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PubMed2005

Coagulopathy in the trauma patient.

PURPOSE OF REVIEW: Homeostasis represents a delicate balance between hemostatic and fibrinolytic processes. This balance permits arrest of hemorrhage after mild injury but prevents thrombosis from occurring under normal circumstances. Trauma disturbs the equilibrium between hemostatic and fibrinolytic processes, frequently producing either a hypocoagulable state or a hypercoagulable state depending on the severity of injury, degree of hemorrhage, and the nature of the resuscitation. The purpose of this review is to describe the epidemiology and pathophysiology of coagulopathy after trauma and to discuss novel methods of treating it. RECENT FINDINGS: Published reports during the past year focus on the pathophysiology of coagulopathy after trauma and novel methods of treatment. Individual effects of hypothermia and acidosis on clotting factors and platelet function have been described. The effects of varying resuscitation fluids on coagulopathy have also been described as well as the course of coagulopathy over time. Recombinant factor VIIa has emerged as a popular therapy for traumatic coagulopathy although a prospective randomized trial has yet to be published. The efficacy of several new dressings for the local control of hemorrhage has been reported. SUMMARY: Changes in coagulation following trauma are characterized by a complex series of events that may result in either a hypocoagulable or a hypercoagulable state. Routinely analyzed coagulation parameters do not adequately describe this state and they are deficient for guiding its therapy. Several promising new agents are available for treating hemorrhage in coagulopathic trauma patients that should result in improved survival.

Disseminated Intravascular Coagulation↗
PubMed2006

Reduced fibrinolysis and increased fibrin generation can be detected in hypercoagulable patients using the overall hemostatic potential assay.

BACKGROUND: Routinely available coagulation assays are not capable of detecting clinically defined hypercoagulable states. A number of global coagulation assays have been developed with the potential to evaluate hypercoagulability, which predisposes to the common clinical events of arterial and venous thromboembolism (VTE). OBJECTIVES: We hypothesized that the overall hemostatic potential (OHP) assay would show abnormal fibrin generation and lysis in patients with clinically defined hypercoagulable states. METHODS: We used the OHP assay as described by Blombäck and colleagues [1,2] in 161 clinically hypercoagulable patients with arterial or VTE, pregnancy complications or autoimmune disease. Eighty patients had associated antiphospholipid antibodies (APLA). Ninety-eight normal plasma donors were tested for comparison. RESULTS: We derived three new assay parameters for correlation with hypercoagulable states: the maximum optical density, maximum slope, and delay in onset of fibrin generation. We found significantly different assay results for all patients' parameters examined when compared with controls, indicating both increased fibrin generation and reduced fibrinolysis in hypercoagulable patients. The findings were similar whether samples were collected in association with an acute thrombotic event or not. Estimated assay sensitivity for detection of a clinically defined hypercoagulable state was 96%. CONCLUSIONS: The OHP assay is a simple, inexpensive global test that is useful for assessing patients with hypercoagulable states including APLA. OHP results are significantly abnormal in hypercoagulable groups compared with controls, indicating that both increased fibrin generation and reduced fibrinolysis contribute to hypercoagulable states. The assay may ultimately assist in tailoring clinical management to patients' individual requirements.

Adolescent↗
PubMed1998

[Potential role of primary hypercoagulability and antiphospholipid antibody as a risk factor of acute pulmonary thromboembolism].

