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PubMed2001

The mechanisms of thrombotic risk induced by hormone replacement therapy.

OBJECTIVES: To review the available information on the action of hormones on the mechanisms involved in thrombotic risk. RESULTS AND CONCLUSIONS: Thrombosis plays a crucial role in the genesis and progression of both coronary heart disease (CHD) and venous thromboembolic disease (VTED), the two main forms of cardiovascular disease. Two main determinants of the thromboembolic phenotype, hypercoagulable state and altered endothelium, accumulate much of the work performed on the influence of hormones on thrombosis. Information has accumulated mainly for oestrogens, but increasing evidences support a role for progestogens. The sensitivity of each of the three components of the hemostatic balance, the coagulation cascade, the anticoagulant system and fibrinolysis, to oestrogens has been widely examined in the literature. Functional tests suggest that HRT is accompanied by a procoagulant state. Much of the work has concentrated on changes induced on reputable indicators of risk for either CHD or VTED. Distinct indicators of increased coagulability, such as resistance to activated C protein, antithrombin or tissue factor pathway inhibitor have been selected for VTED, whereas factor VII, fibrinogen, and defective fibrinolysis, for CHD. Different states of genetic susceptibility have been involved in both forms of the disease. The status of health of endothelium, defines another scenario for attention in CHD. A long-term anti-atherogenic action of oestrogens, which may be associated with short-term risk in cases of atherosclerosis-induced endothelial dysfunction, may most adequately explain much of the clinical observation. In both CHD and VTED, the procoagulant changes initiate soon after HRT administration.

Aged↗
PubMed2000

Stroke treatment-specific considerations.

Unusual causes of stroke account for a minority of all strokes, but they have specific diagnostic and therapeutic implications which must be considered early in the clinical course. This article focuses on arteriopathies such as arterial dissection, vasospasm-induced stroke, and vasculitis; hematological disorders such as hypercoagulable states, disseminated intravascular coagulation, and sickle cell disease; migraine-induced stroke, and cerebral venous thrombosis.

Cerebral Angiography↗
PubMed2001

Epidemiology of venous thromboembolic disease.

From the information presented in this article, it can be concluded that clinical suspicion of VTE should be increased in patients with a history of VTE, recent surgery, spinal cord injury, trauma, or malignancy. A variety of medical illnesses also increase the risk of venous thrombosis, including congestive heart failure, myocardial infarction, stroke with paresis, nephrotic syndrome, cigarette smoking, and obesity. Hypercoagulable states, such as antithrombin III deficiency, protein C deficiency, protein S deficiency, or factor V Leiden mutation should be considered in those patients who develop VTE in the absence of known risk factors. Additionally, the presence of vena caval filters does not exclude the possibility of PE or recurrent DVT. With a careful assessment of risk, physicians can hope to increase the diagnostic yield of VTE and decrease the significant morbidity and mortality of caused by this disease.

Adult↗
PubMed2001

To anticoagulate or not to anticoagulate patients with cardiomyopathy.

The current published literature does not indicate whether the long-term effect of anticoagulant or antiplatelet therapy contributes to mortality reduction in patients with LV dysfunction. Evaluating patients for personal risk for emboli or for ischemic coronary artery events may influence the choice of therapies. As more is learned about the mechanisms of drug effects in different populations, physicians may be better able to direct appropriate therapies. Until that time, one must weigh the risks and benefits of each drug alone and in combination. In NYHA class IV patients, the risk for thrombosis owing to spontaneous clotting increases as does the adverse potential of warfarin and the adverse effects of inhibiting prostaglandin mediated vasodilation by aspirin. In NYHA class I and II patients, the quality of life and convenience of multidrug therapy is weighed against the devastating effect of a major stroke. In less symptomatic patients, the long-term risk for acute coronary events may be higher than previously identified. This would suggest that all patients with depressed LV function should be on some type of antiplatelet or anticoagulant therapy. The current WATCH study will provide much needed information about the outcome differences between these agents. Conclusions based on available data include the following: Heart failure is increasing in incidence and prevalence. Atherosclerotic disease is an important causative factor for the development of heart failure or may be a comorbid condition in these patients. There is a measurable rate of stroke in patients with heart failure, although the cause of death in large studies is more often owing to sudden death or progressive heart failure. Sudden death may be from new ischemic events, asystole, or from ventricular tachyarrhythmias. In patients with heart failure, not all strokes are cardioembolic in origin. The benefits and risks of warfarin may be increased as the EF worsens or heart failure functional class declines. The interactions of aspirin and ACE inhibitors have been best evaluated for the hemodynamic effects. There may be additional factors hitherto not studied. The hemodynamic effect of ACE inhibitors may be more important in NYHA classes III and IV than in less symptomatic patients. Warfarin use has clear indications for patients in atrial fibrillation with mechanical prosthetic valves, in hypercoagulable states, and with a previous history of embolization. Aspirin is inexpensive and commonly available, but its use must be evaluated and articulated by the prescribing physician. The current multicenter prospective trials will provide much needed guidance on this subject. The ongoing trials do not have a placebo arm, however, indicating a consensus among clinicians that patients with cardiomyopathy should be on an antiplatelet or anticoagulant drug until further data emerge.

