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PubMed1999

Recognition, diagnosis, and management of heparin-induced thrombocytopenia and thrombosis.

This case report describes a post-coronary artery bypass graft patient who developed arterial thrombosis and loss of a dominant hand as a result of the common and serious immune complication of heparin anticoagulation, heparin-induced thrombocytopenia and thrombosis. This report underscores the need for all surgeons who use heparin in the course of their practice to be aware of heparin-induced thrombocytopenia and the spectrum of its clinical presentations and management. Thrombocytopenia or thrombosis that occurs in a patient receiving heparin should prompt a surgeon to stop all heparin as soon as possible and seek appropriate hematologic consultation. Because heparin-induced thrombocytopenia and heparin-induced thrombocytopenia and thrombosis are mainly clinical diagnoses, one should not wait for objective test confirmation of heparin-induced thrombocytopenia before stopping all heparin treatment. Alternative anticoagulation, other than low molecular weight heparin, must be considered for the patient who develops either condition. For surgeons who perform hand surgery, it is necessary to be aware of the significance of upper extremity thrombosis in a patient who is receiving heparin when consulted for surgical management.

Angina, Unstable↗

PubMed1999

Mesenteric venous thrombosis.

BACKGROUND: Mesenteric venous thrombosis is an uncommon but often lethal form of intestinal ischemia. METHODS: We reviewed pertinent literature on mesenteric venous thrombosis using MEDLINE search. RESULTS: We found that previous abdominal surgery and hypercoagulable states are the most common conditions associated with mesenteric venous thrombosis. The symptoms and signs related to mesenteric venous thrombosis are not specific. In the majority of cases, the diagnosis is established by a high index of clinical suspicion and noninvasive imaging techniques. Immediate operation is indicated if signs of peritonitis or intestinal infarction are present. Administration of heparin is beneficial for reducing recurrence and mortality. CONCLUSION: Clinicians should consider the possibility of acute mesenteric venous thrombosis when faced with a patient having abdominal pain out of proportion to the physical findings and with a negative workup for the common causes of abdominal pain.

Humans↗

PubMed2001

Factor V Leiden mutation: potential thrombogenic role in renal vein, dialysis graft and transplant vascular thrombosis.

Factor V is an important blood coagulation factor, the procoagulatory activity of which is inhibited by activated protein C. The factor V Leiden mutation is due to a single base-pair change (G1691A), which alters the initial cleavage site for activated protein C. The impaired degradation of factor V by activated protein C yields a hypercoagulable state that confers a lifelong increased risk of thrombosis in heterozygous and homozygous individuals. The factor V Leiden mutation represents the most common cause of inherited thrombophilia, and enhances the risk for venous thrombosis by approximately sevenfold. In normal Western populations, heterozygosity for the factor V Leiden mutation is present in 2-5%, whereas in patients with venous thrombosis and a family history of thrombotic disease this figure may reach 50-60%. The presence of the mutation markedly increases the risk for renal vein thrombosis, particularly in neonates. Heterozygosity for factor V Leiden mutation does not appear to be a major risk factor for dialysis access clotting. The presence of factor V Leiden mutation is most devastating in kidney transplant recipients. In these patients the mutation predisposes to renal transplant vein thrombosis and early graft loss. The risk for acute vascular rejection is also enhanced in transplant recipients who are heterozygous for the mutation. Routine screening for factor V Leiden mutation by polymerase chain reaction, and appropriate perioperative and postoperative anticoagulation after renal transplantation might be a valuable strategy to prevent thromboembolic complications in transplant recipients.

Factor V↗

PubMed2004

Symptomatic thrombosis in Turkish neonates.

