circulating cryofibrinogen were detected in the plasma and the significance of these findings is discussed.

Glomus tumour of the hallux: diagnosis by Doppler-shift ultrasound and digital subtraction angiography.

A case is presented of a glomangioma with typical history and clinical findings, proven by operation and histology. Unique radiographic features are demonstrated including visualization of the tumour on a soft tissue radiograph and associated hyperaemic bone changes, continuous wave Doppler results indicating hyperaemia and an arterio-venous malformation, and the clear demonstration of the tumour in both frontal and lateral views was possible by intra-arterial digital subtraction angiography (DSA) under local anaesthesia. Fibrous dysplasia of a femur was an incidental finding.

Prostaglandin E1 in severe Raynaud's phenomenon.

Twenty-one patients with severe Raynaud's phenomenon were treated on 29 occasions with prostaglandin E1 (PGE1), a potent vasodilator and pyrogen. A history of finger sepsis or necrosis was absent in 8 (group I) and present in 13 (group II). Three group I and eight group II patients had an associated connective tissue disease, and previously eight upper limbs had been sympathectomized in six group I patients and 14 upper limbs in eight group II patients. A total of 12 fingers had been amputated in six group II patients. Treatment comprised antibiotics for sepsis, PGE1 intravenously for 72 hours, and subsequent surgical debridement of septic and necrotic tissue in 30 fingers of eight group II patients under general anesthesia. Finger skin temperature measured half-hourly in a temperature-controlled ward cubicle (23.7 degrees +/- 0.7 degrees C), Doppler-detectable digital arterial flow, and finger/brachial systolic pressure index with local finger cooling to 10 degrees C were not improved by the administration of 0.9% saline for 72 hours, but were all significantly improved after PGE1 administration. Finger skin temperature was significantly elevated 11 weeks after treatment. The symptoms did not improve after PGE1 administration in group I patients but did improve in 12 of 13 group II patients. No finger deteriorated, and all debrided fingers healed after surgery. Nail bed removal in 11 fingers met with patient approval and prevented recurrent sepsis and necrosis. PGE1 provides a means of increasing finger blood flow during acute exacerbations of finger sepsis and necrosis; unlike sympathectomy, it is a minor procedure without prolonged side effects and is repeatable.

Preliminary experience with prostaglandins E1 and I2 in peripheral vascular disease.

Severe extremity ischemia frequently cannot be relieved by surgical means and failure of current drug therapy may then result in prolonged disability or amputation. Prostaglandins E1 (PGE1) and I2 (prostacyclin, PGI2) are potent vasodilators and inhibitors of platelet aggregation which have been reported to be of value in the treatment of peripheral ischemia. Nineteen patents with severe extremity ischemia and one with vasculitic leg ulceration were treated on 25 occasions by intravascular infusion of PGE1 or PGI2 for 72 to 96 hours. Causes of ischemia were arteriosclerosis, Raynaud's phenomenon (secondary), Buerger's disease, and "trash" foot. Prolonged pain relief and promotion of tissue healing occurred mainly in patents with patent proximal axial arteries. Patency of the superficial femoral artery was associated with a good clinical response in eight of nine cases of foot ischemia, and mean hallux temperature rose 4.6 +/- 2.5 degrees C. In contrast, occlusion of the artery was associated with failure in eight of nine cases, and hallux temperature rose 0.6 degrees +/- 1.3 degrees C. PGE1 or PGI2 administered intravenously may be the treatment of choice for severe ischemia in distal arteriopathy, although the exact mechanisms by which these prostaglandins act are far from clear.

Sequential patterns of haemodynamic and metabolic changes in experimental hypovolaemic shock. I. Responses to acute haemorrhage.

