Effect of thermal stimuli on peripheral blood flow in homozygous sickle cell disease: A preliminary study

2011 ◽  
Vol 5 (01) ◽  
pp. 19-23
Author(s):  
Junette Mohan ◽  
Harvey Reid ◽  
Graham Serjeant
Keyword(s):  
Blood Flow ◽  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Peripheral Blood ◽  
Peripheral Blood Flow ◽  
Cell Disease ◽  
Preliminary Study ◽  
Thermal Stimuli ◽  
Homozygous Sickle Cell Disease

scholarly journals The effect of hypnosis on pain and peripheral blood flow in sickle-cell disease: a pilot study

2017 ◽  
Vol Volume 10 ◽  
pp. 1635-1644 ◽  
Author(s):  
Ravi Bhatt ◽  
Sarah Martin ◽  
Subhadra Evans ◽  
Kirsten Lung ◽  
Thomas Coates ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pilot Study ◽  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Peripheral Blood ◽  
Peripheral Blood Flow ◽  
Cell Disease

scholarly journals Peripheral Blood Flow Responses to Pain Following a Hypnosis Intervention in Sickle Cell Disease

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 4853-4853
Author(s):  
Ravi Bhatt ◽  
Subhadra Evans ◽  
Lonnie Zeltzer ◽  
Thomas D. Coates ◽  
Jennie Tsao
Keyword(s):  
Blood Flow ◽  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Peripheral Blood ◽  
Pain Sensitivity ◽  
Pain Threshold ◽  
Pain Tolerance ◽  
Peripheral Blood Flow ◽  
Cell Disease ◽  
Before And After

Abstract Introduction: Vaso-occlusive pain crises are considered the "hallmark" of sickle cell disease (SCD). Persistent occurrence is thought to lead to changes in the peripheral and central nervous system, which can then in turn lead to changes in pain sensitivity. Imaging studies have shown that hypnotic analgesia can reduce activity in supraspinal areas of the "pain matrix." To date there are no published studies looking at the effectiveness of hypnosis in altering pain perception in patients with SCD. The purpose of this study was to investigate changes in peripheral blood flow in response to a 30-minute hypnosis intervention and its relationship to pain sensitivity. Methods: To assess the effectiveness of increasing vasodilation, a laboratory based, single session hypnosis protocol was administered to a sample of 14 SCD patients and 14 healthy controls. Continuous readings for SpO2, pulse rate and pulse waveform was monitored using a pulse oximetry transducer placed on the left thumb. Bio-behavioral pain measures were collected during a standardized pain protocol before and after a hypnosis session, performed by a trained therapist. The protocol consisted of assessing pain tolerance and threshold via a heat probe (˚C) for "pain task 1", preceded by an anticipation period. "Pain task 2" consisted of assessing pain intensity via the same heat probe (˚C) on a 1-100 visual analog scale (VAS), preceded by another anticipation period. Results: To investigate blood-flow responses to their respective baseline (baseline vs. hypnosis), all recorded signal following these two periods was normalized respectively. Independent sample t-tests between both normalized anticipation and pain responses periods revealed controls showed no response to hypnosis for anticipation period 1(t(23.42) = .184, p = .855, d = .072), but SCD patients showed a large increase in blood flow (t(16.99) = 4.189, p = .0006, d = 1.79). Neither controls (t(21.05) = .00, p = .994, d = .003) or SCD patients (t(19.99) =.718, p = .481, d = .305) showed an effect of hypnosis in response to pain task 1. Neither controls (t(23.96) = -.139, p = .890, d = -.05) or SCD patients (t(18.82) = 1.035, p = .313, d = .441) showed a response to anticipation period 2, but the effect size reveals that this may be due to a lack of power. Neither controls (t(16.52) = .258, p = .799, d = .101) or SCD patients (t(19.63) = p = .5375, d = .268) showed no changes in response to hypnosis for pain task 2. Independent sample t-tests revealed no significant difference in pain threshold (t(13) = 0.941, p = .364, d = .251) or tolerance (t(13) = 0.937, p = 0.366, d = 0.250) in SCD patients before and after hypnosis. Differences in pain ratings were marginal but showed a decrease with medium effect (t(13) = -1.5315, p = 0.150, d = 0.409). The same tests revealed significant decreases in controls for pain threshold (t(13) = 2.825, p = 0.01, d = .755), pain tolerance (t(13) = 2.482, p = 0.02, d = 0.664), and pain rating (t(13) = 2.950, p = 0.01, d = .789). Conclusion: Results revealed that hypnosis may be an effective treatment in helping manage vasoconstriction in SCD as a response to cognitive appraisals about pain, as well as reducing pain sensitivity. The data presented provide preliminary clinical evidence of the use of hypnosis as a treatment method to improve vasodilation in SCD patients and decreasing pain crises, thus increasing overall quality of life. Disclosures No relevant conflicts of interest to declare.

