Surgery for pretibial myxoedema.
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Publications and source records attributed to P S Mortimer.
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The control of human forearm cutaneous vascular resistance was examined using a combination of laser Doppler perfusion measurement and continuous Finapres blood pressure measurement. Tests which provoke changes in blood flow via different control mechanisms (local and neural) were applied in a group of ten healthy subjects. The purpose was to select from them a suitable (i.e. statistically significant) group to apply in cases where a disease process is suspected of interfering with the control of the skin circulation. Deep inspiration, immersion of the feet in water at 15 degrees C (both eliciting sympathetic vasoconstrictor nerve activity) and arm dependency (eliciting the local veni-arteriolar response) produced statistically significant, symmetrical increases in cutaneous vascular resistance in both arms (p < 0.05, Wilcoxon's test for paired differences). Similarly, post-ischaemic reactive hyperaemia (mediated by local vasodilator mechanisms) and indirect heating of the body (eliciting increased sympathetic vasodilator nerve activity) resulted in significant decreases in cutaneous vascular resistance (p < 0.01). When deep inspiration was repeated from a vasodilated baseline after indirect heating, the increases in cutaneous vascular resistance were smaller than those obtained before heating. Isometric handgrip exercise failed to produce a significant change in contralateral cutaneous vascular resistance (p > 0.05). There were no differences between right and left arms for any test (p > 0.05). The successful tests were subjected to power analysis in order to predict likely patient sample sizes required to demonstrate altered responsiveness at sites of microcirculatory disturbance compared with normal skin.
BACKGROUND: Few studies have attempted to quantitatively assess in vivo changes in the microvasculature with age. OBJECTIVE: The objective was to assess in vivo structural and functional changes in the cutaneous microvasculature with aging and to analyze the contribution of the microvasculature to skin color. METHODS: Video capillaroscopy, in conjunction with fluorescein angiography, and laser-Doppler flowmetry were used to compare elderly and young normal volunteers. Skin color differences were assessed with a handheld color reflectance meter. A photoexposed site, the forehead, and the relatively photoprotected ventral forearm were studied to differentiate photoaging from chronologic aging. RESULTS: Dermal papillary loops were significantly reduced in old skin compared with young skin (forehead by 40%; forearm by 37%). Horizontal vessels showed increased volume fraction in elderly forehead and forearm skin. Laser-Doppler studies demonstrated no significant differences between young and old skin; indeed, hyperemic responsiveness appeared more rapid in the elderly. Color measurements showed elderly skin, particularly in men, to be significantly darker and redder. CONCLUSION: A marked loss in dermal nutritional vessel density and surface area for exchange is a feature of both chronologic aging and photoaging.
In this prospective study computed tomography (CT) was used to monitor the response of compression therapy in 27 patients with chronic unilateral lymphoedema over a 12 week period. Computed tomography examination of abnormal and normal limbs (proximal and distal portions) was performed in the first, third and 12th weeks of treatment. Changes in cross-sectional area (CSA) and average densities of the different compartments within the proximal and distal portions of the abnormal limb were compared with the normal side. The most significant decrease in CSA occurred within the subcutaneous compartment of the distal portion (P = 0.002); the decrease in CSA of the proximal portion was also significant (P = 0.02) but changes in muscle and bone compartments were not significant. Significant differences in average density measurements of the subcutaneous and muscle compartments remained between normal and abnormal limbs following the conclusion of the study (P = 0.001 and P = 0.01, respectively). This study demonstrates that CT is a useful method for monitoring therapeutic response to compression therapy.
T-cell prolymphocytic leukaemia (T-PLL) is an aggressive leukaemia accounting for over 30% of all mature T-cell malignancies. We describe the clinical manifestations and histology of cutaneous involvement in a series of 92 patients with T-PLL. Of the 92 patients, 26 (28%) had cutaneous involvement, and in 23 this was present at the time of the diagnosis of the leukaemia. Skin manifestations included a diffuse infiltrated erythema, infiltration localized to the face and ears, nodules and erythroderma. Histology showed a perivascular and periappendageal dermal infiltrate of lymphoid cells with the morphology of prolymphocytes. An early skin biopsy in these patients should help to reveal the underlying diagnosis.
Two women with a distinctive rash on the legs are reported. The clinical features of erythema, erosions, crusting and pustular lakes, and the failure to respond to any treatment except very potent topical corticosteroids (Dermovate), are very similar to those of erosive pustular dermatosis of the scalp.
The anthracenedione cytotoxic agent, mitozantrone, has a well-established place in the treatment of acute leukaemia, lymphoma, breast carcinoma and other malignant tumours. In general it is well tolerated apart from myelosuppression and dose-related cardiotoxicity. Alopecia is a common side-effect with mitozantrone but otherwise the skin and its appendages are rarely affected. We present five cases of mitozantrone-induced onycholysis.
Lymphoedema is perceived by clinicians in the UK as a rare condition for which there is no effective treatment. I would like to argue that lymphoedema is in fact a common condition which is misunderstood and often poorly managed. To explain further the basic physiology of oedema has to be considered.