To examine whether primary hypercoagulable states, such as protein C and protein S deficiencies and antiphospholipid antibody, are associated with an increased risk, severity and recurrence of acute pulmonary thromboembolism, the blood levels of antithrombin III, protein C, protein S, lupus anticoagulant, anticardiolipin antibodies were measured in 23 patients with acute pulmonary thromboembolism, 7 men and 16 women (mean age +/- SD, 52 +/- 5 years), admitted to Nippon Medical School Hospital from January, 1990 through December, 1997. Four patients (17.4%) had protein C deficiency, one had protein S deficiency (4.3%), 10 had lupus anticoagulant (43.5%), and 2 had anticardiolipin antibodies (8.7%). Hemodynamic evaluation by Swan-Ganz catheter and venography of the lower extremity to detect deep venous thrombi were carried out in 20 and 21 patients, respectively. There were no differences between the patients with and without primary hypercoagulable states in age (52 +/- 14 vs 52 +/- 19 years), gender, or percentage of patients with deep venous thrombi in the lower extremity (91.7% vs 88.9%). Mean pulmonary arterial pressure (38 +/- 9 vs 26 +/- 4 mmHg, p < 0.05) and total pulmonary vascular resistance (10 +/- 5 vs 6 +/- 2 Wood unit, p < 0.1) were higher in the 13 patients with primary hypercoagulable states compared with the 10 patients without primary hypercoagulable states. Recurrence of pulmonary thromboembolism tended to be higher in the 13 patients with primary hypercoagulable states compared with the 10 patients without primary hypercoagulable states (46.2% vs 10.0%, p < 0.1). These findings suggest that primary hypercoagulable states, such as protein C and S deficiencies and antiphospholipid antibody, are associated with the severity and increased risk and recurrence of acute pulmonary thromboembolism.

Acute Disease↗
PubMed1984

Physiopathological aspects of body overweight in the female climacteric.

The correlation between overweight and the climacteric was studied in 550 menopause clinic patients by investigating certain clinical and sociocultural parameters (age, marital status, educational level, occupation and type of work, calorie intake, smoking habits, parity, blood pressure, previous hormonal therapy and climacteric symptoms), evaluating plasma levels of various hormones (17 beta-oestradiol, follicle-stimulating hormone (FSH), luteinizing (LH), testosterone, hydrocortisone, adrenocorticotrophic hormone (ACTH), triiodothyronine (T3), thyroxine (T4), growth hormone (GH) and insulin), glucose and various lipid fractions (total lipids, total cholesterol, nonesterified fatty acids (NEFA), triglycerides and phospholipids) and exploring the blood-clotting pattern ( Owren 's test, euglobulin lysis time, antithrombin III and prothrombin agglutination time (PAT). The subjects were classified as normal weight or overweight by reference to Broca's Index, as modified by Brusch , and the degree of overweight was determined by means of the Body Mass Index (BMI). Of the subjects examined, 49% were overweight and, in successive years following the menopause, there was a growing bipolarization of the weight increase. The correlation between overweight in the climacteric and the parameters considered was found to be significant only in regard to calorie intake, age and educational level. Post-menopausal gonadotrophin levels in blood were significantly lower in the overweight than in the normal-weight women. With the onset of menopause, the plasma level of testosterone fell in the normal-weight women, while it increased, along with that of hydrocortisone, in the overweight women. In the normal-weight women at menopause, it was found that there was a tendency towards a substantial increase in lipid fractions and glycaemia, as well as a state of hypercoagulability. In the overweight women, the tendency was towards an even more marked increase in both glycaemia and the various lipid fractions, and, besides the hypercoagulative state, there was an associated reduction in fibrinolytic activity. It is concluded that the menopause not only causes metabolic changes but also aggravates the metabolic and endocrine tendencies which characterize overweight subjects and thus, clinically, constitutes an obesity risk factor in those women who already demonstrate a tendency towards overweight in the pre-menopausal phase.

Adult↗
PubMedDate not supplied

Elevation of fibrinogen and thrombin-antithrombin III complex levels of type 2 diabetes mellitus patients with retinopathy and nephropathy.

Diabetes is associated with a hypercoagulable state. Blood hypercoagulability may accelerate atherosclerosis and the diabetic microvascular complications. Thrombin-antithrombin III complex (TAT) and fibrinogen levels are parameters of coagulation and fibrinolysis. In the present study, we examined the risk factors for the diabetic microangiopathy including TAT and fibrinogen levels. To investigate the relationship between the clinical parameters and microangiopathy in type 2 diabetic patients, the clinical parameters of subjects with microangiopathy were compared with those of subjects without microangiopathy. The clinical parameters were as follows: age at examination, duration of diabetes, fasting plasma glucose (FPG) level, HbA(1C) level, insulin level, TAT level, fibrinogen level, lipoprotein (a) (Lp(a)) level, total cholesterol level, triglyceride level, HDL cholesterol level and existence of hypertension. The plasma TAT and fibrinogen levels were significantly higher in patients with retinopathy or nephropathy than in patients without these complications. Moreover, fibrinogen levels of patients with microalbuminuria or background retinopathy were significantly higher than those of patients with normoalbuminuria or no retinopathy. The duration of diabetes was significantly longer in patients with any microangiopathy than in patients without it. Multiple regression analyses showed that duration and fibrinogen level were independent factors associated with the existence of retinopathy or nephropathy. Our data show that the disorder of coagulation and fibrinolysis is significantly associated with diabetic retinopathy and nephropathy and exists at the early stage of microangiopathy.