OBJECTIVE: To investigate the association of two common prothrombotic mutations, factor V G1691A (FV G1691A) and prothrombin G20210A (PT G20210A), in neonates with thrombosis. METHODS: Twenty-six neonates with thrombosis were assessed with the spectrum of assays for thrombophilia, including the two DNA-based prothrombotic factors. RESULTS: Eight patients (31%) had the FV G1691A mutation in heterozygous state. PT G20210A mutation was detected in four patients (15%). Overall, two common prothrombotic factors were detected in 12 neonates (46%) and an underlying disease or a triggering event in 18 neonates (69%). Thrombosis was considered to be idiopathic in five neonates (19%). CONCLUSIONS: The pathogenesis of thrombosis in neonates is multi-factorial. Along with underlying diseases or triggering events, congenital prothrombotic factors (FV G1691A and PT G20210A) showed a trend toward a higher frequency in neonates with thrombosis. These data indicate that mutations associated with underlying disorders in neonates may contribute to the development of thromboembolic disease.

Factor V↗

PubMed1999

Upper extremity deep vein thrombosis.

Upper extremity deep-vein thrombosis has recently been recognized as being a more common and less benign disease than previously reported. It arises generally in the presence of recognizable risk factors, such as central venous catheters and cancer. However, as many as 20% of patients present with apparently spontaneous episodes. The prevalence of inherited coagulation defects in patients with this disease ranges from 10% to 26%. The clinical picture of upper extremity DVT is characterized by pain, edema, and functional impairment, although it may be completely asymptomatic. Because the prevalence of this thrombotic disease is less than 50% among symptomatic subjects, objective diagnosis is mandatory prior to instituting an anticoagulant treatment. When available, compression ultrasonography (alone or associated with Doppler or color Doppler facilities) should be the preferred initial diagnostic test. However, contrast venography may be necessary before anticoagulants are withheld because of negative findings on compression ultrasonography. Pulmonary embolism complicates upper extremity deep-vein thrombosis in up to 36% of patients and may even be the presenting manifestation of this disorder. Its long-term clinical course is complicated by recurrent thromboembolism and post-thrombotic sequelae. Among the therapeutic options advocated for the therapy of upper extremity deep-vein thrombosis, unfractionated or low molecular weight heparin followed by at least 3 months of oral anticoagulants should be regarded as the treatment of choice. Thrombolysis and surgical procedures may be indicated in selected cases. The prevention of this disease requires the institution of appropriate pharmacologic measures (i.e., low-dose unfractionated or low molecular weight heparin or low-dose warfarin) whenever an indwelling central venous catheter is indicated. This review suggests that upper extremity deep-vein thrombosis is at least as serious a disease entity as deep-vein thrombosis of the lower extremities.

Acute Disease↗

PubMed2001

Outpatient treatment of patients with deep-vein thrombosis or pulmonary embolism.

There have been a large number of randomized trials comparing standard unfractionated intravenous heparin with low-molecular-weight heparin for the treatment of deep-vein thrombosis, but only two of these have looked at outpatient therapy. There have been only two randomized trials including patients with symptomatic pulmonary embolism, and neither of these provided outpatient therapy. Postmortem and clinical studies have shown a strong association between pulmonary embolism and the presence of venous thrombosis in the lower limbs. Based on similar rates of venous thromboembolic recurrence and death, these studies suggest that initial treatment should be the same for deep-vein thrombosis and pulmonary embolism. The feasibility of providing outpatient care to many patients seeking treatment for deep-vein thrombosis or acute pulmonary embolism at certain tertiary care hospitals has become evident, but the data suggest that the proportion of eligible patients is institution dependent and may vary from 18% to 91%. In the author's institution, approximately 50% of patients with pulmonary embolism could be treated as outpatients, but there have been no other reports on outpatient therapy for patients with pulmonary embolism. If patients with pulmonary embolism meet criteria demonstrated to result in a higher risk of death, it is, of course, reasonable to not treat such patients on an outpatient basis. Low-molecular-weight heparin followed by oral anticoagulant therapy provides adequate therapy in most patients with deep-vein thrombosis or pulmonary embolism, and many patients can be treated as outpatients.

Administration, Oral↗

PubMedDate not supplied

Antiphospholipid antibody thrombosis. Another source of chronic wounds.