After initial treatment for breast cancer, lymphedema often affects the trunk as well as the arm. Evaluation of truncal swelling by the clinical "pinch test" of the posterior axillary fold is unreliable. Our aim was to develop an objective measurement, using modified Harpenden skinfold calipers. Standard Harpenden skinfold calipers exert a pressure of 12.6 g.mm-2, which rapidly squeezes edema fluid out of the skinfold. Springs were substituted to exert a lighter but relatively constant load (3.7 g.mm-2). Repeated skinfold thickness measurements on the same, normal subject then gave a relative standard deviation (r.s.d.) or coefficient of variation of 5%. The posterior axillary folds of 14 patients (age 56 +/- 13 (s.d.) years) with an average 30% arm swelling were measured using the same procedure. Readings were taken at 10 s, and again after 60 s of sustained application to assess the rate of creep, or deformation with time, attributed to displacement of pressurized interstitial fluid. Two patients had clinically observable axillary fold swelling. Eight patients, including the above two, showed axillary fold swelling by caliper measurement, defined as a 10% increase over the contralateral side (2 r.s.d.'s). Creep was greater on the affected side in all 14 patients. Thus, modified calipers can detect axillary fold edema, and thereby provide an objective method for assessing changes in swelling after lymphedema treatment.
OBJECTIVE: To determine whether there is a reduction in human forearm skin capillary density in essential hypertension. SUBJECTS AND METHODS: We compared the number of capillary loops in the forearm skin of 12 patients with established, uncomplicated essential hypertension (mean blood pressure 180/109 mmHg) with that in carefully matched control subjects, using intravital capillaroscopy and fluorescein angiography. RESULTS: There was a significant reduction in forearm skin capillary density in the hypertensive patients compared with the normotensive subjects. This represents a reduction by approximately 20% in capillary density. Capillary density was inversely correlated with blood pressure in the hypertensive patients alone (r = -0.4, P < 0.05) and in the whole group. CONCLUSION: The present study demonstrates a reduction in capillary density in the forearm of patients with essential hypertension. If this rarefaction in the forearm is also present in other vascular beds, it could result in an approximately 20% increase in peripheral resistance, which might play an important additional role in determining blood pressure.
OBJECTIVE: To determine the effect of inflammatory arthritis on lymphatic function in the upper limb. METHODS: Lymphoscintigraphy was used to measure lymphatic drainage in the upper limbs of 3 groups of patients: Group 1, inflammatory arthritis and edema (N = 10); Group 2, inflammatory arthritis and no edema (N = 18); and Group 3, healthy controls (N = 11). RESULTS: Lymphatic drainage was reduced significantly in Group 1 but was the same in Groups 2 and 3. Multiple regression analysis failed to show any effect of arthritis on lymphatic drainage. CONCLUSION: Inflammatory arthritis alone does not impair lymphatic drainage in the upper limbs. The results suggest that the presence of edema is primarily attributable to an unrelated abnormality influencing lymphatic function.
The essential function of the lymphatic system is to return to the vascular system extravascular molecules and colloids too large to re-enter directly. Quantitative lymphoscintigraphy employs this principle and has proved useful in the differential diagnosis of chronic limb swelling, in the identification of subtle or incipient lymphoedema and in edema of compound origin where a lymphatic component would otherwise go unnoticed. In a study exploring the contribution of lymphatic insufficiency to poor wound healing in chronic venous leg ulceration 32 patients were compared to 22 normal control subjects using quantitative lymphoscintigraphy. In subjects less than 65 years lymphatic function was reduced in the ulcerated limbs compared to normal limbs (p<0.0001). In those aged more than 65 years lymphatic function was lower in ulcerated limbs but not significantly so, owing to a decline in lymph drainage with age in normal controls (r = 0.62, p = 0.0001). In patients with unilateral leg ulceration lymphatic function was reduced in the ulcerated limb compared with the contralateral leg (<65 years, p = 0.05; >65 years, p = 0.03). The finding of impaired lymph drainage with chronic venous insufficiency suggests that lymphatic pathology may be as important as venous pathology in the "chronic venous leg ulcer" and treatment should be aimed at improving lymphatic as well as venous function.
