Arm Ischemia Research Articles

Endovascular Treatment of Acute Type B Dissection and Kommerell’s Diverticulum

A 59-year-old man presented with severe hypertension and resistant interscapular pain. Transesophageal echocardiography and computed tomographic angiogram demonstrated acute type B dissection associated with aberrant right subclavian artery with 3.5 cm Kommerell's diverticulum. Open repair was deemed to be high risk to elevate perioperative mortality and morbidity of this surgical technique. Therefore the patient was managed with an endovascular procedure after 14 days of medical therapy because of resistant thoracic pain. We did not observe intraoperative or perioperative mortality and right arm ischemia or symptomatic subclavian steal.

Indoor Particles Affect Vascular Function in the Aged

Exposure to particulate matter is associated with risk of cardiovascular events, possibly through endothelial dysfunction, and indoor air may be most important. We investigated effects of controlled exposure to indoor air particles on microvascular function (MVF) as the primary endpoint and biomarkers of inflammation and oxidative stress as secondary endpoints in a healthy elderly population. A total of 21 nonsmoking couples participated in a randomized, double-blind, crossover study with two consecutive 48-hour exposures to either particle-filtered or nonfiltered air (2,533-4,058 and 7,718-12,988 particles/cm(3), respectively) in their homes. MVF was assessed noninvasively by measuring digital peripheral artery tone after arm ischemia. Secondary endpoints included hemoglobin, red blood cells, platelet count, coagulation factors, P-selectin, plasma amyloid A, C-reactive protein, fibrinogen, IL-6, tumor necrosis factor-alpha, protein oxidation measured as 2-aminoadipic semialdehyde in plasma, urinary 8-iso-prostaglandin F(2alpha), and blood pressure. Indoor air filtration significantly improved MVF by 8.1% (95% confidence interval, 0.4-16.3%), and the particulate matter (diameter < 2.5 mum) mass of the indoor particles was more important than the total number concentration (10-700 nm) for these effects. MVF was significantly associated with personal exposure to iron, potassium, copper, zinc, arsenic, and lead in the fine fraction. After Bonferroni correction, none of the secondary biomarkers changed significantly. Reduction of particle exposure by filtration of recirculated indoor air for only 48 hours improved MVF in healthy elderly citizens, suggesting that this may be a feasible way of reducing the risk of cardiovascular disease.

Transient Limb Ischemia Induces Remote Preconditioning and Remote Postconditioning in Humans by a K ATP Channel–Dependent Mechanism

Transient limb ischemia administered before a prolonged ischemic insult has systemic protective effects against ischemia-reperfusion (IR) injury (remote ischemic preconditioning [RIPC]). It has been demonstrated that protection from IR can be achieved by brief periods of ischemia applied at a remote site during an injurious ischemic event (remote postconditioning [RPostC]). Using an in vivo model of endothelial IR injury, we sought to determine whether RPostC occurred in humans and whether it shared mechanistic similarities with RIPC. Endothelial function was assessed by flow-mediated dilation before and after IR (20 minutes of arm ischemia followed by reperfusion). RIPC was induced by conditioning cycles of 5 minutes of ischemia and reperfusion on the contralateral arm or leg before IR. For RPostC induction, conditioning cycles were administered during the ischemic phase of IR. Oral glibenclamide was used to determine the dependence of RIPC and RPostC on K(ATP) channels. IR caused a significant reduction in flow-mediated dilation in healthy volunteers (baseline, 9.3+/-1.2% versus post-IR, 3.3+/-0.7%; P<0.0001) and patients with atherosclerosis (baseline, 5.5+/-0.6% versus post-IR, 2.3+/-0.5%; P<0.01). This reduction was prevented by RIPC (post-IR+RIPC: healthy volunteers, 7.2+/-0.5% [P<0.0001 versus post-IR]; patients, 4.5+/-0.3% [P<0.01 versus post-IR]) and RPostC (post-IR+RPostC: 8.0+/-0.5%; P<0.0001 versus post-IR). The protective effects of RIPC and RPostC were blocked by glibenclamide. This study demonstrates for the first time in humans that RPostC can be induced by transient limb ischemia and is as effective as RIPC in preventing endothelial IR injury. RIPC and RPostC share mechanistic similarities, with protection being dependent on K(ATP) channel activation. These results suggest that remote conditioning stimuli could be protective in patients with acute ischemia about to undergo therapeutic reperfusion.