Antiphospholipid antibody thrombosis syndrome is currently not well known and probably underdiagnosed. The risk it presents for recurrent thromboembolism is both life threatening and chronic. Because patients often develop long-standing wounds, it is important for the wound care nurse to identify clients suspect for the disease. Several theories exist speculating on the mechanism of thrombosis involving antiphospholipid antibodies, and each focuses on changes at the interface between the vessel, cell wall membrane, and its interaction with circulating antibodies. As wound care nurses, we should consider antiphospholipid antibody thromboses whenever encountering a recalcitrant wound without obvious underlying cause. Thrombosis can occur anywhere, although 41% of presentations are cutaneous. Recurrent deep vein thrombosis with coexisting venous insufficiency can lead to a missed diagnosis of antiphospholipid thrombosis syndrome, despite evidence of pain and tissue necrosis that is typical of the disease. In any event, long-standing nonhealing wounds are always a signal to revise a diagnosis and seek alternative causes for failure of healing.

Adult↗

PubMed2005

Improving the diagnostic process for deep vein thrombosis in orthopaedic outpatients.

Prompt diagnosis of proximal lower extremity deep vein thrombosis in outpatients is critical because of the risk of pulmonary embolism. Our purpose was to determine the accuracy of orthopaedists' clinical decisions regarding the diagnosis of proximal deep vein thrombosis in outpatients. A nationally representative random sample of 2300 orthopaedists received a survey of six clinical vignettes. They were asked to estimate the probability of proximal lower extremity deep vein thrombosis using defined criteria and to specify their planned diagnostic tests. A clinical decision rule and evidence-based diagnostic test recommendations from the general literature served as the gold standard for comparison. Six-hundred seventy-six (29%) surgeons completed the survey. The orthopaedists' planned diagnostic tests differed from the gold standard, but these differences varied depending on the probability of deep vein thrombosis. For the moderate and high risk vignettes, the diagnostic test recommendations agreed with the gold standard approximately 70% of the time. With the exception of gender, no differences were found between respondents and nonrespondents. Orthopaedists' approach to the diagnosis of deep vein thrombosis in outpatients potentially could be improved by applying a clinical decision rule and current evidence on diagnostic test usage.

Adult↗

PubMed2005

The antithrombotic effect of melagatran in combination with clopidogrel and/or aspirin (carotid artery primary thrombosis study).

Melagatran with aspirin and/or clopidogrel was evaluated for prevention of arterial thrombosis in a model of vessel wall injury. Thirty-five dogs were randomized to receive placebo (n=14), aspirin (7 to 8 mg/kg, p.o. q12 h for three doses with the last dose administered 12 hours before surgery, n=7), clopidogrel (1 mg/kg p.o. QDx3, n=7), or aspirin+clopidogrel (n=7). The right carotid artery (RCA) was the control vessel, whereas the left carotid artery (LCA) was subjected to injury after administration of Melagatran (0.033 mg/kg i.v.+0.1 mg/kg/h). Clopidogrel, but not aspirin pretreatment, increased time (135.6+/-13.5 vs. 116.1+/-27.8 minutes) to RCA thrombosis versus placebo (88.1+/-10.5 minutes). Melagatran prolonged time to occlusion (min) in the LCA (192.4+/-10.9) versus the placebo-treated RCA (88.1+/-10.5). Addition of Melagatran plus aspirin or clopidogrel prevented formation of occlusive thrombosis, in all LCAs. A two-fold increase in tongue bleeding time was observed after aspirin+Melagatran (178.6+/-14.7 to 347.1+/-87.3 seconds) or clopidogrel+Melagatran (279.9+/-97.3 to 437.1+/-142.5 seconds). However, the combination of aspirin and clopidogrel prevented occlusive thrombosis in the RCA and the subsequent addition of Melagatran did not further increase bleeding time. The combination of Melagatran+aspirin or clopidogrel can reduce formation of occlusive arterial thrombosis without eliciting a significant increase in bleeding-time.

Animals↗

PubMed2005

Superior ophthalmic vein thrombosis in a patient with dacryocystitis-induced orbital cellulitis.