Adult↗
PubMedDate not supplied

Exploring the relationships between inflammatory response and coagulation cascade in inflammatory bowel disease.

BACKGROUND: The inflammatory network and the coagulation cascade are strictly correlated biological systems. Inflammatory Bowel Diseases (IBD) are characterised by a prothrombotic state, a hypercoagulability state and an increased prevalence of thromboembolic events. METHODS: We reviewed the IBD literature in which the relationships between inflammation and coagulation were evaluated. RESULTS: Several risk factors and mechanisms have been suggested to be implicated in determining the increased risk for thrombosis of IBD. Even if IBD may be per se a prothrombotic condition, systemic inflammation and vitamin deficiencies appear to play a relevant role in determining such a risk. CONCLUSIONS: A good and continuous control of the intestinal disease and vitamin supplementation are strongly recommended in order to correct some of the risk factors for thrombosis in IBD patients.

Blood Coagulation↗
PubMed1990

[Blood coagulation changes in systemic lupus erythematosus].

Changes of blood coagulation in 32 cases of SLE were investigated. Abnormalities frequently found were elevation of blood fibrinogen, FDP, V111R: Ag levels, prolonged or shortened KPTT time, and depressed AT-III value. Half of the patients with SLE showed laboratory changes compatible with the diagnostic criteria of DIC, but acute DIC was encountered clinically only in 2 cases hypercoagulation state or hypercoagulation with lower fibrinolysis, however were frequently seen. Lupus anticoagulant were detected in 6 patients and deep vein thrombosis of lower extremity in 1 patient. Examination of blood coagulation in patients with SLE was, therefore, of clinical importance.

Adult↗
PubMed1995

[CT examination for renal vein thrombosis in nephrotic syndrome and the effect of thrombolytic therapy].

Renal vein thrombosis (RVT) was diagnosed in 12 of 60 patients with nephrotic syndrome with CT scan and confirmed by selective renal angiography. Of the 60 patients, 50 had primary glomerulonephritis with various pathological findings and 10 lupus nephritis. CT is valuable in screening renal vein thrombosis. Renal vein and cubital vein blood in the 12 patients were drawn for assay of FDP, AT III, VIIIR: AG, fibrinogen; the results indicated the presence of a state of hypercoagulation. Of these, 7 were given 200,000 units of urokinase (UK) in divided doses into renal vein within one hour and 5,200,000 units UK into renal artery in the same way. Patients also received 2.5mg/d warfarin and 75mg/d persantine. Except for the 3 with focal sclerosis, patients received 40mg/d prednisone. After 1 month CT and blood fibrinogen, FDP, AT III, VIIIR: AG studies were repeated. RVT in patients with intraarterial UK had complete dissolution of their thrombi. Complete dissolution occurred in 2 of the 7 receiving UK by renal vein and there was partial dissolution in the other 5. It seems that intraarterial injection yielded better results. Hypercoagulation state was alleviated in all patients with UK therapy.

Adult↗
PubMed1994

[Markers of intravascular activation of coagulation].

New markers of intravascular activation of coagulation have been developed, based on advance in our understanding of the biochemistry of the haemostatic mechanism. These are sensitive methods for measuring of peptides liberated with the generation of thrombin (factor IX activation peptide, factor X activation peptide, peptide F1 + 2), for measuring concentration of enzyme-inhibitor complexes (eg. thrombin-antithrombin III-TAT complexes), as well as for investigating the effect of thrombin on fibrinogen (fibrinopeptide A-FPA) or on protein C (protein C activation peptide). Studies employing these markers indicate that a state of hypercoagulability can be detected in the blood of humans prior to the appearance of thrombotic phenomena. However, further studies will be required to determine whether these methods can identify individuals who are entering a clinically relevant hypercoagulable state as well as to monitor an antithrombotic treatment.