Anticoagulants↗
PubMed1998

Endothelial tissue-type plasminogen activator release in coronary heart disease: Transient reduction in endothelial fibrinolytic reserve in patients with unstable angina pectoris or acute myocardial infarction.

OBJECTIVES: We sought to examine whether the disturbed fibrinolytic system in patients with an acute coronary syndrome is associated with a reduced endothelial fibrinolytic capacity. BACKGROUND: Intracoronary thrombus formation is a frequent finding in acute coronary syndromes. Systemic alterations of coagulation and fibrinolysis are known to occur, but possible disturbances of endothelial fibrinolytic function have not been investigated. METHODS: We compared 42 patients with an acute coronary syndrome (acute myocardial infarction in 11 and unstable angina pectoris in 31) with 25 patients with stable angina. Venous blood was sampled serially for determination of markers of the fibrinolytic system and of hypercoagulability from admission to day 10. An occlusion test to determine the maximal endothelial tissue-type plasminogen activator (t-PA) release was also performed. RESULTS: Both on day 0 and day 10, patients with an acute coronary syndrome had a marked elevation of t-PA mass concentration (mean value +/- SEM 14.4 +/- 1.6 [day 0], 18.9 +/- 2.5 ng/ml [day 10]) and of plasminogen activator inhibitor (PAI) (9.4 +/- 2.2 [day 0], 11.3 +/- 2.6 AU/liter [day 10], p < 0.05 vs. patients with stable angina). There was also a hypercoagulative state with elevated thrombin activity and increased D-dimers (p < 0.05 vs. patients with stable angina). Maximal endothelial t-PA release was initially reduced (p < 0.05 vs. patients with stable angina) to 2.3 +/- 0.9 ng/ml, but levels recovered during follow-up to 4.4 +/- 1.4 ng/ml (vs. 5.7 +/- 1.5 ng/ml in patients with stable angina). CONCLUSIONS: Despite the known prolonged systemic alteration of fibrinolysis in acute coronary syndromes, endothelial fibrinolytic capacity is reduced only during the acute phase and becomes normalized during follow-up, and thus is linked more to intravascular thrombus formation than to steady state levels of markers of the fibrinolytic system.

Angina, Unstable↗
PubMed2002

The effect of long-term methylprednisolone treatment on the femoral head in growing pigs.