Blood Flow Response to Cold Face Stimulation Is Blunted In Patients with Sickle Cell Disease

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2655-2655
Author(s):  
Roberta Miyeko Kato ◽  
Adam Bush ◽  
Suvimol Sangkatumvong ◽  
Daniel Gardner ◽  
Jon Detterich ◽  
...  
Keyword(s):  
Blood Flow ◽  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Peripheral Blood ◽  
Peripheral Blood Flow ◽  
Cell Disease ◽  
Flow Response ◽  
Cold Face ◽  
Flow Changes ◽  
Normal Controls

Abstract Abstract 2655 Sickle cell disease (SCD) is characterized by repeated episodes of vaso-occlusion leading to painful episodes, acute chest syndrome, stroke, end organ damage and death. Blood flow changes that result in decreased perfusion of tissues and organs increase the risk for vaso-occlusion by increasing the residence time of deoxygenated and deformed sickled red blood cells in the capillary bed. Patients with SCD are more likely to have transient decreases in perfusion in response to sighs (unpublished data). We thus hypothesized that SCD patients would have an enhanced vasoconstriction response to other autonomic stimuli, such as the cold face stimulation test, when compared to normal controls and SCD patients who are chronically transfused. Using an IRB approved protocol, we studied 13 normal, ethnic matched, subjects (mean age 30.2 + 14 yrs), 12 SCD subjects (mean age 22.9 + 13.1 yrs) and 7 chronically transfused SCD subjects (mean age 22.5 + 11.5 yrs). Dermal capillary perfusion (DCP) measured by laser Doppler and near infrared regional oxygen saturation (rSO2) of the hand were monitored as continuous measures of peripheral blood flow. Physiologic data including systemic vascular resistance (SVR), respiratory rate, tidal volume, heart rate and mean arterial blood pressure, as well as DCP and rSO2, were continuously monitored and recorded digitally. A cold pack was applied to the forehead for 60 seconds and the perfusion and physiological data were recorded. Baseline physiologic values were calculated as the median from 5 min to 1 min prior to the cold face stimulation and compared to median values during the cold face stimulation. In all three populations (normal controls, chronically transfused SCD, SCD) there was a rapid decrease of DCP from baseline (−38.2%, −26.6%, −22.5% respectively) and rSO2 (−8.8%, −4.8%, −3.3% respectively) during the cold face stimulation. Thus, compared to controls, the vascular response was blunted in both SCD and transfused SCD. The blood flow changes in response to the cold face stimulation in SCD improved with chronic transfusion but did not normalize. SVR increased in all populations (17%, 16%, 9% respectively) but the response was blunted in the non-transfused SCD group. Bradycardia was observed in the control and chronically transfused SCD groups (−5.9%, −3.7%) but not in the non-transfused SCD (−0.21%). Our results indicate that, as expected, there is a decrease in peripheral blood flow during cold exposure in normal controls which also occurs in SCD and chronically transfused SCD; SVR is increased consistent with peripheral vasoconstriction. Interestingly, the peripheral blood flow response to cold face stimulation is significantly blunted in both SCD and SCD with chronic transfusion, and thus transfusion does not correct the abnormality. However, chronic transfusion in SCD normalizes the bradycardiac/parasympathetic response to cold face stimulation. In overview, these findings indicate that chronic transfusion partially improves autonomic function in SCD patients, but does not correct the abnormality in peripheral microvascular reactivity. Disclosures: Coates: Novartis: Research Funding, Speakers Bureau.