Animals↗
PubMed1998

Cerebrovascular disease risk factors: neuroradiologic findings in patients with activated protein C resistance.

PURPOSE: To assess the patterns of abnormal neuroradiologic findings in patients with a hypercoagulable state related to activated protein C (APC) resistance. MATERIALS AND METHODS: Records in 23 patients with a hypercoagulable state related to APC resistance (18 women, five men; average age, 44.5 years) were reviewed for cerebrovascular disease risk factors and other causes of a hypercoagulable state. Computed tomographic scans, magnetic resonance (MR) images, angiograms, and transesophageal echocardiograms were also reviewed. RESULTS: Stroke risk factors or other causes of a hypercoagulable state were found in 12 patients. Arterial infarcts were seen in 18 patients. Hyperintense white matter foci were seen on MR images in six patients. Dural sinus thrombosis was found in four patients. Angiograms of intracranial circulation in six patients showed major artery occlusions in four. MR angiograms in four patients showed internal carotid artery occlusion in one. No major abnormalities were seen in extracranial cerebral vasculature in 15 patients. Transesophageal echocardiograms in 11 patients showed a patent foramen ovale in one patient but no systemic source of embolism. Seven patients had non-central nervous system thrombotic events. CONCLUSION: Patients with APC resistance and stroke appear to differ from the general stroke population in terms of age and frequency of extracranial sources of cerebrovascular disease.

Adolescent↗
PubMed2001

Haemostatic profile in hypothyroidism as potential risk factor for vascular or thrombotic disease.

The influence of thyroid failure on haemostasis is controversial, both hypocoagulable and hypercoagulable states have been reported. Since both subclinical and overt hypothyroidism have been associated with atherosclerosis, a hypercoagulable state in addition might represent a risk factor for thromboembolic disease. We investigated various haemostatic variables in 42 women with subclinical hypothyroidism and compared them to 66 euthyroid controls. Prothrombin time, activated partial thromboplastin time, fibrinogen, factor VII activity (FVII:C), factor VII antigen (FVII:Ag), factor VIII activity, von Willebrand factor (vWF), antithrombin III, heparin cofactor II, protein C, protein S, plasminogen, antiplasmin, plasminogen activator inhibitor and tissue plasminogen activator, as well as common lipid variables, were measured. Factor VII:C (P < 0.02) and the ratio FVII:C/FVII:Ag (P < 0.01) were significantly increased in subclinical hypothyroid patients compared to the control group. Both parameters remained higher in hypothyroid patients after exclusion of 18 women on oestrogen replacement therapy. No differences were found between the groups with respect to vWF or the other haemostatic and lipid variables tested. Patients with subclinical hypothyroidism had significantly higher levels of FVII:C. The greater increase in FVII:C compared to that of FVII:Ag, as shown by the increase in their ratio, might reflect the presence of activated FVIIa. This might mean a hypercoagulable state, which could contribute to the increased prevalence of coronary heart disease reported in such patients. A hypercoagulable state might be another argument in favour of thyroxine replacement treatment in subclinical hypothyroidism, especially in patients with additional risk factors for vascular disease.

Adult↗
PubMed2001

Hemostatic changes in pediatric neurosurgical patients as evaluated by thrombelastograph.