1. Surgery and radiotherapy to axillary lymph nodes during breast cancer treatment is often followed, commonly years later, by chronic postmastectomy oedema (PMO). PMO is considered a 'high protein' oedema due to reduced axillary lymph drainage. Since oedema formation also depends on fluid input (capillary filtration), we studied the Starling pressures in the affected and contralateral arm. Colloid osmotic pressure was measured in patient serum (pi p) and interstitial fluid (pi i). Subcutis fluid was collected from PMO arms by both wick and aspiration methods, and from the control arm by the wick method only. Interstitial hydraulic pressure (P(i)) was measured by the wick-in-needle method. 2. Oedema pi i was 19.2 +/- 4.1 cmH2O (n = 13, wick) to 16.3 +/- 4.4 cmH2O (n = 41, aspirate; difference not significant; mean +/- S.D. throughout). This was significantly lower than pi i in the control arm (21.4 +/- 3.8 cmH2O, n = 14, P < 0.01, analysis of variance). Also, there was a negative correlation between oedema pi i and the percentage increase in arm volume (correlation coefficient r = -0.35, P < 0.05) in contrast to conventional expectation. 3. Oedema P(i) (1.9 +/- 2.0 cmH2O, n = 28) exceeded the subatmospheric control P(i) (-2.8 +/- 3.0 cmH2O; P < 0.01). Venous and arterial pressures were normal but pi p was subnormal (31.1 +/- 2.7 cmH2O, n = 47). 4. Net pressure opposing capillary blood pressure, P(o), was calculated as P(i) + sigma (pi p-pi i) for a reflection coefficient, sigma, of 0.90-0.99.(ABSTRACT TRUNCATED AT 250 WORDS)
Chronic arm oedema following breast cancer treatment is traditionally attributed to lymphatic obstruction, with venous obstruction as an infrequent complicating factor. The axillo-subclavian venous systems of 81 patients with arm swelling following breast cancer treatment were examined with colour Doppler, duplex Doppler and grey scale ultrasound. Over half (57%) had evidence of venous outflow obstruction and a further 14% had signs of venous "congestion". Only 30% of the swollen arms had normal venous outflow. The venous systems of the contralateral non-swollen arms were all normal as were both arms in 28 control patients who had similar treatment but had not developed arm swelling. These findings suggest that venous outflow obstruction is an important contributory factor in the pathophysiology of arm swelling following breast cancer treatment.
Doppler ultrasound was used to estimate the mean arterial flow in the arms of 50 patients with arm oedema following breast cancer treatment (oedema group). They were compared with 26 treated breast cancer patients with no arm swelling (control group). Flows on the treatment side were expressed as a percentage of the flow in the contralateral normal arm. Mean percentage blood flow was 68% higher in the swollen arms than the contralateral normal arms compared to a mean increase of 38% on the breast cancer treatment side in the control group. In both groups there was a significantly higher proportion of patients with increased (> 150%) rather than decreased (< 50%) flow on the treatment side. The ratio of increased to decreased flow was 27:4 in the oedema group and 6:0 in the control group. A neurological deficit on the treatment side was associated with an increased incidence of higher flow on the same side in the oedema group. These findings demonstrate that breast cancer treatment results in a significant increase in arterial flow in the arm on the treatment side, and that this increase is even higher in those patients with swelling. Increased blood flow is likely to contribute to arm swelling. One explanation for increased flow would be neurological deficit with loss of sympathetic vasoconstrictor control.
A 66-year-old woman had a long-standing, scaly erythematous lesion on her left temple which histologically showed features of amelanotic lentigo maligna. It had recurred on numerous occasions over a period of 17 years, in spite of multiple attempts at curative surgery. There were also recurrences within a skin graft which, to our knowledge, has not been documented previously with lentigo maligna. In spite of the prolonged course, and extensive intraepidermal melanocytic proliferation amounting to melanoma in situ, there has been no evidence of dermal invasion. The lack of pigmentation in such lesions means that clinical definition of margins is highly inaccurate. In view of the aggressive horizontal growth phase of this lesion, with rapid recurrence following surgery, it was treated with electron beam therapy, and this has resulted in complete clinical remission. This most unusual case illustrates the potential difficulties in diagnosis and management of amelanotic lentigo maligna.
An instrument (tonometer) was developed to measure objectively the rate as well as depth of pitting of edematous limbs under a sudden local load. Displacement versus time curves were obtained in vivo in postmastectomy edema arms and also in vitro (compression of sponges) and were analyzed in terms of spring and dashpot constants. There was no significant difference between the quasi-instantaneous indentation of tissue in the edematous and normal arms (median 2.9mm), and the two correlated strongly (r = 0.91, p < 0.0001). An exponentially slowing indentation followed. The mean difference between initial and final deformation (X infinity-X0) was greater in the swollen arms (5.7mm) than in the normal arms (1.3mm, p < 0.01). The time constant of indentation (tau) was significantly greater in the swollen arms (227s) than in the normal arms (71s). There was no correlation between the duration of the edema and any of the pitting characteristics. There was a significant negative correlation between glycosaminoglycan concentration of interstitial fluid and rate constant 1/tau (r = 0.9, p < 0.01). The tonometer thus provides an objective way of quantifying the rate and depth of pitting edema.
OBJECTIVE: To determine the cause of upper limb edema in 8 patients with peripheral polyarthritis of rheumatoid-type. METHODS: Objective assessment of lymph function using quantitative lymphoscintigraphy. RESULTS: Seven cases with either rheumatoid or psoriatic arthritis were found to have impaired lymph drainage associated with edema. All cases shared a distal rheumatoid pattern of arthritis but showed no relation between severity of lymphatic impairment and either duration or severity of arthritis. CONCLUSION: Polyarthritis of rheumatoid-type may be associated with lymphedema due to impaired lymphatic function.