Osmundson, Philip J.

A low oxygen tension might contribute to the dermatological changes produced by deep venous insufficiency and venous stasis. Since elastic support is often prescribed for stasis disorders, it would be of value to know whether compression alters the oxygen tension in affected skin. We performed studies in which the transcutaneous Po 2 (TcPo 2 ) was determined for the foot or lower leg in subjects with normal veins (n = 9) or with dermatitis caused by documented deep venous insufficiency (n = 14). Measurements were made using O 2 -sensing electrodes placed 1–2 cm apart; surface temperature was 45°C for one electrode (producing maximal vasodilation of the underlying skin) and 42°C for the other (producing submaximal vasodilation). The vasodilation index (VI = TcPo 2 at 42 °C/TcPo 2 at 45°C) was used as an index of vasomotor tone. In normal limbs, TcPo 2 (mmHg) and VI were affected by the subject's posture (TcPo 2 = 38.8 at 42°C and 61.4 at 45°C when supine; 40.8 at 42°C and 74.6 at 45°C when upright with legs dependent; VI = 0.63 supine and 0.53 upright). In limbs with venous stasis, TcPo 2 and VI were considerably lower (TcPo 2 = 23.6 at 42°C and 51.5 at 45°C when supine; 20.8 at 42°C and 60.5 at 45°C when upright; VI = 0.48 supine and 0.37 upright). Following the application of an elastic wrap to the limbs with stasis, upright values for TcPo 2 and VI were substantially improved (TcPo 2 with compression = 28.8 at 42°C and 62.4 at 45°C; VI = 0.46). We conclude that (1) TcPo 2 is reduced in regions of skin affected by stasis dermatitis, and (2) elastic compression improves TcPo 2 (during upright posture) in limbs with stasis dermatitis.

A case is reported of a man who had an acute painless dissecting hematoma of the aorta, which was diagnosed clinically in the absence of hypertension or known precipitating cause. The successful surgical treatment is described and illustrated. The following diagnostic features were stressed in the absence of pain: sudden onset of symptoms, syncope, acute peripheral arterial occlusion, appearance of aortic insufficiency, and finding of bruits over the course of the aorta. The significance of the symptom of pain in the torso and the possible modes of its production in this condition are considered, and it is suggested that pain in dissecting aneurysm may imply a poor prognosis.

The records of 66 necropsied cases of periarteritis nodosa in which there was no associated collagen disease were reviewed with reference specifically to the heart. Clinically, congestive heart failure and its manifestations were the most important cardiac findings. Congestive heart failure developed some time during the illness in 57 per cent of the patients, and 44 per cent died as a direct result of this cardiac condition. Myocardial infarction was diagnosed clinically in only three cases. The electrocardiogram was abnormal in 35 of 41 cases but was diagnostic of left ventricular hypertrophy in only six cases and of acute myocardial infarction in only three cases; in the other cases the changes were of a nonspecific nature. Pathologically, 41 of the 66 hearts had evidence of necrotizing arteritis of the coronary arteries; in 39 of these the arteritis had been acute, and in two it had healed. Forty-one of the 66 hearts exhibited myocardial infarcts. Evidence of acute pericarditis was found in 22 hearts; nine of these cases were attributed to uremia, one was due to transmural myocardial infarction, three could not be classified, and the remaining nine were attributed directly to the periarteritis nodosa. Forty-one of the 64 hearts that had been weighed were hypertrophied.

The present study presents pertinent clinical and pathologic findings in 20 cases of ruptured mitral chordae tendineae encountered at the Mayo Clinic between 1934 and 1958 inclusive. Mitral insufficiency results from the rupture of chordae tendineae, the severity being related to the number of chordae ruptured. The resulting heart disease may be severe and may progress to cardiac decompensation and death. Bacterial endocarditis was the major etiologic factor in rupture of the chordae tendineae in this study.

Transcutaneous oxygen tension (TcPO 2 ) was measured according to a standard protocol in 43 limbs from 23 subjects, by use of oxygen-sensing electrodes attached to the chest (at a single site) or dorsum of the foot (at proximal and distal sites, located 1-2 cm apart). With the subjects supine, distal foot TcPO 2 differed from proximal by an average of ±7.4 mmHg, and in 80% of all limbs the differences were between -6 mmHg and + 15 mmHg. The two TcPO 2 's were subsequently combined to yield a single "average" value for each foot. TcPO 2 measurements were repeated twenty-four to forty-eight hours later; in the supine position the change in "average" foot TCPO 2 from the first to second measurement was ±6.9 mmHg, and in 80% of limbs the changes were between -11 mmHg and +9 mmHg. Similar reproducibility data were also obtained for ankle/brachial blood pressure indices (ABIs), chest TcPO 2 , and foot TcPO 2 during three minutes of leg elevation at 30 degrees. The authors conclude that: (1) TcPO 2 measurements from adjacent areas on the dorsum of the foot usually differ by 20-25% or less and (2) the short-term reproducibility of TcPO 2 between studies is comparable to that for ABIS.