A 71-year-old-man presented with chronic left-sided epiphora and a 5-day history of progressive left orbital swelling that had started with a "bump" on the left side of his nose. Orbital CT revealed left-sided preseptal and postseptal inflammation, along with marked thickening of the left superior ophthalmic vein. Orbital MRI with gadolinium enhancement and fat suppression revealed a low-intensity signal in the left superior ophthalmic vein, consistent with a superior ophthalmic vein thrombosis. There was no cavernous sinus involvement. A diagnosis was made of left-sided dacryocystitis-induced orbital cellulitis and superior ophthalmic vein thrombosis. Treatment consisted of intravenous vancomycin, followed by early dacryocystorhinostomy and postoperative intravenous dexamethasone. Anticoagulation was not used. Within 1 week after surgery, the orbital congestion had dramatically improved. Though rare, isolated superior ophthalmic vein thrombosis can be a harbinger of cavernous sinus thrombosis; therefore, early detection is the key to avoiding cavernous sinus thrombosis.

Aged↗

PubMed2006

Internal jugular vein thrombosis associated with acute mastoiditis in a pediatric age.

OBJECTIVE: To discuss the clinical aspects and management of internal jugular vein thrombosis associated with acute otitis media. STUDY DESIGN: Case reports and review of the literature. SETTING: University hospital, tertiary referral center. PATIENT: The authors describe two cases of internal jugular vein thrombosis, without sigmoid sinus thrombosis, secondary to acute otomastoiditis. INTERVENTION: Jugular vein thrombosis was diagnosed in both cases by observation of filling defects of the involved jugular bulb on contrast-enhanced computed tomography and confirmed by conventional magnetic resonance and magnetic resonance venography. RESULTS: Both patients recovered after recanalization of the vessel concomitant to anticoagulation and antibiotic treatment associated with a simple mastoidectomy. CONCLUSION: Internal jugular vein thrombosis may be a complication of acute otitis media, without involvement of the sigmoid sinus and with a starting point in the jugular bulb. Anticoagulation associated with antibiotic therapy can be considered a safe and effective treatment. Surgery should only be performed to eliminate the source of infection from the middle ear and mastoid.

Acute Disease↗

PubMedDate not supplied

Short-term in vivo studies of surface thrombosis in a left ventricular assist system.

Thrombosis continues to be a major adverse and at times fatal event in patients with left ventricular assist systems (LVAS). To assess acute thrombosis in an LVAS, multiscale analysis of surface thrombosis was performed on LVAS blood sacs retrieved after implantation in seven calves for 3 days. Two study groups were evaluated: One group was given heparin and warfarin sodium throughout the study; the second received no postoperative anticoagulation. On explantation, the blood sacs were examined for macroscopic thrombi; microscale thrombosis was assessed with the use of scanning electron microscopy. Macroscopic thrombi about 1 mm in diameter were seen in all sacs from both groups. Although macroscopic thrombi occurred in all sac regions, scanning electron microscopy revealed differences in microscale topography between the port regions and the other sac regions. The primary structure was spherical particles approximately 400 nm in diameter, found to occur at a lower density in the ports. In contrast, the highest densities of proteinaceous rough topography and fibrillar structures consistent with fibrin clot were seen in the port regions. The density distribution of these structures was different in the eight sac regions, and anticoagulation therapy appeared to have no effect on surface thrombosis in these short-term LVAS implants.

Acute Disease↗

PubMed2003

Inhibition of microsurgical thrombosis by the platelet glycoprotein IIb/IIIa antagonist SR121566A.