Cerebral Embolic Stroke and Arm Ischemia in a Teenager With Arterial Thoracic Outlet Syndrome: A Case Report

A rare presentation of arterial thoracic outlet syndrome (TOS) is described in a young woman. Arterial TOS caused by a cervical rib produced acute upper extremity ischemia due to subclavian artery aneurysm formation. Clinical presentation also included left hemiparesis caused by right subclavian artery thrombosis and retrograde embolization of thrombus via the common carotid artery to the right middle cerebral artery distribution. Surgical repair of the subclavian artery was performed, but permanent neurologic deficit remained. Acute thrombosis of the right subclavian artery can produce cerebrovascular complication. The assessment of such risk in patients with arterial TOS is warranted and the arterial lesion corrected surgically.

Does Cuff Location for FMD Matter in Smokers?

In Response: We appreciate the interest in our article. Dr Beckman highlights an important issue that we had not discussed, namely the statistical power associated with different methodologies for inducing flow-mediated dilatation (FMD) of the brachial artery. Using upper arm ischemia-reperfusion to induce FMD of the distal brachial artery, we were unable to demonstrate endothelial dysfunction in cigarette smokers, nor its improvement by inhibition of xanthine oxidase.1 In contrast, induction of FMD using ischemia of the forearm distal to the brachial artery allowed us to detect a difference in endothelial function between smokers and nonsmokers and reversal of dysfunction in smokers. As Dr Beckman points out, these results were obtained in a relatively small number of subjects (n=10), which suggests better statistical power for the technique using lower arm occlusion. We agree with Dr Beckman that we may have been able to detect impaired FMD using upper arm ischemia if …

Unusual etiology of upper extremity ischemia in a scleroderma patient: Thoracic outlet syndrome with arterial embolization

Although the causes of digital ischemia and necrosis are diverse in women, the most common etiology is connective tissue disease. We describe a patient with scleroderma who presented with arm ischemia secondary to arterial embolization from thoracic outlet syndrome. Her sublavian artery was compressed by the anterior scalene muscle and a cervical rib, leading to a stenosis with poststenotic dilation of the artery. Within the aneurysmal formation was a thrombus, which was probably the source of the distal embolization. The patient underwent surgical resection of the cervical and first rib. The abnormal portion of the subclavian artery was resected and replaced with an interposition graft.

Rare Presentation of Subclavian Artery Isolation in a Neonate With a Family History of Aortic Arch Anomalies

Isolation of the left subclavian artery is a rare aortic arch anomaly in which the artery originates from the pulmonary artery through a ductus arteriosus rather than the aorta. In neonates it is usually diagnosed incidentally with other aortic or cardiac anomalies and can be associated with chromosomal deletions. We describe an extremely rare presentation whereby subclavian artery isolation was presented with left arm ischemia in a 6-day-old child. There were also a concurrent right aortic arch, ventricular septal defect, persistent left superior vena cava, and both radial and ulnar artery hypoplasia. A family history of aortic arch anomalies with no known chromosomal aberration was also present, whereby all the male family members on the maternal side had undergone aorto-cardiac surgery as neonates. Diagnosis and surgical management are discussed.

Transient upper arm ischemia reduces myocardial injury in patients undergoing cardiac bypass surgery

Transient upper arm ischemia reduces myocardial injury in patients undergoing cardiac bypass surgery

Subclavian flap aortoplasty: still a safe, reproducible, and effective treatment for infant coarctation

Subclavian flap repair of infant coarctation has been criticized and in many centers abandoned in favor of resection with end-to-end anastomosis. The goal of this study was to examine intermediate and long-term results of infant subclavian flap aortoplasty, which has been the preferred technique at our institution over the last two decades. Our patient database identified all infants (age<1 year) who underwent repair of isthmic coarctation via thoracotomy between January 1984 and December 2004. Procedure details and late results were collected by retrospective review of hospital and clinic data. Follow-up was 95.8% complete at a mean of 6.7 years. Between January 1984 and December 2004, 119 infants underwent isolated subclavian flap repair of coarctation. Mean age and weight at operation were 35+/-52 days (range 1-269 days) and 3.5+/-1.3kg (range 0.7-9.3kg), respectively. Concomitant pulmonary artery banding was performed in 22% (26/119). In-hospital mortality was 4% (5/119) and cumulative late mortality was 6% (7/114) of patients with long-term follow-up. Actuarial survival at 1, 5, and 10 years was 91, 85, and 85%, respectively. Overall re-intervention rate for re-stenosis was 11% (12/114); 10 patients (9%) underwent balloon angioplasty while 3 patients (3%) required operative revision. All re-stenoses occurred in the descending aorta, and all occurred in patients who had undergone neonatal repair. At late follow-up, there were no significant neurologic events (left recurrent laryngeal nerve injury, stellate ganglion dysfunction, or paraplegia), no clinically significant ischemic arm complications, and no flap aneurysms. Subclavian flap aortoplasty remains our procedure of choice for isthmic coarctation, as it is a simple, technically straightforward technique with a low incidence of re-stenosis and serious early and late morbidity. Furthermore, subclavian flap re-stenoses are easily treated with percutaneous intervention and seldom require surgical re-intervention via thoracotomy.

