W. Sandmann

Prothrombin and factor V mutations in women with a history of thrombosis during pregnancy and the puerperium

Background Venous thromboembolism is a leading cause of morbidity and mortality during pregnancy and the puerperium. However, the role of mutations in the prothrombin and factor V genes and other thrombophilic abnormalities as risk factors for thromboembolism in women during pregnancy and the puerperium is not known. Methods In a study of 119 women with a history of venous thromboembolism during pregnancy and the puerperium and 233 age-matched normal women, we measured the activity of antithrombin, protein C, protein S, and lupus anticoagulant. We also performed genetic analyses to detect the G1691A mutation in the factor V gene (factor V Leiden), the G20210A mutation in the prothrombin gene, and the C677T mutation in the methylenetetrahydrofolate reductase gene. Blood samples were obtained at least three months post partum or after the cessation of lactation. Results Among the women with a history of venous thromboembolism, the prevalence of factor V Leiden was 43.7 percent, as compared with 7.7 percent ...

The risk of ischemic spinal cord injury in patients undergoing graft replacement for thoracoabdominal aortic aneurysms

PURPOSE We developed a monitoring system to detect spinal cord ischemia during aortic cross-clamping (AXC). This system was used to prospectively determine in which patients ischemia occurs, in which patients reimplantation of intercostal arteries is unnecessary or mandatory, and when reperfusion of intercostal arteries (ICAs) is urgent. METHODS Two hundred sixty patients underwent thoracoabdominal aortic aneurysm (TAA) repair with simple AXC. In 167 patients, two electrocatheters were placed before the onset of anaesthesia at level L1/L2 (stimulation) and level T5/T6 (recording) within the epidural space. During surgery, spinal cord function was monitored by recording spinal somatosensory evoked potentials (sSSEP). According to the extent of aortic replacement, most patients were expected to have a high risk of paraplegia. RESULTS In group A (59 patients), sSSEP remained normal throughout surgery, and in 54 of these patients ICAs were not reattached outside the proximal aortic anastomosis. In the other five patients ICAs were reimplanted separately because of possible anatomic relation to spinal cord blood supply. No patient in group A had postoperative neurologic deficit. In group B (54 patients) sSSEP remained normal until 15 minutes after AXC but were impaired thereafter. Nineteen patients had early reimplantation of ICAs. Of the 19, three had paraparesis and two had paraplegia. Neurologic deficit developed in the patients without early reimplantation of ICAs. In four patients separate reimplantation of ICAs was performed late in the procedure because of incomplete sSSEP recovery. Subsequently, the sSSEP returned to normal and only one of the four patients had mild paraparesis. The total rate of neurologic deficits in this group was 13% (paraplegia, 3.5%; paraparesis, 9.5%). All 54 patients in group C showed rapid loss of sSSEP within 15 minutes of AXC. In 28 patients ICAs were reimplanted only within the proximal anastomosis. Twenty-one of these patients showed prompt signal recovery after blood-flow release into the reimplanted ICAs, and none had neurologic deficit. Seven patients had no or very late and incomplete sSSEP recovery. Of the seven, three had paraplegia and four had paraparesis. In 26 patients ICAs were reimplanted separately to the proximal anastomosis. This was done early during the procedure in 17 patients, of whom 13 had full recovery of sSSEP and normal neurologic status. Four patients had incomplete or no recurrence of sSSEP, followed by paraplegia in one and paraparesis in three. In nine patients ICAs were reimplanted after the aortic replacement had been completed because of sSSEP recovery was not satisfactory. In all patients in this subgroup sSSEP returned to normal. Six patients had a normal neurologic status and three had mild paraparesis. The total neurologic complication rate in group C was 26% (paraplegia, 7.5%; paraparesis, 18.5%). CONCLUSION The risk of ischemic spinal cord injury during replacement for TAA can be assessed continuously by monitoring the sSSEP directly from the spinal cord. Patients without sSSEP changes during aortic reconstruction do not require ICA reattachment and will not have neurologic deficit. Patients who lose sSSEP after AXC are at risk for paraplegia. Patients with impairment or loss of sSSEP >15 minutes after AXC have some collateral vessels, and must have ICAs reimplanted only if sSSEP do not return within normal recovery time after blood-flow release into the proximal anastomosis. Loss of sSSEP within 15 minutes of AXC shows poor collateralization and mandates early restoration of spinal cord blood supply. If the surgeon can achieve the return of sSSEP to normal by subsequent separate reimplantation of ICAS, paraplegia will not occur and paraparesis will be rare and mild. Spinal cord monitoring is a valuable guide to detect whether the spinal cord is at risk and to take measures against par