Increased Procoagulant Activity of Red Blood Cells from Patients with Homozygous Sickle Cell Disease and β-Thalassemia

1996 ◽  
Vol 76 (03) ◽  
pp. 322-327 ◽  
Author(s):  
Dominique Helley ◽  
Amiram Eldor ◽  
Robert Girot ◽  
Rolande Ducrocq ◽  
Marie-Claude Guillin ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Red Blood Cells ◽  
Sickle Cell ◽  
Blood Cells ◽  
Annexin V ◽  
Mean Value ◽  
Procoagulant Activity ◽  
Dependent Manner ◽  
Cell Disease ◽  
Homozygous Sickle Cell Disease

SummaryIt has recently been proved that, in vitro, red blood cells (RBCs) from patients with homozygous β-thalassemia behave as procoagulant cells. The procoagulant activity of β-thalassemia RBCs might be the result of an increased exposure of procoagulant phospholipids (i. e. phosphatidylserine) in the outer leaflet of the membrane. In order to test this hypothesis, we compared the catalytic properties of RBCs of patients with β-thalassemia and homozygous sickle cell disease (SS-RBCs) with that of controls. The catalytic parameters (Km, kcat) of prothrombin activation by factor Xa were determined both in the absence and in the presence of RBCs. The turn-over number (kcat) of the reaction was not modified by normal, SS- or (3-thalassemia RBCs. The Km was lower in the presence of normal RBCs (mean value: 9.1 µM) than in the absence of cells (26 µM). The Km measured in the presence of either SS-RBCs (mean value: 1.6 µM) or β-thalassemia RBCs (mean value: 1.5 pM) was significantly lower compared to normal RBCs (p <0.001). No significant difference was observed between SS-RBCs and p-thalassemia RBCs. Annexin V, a protein with high affinity and specificity for anionic phospholipids, inhibited the procoagulant activity of both SS-RBCs and (3-thalassemia RBCs, in a dose-dependent manner. More than 95% inhibition was achieved at nanomolar concentrations of annexin V. These results indicate that the procoagulant activity of both β-thalassemia RBCs and SS-RBCs may be fully ascribed to an abnormal exposure of phosphatidylserine at the outer surface of the red cells.

scholarly journals Is there a role for selective vasodilation in the management of sickle cell disease?

Blood ◽  
1988 ◽  
Vol 71 (3) ◽  
pp. 597-602 ◽  
Author(s):  
GP Rodgers ◽  
MS Roy ◽  
CT Noguchi ◽  
AN Schechter
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Microvascular Obstruction ◽  
Controlled Study ◽  
Control Group ◽  
Cell Disease ◽  
Retinal Arteriolar

Abstract To test the hypothesis that microvascular obstruction to blood flow at the level of the arteriole may be significant in individuals with sickle cell anemia, the ophthalmologic effects of orally administered nifedipine were monitored in 11 steady-state patients. Three patients with evidence of acute peripheral retinal arteriolar occlusion displayed a prompt reperfusion of the involved segment. Two other patients showed fading of retroequatorial red retinal lesions. Color vision performance was improved in six of the nine patients tested. The majority of patients also demonstrated a significant decrease in the amount of blanching of the conjunctiva which reflects improved blood flow to this frequently involved area. Such improvements were not observable in a control group of untreated stable sickle cell subjects. These findings support the hypothesis that inappropriate vasoconstriction or frank vasospasm may be a significant factor in the pathogenesis of the microvascular lesions of sickle cell disease and, further, that selective microvascular entrapment inhibition may offer an additional strategy to the management of this disorder. We believe a larger, placebo-controlled study with nifedipine and similar agents is warranted.

scholarly journals Clinical findings associated with homozygous sickle cell disease in the Barbadian population – do we need a national SCD registry?

2014 ◽  
Vol 7 (1) ◽  
Author(s):  
Kim R Quimby ◽  
Stephen Moe ◽  
Ian Sealy ◽  
Christopher Nicholls ◽  
Ian R Hambleton ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Clinical Findings ◽  
Cell Disease ◽  
Homozygous Sickle Cell Disease

scholarly journals Concurrent homozygous sickle‐cell disease and severe haemophilia A: Thromboelastography profiles

Haemophilia ◽  
2019 ◽  
Vol 25 (2) ◽  
Author(s):  
Ahmar U. Zaidi ◽  
Latha Rao ◽  
Michael U. Callaghan ◽  
Madhvi Rajpurkar ◽  
Wendy Hollon ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Haemophilia A ◽  
Severe Haemophilia ◽  
Cell Disease ◽  
Homozygous Sickle Cell Disease
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