Vascular thoracic outlet syndrome

In the methods section of the article on vascular thoracic outlet syndrome (TOS) by Geven et al. [1], the authors point out that their indication for the diagnosis of ‘vascular TOS’ was an abnormal PPG study indicating signs of vascular compression of the subclavian artery. I question the labeling of the patients described here as having ‘vascular’ TOS. As the authors point out in their opening paragraph, there are two types of vascular TOS, arterial and venous. Because these two types are totally different from each other, the terms arterial TOS and venous TOS should be employed and the term ‘vascular’ eliminated. Venous TOS is manifested by symptoms of swelling and cyanosis, while arterial TOS by symptoms of ischemic fingers and arm claudication. Neurogenic TOS is identified by symptoms of paresthesia, weakness, and pain, not only in the upper extremity, but usually in the neck as well. Further, arterial TOS is almost always associated with a cervical rib or anomalous first rib. The symptoms of arterial TOS are usually the result of emboli from subclavian artery thrombosis, either from subclavian artery stenosis or subclavian artery aneurysm with mural thrombus. Only 6 of the 32 patients in this study had cervical ribs. Unfortunately, the authors fail to describe their patients’ symptoms which would help define the type of TOS they were treating. However, since all operations were transaxillary rib resections and none were arterial repairs, it can be assumed that none of these patients had arterial TOS and probably the large majority, if not all, of the patients had neurogenic TOS. Confusion regarding the differentiation between arterial and neurogenic TOS is common because many patients with neurogenic TOS have symptoms of coldness and color changes in their hands along with their other symptoms. These symptoms do not establish a diagnosis of arterial or vascular TOS. They are the result arteriolar vasoconstriction brought on by sympathetic nerve stimulation from compression of the sympathetic nerve fibers that accompany the C7 and C8 nerve roots [2]. Thus, these symptoms are those of neurogenic TOS

The Biochemical and Neuroendocrine Bases of the Hyperalgesic Nocebo Effect

Despite the increasing research on placebos in recent times, little is known about the nocebo effect, a phenomenon that is opposite to the placebo effect and whereby expectations of symptom worsening play a crucial role. By studying experimental ischemic arm pain in healthy volunteers and by using a neuropharmacological approach, we found that verbally induced nocebo hyperalgesia was associated to hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, as assessed by means of adrenocorticotropic hormone and cortisol plasma concentrations. Both nocebo hyperalgesia and HPA hyperactivity were antagonized by the benzodiazepine diazepam, suggesting that anxiety played a major role in these effects. The administration of the mixed cholecystokinin (CCK) type-A/B receptor antagonist proglumide blocked nocebo hyperalgesia completely but had no effect on HPA hyperactivity, which suggests a specific involvement of CCK in the hyperalgesic but not in the anxiety component of the nocebo effect. Importantly, both diazepam and proglumide did not show analgesic properties on basal pain, because they acted only on the nocebo-induced pain increase. These data indicate a close relationship between anxiety and nocebo hyperalgesia, in which the CCKergic systems play a key role in anxiety-induced hyperalgesia. These results, together with previous findings showing that placebo analgesia is mediated by endogenous opioids, suggest that the analgesic placebo/hyperalgesic nocebo phenomenon may involve the opposite activation of endogenous opioidergic and CCKergic systems.