Predicting Delirium After Vascular Surgery: A Model Based on Pre- and Intraoperative Data

Objective The aim of the study was to determine pre- and intraoperative risk factors for the development of postoperative delirium among patients undergoing aortic, carotid, and peripheral vascular surgery to predict the risk for postoperative delirium. Summary Background Data Although postoperative delirium after vascular surgery is a frequent complication and is associated with the need for more inpatient hospital care and longer length of hospital stay, little is known about risk factors for delirium in patients undergoing vascular surgery. Methods Pre-, intra-, and postoperative data were prospectively collected, including the first 7 postoperative days with daily follow-up by a surgeon and a psychiatrist of 153 patients undergoing elective vascular surgery. Delirium (Diagnostic and statistical Manual of Mental Disorders IV) was diagnosed by the psychiatrist. Multivariate linear logistic regression and a cross validation analysis were performed to find a set of parameters to predict postoperative delirium. Results Sixty patients (39.2%) developed postoperative delirium. The best set of predictors included the absence of supraaortic occlusive disease and hypercholesterinemia, history of a major amputation, age over 65 years, a body size of less than 170 cm, preoperative psychiatric parameters and intraoperative parameters correlated to increased blood loss. The combination of these parameters allows the estimation of an individual patients’ risk for postoperative delirium already at the end of vascular surgery with an overall accuracy of 69.9%. Conclusions Postoperative delirium after vascular surgery is a frequent complication. A model based on pre- and intraoperative somatic and psychiatric risk factors allows prediction of the patients risk for developing postoperative delirium.

Risk factors for postoperative delirium in vascular surgery.

The aim of this study was to identify psychiatric and somatic risk factors associated with the development, severity and duration of postoperative delirium after vascular surgery. Forty-seven patients underwent aortic, carotid artery and peripheral artery surgery. Both, surgeon and psychiatrist, monitored patients preoperatively with daily follow up. Preoperative psychiatric assessment included standardized psychopathological scales for the detection of psychiatric symptoms and cognitive deficits. We diagnosed delirium using DSM IV criteria. Delirium Rating Scale was used to estimate delirium severity. Surgical parameters included patient history, diagnoses, medication and laboratory parameters. A statistical analysis was performed using multivariate regression analyses to find factors significantly associated with delirium development, severity, and duration. Thirty-six percent of the patients developed postoperative delirium after surgery. Comparison of different parameters revealed that especially preoperative depression symptoms and perioperative transfusions/infusions had significant predictive value for the development as well as for the severity of postoperative delirium.