Despite major improvements in tools and significant refinements of techniques, microsurgical anastomosis still carries a significant risk of failure due to microvascular thrombosis. The key to improving the success of microvascular surgery may lie in the pharmacologic control of thrombus formation. Central to pathologic arterial thrombosis are platelets. Glycoprotein IIb/IIIa is a highly abundant platelet surface receptor that plays a major role in platelet aggregation by binding platelets to each other through the coagulation factor fibrinogen. To explore the ability of antithrombotic agents to prevent microvascular thrombosis, a rabbit ear artery model was used in which a standardized arterial injury results in predictable thrombus formation. This model was used to examine whether SR121566A, a specific and potent glycoprotein IIb/IIIa inhibitor, can successfully prevent microsurgical thrombosis. Using a coded, double-blind experimental design, 20 rabbits (40 arteries) were assigned to four treatment groups: (1) saline injection (n = 10), (2) acetylsalicylic acid 10 mg/kg (n = 10), (3) heparin 0.5 mg/kg bolus with subsequent intermittent boluses of 0.25 mg/kg every 30 minutes (n = 10), and (4) SR121566A 2 mg/kg bolus (n = 10). After vessel damage and clamp release, arteries were assessed for patency at 5, 30, and 120 minutes by the Acland refill test. Coagulation assays, in vivo bleeding times, and ex vivo platelet aggregation studies were also conducted. Scanning electron microscopy was used to examine mural thrombus composition.A significant, fourfold increase in vessel patency following administration of SR121566A over saline control (80 percent versus 20 percent patency, respectively, at 35 minutes after reperfusion, p < 0.01) was noted. This was correlated with marked inhibition of ex vivo platelet aggregation. This antiplatelet treatment did not prolong coagulation assays (mean international normalized ratio: saline, 0.66 +/- 0.04; SR121566A, 0.64 +/- 0.03; mean thromboplastin time: saline, 19.63 +/- 0.67; SR121566A, 17.87 +/- 3.27) and bleeding times (mean bleeding time: saline, 42 +/- 4; SR121566A, 48 +/- 6). Scanning electron microscopy demonstrated extensive platelet and fibrin deposition in control vessel thrombi. In contrast, thrombi from SR121566A-treated vessels demonstrated predominance of fibrin with few platelets when examined under scanning electron microscopy.Administration of SR121566A was associated with a significant increase in vessel patency, without deleterious effects on coagulation assays or bleeding times. The increase in vessel patency was correlated with inhibition of platelet aggregation and decreased platelet deposition, as demonstrated by scanning electron microscopy. Glycoprotein IIb/IIIa antagonists represent a new class of anti-platelet agents that may be suited for inhibiting microsurgical thrombosis. This study supports further investigation into the use of these agents in microsurgery.

Anastomosis, Surgical↗

PubMed2003

Endothelial dysfunction after arterial thrombosis is ameliorated by L-arginine in combination with thrombolysis.

PURPOSE: To assess endothelial function after arterial thrombosis creation and after administration of a novel thrombolytic regimen in a new porcine model. MATERIALS AND METHODS: Untreated arteries that had undergone thrombosis for 90 minutes were compared to arteries treated with tissue plasminogen activator (tPA, 4 mg) and a combination of tPA and L-arginine (L-arg; 600 mmol/L). External iliac artery luminal diameter was measured with use of duplex ultrasonography. Endothelial-dependent relaxation (EDR) and endothelial-independent relaxation (EIR) were measured with use of acetylcholine chloride (ACh) and sodium nitroprusside (NTP), respectively. Endothelial integrity was confirmed by scanning electron microscopy (SEM). Nitric oxide (NO) levels were determined with use of a chemiluminescent assay of its nitrite/nitrate metabolites (NO(x)). RESULTS: After thrombosis, EDR was decreased (69% +/- 9.5; ACh = 15 micro g/min; n = 6). EDR remained unchanged after thrombolysis with tPA despite complete dissolution of thrombus (67% +/- 5.7; ACh = 15 micro g/min; n = 5). Thrombolysis with use of tPA coupled with L-arg resulted in an increase in EDR (95% +/- 4.9; ACh = 15 micro g/min; n = 5; P =.007). EIR was preserved in all groups, with uniform response to NTP. SEM analysis revealed intact endothelium in all groups. Local NO(x) levels were diminished after 90 minutes of thrombosis (49.3 micro mol/L vs 40.8 micro mol/L; P =.0002), but increased to 55.7 micro mol/L after thrombolysis with tPA and L-arg (P = NS). CONCLUSIONS: Thrombus induces arterial dysfunction acutely without altering endothelial integrity. This dysfunction is ameliorated through regional administration of L-arg in combination with standard thrombolytic therapy, which increases local NO levels. This model allows the in-vivo study of thrombosis and alternative thrombolytic regimens. Regional enhancement of NO levels may prove to be an attractive adjunct in thrombolytic therapy.