The effect of long term steroid treatment on coagulation, intraosseous pressure (IOP), femoral head (FH) blood flow, and histology in the normal organism was investigated in this study in growing pigs. From 24 growing female Danish Landrace pigs from 12 litters, 12 animals daily received 100 mg methylprednisolone orally for three months. Their 12 sister pigs served as controls without steroid treatment. Prothrombin time, activated partial thromboplastin time (aPTT), fibrinogen, and antithrombin III levels were recorded in jugular venous blood. Blood flow of the hip regions was measured by means of the radioactive microsphere technique. Metaphyseal and epiphyseal IOP of the left or right proximal femur were measured. Histomorphometry of the left or right FH epiphysis was performed. Major growth inhibition was found in the corticosteroid (CS) treated group. In CS pigs, aPTT was shortened to 50% compared to control pigs. Plasma fibrinogen was higher in the CS animals. Total FH blood flow was not different while regional blood flow in the cranial subregion of the FH epiphysis was higher in the CS group. Metaphyseal and epiphyseal IOP of the proximal femur were not different in the CS animals. Histomorphometrically, cancellous bone volume (23 +/- 1% vs. 34 +/- 2%; p < 0.001) and bone turnover (10 +/- 2% vs. 55 +/- 8%; p < 0.001) of the FH epiphysis was lowerin the CS than in the control group. The FH epiphysis of the CS animals invariably showed an irregular cartilage-bone interface with cartilaginous projections into the subchondral bone mainly in its cranial part. In normal growing pigs, long term high dose CS treatment has induced a hypercoagulable state of plasma via the intrinsic pathway of coagulation, cartilaginous projections into FH subchondral bone, FH osteopenia, and reduced bone turnover. Long-term steroid treatment did not produce FH necrosis or FH IOP alterations in the immature pig model.

Animals↗
PubMed2003

Buerger's disease in a 19-year-old woman.

A 19-year-old female college student had numbness and the sensation of coldness of her left toes. She had a 3-year smoking history. Gangrene of the left foot developed rapidly. Angiography revealed peripheral arterial occlusion of both legs and arms. Detailed laboratory examination excluded collagen disease, a hypercoagulable state, and juvenile atherosclerosis. Below-knee amputation of the left leg was performed. Typical histologic findings of Buerger's disease were observed in the crural arteries and saphenous veins. The clinical course was uneventful after the patient stopped smoking. This is the second case report of Buerger's disease in a woman in the second decade of life. It is important that a correct diagnosis of Buerger's disease be established, because the disease process is benign, compared with collagen disease, if the patient stops smoking.

Adolescent↗
PubMed1994

Mesenteric venous thrombosis: still a lethal disease in the 1990s.

PURPOSE: This study was designed to evaluate progress in diagnosis, management, and clinical outcome of mesenteric venous thrombosis (MVT). METHODS: We retrospectively reviewed the clinical course of 72 patients treated for mesenteric venous thrombosis between 1972 and 1993. RESULTS: Fifty-three patients had acute and 19 had chronic mesenteric venous thrombosis. Fifty-seven patients had secondary mesenteric venous thrombosis; previous abdominal surgical procedure and hypercoagulable states were the most prevalent associated conditions. Computed tomography was abnormal in all patients who underwent this test for acute mesenteric venous thrombosis and in 93% of those who had chronic disease. Angiography diagnosed acute mesenteric venous thrombosis in five (72%) of seven patients. Acute mesenteric venous thrombosis presented most frequently as abdominal pain (83%), anorexia (53%), and diarrhea (43%). Thirty-three (75%) had symptoms longer than 48 hours. Thirty-four (64%) patients with acute mesenteric venous thrombosis underwent a surgical procedure. Bowel resection was necessary in 31 patients. One patient had unsuccessful mesenteric venous thrombectomy. Seven patients with acute mesenteric venous thrombosis underwent anticoagulation without a surgical procedure, and 12 were observed. All patients with chronic mesenteric venous thrombosis were observed; nine of the 19 underwent anticoagulation. The median delay in diagnosis for patients with acute mesenteric venous thrombosis was 48 hours and did not decrease during the last decade. Mesenteric venous thrombosis recurred in 19 (36%) patients. The 30-day mortality was 27%. Long-term survival of patients with acute mesenteric venous thrombosis was significantly worse than that of those with chronic disease (36% vs 83% survival at 3 years). The patients with acute mesenteric venous thrombosis who underwent anticoagulation with and without surgical procedure had improved survival when compared with the observed group. CONCLUSION: Acute mesenteric venous thrombosis remains a lethal disease. Mortality has not improved in the last 22 years. Computed tomography is the most sensitive diagnostic test. Anticoagulation and surgical procedure enhanced survival in the acute subgroup. The underlying disease determined survival in chronic disease.