Progress in carotid artery surgery at the base of the skull

From 1977 to 1984, 752 reconstructions of the supra-aortic arteries were performed at our service. In a group of 31 patients presenting with transient ischemic attacks (13) or minor strokes (15), preoperative multiplane angiograms identified lesions from various causes in extremely high locations (fibromuscular dysplasia, 10; atherosclerosis, 6; traumatic changes, 10; spontaneous dissection, 3; and mycotic aneurysms and others, 4) in 34 internal carotid arteries (aneurysms, 10; and stenosis, 24). Surgery was performed on 30 patients. Flow restoration was achieved by resection and vein graft replacement (20), gradual dilatation (5), thromboendarterectomy (6), and tangential clip for exclusion of a lateral aneurysm (1). Only one patient was treated with an extracranial-intracranial anastomosis because the stenosis extended into the carotid siphon. One patient was treated with heparin. Exposure of the internal carotid artery (ICA) at the base of the skull required dissection of the digastric muscle, careful mobilization of the cranial nerves, and detachment of the styloid process in 29 patients. Partial resection of the mastoid process was helpful in two patients. The carotid bone canal was opened from the lateral side in four cases to allow the most distal anastomosis 1 cm within the carotid canal. Back-bleeding was controlled by a balloon catheter. A shunt was impossible to use and clamping time averaged 62 +/- 40 minutes. Except for one recurrent stroke and two transient ischemic attacks no other neurologic deficits occurred. Cranial nerve damage could not be avoided in 21 cases (nervus recurrens, 7; nervus glossopharyngeus, 16; and nervus facialis, 4) but disappeared clinically within a 1- to 6-month period in all but two. Each surgical patient underwent control angiography, which demonstrated 30 arteries to be patent, two became occluded, and one had an insignificant stenosis. We conclude that standard surgical techniques are unsuitable for repair of highly located lesions of the ICA. Although extracranial-intracranial anastomosis has been proposed in patients with planned ligation of the ICA, the anatomic reconstruction remains advantageous because flow is restored to normal and the source of emboli is eliminated. With the use of a special approach, graft replacement can be performed up to the base of the skull.

In situ replacement of infected vascular prostheses with rifampin-soaked vascular grafts: Early results

Based on the excellent results of experimental studies with antibiotic-bonded vascular prostheses for prevention of graft infection, gelatin-sealed grafts soaked with rifampin were implanted in situ in five patients with vascular infection. All patients were at risk for limb loss or death and could not be treated by standard techniques such as graft excision and extra-anatomic bypass. In one patient an infected aortic stump aneurysm with involvement of both renal and visceral arteries was found. He was treated by implantation of a bifurcation rifampin-soaked graft between the subdiaphragmal aorta and both renal arteries and reimplantation of celiac and superior mesenteric artery into the graft. In four patients with in-flow or runoff problems on angiography, an antibiotic-soaked graft was used for replacement of a partially or totally infected graft. Cultures were positive for Staphylococcus aureus in three and coagulase-negative staphylococci in two patients. Wound healing was uncomplicated; there was no need for amputation. After a follow-up of at least 6 months, all grafts were patent without any evidence of reinfection on computed tomographic scan. We conclude that infected vascular prostheses can be replaced in situ by rifampin-soaked grafts in patients at high risk for death or major amputation.

Expression of Tissue Factor in High-Grade Carotid Artery Stenosis: Association With Plaque Destabilization

Background and Purpose— The procoagulant protein tissue factor (TF) has been implicated in thromboembolic complications associated with advanced atherosclerosis. In this study, we investigated whether TF expression in high-grade stenoses of the internal carotid artery (ICA) is associated with clinical features of plaque destabilization and addressed the relationship between TF expression and plaque inflammation. Methods— In 36 consecutive patients undergoing surgery for high-grade ICA stenosis, clinical evidence of plaque instability was provided by the recent occurrence of ischemic symptoms attributable to the stenosis and the detection of cerebral microembolism by means of transcranial Doppler ultrasound monitoring of the ipsilateral middle cerebral artery. Endarterectomy specimens were stained immunocytochemically for TF expression as well as macrophage (CD68) and T cell (CD3) infiltration. Results— Morphologically, TF immunoreactivity was codistributed with plaque inflammation and predominantly localized to CD68+ macrophages. Accordingly, statistical analysis revealed a significant association of TF expression with plaque infiltration by macrophages (P <0.0001) and T cells (P =0.013). Plaques extensively stained for TF (median of TF+ total section area >40% in semiquantitative assessment) were more frequent in symptomatic (12/27) than in asymptomatic patients (1/9). Conversely, plaques exhibiting little TF expression (median of TF+ section area <20%) were more frequent in asymptomatic (3/9) than in symptomatic (1/27) patients (P =0.016). Likewise, we found a highly significant association of TF expression with the occurrence of cerebral microembolism (P =0.008). Conclusions— Induction of TF at sites of plaque inflammation may play an important role in the destabilization of high-grade ICA stenosis.

Management of arterial stenosis affecting kidney graft perfusion: a single-centre study in 53 patients.