Muscle Oxygenation During Incremental Arm-Cranking Exercise in Healthy and Hypertensive Elderly Humans

PURPOSE: We evaluated the factors limiting aerobic arm exercise performance in compensated hypertensive vs healthy elderly males. We hypothesized that, due to cardiovascular modifications associated with high blood pressure, central factors play a larger role, in the age-related decline in arm exercise capacity, in hypertensive rather than in normotensive subjects. METHODS: Non-smoking elderly (14 normotensive, mean age ± SD 69 ± 5 yrs and 13 hypertensive, 68 ± 5) were compared to 10 young males (29 ± 6 yrs). The subjects performed an incremental arm-cranking test to exhaustion. Ventilation, gas exchange and heart rate (HR) were measured breath by breath (Quark b2, Cosmed, Italy). Changes in concentration of deoxygenated hemoglobin ([deoxyHb], an index of the ratio between O2 consumption and O2 delivery, similar to O2 extraction) were monitored non-invasively by near infrared spectroscopy (HEO-200, Omron, Japan) at the biceps brachii. O2 extraction was expressed as % of the value obtained during arm ischemia (physiological calibration). Peak data were compared for significant differences by one-way analysis of variance. RESULTS: As expected, peak exercise variables were significantly higher in the young compared to the elderly subjects. Yet, no differences in peak values of power output (83 ± 11; 89 ± 14 W), VO2 (1.62 ± 0.29; 1.64 ± 0.41 l*min−1), HR (147 ± 14; 152 ± 11 b*min−1), respiratory quotient (1.18 ± 0.06; 1.18 ± 0.08) and oxygen pulse (11 ± 1.8; 11 ± 2.4 ml*b−1) were detected in the healthy compared to the hypertensive elderly subjects. Δ[deoxyHb] increased as a function of absolute and relative exercise intensity, reaching upon exhaustion 77 ± 17 and 68 ± 13 % of ischemia in healthy and hypertensive subjects, respectively (difference not significant). In both elderly populations, peak O2 extraction, was not significantly different from that of young healthy sedentaries (75 ± 12% of ischemia). CONCLUSIONS: Our data show that arm maximal exercise capacity is reduced to a similar extent in normotensive and hypertensive older compared to young subjects. Since O2 utilization by the working muscles appears unaffected, we suggest that an impairment of O2 delivery is the main responsible for the reduction of arm exercise capacity observed in elderly hypertensive subjects and age-matched healthy sedentaries, compared to young subjects. Furthermore, the relative role of central and peripheral factors in causing the age-related loss of arm exercise capacity is apparently not altered by pathophysiological factors related to compensated hypertension.

Emergency endovascular stent-graft treatment for acute thoracic aortic syndromes

We report the results of our ongoing experience of urgent and emergency stent-graft implantation in acute thoracic aortic syndromes. In the last 5-years, 19 patients were treated for acute thoracic aortic syndromes. Traumatic rupture was diagnosed in 7 patients, complicated acute type B dissection was present in 5 patients, penetrating ulcer in 4, and symptomatic thoracic aortic aneurysm in 3 patients. There were 17 male patients with a mean age of 54 +/-26 years (range 18-87 ; median 63). Patients were treated in the theatre suite under general anesthesia. Stent-graft placement was technically successful in all patients. The early postoperative mortality was 10.5 %. Neurological events or upper arm ischemia due to overstenting of the left subclavian artery were not observed. Average intensive care unit and hospital stay were 18 and 21 days, respectively. Major complications occurred in 6 patients. Follow-up ranged between 3 and 60 months (mean 25) and included clinical examinations and serial CT-angiography at 1, 4 and 12 months, and every year thereafter. Only one type II endoleak was detected and treated by coil embolization of the left subclavian artery. Our experience suggests emergency stent-graft repair in patients with acute thoracic aortic syndromes is a less-invasive attractive alternative, showing encouraging early and mid-term results.