Acute Disease↗
PubMed1995

Essential thrombocytosis: underemphasized cause of large-vessel thrombosis.

PURPOSE: The purpose of this study was to describe the clinical course of patients seen with large-vessel thrombosis in association with essential thrombocytosis (ET). METHODS: This study was a retrospective review of all patients treated for large-vessel thrombosis caused by ET during a 2-year period at University of Washington teaching hospitals. RESULTS: Five patients presented with arterial (femoral-popliteal-tibial: aortic), portal (two cases), or systemic venous (inferior vena cava) thrombosis and required operation. Two were known to have ET; in three others ET was diagnosed after operation when platelet counts persistently in excess of 500,000/mm3 were noted. The diagnosis of ET was established in each case by ruling out causes of reactive thrombocytosis and (in the three new cases) by evidence for megakaryocyte hyperplasia on bone marrow biopsy. Platelet counts in all five patients were reduced to normal levels by cytoreductive therapy, and no further thrombotic episodes have occurred during 18 months (mean) of follow-up. During this 2-year period ET accounted for more large-vessel thrombotic complications in our institutions than all other more frequently described hypercoagulable states combined. CONCLUSIONS: ET is an underemphasized cause of large-vessel thrombosis.

Adult↗
PubMed1996

Prospective comparison of infrainguinal bypass grafting in patients with and without antiphospholipid antibodies.

PURPOSE: The antiphospholipid antibodies (APL)-anticardiolipin antibodies (ACL) and lupus anticoagulant (LA)-are widely believed to be associated with decreased lower extremity bypass graft patency rates. To date, no prospective cohort study has confirmed this assumption. A prospective comparison of the result of infrainguinal revascularization procedures performed since 1990 in patients with and without APL forms the basis of this report. METHODS: Patients who underwent elective infrainguinal bypass procedures from 1990 to 1994 were evaluated for hypercoagulable states (ACL, LA, protein C, protein S, and antithrombin III). Patient data were prospectively entered in a computerized vascular registry, and postoperative follow-up was maintained for life. Graft patency, limb salvage, and patient survival rates were calculated by life-table methods. RESULTS: Three hundred twenty-seven lower extremity bypass grafting procedures were performed in 262 patients. APLs were present in 83 patients (32%); 70 patients (84%) had ACLs only, 11 patients (13%) had LA only, and two patients (3%) had both ACLs and LA. There was no significant difference between APL-positive and APL-negative patients with respect to demographics, associated medical conditions, indication for operations, and type of procedures performed. More patients who had APLs had warfarin treatment after surgery (43% vs 24%, p = 0.002). Life table 4-year primary patency rates showed minimal difference (APL-positive, 43%; APL-negative, 59%; p = 0.087), and no significant difference was noted in assisted primary patency rates (APL positive, 72%; APL negative, 73%; p = NS), limb salvage rates (APL positive, 79%; APL negative, 88%; p = NS), and patient survival rates (APL positive, 67%; APL negative, 66%; p = NS). CONCLUSIONS: APLs were found in a surprising one third of the patients who underwent leg bypass grafting procedures. The majority of APLs identified were ACLs (87%). There was minimal difference in graft primary patency rates, and no difference in assisted primary patency, limb salvage, and survival rates between patients with and without APLs who underwent leg bypass grafting procedures. The extreme morbidity rate associated with APLs in previous reports is not confirmed by this prospective study. APLs should not be regarded as a contraindication to indicated leg bypass grafting procedures.

Aged↗
PubMed1996

A prospective study of the incidence of deep venous thrombosis in hospitalized children.