We assessed clinical and duplex sonographic (CDS) findings, and outcome in patients with stenosis of the transplant renal artery (TRAS) or the aorto‐iliac segment proximal to the graft (Prox‐TRAS) treated with dilatation (PTA), stenting (PTAS) and surgery. From 1988 to 2002, of 1189 patients with renal transplantations, 117 underwent angiography. Fifty‐three patients with TRAS (n = 37)/Prox‐TRAS (n = 16) were found (4.4%).

Prospective randomized trial of operative vs interventional treatment for renal artery ostial occlusive disease (RAOOD)

INTRODUCTION AND OBJECTIVES Patients with either renovascular hypertension (RVH) and/or renal insufficiency (RI) due to renal artery ostial occlusive disease (RAOOD) can successfully undergo an open surgical reconstruction procedure (OSRP), but since the publication of Blum et al(1) percutaneous balloon stent angioplasty (PTRA + stent) leaving a small part of the stent within the aorta has become very popular. However, balloon dilatation and stenting does not remove the atherosclerotic plaque, which is often heavily calcified but leads to disruption of the plaque causing myointimal hyperplasia and recurrent stenosis. Therefore, a comparison of the two treatment modalities concerning complications and durability in a prospective randomized design was felt to bring more insight to the discussion. METHODS From 1998 to 2004, we performed OSRP in 330 patients with RVH and/or RI for various locations of RAOOD. During this time period, 50 patients (female 18, male 32, mean age 64.4 years) with RAOOD of at least 70% stenosis (DSA and duplex criteria) in one or both renal arteries, who did not require other aorto/mesenteric/iliac reconstructive procedures agreed and were randomized to either OSRP (n = 25 patients, 49 arteries) or PTRA + stent (n = 25 patients, 28 arteries). Two patients crossed over to surgical treatment. Patients were followed on a regular basis for 4 years and longer. Endpoints were re-occurrence of RAOOD and impairment of either kidney function or RVH. RESULTS We approached 77 arteries. There was no early mortality in either group, but directly procedure-related morbidity was 13% in the interventional group and 4% in the surgical group. Four-year follow-up mortality was 18% in the interventional group and 25% in the surgical group. Both groups showed significant improvement of RVH (P < .001 in each group) as well as improvement or stabilization in patients with insufficient renal function. Freedom from recurrent RAOOD (>70%) was achieved in 90.1% of the surgical group and 79.9% of the interventional group. CONCLUSION Both treatment modalities showed good early results concerning RVH, kidney function, and renal perfusion. Despite a higher number of bilateral renal artery reconstructions in patients undergoing OSRP, which was probably due to the preferred technique of transaortic endarterectomy eliminating the plaque originating in the aorta and usually extending into both renal arteries, mortality was not higher and procedure-related morbidity was even lower compared to PTRA + stent. These findings and also longer durability of OSRP imply that surgical reconstruction remains the gold standard for patients with RAOOD before PTRA + stent may be considered.

Surgical treatment of septic deep venous thrombosis

BACKGROUND Septic deep venous thrombosis (SDVT) is an uncommon but occasionally lethal disease caused by systemic complications. In most cases reported in the literature SDVT is caused by intravenous drug abuse or transvenous catheter lines. Conservative management with antibiotic drugs and systemic anticoagulation is usually successful, and the surgical approach is regarded as not indicated or unnecessary. Occasionally, however, conservative management fails, thrombosis progresses, and septic embolism develops. METHODS In a 7-year period five patients (three male and two female; mean age, 21.2 years), three with severe systemic complications of SDVT (femoropopliteal, 1; iliofemoral, 1; iliofemoral+vena cava, 3), were treated by venous thrombectomy in addition to intravenous antibiotic administration. Simultaneous transabdominal caval thrombectomy was performed twice. RESULTS Two patients suffered from respiratory failure caused by previous septic embolization. One patient had experienced multiorgan failure before thrombectomy was performed. Intensive care was necessary for all patients (mean, 28 days). All patients survived. CONCLUSIONS In complicated cases of SDVT without improvement or even impairment after conservative management, venous thrombectomy is a lifesaving treatment.