UNLABELLED: Thromboembolic events are a known complication in neurosurgical patients. There is evidence to suggest that a hypercoagulable state may develop perioperatively. Thrombelastograph (TEG) coagulation analysis is a reliable method of evaluating hypercoagulability. We evaluated coagulation by using TEG data in pediatric neurosurgical patients undergoing craniotomy to determine whether a hypercoagulable state develops intraoperatively or postoperatively. Thirty children undergoing craniotomy for removal of a tumor or seizure focus were studied. Blood was analyzed with TEG) data by using native and celite techniques, at three time points for each patient: preoperatively after induction of anesthesia; intraoperatively during closure of the dura; and on the first postoperative day. Compared with preoperative indices, closing and postoperative celite TEG values were indicative of hypercoagulability with shortened coagulation time values (P < 0.001), prolonged alpha angle divergence values (P < 0.001), and above-normal TEG coagulation indices (P < or = 0.002). Reaction time values were shortened, and maximal amplitude of clot strength values were prolonged but did not reach statistical significance. Hypercoagulation develops early after resection of brain tissue in pediatric neurosurgical patients as assessed by using TEG data. Further studies are needed to determine the clinical significance of this hypercoagulable state. IMPLICATIONS: Hypercoagulability in postoperative neurosurgical patients has been demonstrated in the adult population, but few studies have dealt with the pediatric population. We found that children undergoing craniotomy for focal resection, lobectomy, and hemispherectomy are hypercoagulable as detected by thrombelastograph coagulation analysis. Further studies are needed to determine whether this is clinically significant.

Adolescent↗
PubMed1999

Pathophysiology of the thrombophilic state in the cancer patient.

The "hypercoagulable state" of malignancy is due to a complex interaction of tumor cells and their products with host cells, leading to various degrees of impairment of the normal defense mechanisms that ordinarily protect the host against thrombogenesis. Tumor cells can activate directly the blood clotting cascade and cause thrombosis or can induce procoagulant properties and inhibit anticoagulant properties of vascular endothelial cells, platelets, and monocytes and macrophages. In the setting of the local and systemic effects of cancer (e.g., stasis induced by prolonged bed rest and/or vascular invasion by tumor), together with iatrogenic complications of the treatment of cancer (e.g., the use of central vein catheters and angiopathic chemotherapy), this basic pathophysiology conspires to make cancer perhaps the best example of "acquired thrombophilia." In this brief review, we have attempted to describe what is currently known about the mechanisms for the hypercoagulable state of cancer and provide a summary of the evidence that indicates the many levels of defects in patients with malignancies that predispose them to thrombosis. A better understanding of the pathophysiology of thrombophilia in cancer should provide clinicians with an improved rationale for more aggressive and specific anticoagulant strategies in selected patients.

Blood Coagulation↗
PubMed1991

[Coagulation abnormalities in stroke--disseminated intravascular coagulation as a complication of subarachnoid hemorrhage].

To determine the pathogenesis of the symptomatic vasospasm (SV) following subarachnoid hemorrhage (SAH), we compared the difference in coagulation activity between 52 aneurysmal patients with SV and 20 patients without SV. The hypercoagulable state was scored according to the Disseminated Intravascular Coagulation (DIC) scoring system. Our clinical studies showed that severe SAH following aneurysmal rupture caused the hypercoagulable state and there was a good correlation between the degree of the hypercoagulable state, the severity of SV and outcome of the aneurysmal patients. We stressed in this report that the monitoring of the blood coagulation and fibrinolytic activities is very important in severe SAH and that the hypercoagulable state after SAH plays an important role on the occurrence of SV.

Aged↗
PubMed1997

Effects of warfarin on markers of hypercoagulability in patients with heart failure.

Heart failure is associated with a hypercoagulable state. A single-center, randomized, double-blind, placebo-controlled trial was performed to test the hypothesis that warfarin will modify a hypercoagulable state in heart failure. This study included 76 patients with heart failure. At baseline, patients had evidence for a hypercoagulable state with elevated plasma levels of thrombin/antithrombin III (TAT) complexes (3.4 +/- 2.0 ng/ml), prothrombin fragment F1 + 2 (1.5 +/- 0.9 nmol/L), and D-dimers (630 +/- 401 ng/ml). Warfarin therapy (international normalized ratio [INR] 2.7 +/- 1.3) significantly decreased plasma levels of TAT complexes (p < 0.002), F1 + 2 (p < 0.001), and D-dimers (p < 0.001) when compared with baseline values at 1, 2, and 3 months of therapy. In contrast, patients receiving placebo had persistent elevation of TAT complexes (p = not significant [NS]), F1 + 2 (p = NS), and D-dimers (p = NS) during follow-up at 1, 2, and 3 months. The two treatment groups followed different trends over time for all three markers (p < 0.001). The effect of low-intensity warfarin (INR 1.3 +/- 0.08) versus moderate-intensity warfarin (INR 2.3 +/- 1.1 ) on markers of hypercoagulability was evaluated in 14 patients. When compared with baseline, low-intensity warfarin administration decreased plasma levels of TAT complexes (p = NS), F1 + 2 (p = 0.05), and D-dimers (p = 0.04). In these patients F1 + 2 was further reduced with moderate-intensity warfarin (p < 0.001). Our findings suggest that a hypercoagulable state in heart failure can be modified by warfarin therapy.