PURPOSE: It is commonly believed that the incidence of deep venous thrombosis (DVT) in hospitalized children is less than in adults. However, it is possible that the disease is significantly underdiagnosed in children because the index of suspicion of pediatric practitioners is low, a substantial number of patients may have no symptoms, and DVT screening is not routinely performed. We therefore undertook a prospective study to define the incidence of DVT in hospitalized children with no symptoms. METHODS: Patients included in the study were those younger than 18 years of age who were hospitalized for more than 72 hours and were identified to have two or more risk factors for the development of DVT and had at least one screening duplex scan. Risk factors for the development of DVT considered were a history of DVT or pulmonary embolism, recent operation, immobilization, trauma, stroke or acute neurologic deficit, the presence of cancer, sepsis, greater than 150% ideal body weight, a hypercoagulable state, and the presence of a femoral venous catheter. RESULTS: Over the 9-month period ending December 1994, 1997 patients 17 years of age and younger were admitted to the hospital, and 59 patients including 19 girls and 40 boys were enrolled in the study. The one patient with DVT was a 17-year-old boy hospitalized after a motor vehicle accident with blunt head trauma and a neurologic deficit who underwent multiple orthopedic and neurosurgical procedures. CONCLUSIONS: The development of acute DVT in children is unusual. As a result, DVT prophylaxis and screening is unnecessary in young children with only two risk factors for the development of the disease. Young age appears to be an important protective risk factor for the prevention of DVT.

Age Distribution↗
PubMed1999

The progressive nature of peripheral arterial disease in young adults: a prospective analysis of white men referred to a vascular surgery service.

OBJECTIVE: The onset of symptomatic peripheral arterial disease at a young age (premature PAD) has been associated with rapid progression, bypass graft failure, and amputation. This study was performed to document the incidence of these complications and to determine the risk factors for poor outcome in patients with premature PAD. METHODS: This study was designed as a prospective longitudinal analysis, with patients who were ambulatory or hospitalized at a single vascular referral institution. The subjects were 51 white men with onset of PAD symptoms before the age of 45 years (mean age of onset, 41 +/- 0.5 years) and represented consecutive patients who were seen at the vascular surgery service during a 4-year period. Thirty of the study subjects (58%) were recruited during the first 2 years. The main outcome measures were number and type of lower extremity revascularization procedures or amputations that were necessitated during the follow-up period. RESULTS: During a mean follow-up period of 73 +/- 6 months, 15 patients (29%) had PAD that remained stable without interventions and 15 (29%) had PAD that remained stable for a mean of 76 +/- 13 months after a single intervention. Twenty-one patients (41%) required multiple operations or major amputations. In a comparison of the 30 PAD patients whose conditions were stable with or without a single intervention with the 21 PAD patients who required multiple interventions (REDO), there were no differences in smoking, hypertension, diabetes, or dyslipidemias. The REDO group had a younger mean age at the onset of symptoms (39 +/- 1 years vs 43 +/- 2 years; P <.001). At entry, the REDO patients had a higher prevalence of infrainguinal or multilevel disease (57% vs 20%; P =.03), a lower mean ankle brachial index (0. 44 +/- 0.04 vs 0.56 +/- 0.03; P =.02), and more frequent tissue loss (24% vs 0; P =.005). The REDO patients had a higher mean lipoprotein (a) level than did the patients with stable conditions (51 +/- 11 mg/dL vs 27 +/- 5 mg/dL; P =.03), but there were no significant differences in the mean plasma homocysteine levels (19 +/- 2 micromol/L vs 16 +/- 1 micromol/L) or in the proportion of patients with hypercoagulable states (33% vs 30%). The only predictive variables that were selected with stepwise logistic regression analysis were age at onset (P <.002; odds ratio, 1.4; 95% confidence interval, 1.11 to 1.81) and ankle brachial index of less than 0.5 (P <.008; odds ratio, 6.4; 95% confidence interval, 1.5 to 27.3). CONCLUSION: Although 60% of the white men with premature PAD who were referred to a vascular surgery service had conditions that appeared to remain stable, these data show that approximately 40% of the patients will require multiple interventions because of disease progression or bypass graft failure. Clinical indicators, not serum markers, are predictors of poor outcome in patients with premature PAD. The results of this study suggest that patients with onset of PAD before the age of 43 years who have objective evidence of advanced disease are predisposed to multiple interventions.

Adult↗
PubMed1999

Mesenteric and portal vein thrombosis in a young patient with protein S deficiency treated with urokinase via the superior mesenteric artery.