Little is known about cardiorespiratory changes during the development of hypovolaemia. This study attempts to provide such information and compares the period of bleeding with that of established hypovolaemia. Eleven anaesthetized and ventilated greyhounds were bled and analyses of cardiopulmonary function made at fixed intervals both during and after haemorrhage. Six sequential patterns of cardiopulmonary and metabolic change were recognized. It was apparent that bleeding caused the first three phases of change, recovery from the effects of bleeding the next two and steady hypovolaemia the last. The event of bleeding is the main factor that elevates total peripheral resistance and reduces tissue perfusion with consequent lowering of oxygen consumption and alkalosis secondary to impaired carbon dioxide production; when bleeding ceases these changes partially reverse in a manner characteristic of that induced by the reinfusion of shed blood; and hypovolaemia per se has a relatively weak influence. These findings provide an explanation for disparities in previous published reports and have obvious clinical implications.

Sequential patterns of haemodynamic and metabolic changes in experimental hypovolaemic shock. II. Responses to reinfusion of shed blood.

The haemodynamic and metabolic effects which follow the infusion of blood in experimental hypovolaemia have not been studied in detail. The 10 dogs that survived 90 min of hypovolaemia in a study of bleeding (Pardy and Dudley, 1979) were investigated during and shortly after the reinfusion of shed blood using the same techniques. Data from 9 animals were suitable for analysis. As with bleeding, 6 sequential phases were identified; reinfusion of blood was completed in the fifth phase. Initial reinfusion was associated with a rapid improvement in haemodynamic and metabolic status, although mean arterial pH fell because carbon dioxide production increased. Maximum metabolically effective tissue perfusion was probably attained in phase II, but haemodynamic improvement continued until phase IV. Arterial pH did not rise above the pre-infusion value until phase V, and this rise was the result of a fall in PaCO2 secondary to a reduction in physiological dead space and an increase in buffering capacity. Pulmonary artery pressure was superior to systemic artery pressure as a predictor of cardiac output during blood volume restoration. A number of conclusions pertaining to clinical practice are drawn.

Plasma glucagon levels in haemorrhagic shock.

Eleven healthy dogs were subjected to haemorrhagic shock for 90 min. after which shed blood was reinfused. Detailed studies were made of cardiopulmonary function. Samples of blood were taken at frequent intervals for the measurement of glucagon, insulin and glucose. Three dogs had samples taken for catecholamine levels. The glucagon level rose during haemorrhagic shock but there was no relationship between this rise and the change in cardiorespiratory measurement, but there was a relationship between the plasma glucagon level, the blood glucose and the catecholamine level. It is suggested that the release of glucagon in haemorrhagic shock is mediated by sympathetic stimulation of the alpha cell and that the rise in glucagon is in part responsible for the hyperglycaemia which is found in shock.

Post-traumatic pulmonary insufficiency.

Pulmonary insufficiency is occasionally a life-threatening sequel to severe nonthoracic trauma. A similar disturbance of pulmonary function may be a feature of hepatic cirrhosis, fulminant hepatic failure, liver homotransplantation and major hepatic resection for blunt injury. In addition to the respiratory changes, other associations common to both post-traumatic pulmonary insufficiency and liver disease are disturbance of consciousness and susceptibility to infection by organisms normally found in the gastrointestinal tract. If failure of some aspect of liver function is responsible for the development of pulmonary insufficiency, it is likely that it is the hepatic reticulo-endothelial cells rather than the parenchymal cells which are concerned, because hepatic parenchymal cell failure is not a feature of post-traumatic pulmonary insufficiency. It is suggested that the hepatic reticuloendothelial system normally protects the lungs by acting as a prepulmonary filter removing and inactivating noxious macromolecular and particulate matter in the blood, such matter arising mainly from the intestine and the blood coagulation and fibrinolytic systems. Experimental evidence indicates that hypovolemia increases the load of circulating phagocytosable material and depresses activity of the hepatic reticuloendothelial system, while trapping of the pulmonary reticuloendothelial system is considerably enhanced. This noxious material, normally dealt with by the hepatic reticuloendothelial system, may accumulate during and after hypovolemia in active form in the lungs as a result of the action of three mechanisms: direct pulmonary reticuloendothelial phagocytosis from the blood, transfer in hepatic reticuloendothelial cells from liver to lungs and uptake from the blood by polymorphonuclear leukocytes which become sequestered in the lungs. The ensuing pulmonary injury caused by this material may then be manifested by progressive pulmonary insufficiency and the impairment of activity of the hepatic reticuloendothelial system by the presence of gram-negative infection. The reticuloendothelial system has been largely neglected in man, and it is considered that evaluation of reticuloendothelial activity in injured patients may lead to the definition of a syndrome of failure of the reticuloendothelial system of which pulmonary insufficiency may be an integral part.