AMPD1 gene polymorphism and the vasodilatory response to ischemia

Peripheral vasculature resistance can play an important role in affecting blood pressure and the development of cardiovascular disease. A better understanding of the genes that encode vasodilators, such as adenosine, will provide insight into the mechanisms underlying cardiovascular disease. We tested whether the adenosine monophosphate deaminase-1 ( AMPD1) C34T gene polymorphism was associated with the vasodilatory response to ischemia in Caucasian females aged 18–35 years. Blood samples ( n = 58) were analyzed for the C34T variant and resulted in the following genotype groups: CC ( n = 45) and CT ( n = 13). Mean blood pressure (MBP), heart rate, and forearm blood flow (FBF) measured by venous occlusion plethysmography were measured at baseline and at 1 (peak FBF), 2 and 3 min of vasodilation during reactive hyperemia following 5 min of arm ischemia. To control for interindividual variability in baseline FBF and forearm vascular resistance (FVR) the percent change in FBF and FVR were calculated for each min. The percent decrease in FVR was significantly greater in the CT compared to the CC genotype group (− 40 ± 4% vs. − 24 ± 3%, P = 0.01) during the 2nd min of reactive hyperemia. The percent increase in FBF tended to be greater in the CT compared to the CC genotype group (+ 69 ± 9% vs. + 42 ± 9%, P = 0.07) during the 2nd min of reactive hyperemia after adjustment for percent body fat. Consistent with previous findings of increased production of adenosine during exercise in individuals carrying a T allele, our findings suggest that the AMPD1 C34T polymorphism is associated with vasodilatory response to ischemia in the peripheral vasculature because individuals with the T allele had a greater vasodilatory response to ischemia.

Postconditioning Protects Against Endothelial Ischemia-Reperfusion Injury in the Human Forearm

Hypoxic cell death follows interruption of blood supply to tissues. Although successful restoration of blood flow is mandatory for salvage of ischemic tissues, reperfusion can paradoxically place tissues at risk of further injury. Brief periods of ischemia applied at the onset of reperfusion have been shown to reduce ischemia-reperfusion (IR) injury, a phenomenon called postconditioning. The aim of this study was to determine whether postconditioning protects against endothelial IR injury in humans, in vivo. Brachial artery endothelial function was assessed by vascular ultrasound to measure flow-mediated dilation (FMD) in response to forearm reactive hyperemia. FMD was measured before and after IR (20 minutes of arm ischemia followed by 20 minutes of reperfusion) in healthy volunteers. To test the protective effects of postconditioning, 3 cycles of reperfusion followed by ischemia (each lasting 10 or 30 seconds) were applied immediately after 20 minutes of arm ischemia. To determine whether postconditioning needs to be applied at the onset of reperfusion, a 1-minute period of arm reperfusion was allowed before the application of the 10-second postconditioning stimulus. IR caused endothelial dysfunction (FMD 9.1+/-1.2% pre-IR, 3.6+/-0.7% post-IR, P<0.001; n=11), which was prevented by postconditioning applied as 10-second cycles of reperfusion/ischemia (FMD 9.9+/-1.7% pre-IR, 8.3+/-1.4% post-IR, P=NS; n=11) and 30-second cycles of reperfusion/ischemia (FMD 10.8+/-1.7% pre-IR, 9.5+/-1.5% post-IR, P=NS; n=10) immediately at the onset of reperfusion. No protection was observed when the application of the 10-second postconditioning stimulus was delayed for 1 minute after the onset of reperfusion (FMD 9.8+/-1.2% pre-IR, 4.0+/-0.9% post-IR, P<0.001; n=8). This study demonstrates for the first time that postconditioning can protect against endothelial IR injury in humans. Postconditioning might reduce tissue injury when applied at the onset of reperfusion by modifying the reperfusion phase of IR.

Endograft exclusion of acute and chronic descending thoracic aortic dissections

To analyze the results of endograft exclusion of acute and chronic descending thoracic aortic dissections (Stanford type B) with the AneuRx (n = 5) and Talent (n = 37) thoracic devices and to compare postoperative outcomes of endograft placement acutely (<2 weeks) and for chronic interventions. Patients treated for acute or chronic thoracic aortic dissections (Stanford type B) with endografts were included in this study. All patients (n = 42) were enrolled in investigational device exemption protocols from August 1999 to March 2005. Three-dimensional computed tomography reconstructions were analyzed for quantitative volume regression of the false lumen and changes in the true lumen over time (complete >95%, partial >30%). Forty-two patients, all of whom had American Society of Anesthesiologists (ASA) risk stratification > or =III and 71% with ASA > or = IV, were treated for Stanford type B dissections (acute = 25, chronic = 17), with 42 primary and 18 secondary procedures. All proximal entry sites were identified intraoperatively by intravascular ultrasound (IVUS). The procedural stroke rate was 6.7% (4/60), with three posterior circulation strokes. Procedural mortality was 6.7% (4/60). The left subclavian artery was occluded in 11 patients (26%) with no complaints of arm ischemia, but there was an association with posterior circulation strokes (2/11) (18%). No postoperative paraplegia was observed after primary or secondary intervention. Complete thrombosis of the false lumen at the level of endograft coverage occurred in 25 (61%) of 41 patients < or =1 month and 15 (88%) of 17 patients at 12 months. Volume regression of the false lumen was 66.4% (acute) and 91.9% (chronic) at 6 months. Lack of true lumen volume (contrast) increase and increasing false lumen volume (contrast) suggests continued false lumen pressurization and the need for secondary reintervention. Thirteen patients (31%) required 18 secondary interventions for proximal endoleaks in 6, junctional leaks in 3, continued perfusion of the false lumen from distal re-entry sites in 3, and surgical conversion in 4 for retrograde dissection. Preliminary experience with endografts to treat acute and chronic dissections is associated with a reduced risk of paraplegia and lower mortality compared with open surgical treatment, the results of medical treatment alone, or a combination.