A 32-year-old man, who was previously healthy, had acute abdominal pain without peritonitis. Diffuse mesenteric and portal vein thrombosis were shown by means of a computed tomography scan. A protein s deficiency was found by means of an extensive workup for hypercoagulable state. Successful treatment was achieved with urokinase infusion via the superior mesenteric artery without an operation. This represents an attractive alternative approach to treating patients with this disease. The previous standard of operative intervention(1) can now be reserved for complications, such as bowel infarction with peritonitis, or for those patients with absolute contraindications to thrombolytic therapy.

Abdominal Pain↗
PubMed2001

Pulmonary embolism in the elderly.

The elderly are at increased risk for pulmonary embolism because of both the conditions common to this age group, and the immobility that often accompanies them. Whether aging alone represents a hypercoagulable state is unclear. The incidence of pulmonary embolism rises with age, however, as does pulmonary embolism mortality. The diagnosis of pulmonary embolism is difficult and frequently missed because elderly patients and their physicians may attribute nonspecific symptoms to underlying cardiopulmonary disease or to age itself. Routine laboratory examinations are also nonspecific. Lower extremity studies to diagnose DVT should always be pursued because a positive study results in identical treatment, without the need for further testing. D-dimer concentrations are useful when low, but are commonly elevated in the elderly because of other comorbid conditions. Lung scanning remains the most common initial study to diagnose pulmonary embolism, although spiral CT is as sensitive and specific. Pulmonary angiography should always be considered when the initial studies are nondiagnostic and clinical suspicion is high, and this test is well tolerated in the elderly. The role of newer diagnostic techniques, such as MR imaging, cannot be determined until well-designed outcomes trials are completed. Prophylaxis with appropriate pharmacologic agents or mechanical measures should be administered not only to patients undergoing hip or knee reconstruction surgery, but to all bed-ridden elderly medical and general surgery patients. Treatment for pulmonary embolism with anticoagulation reduces the mortality rate and should be administered in all elderly patients without contraindications. In addition, thrombolysis should be considered for all hemodynamically unstable patients with pulmonary embolism, regardless of age. Vena caval filters are warranted when anticoagulation is contraindicated, although evidence of the long-term benefit of these devices is lacking. At present, pulmonary embolism is underdiagnosed and undertreated in the elderly. By heightening awareness of this diagnosis and its appropriate management in this age group, considerable morbidity and mortality may be avoided.

Adolescent↗
PubMed2002

The equine metabolic syndrome peripheral Cushing's syndrome.

Certain management practices tend to promote the development of obesity (metabolic syndrome) in mature horses as they enter their teenage years. These management practices include the provision of starch-rich (high glycemic index) and fat-supplemented rations to healthy horses that are relatively inactive. Some horse breeds and ponies appear to be genetically predisposed to metabolic syndrome. The accretion of intra-abdominal adiposity by equids is associated with the development of insulin insensitivity (hyperinsulinemia), glucose intolerance, dyslipidemia, hypertension, and insidious-onset laminitis. Omental adipocytes are metabolically active, secreting free fatty acids and hormonally active mediators including cortisol, leptin, and resistin that might contribute to persistence and worsening of insulin refractoriness and the obese phenotype. We have hypothesized that obesity-associated laminitis arises as a consequence of vascular changes and a hypercoagulable state, similar to the development of atherosclerosis in human type 2 diabetes. Several molecular mechanisms that might serve to explain the development of insulin insensitivity as a result of excessive adiposity have been incriminated. Little investigation into the relationship between obesity, insulin insensitivity, and laminitis in horses has been reported to date. Insulin sensitivity and glucose tolerance can be improved by dietary restriction and exercise aimed at reversing omental obesity. Management practices that promote the development of obesity are likely initiated during the first 10 years of the horse's life. Veterinarians and horse owners must recognize that mature-onset obesity in adult horses is associated with a risk for development of laminitis. Obesity and insulin insensitivity might be prevented if horse owners can be educated to feed rations with a relatively lower glycemic index to inactive horses. Investigative research pertaining to the development of antiobesity drugs for human patients is continuing. Greater than 30 new pharmaceuticals are in various stages of research. However, it will likely take many years before any of these drugs are shown to be useful and safe in horses. Lifestyle changes in the form of diet and exercise patterns are still the crux of therapy for both human and equine patients.