Hepatic reticuloendothelial protection against bacteremia in experimental hemorrhagic shock.

Gram-negative septicemia is an increasingly common problem, and various suggestions have been made about the cause. One not often considered is that it may be the result of failure of hepatic removal of organisms which have crossed the intestinal mucosal barrier from the large bowel lumen to the portal blood stream. Splanchnic hypoperfusion both increases mucosal permeability and reduces the ability of the hepatic reticuloendothelial system (RES) to remove particulate matter from the blood. If RES funciton is reduced further by blockade with colloidal carbon, then any tnedency for bacteremia to occur in shock might be enhanced. Splenectomized greyhounds, who had received a portal perfusion of either colloidal carbon or saline, were subjected to a period of hypovolemia and then were resucitated. Peripheral blood cultures were sterile at all times in the control animals and before bleeding in the dogs that recived carbon. However, all the RE-blockaded animals developed bacteremia during shock, It was condluded that hepatic RES funciton was essential in the prevention of bacteremia in the hypovolemic dog and that investigation should be directed toward studies of RES function in man with a view to determining the importance or otherwise of the RES in relation to gram-negative bacteremia.

Comparison of pulmonary artery pressures and mixed venous oxygen tension with other indices in acute haemorrhage: an experimental study.

A pulmonary artery cannula allows the determination of free and wedge pulmonary artery pressures and mixed venous oxygen tension. These indices have been reported to provide useful information in the assessment of the haemodynamic status of the ill patient. The purpose of this study was to compare them with systemic arterial and central venous pressures as predictors of cardiac output during acute continuous haemorrhage in the dog. Pulmonary artery pressure changed almost linearly with cardiac ouput, and the percentage changes in each were similar; by contrast, systemic arterial pressure was an inferior predictor of cardiac output. Pulmonary artery wedge pressure fell rapidly in the initial phase of bleeding, but right atrial pressure more gradually. The oxygen tension of blood in the pulmonary artery fell steadily during haemorrhage. These findings suggest that data derived from the use of a pulmonary artery cannula may be more useful than systemic arterial and central venous pressures in the detection of hypovolaemia and reduced cardiac output; more frequent use of a pulmonary artery cannula should be made in patients in whom blood volume may fluctuate rapidly.

Experimental fat embolism: a dynamic assessment of pulmonary fat-handling characteristics.

Injection 125I-glyceryl trioleate (0-5 mg/kg) into the right atrium of anaesthetized greyhounds caused the following changes: sequestration of far in the right side of the heart; 95 per cent removal by the lungs in a single passage through the pulmonary circulation; subsequent release of fat into the systemic circulation; rapid overall turnover of fat trapped in the lungs and slow removal of recirculating fat by other tissues. We believe that if there is release of unemulsified fat into the circulation in traumatic fat embolism these findings are of significance in interpreting the subsequent pulmonary events.

The pathophysiological changes of experimental fat embolism: early pre-hypoxaemic changes.

Glyceryl trioleate has been injected into greyhounds as a model of the fat embolism syndrome. Pulmonary vascular pressures, systemic arterial pressure and cardiac output were determined at regular intervals over an 8-hour period. It has been shown that glyceryl tioleate causes an increased pulmonary vascular resistance and a fall in cardiac output. These effects are mediated partly by a direct mechanical block of pulmonary vessels and partly through a thrombogenic property of the injected fat. The relevance of these findings to the clinical situation is discussed and a sequence of events for the fat embolism syndrome is proposed.