Animals↗

PubMed2004

The natural history of pancreatitis-induced splenic vein thrombosis.

OBJECTIVE: To determine the natural history of pancreatitis-induced splenic vein thrombosis with particular attention to the risk of gastric variceal hemorrhage. SUMMARY BACKGROUND DATA: Previous studies have suggested that splenic vein thrombosis results in a high likelihood of gastric variceal bleeding and that splenectomy should be performed to prevent hemorrhage. Recent improvements in cross-sectional imaging have led to the identification of splenic vein thrombosis in patients with minimal symptoms. Our clinical experience suggested that gastric variceal bleeding in these patients was uncommon. METHODS: A computerized index search from 1993 to 2002 for the medical records of patients with a diagnosis of pancreatitis was performed. Fifty-three patients with a diagnosis of pancreatitis and splenic vein thrombosis were identified. The medical records of these patients were reviewed, and follow-up was completed, including the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC-QLQ). RESULTS: Gastrosplenic varices were identified in 41 patients (77%) with varices evident on computed tomography (CT) in 40 of 53 patients, on esophagogastroduodenoscopy (EGD) in 11 of 36 patients, and on both CT and EGD in 10 of 36 patients. This risk of variceal bleeding was 5% for patients with CT-identified varices and 18% for EGD-identified varices. Overall, only 2 patients (4%) had gastric variceal bleeding and required splenectomy. Functional quality of life was better than historical controls surgically treated for chronic pancreatitis. CONCLUSION: Gastric variceal bleeding from pancreatitis-induced splenic vein thrombosis occurs in only 4% of patients; therefore, routine splenectomy is not recommended.

Adult↗

PubMed2005

Mesenteric venous thrombosis in a patient with pancreatitis and protein C deficiency.

Mesenteric vein thrombosis is an uncommon manifestation of hypercoagulable states. A case is reported of superior mesenteric vein (SMV) thrombosis in a patient with pancreatitis and protein C deficiency. A discussion of SMV thrombosis identification, management, and outcomes is included. The patient presented with a significant history of alcohol abuse and constant, midepigastric abdominal pain associated with nausea and vomiting. Amylase and lipase were elevated, and the patient was treated for pancreatitis. His symptoms initially responded to intravenous fluid hydration, but soon his clinical picture worsened, with increased nausea and vomiting, abdominal pain, and distension. Contrasted computed tomography of the abdomen revealed SMV thrombosis. A hypercoagulable workup revealed protein C deficiency. After a 3-month course of oral anticoagulant therapy, the SMV thrombosis resolved.

Abdominal Pain↗

PubMed2006

A case of postpartum cerebral venous thrombosis.

Cerebral venous thrombosis, also known as cortical venous, cerebral sinus, cerebral venous sinus, or dural sinus thrombosis, results from clot formation in one of the many outflow tracts of the brain. Obstruction of flow causes venous hypertension, which is responsible for clinical findings associated with this condition. Signs and symptoms of cerebral venous thrombosis include headache, nausea, mental status changes, seizures, and focal neurologic deficits. Although cerebral venous thrombosis can occur at any time during life, women are particularly vulnerable before delivery and during the postpartum period because of the hypercoagulable state that accompanies pregnancy. This case study describes the challenging clinical course of one postpartum patient who developed venous thrombosis of the sagittal sinus.

Adult↗

PubMed2005

Review article: portal vein thrombosis -- new insights into aetiology and management.

Portal vein thrombosis may occur in the presence or absence of underlying liver disease, and a combination of local and systemic factors are increasingly recognized to be important in its development. Acute and chronic portal vein thrombosis have traditionally been considered separately, although a clear clinical distinction may be difficult. Gastrooesophageal varices are an important complication of portal vein thrombosis, but they follow a different natural history to those with portal hypertension related to cirrhosis. Consensus on optimal treatment continues to be hampered by a lack of randomized trials, but recent studies demonstrate the efficacy of thrombolytic therapy in acute thrombosis, and the apparent safety and benefit of anticoagulation in patients with chronic portal vein thrombosis.

Acute Disease↗