Animals↗
PubMed1999

Disseminated intravascular coagulation.

OBJECTIVES: To provide an overview of the pathophysiology, manifestations, diagnosis, and treatment of disseminated intravascular coagulation (DIC) as it occurs in cancer. DATA SOURCES: Published articles, research reports, and book chapters. CONCLUSIONS: The syndrome of DIC is a serious hypercoagulation state that in its acute form may be life-threatening. The hemorrhage and intravascular coagulation that occur with DIC may lead to irreversible morbidity and mortality. Prompt recognition and emergency treatment are necessary to help minimize morbidity and mortality. IMPLICATIONS FOR NURSING PRACTICE: Nurses can play an important role in early recognition of DIC to allow for prompt intervention. Nurses caring for patients affected by DIC will be providing complex nursing care, in addition to psychosocial support to patients and families.

Adenocarcinoma↗
PubMed2002

[Coronary thrombosis on patient with the factor V Leiden mutation].

We report a documented observation of coronary thrombosis occurring in a 25-year-old patient with no risk factor, presenting a hereditary thrombophilia (facteur V Leiden) diagnosed a few months earlier in a context of venous thrombosis. This patient had a spread out anterior myocardial infarction with cardiac arrest due to a ventricular fibrillation; although he was quickly rescued by the mobile intensive Care Unit, the patient died 48 hours later, after cerebral anoxia. The mutation called factor V Leiden is a widely spread hereditary family thrombophilia (5 to 6% of the population) and is characterized by a resistance to activated C protein provoking a hypercoagulable state. The unexpected arterial thrombosis, very rare in that case, can be extremely serious and raises the question of a preventive medication such as antiplatelet agent or low-molecular-weight heparin as soon as the genetic abnormally has been proved to be symptomatic.

Adult↗
PubMed2002

[Effects of plasma substitutes on hemostasis].

OBJECTIVE: Data synthesis on haemostasis effects of cristalloids and colloids and clinical implications for their use for plasma volume replacement. DATA SOURCES: Data were searched in the Medline database from 1954 to 2000 using the following key-words: cristalloids, colloids, albumin, gelatin, dextran, hydroxyethyl starch, haemostasis, von Willebrand disease, haemodilution. DATA EXTRACTION: Publications from 1954 to 1990 were selected depending on the quality of their methodology. Most of articles published after 1990 and all types including case report were accepted. DATA SYNTHESIS: Cristalloids induces a moderate hypercoagulable state with 10 to 30% haemodilution. Hypocoagulation is observed above 50% haemodilution. Albumin does not impair hemostasis except with a 50% or more haemodilution where hypocoagulation is observed. Dextran dramatically impairs haemostasis and fibrinolysis. With increasing dose, a progressive decrease of all von Willebrand multimers, mostly the largest, is observed. Till 50% haemodilution, gelatin has a moderate impact on hemostasis, but platelet aggregation is moderately modified. However this moderate impairment of haemostasis may potentiate the haemostatic effect of other colloids when used in association with gelatin. More than 30% haemodilution with hydroxyethyl starch (HES) has a serious effect in vitro on platelet function and fibrinoformation. In most studies in human, less than 20 ml.kg-1 plasma volume replacement has no clinical impact, but in some evaluations postoperative bleeding is more important with HES, particularly HES 450, in comparison to other colloids. With HES 450 and HES 200 highly substituted (0.6 of degree of substitution) intravascular cumulation of large molecules leads to type I von Willebrand syndrome when doses overtake 80 ml.kg-1. Dextran and HES are prohibited in patients with impaired haemostasis due to congenital disease (haemophilia and von Willebrand disease) or acquired defect (thrombocytopenia). Caution is required in patients with renal failure or receiving antithrombotic or non-steroidal anti-inflammatory agents. Patients without a haemorrhagic diathesis must not received more than 1.5 g.kg-1.j-1 of dextran and restrictive conditions of use must be respected with HES. CONCLUSION: Except isotonic cristalloids, all colloids induce haemostastic changes particularly for haemodilution over 30%. Effects are more pronounced with HES and dextran.

Blood Coagulation↗