Adult↗
PubMed1994

Paraneoplastic cholestasis and hypercoagulability associated with medullary thyroid carcinoma. Resolution with tumor debulking.

The authors report a 69-year-old woman with a hypercoagulable state manifesting as superior sagittal sinus thrombosis, thrombocytosis, right lower extremity deep venous thrombosis, and subsequent pulmonary embolus. The liver enzyme values were elevated in a cholestatic pattern. Carcinoembryonic antigen level was markedly elevated. Evaluation revealed that her longstanding "goiter" had slowly enlarged during the past 6 years. The serum calcitonin level was markedly elevated. Subsequent biopsy revealed medullary thyroid carcinoma. Surgical debulking of the tumor and lymph nodes resulted in substantial reduction of the calcitonin and carcinoembryonic antigen levels in a matter of days. Long-term follow-up revealed normalization of cholestasis and resolution of the hypercoagulable state. Review of the literature revealed no previously reported cholestasis or hypercoagulable state associated with medullary thyroid carcinoma. The literature on paraneoplastic cholestasis, carcinoembryonic antigen production, and hypercoagulable states is reviewed.

Aged↗
PubMed1986

[Cerebral venous thrombosis associated with the use of oral contraceptives].

The entity of cerebrovascular diseases associated with the use of oral contraceptives is well known but quite rare in Japan in contrast to Western countries. We recently encountered a 38 years old female with cerebral venous thrombosis considered to be caused by oral contraception. This patient took oral contraceptives for 17 days following therapeutic abortion, and was transferred to our hospital because of disturbed consciousness. CT scans disclosed a right temporo-occipital subcortical hemorrhagic infarction and bilateral thalamic infarction. Cerebral angiograms showed non-filling of cortical veins in the same area. The internal cerebral vein, vein of Galen and right transverse sinus were not visualized either. The hematoma and necrotic tissue were removed to avoid farther neurological deterioration. The brain was swollen and hyperemic, and thrombosed cortical veins were clearly recognized at operation. Twelve cases, including ours, of cerebrovascular diseases associated with oral contraception were reported up to now in Japan, and only 3 of them were diagnosed objectively as venous or sinus thrombosis. The average age of these 12 cases was 34 years old and many of them experienced abortion or therapeutic abortion. There was no relationship between the dose of estrogen and the onset of cerebrovascular diseases. We believe that the onset of this pathological state is based on gynecological hypercoagulable state, and the oral contraception may play a role of a trigger. Oral contraception should be contraindicated in patients with gynecological hypercoagulable state, hypertension and/or smoking habit.

Adult↗
PubMed1996

The coagulofibrinolytic state of patients with primary varicose veins of the lower legs.

The relationship between a local hypercoagulable state and primary varicose veins of the lower legs was investigated by measuring the plasma levels of D-dimer (DD) and the thrombin-antithrombin-III complex (TAT) in 122 consecutive patients before treatment, and in 46 patients after surgical intervention and compression sclerotherapy. Elevated levels of DD and TAT were found in 25% and 20%, respectively, of the 122 patients, being significantly elevated in the patients with thrombophlebitis compared to the patients with no dermal symptoms, pigmentation, or stasis dermatitis. There was no significant difference in either parameter among eight groups of patients classified according to their valvular incompetence. The levels of DD and TAT were elevated before treatment in 25% and 20%, respectively, of 45 treated patients, but became significantly reduced after treatment. These results indicate that even though the local hypercoagulable state in varicose veins without thrombophlebitis is too subtle to be detected by systemic parameters such as DD and TAT, a local hypercoagulable state can be detected in a certain proportion of patients with venous stasis by these parameters.

Adult↗