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Abnormal venous function in patients with homozygous sickle cell (SS) disease and chronic leg ulcers
J S Mohan1, J E Vigilance, J M Marshall
1Department of Basic Medical Sciences (Physiology Section), Faculty of Medical Sciences, University of West Indies, Kingston, Jamaica.
Insights
Sickle cell disease patients with leg ulcers show abnormal venous function, specifically in ankle valves. This may cause increased venous pressure, contributing to slow healing and ulcer development.
Area of Science:
- Vascular Medicine
- Hematology
- Wound Healing
Background:
- Chronic leg ulceration is a significant complication in homozygous sickle cell (SS) disease.
- These ulcers share characteristics with venous ulcers in individuals with normal hemoglobin (AA).
Purpose of the Study:
- To investigate potential abnormal venous function in the legs of Jamaican patients with SS disease and leg ulcers.
- To compare venous function between SS patients with ulcers, SS patients without ulcers, and healthy AA individuals.
Main Methods:
- Air plethysmography was used to assess venous capacitance, outflow, and emptying time.
- Ambulatory volume changes and venous refilling times were measured at the ankle and calf.
- Laser Doppler flowmetry evaluated cutaneous red blood cell flux recovery time after exercise.
Main Results:
- No significant differences in deep venous obstruction (SVC, MVO, VET) were found between groups.
- While calf venous refilling (RTc) and ambulatory volume changes were similar, ankle venous refilling time (RTa) and flux recovery time (FRT) were significantly reduced in SS patients with ulcers.
- These reductions in RTa and FRT were more pronounced in SS patients with ulcers compared to SS patients without ulcers, independent of anemia levels.
Conclusions:
- Abnormal venous function, particularly ankle venous valve incompetence, is suggested in SS patients with leg ulcers.
- This venous incompetence may lead to elevated venous pressure, contributing to delayed healing and the initiation of leg ulcers in sickle cell disease.
Abstract:
Chronic leg ulceration is a major cause of morbidity in homozygous sickle cell (SS) disease in Jamaica. These ulcers have features in common with venous ulcers in patients with a normal haemoglobin genotype (AA). Thus we sought to determine whether there is abnormal venous function in the legs of patients with SS disease who have ulcers. Experiments were performed on 15 SS patients with ulcers, and on 15 SS patients and 15 AA subjects with no history of leg ulcers. Changes in venous blood volume of the bottom one-third of the leg induced by venous occlusion and release were studied by air plethysmography, providing indices of segmental venous capacitance (SVC), maximal venous outflow (MVO) and venous emptying time (VET). The changes in volume (ambulatory volume change; AVC) induced by a period of leg exercise were also measured at the ankle (AVCa) and calf (AVCc); venous refilling times at these sites (RTa and RTc respectively) were also measured. Finally, cutaneous red blood cell flux recovery time (FRT) after ankle exercise was assessed by laser Doppler flowmetry. Measurements were also made of haematological variables. SVC, MVO and VET did not differ between the groups, indicating no deep venous obstruction in the SS patients with ulcers. AVCc, AVCa and RTc did not differ among the three subject groups. However, compared with AA subjects, SS patients with ulcers had reduced RTa and FRT. Moreover, RTa and FRT were further shortened in SS patients with ulcers relative to SS patients without ulcers. Since the levels of anaemia were similar in SS patients with and without ulcers, these differences cannot be attributed to differences in arterial flow secondary to anaemia. These results suggest abnormal venous function in SS patients with ulcers, relative to both AA subjects and SS patients without ulcers. We propose that there is incompetence of venous valves draining the ankle region of SS patients with ulcers: the consequent raised venous pressure contributes to the slow healing and, possibly, to the onset of leg ulceration in SS disease.