Plethysmography can be used to detect and assess venous incompetence in the lower extremities. The authors recently evaluated a new device designed for this purpose that uses strain gauges to determine changes in lower extremity cir cumference occurring with (and immediately after) exercise. The device plots a curve of volume against time for each limb and automatically calculates key values such as the volume of blood expelled from the lower limb veins during exercise and the time required for the veins to refill following exercise. The ap paratus was incorporated into their noninvasive vascular laboratory and used (along with other standard tests) to study patients referred for suspected venous incompetence. They observed the following: (1) A shortened postexercise refilling time ac curately identified limbs with venous incompetence. (2) The clinical severity of venous incompetence was inversely related to the refilling time. (3) Exercise- induced changes in lower extremity volume correlated well with simultaneously determined changes in venous pressure. (4) Valvular incompetence could be local ized to the deep or superficial veins based upon the improvement in refilling times seen following placement of elastic tourniquets around the lower limb. (5) The type of exercise performed (knee bends while the patient was standing versus ankle reflexes while sitting) had little effect on results. The authors conclude that exercise venous plethysmography is a useful noninvasive tool for assessing low er limb venous incompetence.

The authors evaluated the relationship between sympathetic nerve activity and transcutaneous oxygen tension (TcpO 2 ) in normal and ischemic lower extremities. Dorsal foot TcpO 2 was measured by using oxygen-sensing electrodes with surface temperatures of 42 ° C and 45°C; in theory, changes in sympathetic activity should affect vasomotor tone and TcpO 2 in skin beneath an electrode at 42 °C (submaximal vasodilation), but not at 45°C (maximal vasodilation). The vasodilation index (TcpO 2 at 42°C/TcpO 2 at 45°C) was created as an index of vasomotor tone (vasodilation index increases as tone decreases). In normal limbs (n=24) averages for TcpO 2 at 42°C, TcpO 2 at 45°C, and vasodilation index were 30.3 mmHg, 62.1 mmHg, and 0.47, respectively. In subjects (n=5) with quadriplegia and reduced sympathetic tone secondary to cervical cord trauma, TcpO 2 at 42 ° C and vasodilation index were increased (45.0 mmHg and 0.61); TcpO 2 at 45 ° C did not change. When normal subjects (n=7) were chilled for twenty minutes with a cooling blanket at 5 ° C (to increase sympathetic tone) average vasodilation index dropped from 0.50 to 0.29. Among ischemic limbs (n = 34) vasodilation index was highly variable (range: 0-0.77); in general, vasodilation index fell as the ischemia worsened. In a subset of patients with ischemic limbs, the vasodilation index increased after the limb was wrapped in a warm dressing (average vasodilation index=0.25without dressing, 0.37 with dressing). The authors conclude: (1) TcpO 2 can be used to assess the degree of vasomotor tone (and sympathetic activity) in skin; (2) tone generally increases as ischemia worsens; and (3) local warmth can improve cutaneous circulation in ischemic limbs.

To determine comparative rates of development and progression of peripheral occlusive arterial disease, 110 healthy nondiabetic control subjects, 112 patients with peripheral occlusive arterial disease (POAD), 240 patients with diabetes mellitus (DM), and 100 patientswith diabetes mellitus and peripheral occlusive arterialdisease (DM + POAD) were studied over 4 yr with noninvasive techniques. The presence of peripheral occlusive arterial disease was determined by postexercise ankle-brachial index (ABI) values; progression of peripheral occlusive arterial disease was determined by the rate of change in postexercise ABI. Patients who underwent peripheral arterial reconstructive surgery or amputation were also classified as having progression of their peripheral occlusive arterial disease. On this basis, follow-up revealed that peripheral occlusive arterial disease developed and therefore progressed in 1 (1%) of the control group and 22 (9%) of the DM. Peripheral occlusive arterial disease progressed in 31 (28%) of the POAD and 26 (26%) of the DM + POAD. The presence of peripheral occlusive arterial disease predisposes to progression of disease, and peripheral occlusive arterial disease is more likely to develop in diabetic patients who do not have peripheral occlusive arterial disease than in nondiabetic control subjects. However, the presence of diabetes mellitus in patients with peripheral occlusive arterial disease does not seem to increase the risk of progression.