Endovascular repair of the thoracic aorta necessitating anchoring of the stent graft across the arch vessels

The purpose of the study was to determine technical and clinical results in endovascular repair of thoracic aortic diseases necessitating stent-graft anchoring across the arch vessels. The causes for endovascular treatment in 58 patients (aged 20 to 84 years) were aneurysms (n = 32), acute type A (n = 2) and type B dissections (n = 17), posttraumatic transections (n = 4), iatrogenic dissection (n = 1), and penetrating ulcers with an intramural hematoma (n = 2). Surgical revascularization of arch vessels was performed in 26 patients before stent-graft implantation. Intentional overstenting of the left subclavian artery resulted in complete occlusion in 8 and was partial in 24 patients. The 30-day mortality rate was 3.4%. Overall, 19 major postprocedural complications occurred in 14 (24%) patients. Among patients with left subclavian artery occlusion, 2 patients had major (1 paraplegia, 1 critical arm ischemia), and 3 minor (2 temporary vertebrobasilary symptoms, 1 transient arm claudication) complications. Fourteen (25%) patients had an early endoleak, of whom 5 were treated successfully with a secondary endovascular procedure, 2 necessitated open surgical conversion, and 7 were treated conservatively, with spontaneous sealing of the endoleak in 3. In 53 (91%) in whom computed tomographic follow-up was longer than 3 months (mean, 30.1 months, range, 3 to 85), the aortic diameter along the stented segment decreased in 24, was stable in 19, and increased in 10 patients. Fixation of the stent graft in the aortic arch can expand the applicability of endovascular repair. Intentional overstenting should be performed with caution to avoid ischemic problems after complete occlusion of left subclavian artery.

Acute Subclavian Artery Occlusion by Blunt Trauma: A Case Report

We report a case of acute left subclavian artery occlusion after blunt trauma, presenting with symptoms of acute left upper arm ischemia. Angiography was performed to confirm the injury. The injured left subclavian artery was approached via left thoracotomy, and an interposition graft was placed. The patient recovered without any complications.

Diffuse Vasospasm of All Four Extremities Resulting to Acute Arm and Legs' Ischaemia Due to Cafergot Abuse

Ergotism is a rare cause of vasospasm which occurs in 0.001–0.002% of patients receiving ergot derivatives primarily for treatment of migraine [Dagher FJ, Sidawy AN. Ergotism, current treatment in vascular surgery. 4th ed. Ernst-Stanley. p. 154–157]. Vasospasm though diffuse affects usually the lower limbs.We present the case of a 38 year old woman with truly diffuse vasospasm, due to Cafergot suppositories abuse, of all four extremities causing severe ischaemia to her left arm and bilateral intermittent calf claudication.The patient was treated successfully and recovered from vasospasm 72h later.

Diffuse Vasospasm of All Four Extremities Resulting to Acute Arm and Legs' Ischaemia Due to Cafergot Abuse

Ergotism is a rare cause of vasospasm which occurs in 0.001–0.002% of patients receiving ergot derivatives primarily for treatment of migraine [Dagher FJ, Sidawy AN. Ergotism, current treatment in vascular surgery. 4th ed. Ernst-Stanley. p. 154–157]. Vasospasm though diffuse affects usually the lower limbs.We present the case of a 38 year old woman with truly diffuse vasospasm, due to Cafergot suppositories abuse, of all four extremities causing severe ischaemia to her left arm and bilateral intermittent calf claudication.The patient was treated successfully and recovered from vasospasm 72h later.